MYOCARDIAL INFARCTION AND OTHER

CORONARY ARTERY DISEASE ISSUES

INTRODUCTION

Patients infected with the virus SARS-CoV-2 and its clinical disease COVID-19 are
often minimally symptomatic or asymptomatic. More severe presentations include
pneumonia and acute respiratory distress syndrome.

In some patients, the heart may be affected, and this can occur in individuals with or
without a prior cardiovascular diagnosis. Evidence of myocardial injury, as defined as
an elevated troponin level, is common among patients hospitalized with COVID-19,
with putative causes including stress cardiomyopathy, hypoxic injury, ischemic injury
(caused by cardiac microvascular damage or epicardial coronary artery disease), and
systemic inflammatory response syndrome (cytokine storm). A minority of patients with
an elevated troponin level present with symptoms and signs suggestive of an acute
coronary syndrome. (See "Coronavirus disease 2019 (COVID-19): Myocardial
injury" and "Diagnosis of acute myocardial infarction", section on 'Clinical
manifestations' and "Clinical manifestations and diagnosis of cardiogenic shock in acute
myocardial infarction", section on 'Clinical presentation' and "Approach to diagnosis
and evaluation of acute decompensated heart failure in adults", section on 'Clinical
manifestations'.) 

Patients with cardiovascular disease, hypertension, obesity, and diabetes are at increased
risk of a poor prognosis. In addition, patients with myocardial injury, irrespective of
cause, have a poorer prognosis.

This topic will address our approach to the diagnosis and management of patients with
either an acute coronary syndrome or stable coronary artery disease (CAD) who are
suspected of or who have confirmed COVID-19 infection. Our approach and
recommendations only apply during the pandemic and are superseded by routine care
thereafter.

EPIDEMIOLOGY

The prevalence of CAD in particular, and cardiovascular disease in general, varies from
population to population. Thus, among patients who are diagnosed with COVID-19,
there is a broad range for prevalent CAD. Rates between 4.2 and 25 percent have been
reported, with most series from China [1-5]. Among patients admitted to intensive care
units or those who died [5], the percent is higher. 

The frequency of myocardial injury (as reflected by elevation in cardiac troponin levels)
is variable among hospitalized patients with COVID-19, with reported frequencies of 7
to 28 percent. (See "Coronavirus disease 2019 (COVID-19): Myocardial injury", section
on 'Prevalence'.)
Decline in hospitalization rates — Multiple studies have found that the incidence of
hospitalization for acute myocardial infarction (MI) and admissions for most diagnoses
have decreased by as much as 40 to 50 percent during the pandemic [6-10]. The
following two large studies are representative:
●A study from Northern California compared weekly incidence rates of
hospitalization for acute MI (ST-elevation MI [STEMI] and non-ST-elevation MI
[NSTEMI]) before and after March 4 th, 2020, when the first reported death from
COVID-19 occurred in Northern California [8]. These data were also compared
with data from the same time period in 2019. The weekly rates of hospitalization
decreased by about 48 percent during the COVID-19 period (during the period of
January 1st to March 3rd, 2020, the incidence rate was 4.1 per 100,000 person-weeks
and from April 8th to April 14th, the incidence rate was 2.1 per 100,000 person-
weeks [incidence rate ratio 0.52, 95% CI 0.40-0.68]). This decrease occurred in
patients with NSTEMI (incidence rate ratio 0.51, 95% CI 0.38-0.68) and probably
in patients with STEMI (incidence rate ratio 0.60, 95% CI 0.33-1.08). Compared
with 2019, the incidence of hospitalization for acute MI was significantly lower in
2020 only after March 4th, demonstrating that the decrease could not be explained
by seasonal variation. 
●A study from Italy compared admissions for acute MI to coronary care units from
March 12th to 19th in 2020 with those during the equivalent week in 2019 [9]. There
was a 49.4 percent reduction (p<0.001 percent), and the reduction was significant
for both STEMI and NSTEMI. The STEMI case fatality rate was higher,
comparing 2020 with 2019 (risk ratio 3.3, 95% CI 1.7-6.6). 

Possible explanations for the decreased hospitalization rate include patient fear of being
infected if hospitalized (avoidance of medical care) and a redistribution of health care.

IMPACT ON THE CARDIOVASCULAR SYSTEM

It is likely that COVID-19 directly and indirectly affects the cardiovascular system and
the heart in particular. Potential mechanisms of cardiovascular injury have been
identified and include direct myocardial injury from hemodynamic derangement or
hypoxemia, inflammatory myocarditis, stress cardiomyopathy, microvascular
dysfunction or thrombosis due to hypercoagulability, or systemic inflammation
(cytokine storm), which may also destabilize coronary artery plaques [11]. Pneumonia
and influenza infections have been associated with sixfold increased risk of acute MI
[12-14]. Patients with severe COVID-19, such as those with high fever or hypoxia due
to lung disease, may need a significant increase in cardiac output. Type II myocardial
ischemia, therefore, may result in patients with obstructive CAD. (See "Diagnosis of
acute myocardial infarction", section on 'Definitions'.) 

