Overview

Acute coronary syndrome is a term used to describe a range of conditions associated

with sudden, reduced blood flow to the heart.

One such condition is a heart attack (myocardial infarction) — when cell death results in
damaged or destroyed heart tissue. Even when acute coronary syndrome causes no
cell death, the reduced blood flow changes how your heart works and is a sign of a high
risk of heart attack.

Acute coronary syndrome often causes severe chest pain or discomfort. It is a medical
emergency that requires prompt diagnosis and care. The goals of treatment include
improving blood flow, treating complications and preventing future problems.

Symptoms

The signs and symptoms of acute coronary syndrome usually begin abruptly. They
include:

 Chest pain (angina) or discomfort, often described as aching, pressure, tightness

or burning

 Pain spreading from the chest to the shoulders, arms, upper abdomen, back, neck
or jaw

 Nausea or vomiting

 Indigestion

 Shortness of breath (dyspnea)

 Sudden, heavy sweating (diaphoresis)

 Lightheadedness, dizziness or fainting

 Unusual or unexplained fatigue

 Feeling restless or apprehensive

Chest pain or discomfort is the most common symptom. However, signs and symptoms
may vary significantly depending on your age, sex and other medical conditions. You're
more likely to have signs and symptoms without chest pain or discomfort if you're a
woman, older adult or have diabetes.

When to see a doctor

Acute coronary syndrome is a medical emergency. Chest pain or discomfort can be a

sign of any number of serious, life-threatening conditions. Get emergency help for a
prompt diagnosis and appropriate care. Do not drive yourself to the hospital.

Request an Appointment at Mayo Clinic

Causes

Acute coronary syndrome usually results from the buildup of fatty deposits (plaques) in
and on the walls of coronary arteries, the blood vessels delivering oxygen and nutrients
to heart muscles.

When a plaque deposit ruptures or splits, a blood clot forms. This clot blocks the flow of
blood to heart muscles.

When the supply of oxygen to cells is too low, cells of the heart muscles can die. The
death of cells — resulting in damage to muscle tissues — is a heart attack (myocardial
infarction).

Even when there is no cell death, the decrease in oxygen still results in heart muscles
that don't work the way they should. This change may be temporary or permanent.
When acute coronary syndrome doesn't result in cell death, it is called unstable angina.

Risk factors

The risk factors for acute coronary syndrome are the same as those for other types of
heart disease. Acute coronary syndrome risk factors include:

 Aging
  High blood pressure

 High blood cholesterol

 Cigarette smoking

 Lack of physical activity

 Unhealthy diet

 Obesity or overweight

 Diabetes

 Family history of chest pain, heart disease or stroke

 History of high blood pressure, preeclampsia or diabetes during pregnancy

Overview

Acute coronary syndrome is a term used to describe a range of conditions associated

with sudden, reduced blood flow to the heart.

One such condition is a heart attack (myocardial infarction) — when cell death results in
damaged or destroyed heart tissue. Even when acute coronary syndrome causes no
cell death, the reduced blood flow changes how your heart works and is a sign of a high
risk of heart attack.

Acute coronary syndrome often causes severe chest pain or discomfort. It is a medical
emergency that requires prompt diagnosis and care. The goals of treatment include
improving blood flow, treating complications and preventing future problems.

Symptoms

The signs and symptoms of acute coronary syndrome usually begin abruptly. They
include:

 Chest pain (angina) or discomfort, often described as aching, pressure, tightness

or burning
  Pain spreading from the chest to the shoulders, arms, upper abdomen, back, neck
or jaw

 Nausea or vomiting

 Indigestion

 Shortness of breath (dyspnea)

 Sudden, heavy sweating (diaphoresis)

 Lightheadedness, dizziness or fainting

 Unusual or unexplained fatigue

 Feeling restless or apprehensive

Chest pain or discomfort is the most common symptom. However, signs and symptoms
may vary significantly depending on your age, sex and other medical conditions. You're
more likely to have signs and symptoms without chest pain or discomfort if you're a
woman, older adult or have diabetes.

When to see a doctor

Acute coronary syndrome is a medical emergency. Chest pain or discomfort can be a

sign of any number of serious, life-threatening conditions. Get emergency help for a
prompt diagnosis and appropriate care. Do not drive yourself to the hospital.

Request an Appointment at Mayo Clinic

Causes

Acute coronary syndrome usually results from the buildup of fatty deposits (plaques) in
and on the walls of coronary arteries, the blood vessels delivering oxygen and nutrients
to heart muscles.

When a plaque deposit ruptures or splits, a blood clot forms. This clot blocks the flow of
blood to heart muscles.
When the supply of oxygen to cells is too low, cells of the heart muscles can die. The
death of cells — resulting in damage to muscle tissues — is a heart attack (myocardial
infarction).

Even when there is no cell death, the decrease in oxygen still results in heart muscles
that don't work the way they should. This change may be temporary or permanent.
When acute coronary syndrome doesn't result in cell death, it is called unstable angina.

Risk factors

The risk factors for acute coronary syndrome are the same as those for other types of
heart disease. Acute coronary syndrome risk factors include:

 Aging

 High blood pressure

 High blood cholesterol

 Cigarette smoking

 Lack of physical activity

 Unhealthy diet

 Obesity or overweight

 Diabetes

 Family history of chest pain, heart disease or stroke

 History of high blood pressure, preeclampsia or diabetes during pregnan

Acute coronary syndrome

From Wikipedia, the free encyclopedia
Jump to navigationJump to search

Acute coronary syndrome

 Blockage of a coronary artery

Specialty Cardiology

Acute coronary syndrome (ACS) is a syndrome (set of signs and symptoms) due to
decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function
properly or dies.[1] The most common symptom is chest pain, often radiating to the left shoulder[2] or
angle of the jaw, crushing, central and associated with nausea and sweating. Many people with
acute coronary syndromes present with symptoms other than chest pain, particularly, women, older
patients, and patients with diabetes mellitus.[3]
Acute coronary syndrome is commonly associated with three clinical manifestations, named
according to the appearance of the electrocardiogram (ECG):[4] ST elevation myocardial
infarction (STEMI, 30%), non-ST elevation myocardial infarction (NSTEMI, 25%), or unstable
angina (38%).[5] There can be some variation as to which forms of myocardial infarction (MI) are
classified under acute coronary syndrome.[6]
ACS should be distinguished from stable angina, which develops during physical activity or stress
and resolves at rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or
with minimal exertion, or at lesser degrees of exertion than the individual's previous angina
("crescendo angina"). New-onset angina is also considered unstable angina, since it suggests a new
problem in a coronary artery.

Contents

 1Signs and symptoms

 2Pathophysiology
 3Diagnosis
o 3.1Electrocardiogram
o 3.2Imaging and blood tests
o 3.3Prediction scores
 4Prevention
 5Treatment
o 5.1STEMI
 o 5.2NSTEMI and NSTE-ACS
 6Prognosis
o 6.1TIMI score
o 6.2Global Registry of Acute Coronary Events (GRACE) score
o 6.3Killip class
o 6.4Biomarkers for diagnosis
o 6.5Biomarkers for risk determination
o 6.6Day of admission
 7See also
 8References
 9External links

Signs and symptoms[edit]

The cardinal symptom of critically decreased blood flow to the heart is chest pain, experienced as
tightness around or over the chest and (often, but not always) radiating to the left arm and the left
angle of the jaw. This may be associated with diaphoresis (sweating), nausea and vomiting, as well
as shortness of breath. In many cases, the sensation is "atypical", with pain experienced in different
ways or even being completely absent (which is more likely in female patients and those
with diabetes). Some may report palpitations, anxiety or a sense of impending doom (angor animi)
and a feeling of being acutely ill. The description of the chest discomfort as a pressure has little utility
in aiding a diagnosis as it is not specific for ACS.[7]
Though ACS is usually associated with coronary thrombosis, it can also be associated
with cocaine use.[8] Chest pain with features characteric of cardiac origin (angina) can also be
precipitated by profound anemia, brady- or tachycardia (excessively slow or rapid heart
rate), low or high blood pressure, severe aortic valve stenosis (narrowing of the valve at the
beginning of the aorta), pulmonary artery hypertension and a number of other conditions.[9]

Pathophysiology[edit]
In those who have ACS, atheroma rupture is most commonly found 60% when compared to
atheroma erosion (30%), thus causes the formation of thrombus which block the coronary arteries.
Plaque rupture is responsible for 60% in ST elevated myocardial infarction (STEMI) while plaque
erosion is responsible for 30% if the STEMI and vice versa for Non ST elevated myocardial infarction
(NSTEMI). In plaque rupture, the content of the plaque are lipid rich, collagen poor, with abundant
inflammation which is macrophagepredominant, and covered with a thin fibrous cap. Meanwhile, in
plaque erosion, the plaque is rich with extracellular matrix, proteoglycan, glycoaminoglycan, but
without fibrous caps, no inflammatory cells, and no large lipid core. After the coronary arteries are
unblocked, there is a risk of reperfusion injury due spreading inflammatory mediators throughout the
body. Investigations is still underway on the role of Cyclophilin D in reducing the reperfusion injury.[10]

Diagnosis[edit]
Classification of acute coronary syndromes.[11]

Electrocardiogram[edit]
In the setting of acute chest pain, the electrocardiogram is the investigation that most reliably
distinguishes between various causes.[12] The ECG should be done as early as practicable, including
in the ambulance if possible.[13] If this indicates acute heart damage (elevation in the ST segment,
new left bundle branch block), treatment for a heart attack in the form
of angioplasty or thrombolysis is indicated immediately (see below). In the absence of such changes,
it is not possible to immediately distinguish between unstable angina and NSTEMI.
Imaging and blood tests[edit]
As it is only one of the many potential causes of chest pain, the patient usually has a number of tests
in the emergency department, such as a chest X-ray, blood tests (including myocardial markers such
as troponin I or T, and H-FABP and/or a D-dimer if a pulmonary embolism is suspected), and
telemetry (monitoring of the heart rhythm).
Combination of troponin levels (less than 5 ng/l) with low TIMI scores can help to predict those with
low possibility of myocardial infarction and discharge them safely from the emergency
department.[10] Coronary CT angiography combined with Troponin levels is also helpful
to triage those who are susceptible to ACS. F-fluoride positron emission tomography is also helpful
in identifying those with high risk, lipid-rich coronary plaques.[10]
Prediction scores[edit]
The ACI-TIPI score can be used to aid diagnosis; using seven variables from the admission record,
this score predicts crudely which patients are likely to have myocardial ischemia.[14] For example,
according to a randomized controlled trial, males having chest pain with normal or non
diagnostic ECG are at higher risk for having acute coronary syndrome than women.[15] In this study,
the sensitivity was 65.2% and specificity was 44%. This particular study had an 8.4% prevalence of
acute coronary syndrome, which means the positive predictive value of being a male with chest pain
and having coronary syndrome is 9.6% and negative predictive value is 93.2% ( click here to adjust
these results for patients at higher or lower risk of acute coronary syndrome).
In a second cohort study, exercise electrocardiography was similarly found to be a poor predictor of
acute coronary syndrome at follow-up.[16] Of the patients who had a coronary event at 6 years of
follow up, 47% had a negative ECG at the start of the study. With an average follow up of 2.21 years
the receiver operating characteristic curves gave resting ECG a score of 0.72 and exercise ECG a
score of 0.74.
There are not only prediction scores for diagnosis of ACS, but also prognosis. Most notably, the
GRACE ACS Risk and Mortality score helps diagnose, and based upon that score predicts mortality
rate of a given patient. It takes into account both clinical (blood pressure, heart rate, EKG findings)
and medical history in its scoring system.[17]

Prevention[edit]
Acute coronary syndrome often reflects a degree of damage to the coronaries by atherosclerosis.
Primary prevention of atherosclerosis is controlling the risk factors: healthy eating, exercise,
treatment for hypertension and diabetes, avoiding smoking and controlling cholesterol levels; in
patients with significant risk factors, aspirin has been shown to reduce the risk of cardiovascular
events. Secondary prevention is discussed in myocardial infarction.
After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006,
there was a 17% reduction in hospital admissions for acute coronary syndrome. 67% of the
decrease occurred in non-smokers.[18]

Treatment[edit]
Main article: Management of acute coronary syndrome
People with presumed ACS are typically treated with aspirin, clopidogrel or ticagrelor, nitroglycerin,
and if the chest discomfort persists morphine.[19] Other analgesics such as nitrous oxide are of
unknown benefit.[19] Angiography is recommended in those who have either new ST elevation or a
new left bundle branch block on their ECG.[1] Unless the person has low oxygen levels additional
oxygen does not appear to be useful.[20]
STEMI[edit]
If the ECG confirms changes suggestive of myocardial infarction (ST elevations in specific leads, a
new left bundle branch block or a true posterior MI pattern), thrombolytics may be administered
or primary coronary angioplasty may be performed. In the former, medication is injected that
stimulates fibrinolysis, destroying blood clots obstructing the coronary arteries. In the latter, a flexible
catheter is passed via the femoral or radial arteries and advanced to the heart to identify blockages
in the coronaries. When occlusions are found, they can be intervened upon mechanically
with angioplasty and usually stent deployment if a lesion, termed the culprit lesion, is thought to be
causing myocardial damage. Data suggest that rapid triage, transfer and treatment is
essential.[21] The time frame for door-to-needle thrombolytic administration according to American
College of Cardiology (ACC) guidelines should be within 30 minutes, whereas the door-to-balloon
Percutaneous Coronary Intervention (PCI) time should be less than 90 minutes. It was found
that thrombolysis is more likely to be delivered within the established ACC guidelines among
patients with STEMI as compared to PCI according to a case control study.[22]
NSTEMI and NSTE-ACS[edit]
If the ECG does not show typical changes, the term "non-ST segment elevation ACS" is applied. The
patient may still have suffered a "non-ST elevation MI" (NSTEMI). The accepted management of
unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, a
second platelet inhibitor such as clopidogrel, prasugrel or ticagrelor, and heparin (usually a low-
molecular weight heparin), with intravenous nitroglycerin and opioids if the pain persists. The
heparin-like drug known as fondaparinux appears to be better than enoxaparin.[23]
A blood test is generally performed for cardiac troponins twelve hours after onset of the pain. If this
is positive, coronary angiography is typically performed on an urgent basis, as this is highly
predictive of a heart attack in the near-future. If the troponin is negative, a treadmill exercise test or a
thallium scintigram may be requested.
If there is no evidence of ST segment elevation on the electrocardiogram, delaying
urgent angioplasty until the next morning is not inferior to doing so immediately.[24] Using statins in
the first 14 days after ACS reduces the risk of further ACS.[25]
In a cohort study comparing NSTEMI and STEMI, people with NSTEMI had a similar risk of death at
one year after PCI as compared to people with STEMI (3.4% vs 4.4%).[26]However, NSTEMI had
significantly more "major cardiac events" (death, myocardial infarction, disabling stroke, or
requiring revascularization) at one year (24.0% vs 16.6%).
Cocaine associated ACS should be managed in a manner similar to other patients with acute
coronary syndrome except beta blockers should not be used and benzodiazepinesshould be
administered early.[27]

Prognosis[edit]
TIMI score[edit]
The TIMI risk score can identify high risk patients in non-ST segment elevation MI ACS[28] and has
been independently validated.[29][30]
Global Registry of Acute Coronary Events (GRACE) score [edit]
Based on a global registry of 102,341 patients, the GRACE score estimates in-hospital, 6 months, 1
year, and 3 year mortality risk after a heart attack. GRACE Score 2.0 Calculator.[17]
Killip class[edit]
The Killip classification consists of 4 classes based on clinical symptoms. It predicts 30-day mortality
after myocardial infarction.[31]
Biomarkers for diagnosis[edit]
The aim of diagnostic markers is to identify patients with ACS even when there is no evidence of
heart muscle damage.

 Ischemia-Modified Albumin (IMA) – In cases of Ischemia – Albumin undergoes a conformational

change and loses its ability to bind transitional metals (copper or cobalt). IMA can be used to
assess the proportion of modified albumin in ischemia. Its use is limited to ruling out ischemia
rather than a diagnostic test for the occurrence of ischemia.
 Myeloperoxidase (MPO) – The levels of circulating MPO, a leukocyte enzyme, elevate early
after ACS and can be used as an early marker for the condition.
 Glycogen Phosphorylase Isoenzyme BB-(GPBB) is an early marker of cardiac ischemia and is
one of three isoenzyme of Glycogen Phosphorylase.
 Troponin is a late cardiac marker of ACS
Biomarkers for risk determination[edit]
The aim of prognostic markers is to reflect different components of pathophysiology of ACS. For
example:

 Natriuretic peptide – Both B-type natriuretic peptide (BNP) and N-terminal Pro BNP can be
applied to predict the risk of death and heart failure following ACS.
 Monocyte chemo attractive protein (MCP)-1 – has been shown in a number of studies to identify
patients with a higher risk of adverse outcomes after ACS.
Day of admission[edit]
Studies have shown that for ACS patients, weekend admission is associated with higher mortality
and lower utilization of invasive cardiac procedures, and those who did undergo these interventions
had higher rates of mortality and complications than their weekday counterparts. This data leads to
the possible conclusion that access to diagnostic/interventional procedures may be contingent upon
the day of admission, which may impact mortality.[32][33] This phenomenon is described as weekend
effec

lassification
Acute coronary syndromes include

 Unstable angina

 Non–ST-segment elevation myocardial infarction (NSTEMI)

 ST-segment elevation myocardial infarction (STEMI)

These syndromes all involve acute coronary ischemia and are distinguished based on symptoms, ECG
findings, and cardiac marker levels. It is helpful to distinguish the syndromes because prognosis and
treatment vary.

Unstable angina (acute coronary insufficiency, preinfarction angina, intermediate syndrome) is defined as
one or more of the following in patients whose cardiac biomarkers do not meet criteria for myocardial
infarction (MI):
 Rest angina that is prolonged (usually > 20 min)
 New-onset angina of at least class 3 severity in the Canadian Cardiovascular Society (CCS)
classification (see table Canadian Cardiovascular Society Classification System for Angina Pectoris)
 Increasing angina, ie, previously diagnosed angina that has become distinctly more frequent, more
severe, longer in duration, or lower in threshold (eg, increased by ≥ 1 CCS class or to at least CCS
class 3)
ECG changes such as ST-segment depression, ST-segment elevation, or T-wave inversion may occur during
unstable angina but they are transient. Of cardiac markers, CK is not elevated but cardiac troponin,
particularly when measured using high-sensitivity troponin tests (hs-cTn), may be slightly increased.
Unstable angina is clinically unstable and often a prelude to myocardial infarction or arrhythmias or, less
commonly, to sudden death.

Non–ST-segment elevation MI (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by

cardiac markers in blood; troponin I or troponin T and CK will be elevated) without acute ST-segment
elevation. ECG changes such as ST-segment depression, T-wave inversion, or both may be present.
ST-segment elevation MI (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-
segment elevation that is not quickly reversed by nitroglycerin or showing new left bundle branch block.
Troponin I or troponin T and CK are elevated.
Both types of MI may or may not produce Q waves on the ECG (Q wave MI, non-Q wave MI).

Etiology
The most common cause of acute coronary syndromes is
 An acute thrombus in an atherosclerotic coronary artery

Atheromatous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing
thrombogenic material, which activates platelets and the coagulation cascade and produces an acute
thrombus. Platelet activation involves a conformational change in membrane glycoprotein (GP) IIb/IIIa
receptors, allowing cross-linking (and thus aggregation) of platelets. Even atheromas causing minimal
obstruction can rupture and result in thrombosis; in > 50% of cases, pre-event stenosis is < 40%. Thus,
although the severity of stenosis helps predict symptoms, it does not always predict acute thrombotic events.
The resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous
thrombolysis occurs in about two thirds of patients; 24 h later, thrombotic obstruction is found in only about
30%. However, in virtually all cases, obstruction lasts long enough to cause varying degrees of tissue
necrosis.
Rarer causes of acute coronary syndromes are
 Coronary artery embolism

 Coronary spasm

 Coronary artery dissection

Coronary arterial embolism can occur in mitral stenosis, aortic stenosis, infective endocarditis, marantic
endocarditis, or atrial fibrillation.
Cocaine use and other causes of coronary spasm can sometimes result in myocardial infarction. Spasm-
induced MI may occur in normal or atherosclerotic coronary arteries.
Coronary artery dissection is a non-traumatic tear in the coronary intima with creation of a false lumen.
Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen
sometimes causing coronary ischemia or infarction. Dissection may occur in atherosclerotic or non-
atherosclerotic coronary arteries. Non-atherosclerotic dissection is more likely in pregnant or postpartum
women and/or patients with fibromuscular dysplasia or other connective tissue disorders.

Pathophysiology
Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia
to infarction. Measurement of newer, more sensitive markers indicates that some cell necrosis probably
occurs even in mild forms; thus, ischemic events occur on a continuum, and classification into subgroups,
although useful, is somewhat arbitrary. Sequelae of the acute event depend primarily on the mass and type
of cardiac tissue infarcted.

Myocardial dysfunction
Ischemic (but not infarcted) tissue has impaired contractility and relaxation, resulting in hypokin etic or
akinetic segments; these segments may expand or bulge during systole (called paradoxical motion). The size
of the affected area determines effects, which range from minimal to mild heart failure to cardiogenic shock;
usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. Some
degree of heart failure occurs in about two thirds of hospitalized patients with acute myocardial infarction. It
is termed ischemic cardiomyopathy if low cardiac output and heart failure persist. Ischemia involving the
papillary muscle may lead to mitral valve regurgitation. Dysfunctional wall motion can allow mural
thrombus formation.

Myocardial infarction (MI)

Myocardial infarction is myocardial necrosis resulting from abrupt reduction in coronary blood flow to part
of the myocardium. Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially
reversible ischemia adjacent to infarcted tissue. MI affects predominantly the left ventricle (LV), but
damage may extend into the right ventricle (RV) or the atria.
Infarction may be

 Transmural: Transmural infarcts involve the whole thickness of myocardium from epicardium to
endocardium and are usually characterized by abnormal Q waves on ECG.

 Nontransmural (subendocardial): Nontransmural infarcts do not extend through the ventricular wall
and cause only ST-segment and T-wave (ST-T) abnormalities.

Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually
classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the
ECG.