The clinical impact of SARS-CoV-2 infection will, across a population, be greater in

those with prior disease and increasing age. In one study, patients with prior
cardiovascular disease made up 22.7 percent of all fatal cases, and the case fatality rate
was 10.5 percent [15]. 
 ASSOCIATION BETWEEN BASELINE CVD AND COVID-

There is substantial evidence of an association between cardiovascular disease (CVD)

risk factors of hypertension, diabetes, prior CAD, and the risk and severity of COVID-
19 infection [2,3,16-19]. (See "Coronavirus disease 2019 (COVID-19): Clinical features
and diagnosis", section on 'Risk factors for severe illness'.)

The following two observational studies illustrate the magnitude of the relationship:

●In a report from the Chinese Center for Disease Control and Prevention, 72,314
cases (44,672 confirmed) reported by February 11, 2020 were reviewed [20]. The
crude mortality rate was 2.3 percent. For age over 80, the case fatality rate was
14.8 percent. History of coronary heart disease (CHD) was present in 4.2 percent
of all cases, but in 22.7 percent of fatal cases. Case fatality rates were 10.5 percent
for CHD, 7.3 percent for diabetes, and 6 percent for hypertension. Another report
evaluated 1099 cases from 30 provinces within mainland China [19]. Of these,
15.7 percent were classified as severe, and 6.1 percent had a primary endpoint,
defined as intensive care unit admission, mechanical ventilation, or death. The
presence of diabetes (severe versus nonsevere disease, 16.2 versus 5.7 percent;
primary endpoint versus no primary endpoint, 26.9 versus 6.1 percent),
hypertension (23.7 versus 13.4 percent; 35.8 versus 13.7 percent), or CHD (5.8
versus 1.8 percent; 9 versus 2 percent) was significantly more frequent among
patients with severe disease versus nonsevere disease and with a primary endpoint
versus no primary endpoint. In a report of 191 patients from Wuhan province who
were diagnosed before January 31, 2020, there were significant univariate
associations with death outcome for diabetes (31 versus 14 percent, p = 0.005),
hypertension (48 versus 23 percent, p = 0.0008), and CHD (24 versus 1 percent,
p<0.0001) [3]. In a multivariable analysis, only advancing age, Sequential Organ
Failure Assessment Score, and D-Dimer were associated with mortality. 
●Another study found that the presence of acute injury determined by troponin
elevation was a significant factor in the association of CVD and mortality [21]
(see 'Troponin' below). Among 187 patients with confirmed COVID-19, a history
of CVD (defined as CHD, hypertension, or cardiomyopathy) was present in 66 (35
percent), and troponin was elevated in 52 (28 percent). Troponin elevation was
more frequent in patients with CVD (55 percent, 36 of 66). Among patients with
CVD and elevated troponin, the mortality rate was 69 percent (25 of 36). The
mortality rate was 7.6 percent among patients without CVD and normal troponin,
13.3 percent among those with CVD and normal troponin, 37.5 percent among
those without CVD and elevated troponin, and 69.4 percent among those with
CVD and elevated troponin. Furthermore, troponin elevation correlated with
elevations in C-reactive protein, and higher troponin elevations predicted higher
mortality. Although the number of patients included limits to interpretation, there
is a suggestion that patients with underlying CVD (including hypertension) are
both at increased risk for acute injury and worsened survival in the setting of
injury. The cause of this association and whether injury indicates increased risk for
MI or myocarditis will require additional investigation. 

Until more data with larger numbers of patients are available, it seems reasonable to
consider all patients with history of CVD, hypertension, or diabetes at higher risk. We
consider this risk likely to be highest for patients with these risk factors, older age,
known history of heart failure, or clinically significant valvular disease. For now, there
are no specific measures based on this risk stratification, but we advise all of our
patients with these risk factors to be especially cautious regarding public health
measures of social distancing, including with close family members. Furthermore, given
the association with more severe disease and increased risk for acute myocardial injury,
we advise early clinical evaluation for any suspect symptoms.

ACUTE CORONARY SYNDROME PATIENTS

Definitions — The term acute coronary syndrome (ACS) is applied to patients in whom

there is a suspicion or confirmation of myocardial injury. ACS patients may have either
STEMI or non-ST-elevation ACS, which includes NSTEMI or unstable angina.
According to the Fourth Universal Definition of MI (see "Diagnosis of acute myocardial
infarction", section on 'Definitions'), the term acute MI should be used when there is
acute myocardial injury with clinical evidence of acute myocardial ischemia and with
detection of a rise and/or fall of cardiac troponin values with at least one value above
the 99th percentile upper reference limit and at least one of the following [22]:
●Symptoms of myocardial ischemia.
●New ischemic ECG changes. (See 'Diagnosis and differential diagnosis' below.)
●Development of pathological Q waves.
●Imaging evidence of new loss of viable myocardium or new regional wall motion
abnormality in a pattern consistent with an ischemic etiology.
●Identification of a coronary thrombus by angiography or autopsy (not for type 2
or 3 MI).