Necrosis of a significant portion of the interventricular septum or ventricular wall may rupture, with dire
consequences. A ventricular aneurysm or pseudoaneurysm may form.

Electrical dysfunction
Electrical dysfunction can be significant in any form of acute coronary syndrome. Ischemic and necrotic
cells are incapable of normal electrical activity, resulting in various ECG changes (predominantly ST-T
abnormalities), arrhythmias, and conduction disturbances. ST-T abnormalities of ischemia include ST-
segment depression (often downsloping from the J point), T-wave inversion, ST-segment elevation (often
referred to as injury current), and peaked T waves in the hyperacute phase of infarction. Conduction
disturbances can reflect damage to the sinus node, the atrioventricular (AV) node, or specialized conduction
tissues. Most changes are transient; some are permanent.

Symptoms and Signs

Symptoms of acute coronary syndromes depend somewhat on the extent and location of obstruction and are
quite variable. Painful stimuli from thoracic organs, including the heart, can cause discomfort described as
pressure, tearing, gas with the urge to eructate, indigestion, burning, aching, stabbing, and sometimes sharp
needle-like pain. Many patients deny they are having pain and insist it is merely “discomfort.” Except when
infarction is massive, recognizing the amount of ischemia by symptoms alone is difficult.

Symptoms of ACS are similar to those of angina and are discussed in more detail in sections on unstable
angina and acute myocardial infarction.

Complications
After the acute event, many complications can occur. They usually involve
 Electrical dysfunction (eg, conduction defects, arrhythmias)

 Myocardial dysfunction (eg, heart failure, interventricular septum or free wall rupture, ventricular
aneurysm, pseudoaneurysm, mural thrombus formation, cardiogenic shock)

 Valvular dysfunction (typically mitral regurgitation)

Electrical dysfunction can be significant in any form of ACS, but usually, large parts of myocardium must
be ischemic to cause significant myocardial dysfunction. Other complications of ACS include recurrent
ischemia and pericarditis. Pericarditis that occurs 2 to 10 wk after an MI is known as post-MI syndrome, or
Dressler syndrome.
Diagnosis
 Serial ECGs

 Serial cardiac markers

 Immediate coronary angiography for patients with STEMI or complications (eg, persistent chest pain,
hypotension, markedly elevated cardiac markers, unstable arrhythmias)

 Delayed angiography (24 to 48 h) for patients with NSTEMI or unstable angina without
complications noted above
Acute coronary syndromes should be considered in men > 30 yr and women > 40 yr (younger in patients
with diabetes) whose main symptom is chest pain or discomfort. Pain must be differentiated from the pain
of pneumonia, pulmonary embolism, pericarditis, rib fracture, costochondral separation, esophageal spasm,
acute aortic dissection, renal calculus, splenic infarction, or various abdominal disorders. In patients with
previously diagnosed hiatus hernia, peptic ulcer, or a gallbladder disorder, the clinician must be wary of
attributing new symptoms to these disorders. (For approach to diagnosis, see also Chest Pain.)
The approach is the same when any ACS is suspected: initial and serial ECG and serial cardiac marker
measurements, which distinguish among unstable angina, NSTEMI, and STEMI. Every emergency
department should have a triage system to immediately identify patients with chest pain for rapid assessment
and ECG. Pulse oximetry and chest x-ray (particularly to look for mediastinal widening, which suggests
aortic dissection) is also done.

ECG
ECG is the most important test and should be done within 10 min of presentation. It is the center of the
decision pathway because fibrinolytics benefit patients with STEMI but may increase risk for those with
NSTEMI. Also, urgent cardiac catheterization is indicated for patients with acute STEMI but not for those
with NSTEMI.

For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more
contiguous leads subtending the damaged area (see figure Acute lateral left ventricular infarction).
Acute lateral left ventricular infarction (tracing obtained within a few hours of onset of
illness)

There is striking hyperacute ST-segment elevation in leads I, aVL, V 4, and V6 and reciprocal depression in other leads.

Pathologic Q waves are not necessary for the diagnosis. The ECG must be read carefully because ST-
segment elevation may be subtle, particularly in the inferior leads (II, III, aVF); sometimes the reader’s
attention is mistakenly focused on leads with ST-segment depression. If symptoms are characteristic, ST-
segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing MI. Serial
tracings (obtained every 8 h for 1 day, then daily) showing a gradual evolution toward a stable, more normal
pattern or development of abnormal Q waves over a few days (see figure Inferior (diaphragmatic) left
ventricular infarction) tends to confirm the diagnosis.
Inferior (diaphragmatic) left ventricular infarction (after the first 24 h)
Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF.

Because nontransmural (non–Q wave) infarcts are usually in the subendocardial or midmyocardial layers,
they do not produce diagnostic Q waves or distinct ST-segment elevation on the ECG. Instead, they
commonly produce only varying degrees of ST-T abnormalities that are less striking, variable, or
nonspecific and sometimes difficult to interpret (NSTEMI). If such abnormalities resolve (or worsen) on
repeat ECGs, ischemia is very likely. However, when repeat ECGs are unchanged, acute MI is unlikely and,
if still suspected clinically, requires other evidence to make the diagnosis. A normal ECG taken when a
patient is pain free does not rule out unstable angina; a normal ECG taken during pain, although it does not
rule out angina, suggests that the pain is not ischemic.

If right ventricular (RV) infarction is suspected, a 15-lead ECG is usually recorded; additional leads are
placed at V4R, and, to detect posterior infarction, V8 and V9.

ECG diagnosis of myocardial infarction is more difficult when a left bundle branch block configuration is
present because the ECG changes resemble changes due to STEMI (see figure Left bundle branch block).
ST-segment elevation concordant with the QRS complex strongly suggests MI as does > 5-mm ST-segment
elevation in at least 2 precordial leads. But generally, any patient with suggestive symptoms and new-onset
(or not known to be old) left bundle branch block is treated as for STEMI.
Left bundle branch block

CLINICAL CALCULATOR:

M.I. Prediction Decision TreeCalc

CLINICAL CALCULATOR:

Non Q Wave Myocardial Infarction Prediction

CLINICAL CALCULATOR:

M.I. Prediction Decision TreeCalc

Cardiac markers
Cardiac markers (serum markers of myocardial cell injury) are

 Cardiac enzymes (eg, CK-MB)

 Cell contents (eg, troponin I, troponin T, myoglobin)

These markers are released into the bloodstream after myocardial cell necrosis. The markers appear at
different times after injury, and levels decrease at different rates. Sensitivity and specificity for myocardial
cell injury vary significantly among these markers, but the troponins (cTn) are the most sensitive and
specific and are now the markers of choice. Recently, several new, highly sensitive assays of cardiac
troponin (hs-cTn) that are also very precise have become available. These assays can reliably measure
troponin levels (T or I) as low as 0.003 to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as
0.001 ng/mL (1 pg/mL).

Previous, less sensitive cTn tests were unlikely to detect cTn except in patients who had an acute cardiac
disorder. Thus, a "positive" cTn test (ie, above the limit of detection) was very specific. However, the newer
hs-cTn tests can detect small amounts of cTn in many healthy people. Thus, troponin levels detected with
hs-cTn tests need to be referenced to the normal range, and are defined as "elevated" only when higher than
99% of the reference population. Furthermore, although an elevated troponin level indicates myocardial cell
injury, it does not indicate the cause of the damage (although any troponin elevation increases the risk of
adverse outcomes in many disorders). In addition to acute coronary syndromes, many other cardiac and non-
cardiac disorders can elevate cTn levels (see table Causes of Elevated Troponin Levels); not all elevated
levels detected with hs-cTn represent myocardial infarction, and not all myocardial necrosis results from an
acute coronary syndrome event even when the etiology is ischemic. However, by detecting lower levels of
troponin, hs-cTn assays enable earlier identification of MI than other assays, and have replaced other cardiac
marker tests in many centers.
Patients suspected of having an ACS should have an hs-cTn assay done on presentation and 3 h later.
Troponin should be measured at 0 and 6 h if a standard cTn assay is used.
An hs-cTn level must be interpreted based on the patient's pre-test probability of disease, which is estimated
clinically based on

 Risk factors for ACS

 Symptoms

 ECG findings

A high pre-test probability plus an elevated level detected with an hs-cTn assay is highly suggestive of ACS,
whereas a low pre-test probability plus a normal hs-cTn assay result is unlikely to represent ACS. Diagnosis
is more challenging when test results are discordant with pre-test probability, in which case serial hs-cTn
assays often help. A patient with low pre-test probability and an initially slightly elevated troponin level
detected with hs-cTn that remains stable on repeat testing probably has non-ACS cardiac disease (eg, heart
failure, stable coronary artery disease). However, if the repeat level rises significantly (ie, > 20 to 50%) the
likelihood of ACS becomes much higher. If a patient with high pre-test probability has a normal troponin
level detected with hs-cTn and that rises > 50% on repeat testing, ACS is likely; continued normal levels
(often including at 6 h and beyond when suspicion is high) suggest need to pursue an alternate diagnosis.

TABLE

Causes of Elevated Troponin Levels

Coronary angiography
Coronary angiography most often combines diagnosis with percutaneous coronary intervention (PCI—ie,
angioplasty, stent placement). When possible, emergency coronary angiography and PCI are done as soon as
possible after the onset of acute myocardial infarction (primary PCI). In many tertiary centers, this approach
has significantly lowered morbidity and mortality and improved long-term outcomes. Frequently, the
infarction is actually aborted when the time from pain to PCI is short (< 3 to 4 h).
Angiography is obtained urgently for patients with STEMI, patients with persistent chest pain despite
maximal medical therapy, and patients with complications (eg, markedly elevated cardiac markers, presence
of cardiogenic shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias). Patients
with uncomplicated NSTEMI or unstable angina whose symptoms have resolved typically undergo
angiography within the first 24 to 48 h of hospitalization to detect lesions that may require treatment.
After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing
ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias,
and other abnormalities that suggest recurrence of ischemic events. Some experts also recommend that
angiography be done before hospital discharge in STEMI patients with inducible ischemia on stress imaging
or an ejection fraction < 40%.
Other tests
Routine laboratory tests are nondiagnostic but, if obtained, show nonspecific abnormalities compatible with
tissue necrosis (eg, increased ESR, moderately elevated WBC count with a shift to the left). A fasting lipid
profile should be obtained within the first 24 h for all patients hospitalized with ACS.

Myocardial imaging is not needed to make the diagnosis if cardiac markers or ECG is positive. However,
in patients with myocardial infarction, bedside echocardiography is invaluable for detecting mechanical
complications. Before or shortly after discharge, patients with symptoms suggesting an ACS but
nondiagnostic ECGs and normal cardiac markers should have a stress imaging test (radionuclide or
echocardiographic imaging with pharmacologic or exercise stress). Imaging abnormalities in such patients
indicate increased risk of complications in the next 3 to 6 mo and suggest need for angiography, which
should be done before discharge or soon thereafter, with PCI or CABG done as necessary.
Right heart catheterization using a balloon-tipped pulmonary artery catheter can be used to measure right
heart, pulmonary artery, and pulmonary artery occlusion pressures and cardiac output. This test is not
routinely recommended and should be done only if patients have significant complications (eg, severe heart
failure, hypoxia, hypotension) and by doctors experienced with catheter placement and management
protocols.
Prognosis
Global risk should be estimated via formal clinical risk scores (Thrombosis in Myocardial Infarction
[TIMI], Global Registry of Acute Coronary Events [GRACE], Platelet Glycoprotein IIb/IIIa in Unstable
Angina: Receptor Suppression Using Integrilin Therapy [PURSUIT]—1) or a combination of the following
high-risk features:
 Recurrent angina/ischemia at rest or during low-level activity

 Heart failure

 Worsening mitral regurgitation

 High-risk stress test result (test stopped in ≤ 5 min due to symptoms, marked ECG abnormalities,
hypotension, or complex ventricular arrhythmias)

 Hemodynamic instability

 Sustained ventricular tachycardia

 Diabetes mellitus

 PCI within past 6 mo

 Prior CABG
  LV ejection fraction < 0.40

CLINICAL CALCULATOR:

Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable Angina Non ST Elevation Myocardial
Infarction

CLINICAL CALCULATOR:

Thrombolysis in Myocardial Infarction (TIMI) Score for ST Elevation Acute Myocardial Infarction

Prognosis reference
 1. Boersma E, Pieper KS, Steyerberg EW, et al: Predictors of outcome in patients with acute coronary
syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The
PURSUIT Investigators. Circulation 101(22): 2557–2567, 2000.
Treatment
 Prehospital care: Oxygen, aspirin, and nitrates and triage to an appropriate medical center
 Drug treatment: Antiplatelet drugs, antianginal drugs, anticoagulants, and in some cases other drugs

 Often, angiography to assess coronary artery anatomy

 Often, reperfusion therapy: Fibrinolytics, percutaneous coronary intervention or coronary artery

bypass surgery

 Supportive care

 Post discharge rehabilitation and chronic management of coronary artery disease

Treatment, including drug treatment, is designed to relieve distress, interrupt thrombosis, reverse ischemia,
limit infarct size, reduce cardiac workload, and prevent and treat complications. An acute coronary
syndrome is a medical emergency; outcome is greatly influenced by rapid diagnosis and treatment.
Treatment occurs simultaneously with diagnosis.

Contributing disorders (eg, anemia, heart failure) are aggressively treated.

Because the chest pain of myocardial infarction usually subsides within 12 to 24 h, any chest pain that
remains or recurs later is investigated. It may indicate such complications as recurrent ischemia, pericarditis,
pulmonary embolism, pneumonia, gastritis, or ulcer.
Prehospital care
 Oxygen

 Aspirin
 Nitrates

 Triage to appropriate medical center

A reliable IV route must be established, oxygen given (typically 2 L by nasal cannula), and continuous
single-lead ECG monitoring started. Prehospital interventions by emergency medical personnel—including
ECG, chewed aspirin (325 mg), pain management with nitrates (see table Drugs for Coronary Artery
Disease), early thrombolysis when indicated and possible, and triage to the appropriate hospital where
primary PCI is available—can reduce risk of mortality and complications.
Although opioids have long been used to treat pain in patients with acute coronary syndromes, new data
suggest that morphineattenuates activity of some P2Y12 receptor inhibitors and may contribute to worse
patient outcomes (1, 2).
Early diagnostic data and response to treatment can help determine the need for and timing
of revascularization when primary percutaneous coronary intervention is not possible.

Hospital admission
 Drug therapy with antiplatelet drugs, anticoagulants, and other drugs based on reperfusion strategy

 Risk-stratify patient and choose a reperfusion strategy (fibrinolytics or cardiac angiography with PCI
or CABG for patients with STEMI and cardiac angiography with PCI or CABG for patients with
unstable angina or NSTEMI)

On arrival to the emergency room, the patient's diagnosis is confirmed. Drug therapy and choice of
revascularization depend on the type of acute coronary syndrome as well as the clinical picture (see
figure Approach to acute coronary syndromes). Choice of drug therapy is discussed in Drugs for Acute
Coronary Syndrome, and choice of reperfusion strategy is further discussed in Revascularization for Acute
Coronary Syndromes.
Approach to acute coronary syndromes
* Morphine should be used judiciously (eg, if nitroglycerin is contraindicated or if the patient has symptoms despitenitroglyce
†Complicated means that the hospital course was complicated by recurrent angina or infarction, heart failure, or sustained rec
arrhythmias. Absence of any of these events is termed uncomplicated.
‡Although
some recent trials raise questions, CABG is generally preferred to PCI for patients with the following:
 Left main or left main equivalent disease

 Left ventricular dysfunction

 Treated diabetes

Also, lesions that are long or near bifurcation points are often not amenable to PCI.
CABG = coronary artery bypass grafting; GP = glycoprotein; LDL = low density lipoprotein; NSTEMI = non -ST-segment ele
myocardial infarction; PCI = percutaneous intervention; STEMI = ST-segment elevation MI.

When the diagnosis is unclear, bedside cardiac marker tests can help identify low-risk patients with a
suspected ACS (eg, those with initially negative cardiac markers and nondiagnostic ECGs), who can be
managed in 24-h observation units or chest pain centers. Higher-risk patients should be admitted to a
monitored inpatient unit or coronary care unit (CCU). Several validated tools can help stratify risk.
Thrombolysis in MI (TIMI) risk scores may be the most widely used.

Patients with suspected NSTEMI and intermediate or high risk should be admitted to an inpatient care unit
or CCU. Those with STEMI should be admitted to a CCU.

Only heart rate and rhythm recorded by single-lead ECG are consistently useful for routine, continuous
monitoring. However, some clinicians recommend routine multilead monitoring with continuous ST -
segment recording to identify transient, recurrent ST-segment elevations or depressions. Such findings, even
in patients without symptoms, suggest ischemia and identify higher-risk patients who may require more
aggressive evaluation and treatment.

Qualified nurses can interpret the ECG for arrhythmia and initiate protocols for its treatment. All staff
members should know how to do CPR.

CLINICAL CALCULATOR:

Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable Angina Non ST Elevation Myocardial
Infarction

CLINICAL CALCULATOR:

Thrombolysis in Myocardial Infarction (TIMI) Score for ST Elevation Acute Myocardial Infarction

Supportive care
The care unit should be a quiet, calm, restful area. Single rooms are preferred; privacy consistent with
monitoring should be ensured. Usually, visitors and telephone calls are restricted to family members during
the first few days. A wall clock, a calendar, and an outside window help orient the patient and prevent a
sense of isolation, as can access to a radio, television, newspaper and/or digital devices.

On day 1, patients without complications (eg, hemodynamic instability, ongoing ischemia), including those
in whom reperfusion with fibrinolytics or PCI is successful, can sit in a chair, begin passive exercises, and
use a commode. Walking to the bathroom and doing nonstressful paperwork are allowed shortly thereafter.
Patients with successful, uncomplicated primary PCI for acute MI may be ambulated quickly and be safely
discharged in 3 to 4 days.

If reperfusion is not successful or complications are present, patients require longer bed rest, but they
(particularly elderly patients) are mobilized as soon as possible. Prolonged bed rest results in rapid physical
deconditioning, with development of orthostatic hypotension, decreased work capacity, increased heart rate
during exertion, and increased risk of deep venous thrombosis. Prolonged bed rest also intensifies feelings
of depression and helplessness.
Anxiety, mood changes, and denial are common. A mild tranquilizer (usually a benzodiazepine) is often
given, but many experts believe such drugs are rarely needed. Reactive depression is common by the 3rd
day of illness and is almost universal at some time during recovery.
 After the acute phase of illness, the most important tasks are often management of depression, rehabilitation,
and institution of long-term preventive programs. Overemphasis on bed rest, inactivity, and the seriousness
of the disorder reinforces anxiety and depressive tendencies, so patients are encouraged to sit up, get out of
bed, and engage in appropriate activities as soon as possible. The effects of the disorder, prognosis, and
individualized rehabilitation program should be explained to the patient.
Maintaining normal bowel function with stool softeners (eg, docusate) to prevent straining is important.
Urinary retention is common among elderly patients, especially after several days of bed rest or
if atropine was given. A catheter may be required but can usually be removed when the patient can stand or
sit to void.
Because smoking is prohibited, a hospital stay should be used to encourage smoking cessation. All
caregivers should devote considerable effort to making smoking cessation permanent.
Although acutely ill patients have little appetite, tasty food in modest amounts is good for morale. Patients
are usually offered a soft diet of 1500 to 1800 kcal/day with sodium reduction to 2 to 3 g. Sodium reduction
is not required after the first 2 or 3 days if there is no evidence of heart failure. Patients are given a diet low
in cholesterol and saturated fats, which is used to teach healthy eating.

For patients with diabetes and STEMI, intensive glucose control is no longer recommended; guidelines call
for an insulin-based regimen to achieve and maintain glucose levels <180 mg/dL while avoiding
hypoglycemia.

Treatment references
 1. Meine TJ, Roe MT, Chen AY, et al: Association of intravenous morphine use and outcomes in acute
coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J 149(6):1043-
1049, 2005. doi 10.1016/j.ahj.2005.02.010.
 2. Kubica J, Adamski P, Ostrowska M, et al: Morphine delays and attenuates ticagrelor exposure and action
in patients with myocardial infarction: the randomized, double-blind, placebo-controlled IMPRESSION
trial. Eur Heart J 37(3): 245–252, 2016. doi: 10.1093/eurheartj/ehv547.
Rehabilitation and Postdischarge Treatment
 Functional evaluation

 Changes in lifestyle: Regular exercise, diet modification, weight loss, smoking cessation

 Drugs: Continuation of antiplatelet drugs, beta-blockers, ACE inhibitors, and statins

Functional evaluation
Patients who did not have coronary angiography during admission, have no high-risk features (eg, heart
failure, recurrent angina, ventricular tachycardia or ventricular fibrillation after 24 h, mechanical
complications such as new murmurs, shock), and have an ejection fraction > 40% whether or not they
received fibrinolytics usually should have stress testing of some sort before or shortly after discharge (see
table Functional Evaluation After Myocardial Infarction).
TABLE

Functional Evaluation After Myocardial Infarction

Activity
Physical activity is gradually increased during the first 3 to 6 wk after discharge. Resumption of sexual
activity, often of great concern to the patient and partner, and other moderate physical activities may be
encouraged. If good cardiac function is maintained 6 wk after acute myocardial infarction, most patients can
return to all their normal activities. A regular exercise program consistent with lifestyle, age, and cardiac
status reduces risk of ischemic events and enhances general well-being. Supervised cardiac rehabilitation
programsdecrease mortality after revascularization (1)

Risk factor modification

The acute illness and treatment of ACS should be used to strongly motivate the patient to modify risk
factors. Evaluating the patient’s physical and emotional status and discussing them with the patient, advising
about lifestyle (eg, smoking, diet, work and play habits, exercise), and aggressively managing risk factors
may improve prognosis.

Drugs
Several drugs clearly reduce mortality risk post-MI and are used unless contraindicated or not tolerated:

 Aspirin and other antiplatelet drugs

 Beta blockers

 ACE inhibitors

 Statins

Aspirin and other antiplatelet drugs reduce mortality and reinfarction rates in patients after myocardial
infarction. Enteric-coated aspirin 81 mg once/day is recommended long-term. Data suggest
that warfarin with or without aspirin reduces mortality and reinfarction rates.
Beta-blockers are considered standard therapy. Most available beta-blockers
(eg, acebutolol, atenolol, metoprolol, propranolol, timolol) reduce post-MI mortality rate by about 25% for
at least 7 yr.
ACE inhibitors are also considered standard therapy and are given to all post-MI patients if possible
particularly if ejection fraction post MI is < 40%. These drugs may provide long-term cardioprotection by
improving endothelial function. If an ACE inhibitor is not tolerated because of cough or rash (but not
angioedema or renal dysfunction), an angiotensin II receptor blocker may be substituted.
 Statins are also standard therapy and are routinely prescribed regardless of lipid levels. Reducing cholesterol
levels after MI reduces rates of recurrent ischemic events and mortality in patients with elevated or normal
cholesterol levels. Statins appear to benefit post-MI patients regardless of their initial cholesterol level. Post-
MI patients whose primary problem is a low HDL level or an elevated triglyceride level may benefit from a
fibrate, but evidence of benefit is less clear. The statin should be continued indefinitely, unless significant
adverse effects occur, and dose should be increased to the maximally tolerated dose.

Rehabilitation and postdischarge treatment reference

 1. Goel K, Lennon RJ, Tilbury RT, et al: Impact of Cardiac Rehabilitation on Mortality and Cardiovascular
Events After Percutaneous Coronary Intervention in the Community. Circulation 123:2344–2352, 20111.
doi: 10.1161/CIRCULATIONAHA.110.983536.
Key Points
 Unstable angina, NSTEMI, and STEMI represent worsening degrees of myocardial ischemia
and necrosis; the distinctions help differentiate prognosis and guide treatment.

 Diagnosis is based on serial ECG and cardiac marker levels, particularly using new, highly
sensitive troponin T tests.

 Immediate medical treatment depends on the specific syndrome and patient characteristics but
typically involves antiplatelet drugs, anticoagulants, beta-blockers, and nitrates as needed (eg,
for chest pain, hypertension, pulmonary edema), and a statin to improve prognosis.

 For unstable angina and NSTEMI, do angiography within 24 to 48 h of hospitalization to

identify coronary lesions requiring PCI or CABG; fibrinolysis is not helpful.

 For STEMI, do emergency PCI when door to balloon-inflation time is < 90 min; do fibrinolysis
if such timely PCI is not available.
 Following recovery, initiate or continue aspirin and other antiplatelet drugs, beta-blockers,
ACE inhibitors, and statins in most cases unless contraindicated.
Last full review/revision December 2018 by Ranya N Sweis, MD, MS; Arif Jivan, MD, PhD
NOTE: This is the Professional Version. CONSUMERS: Click here for the Consumer Version

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f you or a loved one has coronary artery disease (CAD), you may have heard the term “acute
coronary syndrome,” also referred to as ACS. ACS is a relatively new term used by
cardiologists, and it can be a little confusing. However, because it represents the new way of
thinking about CAD, it can be useful to take a few minutes to understand it.

Acute coronary syndrome is pretty much what it sounds like. It is an urgent condition affecting
the coronary arteries; an emergency. It indicates that a person’s CAD has suddenly become
unstable, and that permanent cardiac damage is either happening right now or is likely to happen
at any time.

What Is ACS?
ASC occurs when a blood clot suddenly forms within a coronary artery, usually due to the acute
rupture of an atherosclerotic plaque. Plaque rupture can occur at any time, often completely
without warning. The blood clot may produce partial or complete blockage of the artery, either
way placing the heart muscle supplied by that artery in immediate jeopardy.

Any plaque in any coronary artery is subject to rupture, even small plaques that are usually
ignored by cardiologists during cardiac catheterizations. This is why you will often hear of
people who have a myocardial infarction (MI, or heart attack), shortly after being told their CAD
is "insignificant."
Symptoms
The symptoms of ACS are similar to those of stable angina but are often much more intense,
frequent and persistent. The chest discomfort in ACS is often accompanied by other disturbing
symptoms such as sweating, dizziness, nausea, extreme anxiety, and what is often described as a
"feeling of impending doom." The chest pain may be untouched by nitroglycerin (which usually
relieves stable angina). On the other hand, some people who have ACS will have only mild
symptoms, may even fail to notice any symptoms at all — at least initially.

Unfortunately, the permanent heart damage that often results from ACS will, sooner or later,
produce symptoms.

Types
Cardiologists divide ACS into three distinct clinical patterns. Two of them represent different
forms of MI, and one represents a particularly severe form of angina, called "unstable angina."
All three are caused by acute blood clots in the coronary arteries.

If the blood clot is large enough and persists for more than just a few minutes, some of the heart
muscle cells begin to die. The death of heart muscle is what defines an MI. Two types of MI that
can be produced by ACS.

1. ST-Elevation myocardial infarction (STEMI), so named because the "ST segment" on

the ECG appears "elevated,” occurs when a coronary artery is completely blocked so that
a large proportion of the heart muscle being supplied by that artery begins to die.
A STEMI is the most severe form of ACS.
2. Non-ST-Elevation myocardial infarction (NSTEMI), in which the "ST segment" is not
elevated, occurs when the blockage in the coronary artery is “only” partial. Enough
blockage is occurring to damage some of the heart muscle cells being supplied by the
diseased artery, but the damage tends to be less extensive than with a STEMI. One
problem with an NSTEMI, however, is that with inadequate treatment the blockage is
likely to become complete, and the NSTEMI will become a STEMI.
3. Sometimes ACS produces a blood clot that is not yet large enough. or does not persist
long enough, to produce any permanent heart muscle damage. (The body's protective
mechanisms try to dissolve blood clots that form within blood vessels.) When an ACS is
producing symptoms without yet causing the heart muscle to die, it is termed unstable
angina. People with unstable angina have a high risk of progressing to an NSTEMI or a
STEMI.

Both NSTEMI and unstable angina can be considered as “incomplete” heart attacks. These two
forms of ACS need similar, aggressive medical management in order to reduce the likelihood
that they will progress to a STEMI — which cardiologists often call a “completed” MI.

Making the Right Diagnosis

To summarize, once a blood clot forms in a coronary artery, if extensive heart muscle damage
has already occurred a STEMI is diagnosed. If a "little" heart muscle damage occurs, an
NSTEMI is diagnosed. If no measurable heart muscle damage occurs, unstable angina is
diagnosed.

If you are having ACS, usually your symptoms, physical examination, medical
history and cardiac risk factors will immediately steer the doctor to strongly suspect the
diagnosis. From that point, he or she will quickly examine your ECG and measure your cardiac
enzymes. Cardiac enzymes are released into the bloodstream by dying heart muscle cells, so an
elevation in the cardiac enzymes means that heart cell damage is occurring.

So: The appearance of the ECG (i.e., the presence or absence of "elevation" in the ST segments)
will distinguish between STEMI and NSTEMI. And the presence or absence of elevated cardiac
enzymes will distinguish between NSTEMI and unstable angina.

The Significance of ACS

The three types of ACS represent the spectrum of the clinical conditions that can occur when a
plaque ruptures within a coronary artery. In fact, there is actually no clear line that inherently
divides STEMI, NSSTEMI, and unstable angina. Where cardiologists draw the line between a
STEMI and an NSTEMI, or between an NSTEMI and unstable angina, is a relatively arbitrary
decision. Indeed, the definitions of these three types of ACS have changed substantially over the
years, as our knowledge — specifically our ability to interpret ECGs and detect heart cell
damage with enzyme tests — have improved.

The important point is that every case of ACS (no matter how it is categorized) is a medical
emergency, and requires immediate medical care to try to accomplish two things: 1) to limit the
heart muscle damage being done acutely by the blood clot within the coronary artery, and 2) to
limit the possibility that the plaque — which has now shown itself to be unstable and prone to
rupture — will rupture again.

Stress test

While the exercise stress test itself usually takes around 10 or 15 minutes, part one of
the test takes about 30 or 45 minutes total. Dr. Willke suggests blocking off most of your
morning, because you will need to go in for follow-up photos about two hours later, for the
second part of the test.
A standard exercise stress test uses an EKG (electrocardiogram) to monitor changes in your
heart's electrical activity. Imaging stress tests take pictures of blood flow throughout your heart.
... Abnormal test results may be due to coronary heart disease (CHD) or other factors, such as
poor physical fitness.
An echo or nuclear stress test may not reveal certain conditions, such as microvascular
angina. ... This condition can cause chest discomfort with a normalstress test result. A
normal stress test result only shows that there is not a significant coronary artery blockage.
A stress test, also called an exercise stress test, shows how your heart works during
physical activity. Because exercise makes your heart pump harder and faster, an
exercise stress test can reveal problems with blood flow within your heart.

A stress test usually involves walking on a treadmill or riding a stationary bike your heart
rhythm, blood pressure and breathing are monitored. Or you'll receive a drug that
mimics the effects of exercise.

Your doctor may recommend a stress test if you have signs or symptoms of coronary
artery disease or an irregular heart rhythm (arrhythmia). The test may also guide
treatment decisions, measure the effectiveness of treatment or determine the severity if
you've already been diagnosed with a heart condition.

Why it's done

Your doctor may recommend a stress test to:

 Diagnose coronary artery disease. Your coronary arteries are the major blood
vessels that supply your heart with blood, oxygen and nutrients. Coronary artery
disease develops when these arteries become damaged or diseased — usually
due to a buildup of deposits containing cholesterol and other substances (plaques).

 Diagnose heart rhythm problems (arrhythmias). Heart arrhythmias occur when

the electrical impulses that coordinate your heart rhythm don't function properly,
causing your heart to beat too fast, too slowly or irregularly.

 Guide treatment of heart disorders. If you've already been diagnosed with a

heart condition, an exercise stress test can help your doctor find out how well
treatment is working. It may also be used to help establish the treatment plan for
you by showing how much exercise your heart can handle.

Your doctor may use a stress test to help determine the timing of cardiac surgery,
such as valve replacement. In some people with heart failure, stress test results
may help the doctor determine whether you need a heart transplant or other
advanced therapies.
 Your doctor may recommend a test with imaging, such as a nuclear stress test or
echocardiographic stress test, if an exercise stress test doesn't pinpoint the cause of
your symptoms.

More Information

 Angina

 Arteriosclerosis / atherosclerosis

 Atrial flutter
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Risks

A stress test is generally safe, and complications are rare. But, as with any medical
procedure, there is a risk of complications, including:

 Low blood pressure. Blood pressure may drop during or immediately after
exercise, possibly causing you to feel dizzy or faint. The problem should go away
after you stop exercising.

 Abnormal heart rhythms (arrhythmias). Arrhythmias brought on by an exercise

stress test usually go away soon after you stop exercising.

 Heart attack (myocardial infarction). Although exceedingly rare, it's possible that
an exercise stress test could cause a heart attack.

How you prepare

Your doctor will give you specific instructions on how to prepare for your stress test.

Food and medications

You may be asked not to eat, drink or smoke for a period of time before a stress test.
You may need to avoid caffeine the day before and the day of the test.
Ask your doctor if it's safe for you to continue taking all of your prescription and over-
the-counter medications before the test, because they might interfere with certain stress
tests.

If you use an inhaler for asthma or other breathing problems, bring it to the test. Make
sure your doctor and the health care team member monitoring your stress test know
that you use an inhaler.

Clothing and personal items

Wear or bring comfortable clothes and walking shoes. If you're having a nuclear stress
test, don't apply oil, lotion or cream to your skin that day.

What you can expect



Exercise stress test

Your stress test will take around an hour, including both your prep time and the time it
takes to perform the actual test. The actual test takes only around 15 minutes. You may
have an exercise stress test in which you walk on a treadmill or pedal a stationary
bicycle. If you aren't able to exercise, you'll receive a drug through an IV that mimics
exercise by increasing blood flow to your heart.

Before a stress test

First, your doctor will ask you some questions about your medical history and how often
and strenuously you exercise. This helps determine the amount of exercise that's
appropriate for you during the test. Your doctor will also listen to your heart and lungs
for any abnormalities that might affect your test results.

During a stress test

A nurse or technician will place sticky patches (electrodes) on your chest, legs and
arms. Some areas may need to be shaved to help them stick. The electrodes have
wires connected to an electrocardiogram machine, which records the electrical signals
that trigger your heartbeats. A cuff on your arm checks your blood pressure during the
test. You may be asked to breathe into a tube during the test to show how well you're
able to breathe during exercise.

If you're not exercising, your doctor will inject the drug into your IV that increases blood
flow to your heart. You might feel flushed or short of breath, just as you would if you
were exercising. You might get a headache.

You'll probably exercise on a treadmill or stationary bike, starting slowly. As the test
progresses, the exercise gets more difficult. You can use the railing on the treadmill for
balance. Don't hang on tightly, as this may skew the results.

You continue exercising until your heart rate has reached a set target or until you
develop symptoms that don't allow you to continue. These signs and symptoms may
include:

 Moderate to severe chest pain

 Severe shortness of breath

 Abnormally high or low blood pressure

 An abnormal heart rhythm

 Dizziness

 Fatigue

 Certain changes in your electrocardiogram

You and your doctor will discuss your safe limits for exercise. You may stop the test
anytime you're too uncomfortable to continue exercising.
After a stress test

After you stop exercising, you may be asked to stand still for several seconds and then
lie down for a period of time with the monitors in place. Your doctor can watch for any
abnormalities as your heart rate and breathing return to normal.

When your exercise stress test is complete, you may return to your normal activities
unless your doctor tells you otherwise.

Results

If the information gathered during your exercise stress test shows your heart function to
be normal, you may not need any further tests.

However, if the results are normal and your symptoms continue to worsen, your doctor
might recommend a nuclear stress test or another stress test that includes an
echocardiogram before and after exercise or medications to increase blood flow to your
heart. These tests are more accurate and provide more information about your heart
function, but they are also more expensive.

If your stress test results suggest that you might have coronary artery disease or show
an arrhythmia, your doctor will use the information to develop a treatment plan. You
may need additional tests, such as a coronary angiogram.

If you had a stress test to help determine treatment for a heart condition, your doctor will
use the results to plan or change your treatment.

Clinical trials

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means
to prevent, detect, treat or manage this disease.

By Mayo Clinic Staff

Myocardial Perfusion Imaging (MPI) Test

What is a myocardial perfusion imaging test?
Myocardial perfusion imaging (MPI) is a non-invasive imaging test that shows how well
blood flows through (perfuses) your heart muscle. It can show areas of the heart muscle
that aren’t getting enough blood flow. This test is often called a nuclear stress test. It
can also show how well the heart muscle is pumping.

There are 2 techniques for MPI: single photon emission computed tomography
(SPECT) and positron emission tomography (PET).

MPI is useful in patients with chest discomfort to see if the discomfort comes from lack
of blood flow to the heart muscle caused by narrowed or blocked heart arteries
(angina). Myocardial perfusion imaging doesn’t show the heart arteries themselves, but
can tell your doctor with good certainty if any heart arteries are blocked and how
many. MPI can also show if you’ve previously had a heart attack.

Depending on circumstances, for example if you have chest pain and an abnormal MPI
study, the next step may be performing a coronary angiogram (PDF). On the other
hand, if the MPI study is normal, your doctor can confidently look into other causes of
chest pain that aren’t related to the heart.

Quick facts

 An MPI test examines blood flow through your heart during exercise on a
treadmill or exercise bicycle (“physical stress”) and while you rest. If you can’t
exercise well, you’ll get a medicine (“chemical/pharmacologic stress”) to increase
the blood flow to your heart muscle as if you were exercising.
 The test uses radioactive material called tracers. Tracers mix with your blood and
are taken up by your heart muscle as the blood flows through your heart arteries.
 A special “gamma” camera takes pictures of your heart to show how well your
heart muscle is perfused (supplied with blood)
 The pictures will help your doctor see if your heart muscle is getting enough
blood, or if blood flow is reduced to parts of the heart muscle because of
narrowed arteries. MPI can also tell if there are areas of dead cells (scars) from a
past heart attack. Some forms of MPI can also tell your doctor if portion of the
heart muscle that aren’t working well after a heart attack have a chance of going
back to normal if a coronary stent is place or bypass surgery is done (“viability
imaging”)
 The amount of radiation you get from an MPI test is small.

Why do people have MPI tests?

An MPI test shows how well blood flows through your heart muscle. If the test shows a
lack of blood flow during exercise or stress, but is normal at rest, it could mean that an
artery that carries blood to your heart is narrowed or blocked. If the test shows a lack of
blood flow to a portion of the heart muscle during exercise or stress and at rest, it could
mean that your heart muscle is scarred, possibly from a past heart attack.

MPI tests can help your doctor:

 Find out if there are narrowings or blockages in your coronary (heart) arteries if
you have chest discomfort
 If you have heart damage from a heart attack if your heart is not working normally
 Determine if you should undergo a coronary angiogram
 Decide whether you would benefit from coronary stent or bypass surgery to treat
your chest discomfort or help an abnormal pumping function go back to normal
 If a heart procedure you had to improve blood flow (stent, bypass) is working
 How well your heart can handle physical activity

What are the risks of an MPI test?

MPI tests are generally safe for most people. MPI studies expose you to a low dose of
X-rays. Experts disagree if X-rays at such low doses can cause cancer, but the
possibility exists that no dose of X-rays, however low, is completely safe. Don’t take the
test if your risk for a heart attack is low, or if there is no other reason (chest discomfort)
to think that you have heart trouble. If you’re pregnant or think you might be pregnant, or
if you’re a nursing mother, tell your doctor before you have this test. It could harm your
baby.

How do I prepare for my MPI test?

 Tell your doctor about any medicines you take, including over-the-counter
medicines, herbs and vitamins. He or she may ask you not to take them before
the test. Don’t stop taking your medicine until your doctor tells you to.
 Your doctor may also ask you not to eat certain foods, such as caffeine-
containing beverages (i.e. coffee, tea, soft drinks) or chocolate, for 24 hours
before your test. The test may have to be postponed or cancelled if you did drink
caffeine.
 Don’t eat, and drink only water for 4 to 6 hours before your test.
 Wear comfortable, loose-fitting clothing and comfortable shoes to exercise in.

What happens during my MPI test?

Specially trained technicians usually perform the test in a hospital or clinic with special
equipment.

 The technician places small metal disks (electrodes) on your chest, arms and
legs. The disks have wires that hook up to a machine to record your
electrocardiogram (ECG). The ECG keeps track of your heartbeat during your
test and is used to tell the camera when to take a picture.
  You’ll wear a cuff around your arm to keep track of your blood pressure.
 The technician will put an intravenous line (IV) in your arm.
 You’ll exercise on either a treadmill or exercise bicycle
 If you cannot exercise, your IV line will be connected to a bag that has a
medicine to increase the blood flow to your heart, similar to when you exercise,
or make your heart go faster. This is called a chemical or pharmacologic stress
test. These medicines may include adenosine, dipyridamole (Persantine) or
dobutamine.
 When you reach your peak activity level, you’ll stop and receive a small amount
of radioactive material (tracer) through the IV line.
 You’ll lie still on a table for 10- 30 minutes while the gamma camera takes
pictures of your heart. Several scans are done during that time to provide
pictures of thin slices of your entire heart from all angles. It’s very important to
hold completely still with your arms above your head while the pictures are being
taken.
 During the resting part of the test, you’ll receive more tracer and another set of
pictures will be taken. This set of images will be compared to the images taken
after exercise or stress.
 Some forms of the test do not use stress or exercise, but take 2 sets of rest
images with 2 different tracers.

The test takes between 3 and 4 hours. Some labs may do the resting part of the test
first, or do the resting and exercise tests on different days.

What happens after my MPI test?

 You can usually go back to your normal activities right away.
 Drink plenty of water to flush the radioactive material from your body.
 Make an appointment with your doctor to discuss the test results and next steps.

“My doctor showed me the pictures from my test and I could see where I had a lack of
blood supply in my heart.” Mitch, age 49.

How can I learn more about a MPI test?

Talk with your doctor. Here are some good questions to ask:

 Why are you doing this test rather than a different one without radiation?
 Do you think the small possible risk of cancer related to X-rays is justified
compared to my condition and my risk of having heart trouble?
 What do I need to do to get ready for this test?
 When will I get the results of my test?
 Will I need to have more tests after this?
 What if I get chest pain or shortness of breath during the test?
 Percutaneous transluminal angioplasty (PTA) is a procedure that can open up a blocked
blood vessel using a small, flexible plastic tube, or catheter, with a "balloon" at the end of it.
When the tube is in place, it inflates to open the blood vessel, or artery, so that normal blood
flow is restored.

Percutaneous Transluminal Angioplasty

Percutaneous Transluminal Angioplasty (PTA)
What is a PTA?
Percutaneous transluminal angioplasty (PTA) is a procedure that can open up a blocked blood
vessel using a small, flexible plastic tube, or catheter, with a "balloon" at the end of it. When the
tube is in place, it inflates to open the blood vessel, or artery, so that normal blood flow is
restored.
Why is it necessary?
Fatty deposits can build up in your blood vessels, reducing blood flow and in some cases,
blocking it completely. The biggest danger from fat build up is that pieces may break off, form
clots, and cause a heart attack or stroke. The PTA can open blocked arteries and reduce these
risks.
How is it done?
The radiologist will insert a balloon-type catheter into an artery in your groin or arm. The doctor
will inflate the balloon several times, for about one minute each time, in order to "push" the fatty
deposits against the artery wall. The technologists working with the doctor will take X-ray
pictures to make sure the blockage is opened. When blood is flowing freely through the artery,
the balloon catheter is taken out.
What should you expect?
Before the procedure:
 The procedure may be performed immediately after your diagnostic leg arteriogram, which was used to
find the fatty build-up, or it may be done the following day.
 You may need to be admitted to the hospital for overnight observation.
During the procedure:
 The balloon catheter is guided to the exact site of the blockage. The balloon is then inflated slowly with a
pump that is filled with dye, which lets your doctor see the artery on a special monitor screen.
 The balloon may be inflated several times, 30 to 60 seconds each time, until the blockage is opened.
 You may have some discomfort when the balloon is inflated. It will go away when the balloon is
deflated. Let your the doctor know if you feel discomfort.
 The balloon is taken out and pictures are made to make sure the blood is flowing smoothly. If not, the
balloon will be used again.
 The catheter and wire are removed once the pictures show that blood is flowing well.
 A small tube called a sheath may stay in the artery, connected to a monitoring system, after the procedure
for two to four hours. In some cases, it may stay in overnight. This is to make sure the blood is flowing
smoothly.
 The procedure takes about an hour and a half.
After the procedure:
 You may go to the recovery area or to your hospital room.
 You must lie flat on your back while the sheath is in place. The head of the bed may be tilted up a little to
help you rest. You will be able to bend the other leg to relieve pressure on your back, or the nurse may
roll you on your side. If you feel back pain, your doctor can prescribe medication to make you
comfortable.
 When it is safe to remove the sheath, the doctor or nurse will apply pressure to the area for 20 to 30
minutes. A sand bag and dressing may be applied after this.
 You must stay in bed for another twelve hours. Within a few hours, the nurse will raise the head of the
bed a little higher for your comfort.
 Most patients go home the next day.
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Coronary artery bypass grafting (CABG) is a type of surgery that improves blood flow to
the heart. Surgeons use CABG to treat people who have severe coronary heart
disease (CHD).
CHD is a disease in which a waxy substance called plaque (plak) builds up inside the
coronary arteries. These arteries supply oxygen-rich blood to your heart.

Over time, plaque can harden or rupture (break open). Hardened plaque narrows the
coronary arteries and reduces the flow of oxygen-rich blood to the heart. This can cause
chest pain or discomfort called angina (an-JI-nuh or AN-juh-nuh).

If the plaque ruptures, a blood clot can form on its surface. A large blood clot can
mostly or completely block blood flow through a coronary artery. This is the most
common cause of a heart attack. Over time, ruptured plaque also hardens and narrows
the coronary arteries.

CABG is one treatment for CHD. During CABG, a healthy artery or vein from the body is
connected, or grafted, to the blocked coronary artery. The grafted artery or vein
bypasses (that is, goes around) the blocked portion of the coronary artery. This creates
a new path for oxygen-rich blood to flow to the heart muscle.

Surgeons can bypass multiple coronary arteries during one surgery.

hat is robotically-assisted heart surgery?

Robotically-assisted heart surgery, also called closed-chest heart surgery, is a type

of minimally invasive heart surgery performed by a cardiac surgeon. The surgeon uses
a specially-designed computer console to control surgical instruments on thin robotic
arms.

Robotically-assisted surgery has changed the way certain heart operations are being
performed. This technology allows surgeons to perform certain types of complex heart
surgeries with smaller incisions and precise motion control, offering patients improved
outcomes.

Types of robotically assisted heart surgeries:

 Mitral valve repair

 Tricuspid valve repair (with mitral valve repair)
 Atrial septal defect (ASD) repair
 Patent foramen ovale (PFO) repair
 Removal of cardiac tumors (Myxoma, Fibroelastoma)

Who is a candidate for robotically assisted heart surgery?

Diagnostic tests are performed to determine if you are an appropriate candidate for
robotically-assisted surgery, including a cardiac catheterization and chest x-ray. An
echocardiogram and/or a computed tomography scan also may be required to provide
more information about your medical condition.
Your surgeon will review the results of these diagnostic tests to determine if you are an
appropriate candidate for robotically-assisted surgery. The type of treatment
recommended for your condition will depend on several factors, including the type and
severity of heart disease, your age, medical history and lifestyle.

Next: Procedure Details

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What is robotic cardiac surgery?

Robotic cardiac surgery is heart surgery done through very small cuts in the chest. With
the use of tiny instruments and robot-controlled tools, surgeons are able to do heart
surgery in a way that is much less invasive than open-heart surgery. The procedure is
sometimes called da Vinci surgery because that is the name of the manufacturer of the
robot often used for this procedure.

Robotic surgeries have been used for a number of different heart-related procedures,
including valve surgery, coronary artery bypass, cardiac tissue ablation, heart defect
repair, and tumor removal.

Why might I need robotic cardiac surgery?

The main benefit of robotic cardiac surgery is that it is minimally invasive compared with
open-heart surgery. Smaller incisions mean that you can heal faster and return to
activities more quickly.

Your healthcare provider may recommend robotic cardiac surgery if you need an artery
bypass procedure to improve blood flow to the heart. It may also be used to:

 Repair or replace stiff or leaky heart valves

 Correct atrial fibrillation, a common type of arrhythmia
  Remove a tumor in the heart
 Treat congenital heart conditions

Your healthcare provider may have other reasons to recommend robotic cardiac
surgery.

What are the risks of robotic cardiac surgery?

One of the main benefits of robotic cardiac surgery is that it has fewer risks than open-
heart surgery. The surgeon does not have to cut through the breastbone to open your
chest. This removes many of the complications of open-heart surgery.

Robotic cardiac surgery still requires anesthesia and, as with any kind of surgery, there
are always risks involved, including:

 Heart attack
 Stroke
 Infection
 Death

In some cases, your doctor may not be able to complete the surgery with the robot. In
this case, you would need open-heart surgery.

You may have other risks, based on your specific medical condition. Be sure to talk with
your healthcare provider about any concerns you have before your procedure.

How do I get ready for robotic cardiac surgery?

To see if you are a good candidate for this procedure, your healthcare provider will
review your medical history, and lifestyle, as well as the overall severity of the disease.

 Your healthcare provider will explain the procedure and you can ask questions.
  You will be asked to sign a consent form that gives permission to do the
procedure. Read the form carefully and ask questions if something is unclear.
 Along with a complete medical history, your healthcare provider(s) may do a
physical exam to ensure you are in otherwise good health before you undergo
the procedure. You may also have blood tests and other diagnostic tests.
 Your healthcare provider(s) may recommend taking an aspirin before the
procedure.
 If you are pregnant or think you may be, tell your healthcare provider(s).
 Tell your healthcare provider(s) if you are sensitive to or are allergic to any
medicines, latex, iodine, tape, contrast dyes, and anesthetic agents (local or
general).
 Tell your healthcare provider(s) of all medicines (prescribed and over-the-
counter) and herbal supplements that you are taking.
 Tell your healthcare provider(s) if you have a history of bleeding disorders or if
you are taking any anticoagulant (blood-thinning) medicines, aspirin, or other
medicines that affect blood clotting. You may need to stop these medicines
before the procedure.
 Tell your healthcare provider(s) if you have a pacemaker or other implanted heart
device.
 If you smoke, stop smoking as soon as possible before the procedure. This will
improve your chances for a successful recovery from surgery and your overall
health status.
 You will be asked to fast for 8 hours before the procedure, generally stopping
eating, drinking, or any oral medicines after midnight

Based on your medical condition, your healthcare provider(s) may request other specific
preparation.

What happens during robotic cardiac surgery?

The following is the general sequence of events that will most likely occur during robotic
cardiac surgery:

 You may receive a sedative before the procedure to help you relax.
 You will be placed under general anesthesia for the procedure and you will have
a breathing tube.
 A surgeon will make a series of keyhole-sized incisions on the side of your chest.
These incisions will align with the openings between your ribs.
 You may need to be placed on the heart-lung machine for the procedure.
  Depending on the procedure being done, your surgeon will insert several
precision-guided robotic arms into these incisions.
 These robotic arms hold and manipulate tiny instruments to do the required tasks
on the heart or surrounding arteries.
 A tiny video camera will be inserted into another incision to provide a magnified,
three-dimensional image of the operating site.
 The surgeon will control the robotic arms and camera from a console located
within the operating room.
 Once complete, the surgeon will remove the instruments and close the incisions.

Talk with your healthcare provider about what you will experience during your
procedure.

What happens after robotic cardiac surgery?

Once the surgery is done, you will be moved to the recovery area to be monitored. You
can expect a relatively short hospital stay to follow, usually half as long as that
after conventional open-heart surgery. Your healthcare provider will typically discharge
you once your pain is under control, you can keep liquids down without nausea and
vomiting, and your lab tests appear near normal or near your baseline before the
procedure.

You can also expect less scarring on your chest. Open-heart surgery may leave a 10-
inch scar on your chest. Robotic cardiac surgery just leaves a few smaller scars on the
side of your chest.

After being discharged from the hospital, most people can manage their pain with over-
the-counter pain relievers like acetaminophen or ibuprofen. Pain also tends to go away
much faster than with open-heart procedures.
Keep your incisions clean and dry. Do not use powders, lotions, or ointments on the
incision lines as this can irritate the skin and cause prolonged healing and increase the
risk for infection. Do not soak the incisions in water until your doctor says it's OK.

Make plans to have someone give you a ride home from the hospital.

You may also return to normal activities more quickly than you would after open-heart
surgery. Most people can resume their normal activities after a few weeks. Your
healthcare provider will provide specific recommendations for activity.

Your healthcare provider will typically schedule follow-up appointments to check your
progress. Be sure to tell your healthcare provider right away if any symptoms occur after
the procedure, such as chest pain or discomfort. Complications are rare after robotic
heart surgery, but possible, so it is important to carefully monitor for any symptoms and
report them to your healthcare provider.

Remember to take all or your medicines as prescribed.

Next steps
Before you agree to the test o

What is off-pump CABG?

Coronary artery bypass surgery, commonly known as CABG, is a type of heart surgery.
Surgeons perform this type of surgery to bypass blockages in the coronary arteries. An
“off-pump CABG” is a CABG performed without the use of a heart-lung machine
(cardiopulmonary bypass). This means the heart continues to provide blood to the rest
of the body during the surgery. It is sometimes referred to as “beating heart surgery.” In
another method used during surgery, a machine takes over the functions of the heart
and the lungs and the heart is still.

The coronary arteries deliver nutrients and oxygenated blood to the heart.
Atherosclerosis is a disease that can cause hardened plaque to build up in the coronary
arteries. This plaque narrows the arteries over time. This can limit the flow of blood to
the heart and cause chest pain (angina). The plaque can also make blood clots more
likely to form. These clots may completely block the blood flow through one of the
arteries and cause a heart attack.

Off-pump CABG is one of the procedures that surgeons use to restore blood flow to the
coronary arteries. The surgeon takes an artery or a vein from another place in the body.
The surgeon then uses the vessel to “bypass” the blocked part of the vessel and restore
normal blood flow to the heart. Your healthcare provider may plan the surgery in
advance, or you might need it in an emergency if a vessel suddenly becomes blocked.
Sometimes surgeons perform off-pump CABG with the traditional, standard surgical
approach. In this type of CABG, the surgeon makes a large cut down the front of the
chest through the breastbone (sternotomy). Recently, some surgeons have started
using smaller incisions to perform off-pump CABG. In this case, the surgeon makes a
much smaller incision through the ribs to perform the surgery. This is a type of minimally
invasive surgery. It is performed to reduce pain and recovery time.

Why might I need off-pump CABG?

If you have coronary artery disease, you may be able to manage your condition with
lifestyle changes and medicines. Sometimes, a nonsurgical procedure called coronary
angioplasty (also called coronary stenting) is a choice for some people.

If you have severe coronary artery disease, you are more likely to need coronary
angioplasty or some type of CABG surgery. These treatments can help reduce chest
pain and the risk of a heart attack as well as improve survival. It is possible that your
type of blockages will not respond as well to treatment with angioplasty. In this case,
you may need CABG surgery. Certain types of blockages may respond better to CABG
than to angioplasty. For certain people one procedure or the other is clearly the best
choice. Talk with your healthcare provider about the risks and benefits of both. Also ask
if you have any choice in which surgery to have.

Once you and your healthcare provider have decided on CABG, you will need to decide
what type of surgery is right for you. Certain types of people at high risk may be more
likely to benefit from off-pump CABG. These include people with advanced
atherosclerosis of the aorta, kidney problems, or chronic lung disease. Off-pump CABG
may reduce the risks of postoperative inflammation, infection and irregular heart
rhythms. It is important to have off-pump CABG performed by a surgeon with
experience in the approach. Different surgical centers and different surgeons may prefer
one technique over the other. Ask your healthcare provider about your risks and
benefits of CABG with or without a heart-lung machine.

What are the risks of off-pump CABG?

Off-pump CABG may provide a slightly lower risk of complications than CABG
performed with a heart-lung machine. Your particular risks will vary according to your
particular medical conditions, your age, and other factors. In the off-pump technique,
there may be a higher risk of needing another procedure to improve the hearts blood
supply in the future. Be sure to talk with your healthcare provider about any concerns
that you have.

Most people who have off-pump CABG will have a successful outcome. However, there
are some possible risks. These include:

 Infection
  Bleeding
 Irregular heart rhythms
 Blood clots leading to stroke or heart attack
 Complications from anesthesia
 Kidney failure

Certain factors increase the risk of complications. These include increased age and
other medical conditions.

How do I get ready for an off-pump CABG?

Talk with your healthcare provider about how to get ready for your upcoming surgery.
Remember the following:

 Avoid eating or drinking anything after midnight before your surgery.

 If you smoke, try to stop smoking before your operation.
 You may need to stop taking certain medicines, such as warfarin, before your
surgery.
 Follow your healthcare provider’s instructions regarding medicine use before
surgery.

You may need some routine tests before the procedure to assess your health before
surgery. These may include:

 Chest X-ray
 Electrocardiogram (EKG), to assess the heart rhythm
 Blood tests
 Echocardiogram (to assess the structure and pump function of the heart)
 Cardiac stress testing (to evaluate the blood perfusion to the heart)

If needed, someone will shave your skin above the area of operation. About an hour
before the operation, someone will give you medicines to help you relax.

What happens during an off-pump CABG?

Check with your healthcare provider about the details of your procedure. In general,
during your off-pump CABG:

 A healthcare provider will give you anesthesia before the surgery starts. This will
cause you to sleep deeply and painlessly during the operation. Afterwards you
won’t remember the operation.
 The operation will take several hours.
 Your surgeon will make an incision to remove a vessel. Often this is a vessel
taken from your chest wall or your leg.
  If you are having traditional off-pump CABG, your healthcare provider will make
an incision down the middle of your chest to separate your breastbone.
 If you are having a minimally invasive off-pump CABG, your surgeon may make
a small incision down the middle of your chest and separate part of your
breastbone. Sometimes surgeons use special instruments and a camera to do
the surgery. In this approach, your healthcare provider will make several small
holes in your chest, between the ribs. Some surgeons use robot-controlled arms
to perform the surgery.
 Your heart will keep beating during the surgery.
 Your surgeon will surgically attach the removed vessel to the aorta, the main
blood vessel going out to the body. Your surgeon will attach the other end of the
vessel to the blocked coronary artery, to bypass the blockage. An artery inside
the chest wall is typically used as the first bypass vessel of choice because it has
been shown to stay open the longest.
 Once the bypass grafts are complete, a surgery team will wire your breastbone
back together (if necessary).
 The surgery team will then sew or staple the incisions on your skin.

What happens after an off-pump CABG?

After your off-pump CABG:

 You might wake up a bit confused at first. You might wake up a couple of hours
after the surgery, or a little later.
 The surgery team will carefully monitor your vital signs, such as your heart rate.
They may hook you up to several machines to assist in monitoring these
continuously.
 You may have a tube in your throat to help you breathe. This may be
uncomfortable, and you won’t be able to talk. This will usually be removed within
24 hours.
 You may have a chest tube to drain excess fluid from your chest.
 You will feel some soreness, but you shouldn’t feel severe pain. If you need it,
you can ask for pain medicine.
 You should be able to sit in a chair and walk with help within a day or two.
 You may perform therapy to help remove fluids that collect in your lungs during
surgery.
 You will probably be able to drink the day after surgery. You can have regular
foods as soon as you can tolerate them.
 You will probably need to stay in the hospital around 5 days.

After you leave the hospital:

  Make sure you have someone to drive you home from the hospital. For a while,
you will also need some help at home.
 You will probably have your stitches or staples removed in a follow-up
appointment in 7 to 10 days. Be sure to keep all follow-up appointments.
 You may still tire easily, but you will gradually start to recover your strength. It
may be several weeks before you fully recover.
 Do not drive until your healthcare provider says it is safe for you to do so.
 Avoid lifting anything heavy for several weeks.
 Follow all the instructions your healthcare provider gives you for medicines,
exercise, diet, and wound care.
 Your healthcare provider may refer you to a cardiac rehab program to help in
rebuilding your strength after surgery.

Next steps

Acute coronary syndrome:

What you need to know
Last reviewed Fri 20 January 2017
By Brian Wu
Reviewed by Debra Sullivan, PhD, MSN, RN, CNE, COI

1. Types

2. Symptoms

3. Risk factors

4. Diagnosis

5. Treatment
Acute coronary syndrome describes a range of conditions associated with
sudden, reduced blood flow to the heart.
The blockage can be sudden and occur in one instant, or it may come and go
over a period of time.
 The condition occurs due to the buildup of fatty deposits in and on the walls of
the coronary arteries. These arteries are responsible for delivering oxygen
and nutrients to heart muscles.

Heart muscles need a steady and constant supply of oxygen-rich blood to

function. A blood clot is the most common cause of a blocked coronary artery.

Types

Angina and heart attacks are types of acute coronary syndrome.

Acute coronary syndrome is used to describe three types of coronary artery

disease:

 Unstable angina
 Non-ST-segment elevation myocardial infarction or heart attack (NSTEMI)

 ST-segment elevation myocardial infarction or heart attack (STEMI)

If the supply of oxygen to the cells becomes too low, the cells of the heart
muscles can die.

The lack of blood supply to any tissue is called ischemia. The death of the
cells results in damage to muscle tissue, and this is a heart attack or
myocardial infarction.

In some cases, the cells do not die, but damage due to an inadequate supply
of oxygen results in heart muscles that do not work correctly or efficiently. The
problem may be temporary or permanent. Unstable angina is the term used to
describe the condition when acute coronary syndrome does not lead to cell
death.

The location of the blockage, the length of time that the blood flow is blocked,
and the amount of damage that occurs determines the type of acute coronary
syndrome. Doctors classify the coronary syndromes based on:

 The presence of certain substances in the blood released by the damaged

heart

 Symptoms

 Electrocardiography (ECG) results

Proper classification is especially important when it comes to choosing the
right treatment.
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Symptoms
 Risk factors associated with acute coronary syndrome include smoking and obesity.

The signs and symptoms of acute coronary syndrome generally begin quickly,
sometimes without warning, and can alert a person that something is wrong.
Common symptoms include:

 Chest pain or discomfort

 Pain or discomfort in one or both arms, the back, jaw, neck, or stomach

 Shortness of breath

 Dizziness or feeling lightheaded

 Indigestion

 Nausea or vomiting
 Sweating
These symptoms are very serious and a person should seek emergency
treatment immediately. Chest pain caused by acute coronary syndromes can
come on suddenly without warning, which occurs during a heart attack.

In other cases, the pain can be unpredictable and get noticeably worse even
after rest, which is a symptom of unstable angina. Chest pain or discomfort is
typically the most common symptom of acute coronary syndrome, but signs
and symptoms vary depending on age, sex, and the presence of other
medical conditions.

Risk factors
There are certain risk factors associated with acute coronary syndrome that
people should be aware of. Risk factors include:

 Older age - men of 45 years or older, women aged 55 years or older

 High blood pressure or cholesterol

 Smoking

 Lack of physical activity

 Unhealthy diet, obesity, or overweight

 Diabetes

 Family history

Diagnosis
To make a quick and accurate diagnosis, a doctor will perform tests as well as
inquire about any symptoms and previous medical history. Typical tests
include:
 Electrocardiogram (ECG): This test measures the electrical activity in the
heart via electrodes attached to the skin. Abnormal or irregular impulses may
indicate poor heart function due to a lack of oxygen to the heart. Certain
electrical signal patterns may also help to indicate the location of a blockage.

 Blood tests: Certain enzymes may be detectable in the blood if cell death
results in damage to the heart tissue. A positive result indicates a heart
attack.

 Cardiac perfusion scan: This scan can show if the heart is getting enough
blood and can check areas of damage after a heart attack.
Information from these tests, as well as the actual signs and symptoms, are
used to help diagnose acute coronary syndrome and determine whether it
should be classified as a heart attack or unstable angina.

Doctors may use other tests to determine if additional treatment is needed or

if there are additional heart problems present.

Some doctors may order a person to wear a Holter monitor, which records the
heart's electrical activity for 24 hours. The monitor helps to detect whether the
person has abnormal heart rhythms or periods of inadequate blood supply
that may not have any symptoms.

Additional tests may be ordered to rule out other causes as well as help to
treat the person better.

Treatment
 Acute coronary syndrome is a medical emergency and medical attention should be sought immediately.

This is a medical emergency. Immediate treatment is ordered for acute

coronary syndrome. The short-term goals include relieving pain and improving
blood flow to help restore heart function as quickly as possible.

Long-term goals include improving overall heart function, managing risk

factors, and lowering the risk of a heart attack. Typical treatment includes a
combination of medical drugs and surgical procedures.

Medications include:

 Nitroglycerin

 Antiplatelet drugs

 Beta blockers

 Angiotensin-converting enzyme (ACE) inhibitors

 Angiotensin receptor blockers (ARBs)

 Statins
People who call the emergency services may be instructed to take or be
given aspirin in the ambulance. If medications fail to alleviate the problems
and restore proper blood function, angioplasty and stenting as well as
coronary bypass surgery may be necessary.

Lifestyle changes
In some people, acute coronary syndrome may be prevented. Heart
disease can lead directly to acute coronary syndrome, but those who do not
have heart disease can protect themselves by practicing a healthy lifestyle:

 Following a heart-healthy diet: Eating a diet that includes fruits, vegetables,

whole grains, and lean protein.

 Not smoking: Those who smoke can try medicines and counseling to help
them quit.

 Being active: Engaging in regular exercise to stay physically fit. People

should aim for moderate exercise at least 2-3 hours a week.

 Paying attention to the numbers: People should know their blood

pressure and cholesterol levels and understand what the numbers mean as
well as the optimum range.

 Maintaining a healthy weight.

 Drinking alcohol in moderation: Drinking more than one or two alcoholic

drinks per day can raise blood pressure.
People who have had problems such as a heart attack in the past may also be
instructed to take one baby aspirin in addition to their daily medication. Aspirin
helps to prevent platelets from forming clots and helps to reduce the risk of a
second heart attack by around 22 percent.
With lifestyle changes and the right medication, it is possible to prevent acute
coronary syndrome or to treat it and lead a normal life.

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