The Fourth Universal Definition of MI includes a clinical classification according to the

assumed proximate cause of the myocardial ischemia:

●Type 1: MI caused by acute atherothrombotic CAD and usually precipitated by

atherosclerotic plaque disruption (rupture or erosion).
●Type 2: MI consequent to a mismatch between oxygen supply and demand.

With COVID-19 infection, the majority of MIs are type 2 and related to the primary
infection, hemodynamic, and respiratory derangement. As such, the primary disorders
should be treated, and in most cases the patient can be treated conservatively with
regard to coronary disease. If a type 1 infarction is thought to be the primary etiology of
the MI, standard therapies can be considered. (See "Overview of the acute management
of non-ST elevation acute coronary syndromes" and "Overview of the acute
management of ST-elevation myocardial infarction".)

Clinical manifestations — The vast majority of patients presenting with a systemic

illness consistent with COVID-19 will not have symptoms or signs of CAD. Patients
may be tachycardic (with or without palpitations) in the setting of other illness-related
symptoms. 

In patients with COVID-19, the clinical manifestations of acute CAD are likely similar
to those without the virus. (See "Diagnosis of acute myocardial infarction", section on
'Clinical manifestations'.)
Few patients hospitalized with COVID-19 have complained of chest pain on admission,
but the true prevalence and characteristics of chest pain among COVID-19 patients are
unknown [1,23].

Physicians report that there are fewer ACS patients presenting to the hospital during the
pandemic (see 'Epidemiology' above). In addition, there is concern that patients with
ACS are presenting later to emergency departments or not coming at all due to fear of
exposure to patients with COVID-19. These patients will suffer unnecessary morbidity
and mortality without proper ACS management. Health care providers should make
every effort to persuade patients with complaints suggestive of ACS to seek proper
evaluation while ensuring that appropriate screening and protection are available to
avoid patient and provider concerns regarding nosocomial spread of the infection. If
admitted, it is prudent to screen all patients for symptoms of COVID-19 (eg, fever,
cough, dyspnea, sore throat, gastrointestinal disturbance) regardless of the primary
complaint. (See "Coronavirus disease 2019 (COVID-19): Clinical features and
diagnosis", section on 'Clinical manifestations'.)

The pandemic varies in terms of intensity between regions. There are epicenters with
extreme COVID-19-associated disease burden, whereas other areas continue to see
more regular ACS and only rarely COVID-19 patients. 

Assessment of COVID-19 status — ACS patients with unknown COVID-19 status are

treated as potential COVID-19 patients since aerosolization during intubation or
cardiopulmonary resuscitation in the catheterization laboratory is possible. 

Testing for COVID-19 is recommended for NSTEMI patients who are stable prior to
transfer or catheterization. 

ST-elevation myocardial infarction — Irrespective of COVID-19 status, urgent or

emergent diagnosis and treatment are essential to improve outcomes in patients with
STEMI. Patients calling the health care system with ischemic-type chest pain or anginal
equivalent should be urged to present to an emergency department. (See 'Acute
coronary syndrome patients' above.)

Patient and health care system factors have led to delays in the presentation of patients
with STEMI. Later presentation has likely led to worse outcomes [24].

There have been reports of increased coronary artery thrombus burden in patients with
STEMI [24]. This is consistent with an increased frequency of thrombotic strokes,
particularly in young people, during the pandemic. Alterations in the coagulation
system, abnormal platelet function, or abnormal endothelial function have been
postulated [25]. (See "Coronavirus disease 2019 (COVID-19): Hypercoagulability".) 

Our approach to ST-elevation myocardial infarction — Our approach, which is

summarized below, is generally in agreement with a provided algorithm (algorithm 1).
The only way in which we differ slightly from the algorithm is that if we think STEMI
with an occluded vessel is more likely than not, and that the benefit of a confirmed open
artery is likely to impact overall recovery, we favor primary PCI.

The following bullets summarize information contained in the next two sections.
(See 'Diagnosis and differential diagnosis' below and 'Management' below.)
For COVID-19 patients or those under investigation [26]:

●In patients who are critically ill due to COVID-19 infection (eg, acute respiratory
distress syndrome multiorgan failure), the decision to reperfuse (with either
primary PCI or fibrinolysis) or not should be managed on a case-by-case basis. 
●If the patient is not critically ill, we attempt reperfusion, and we perform primary
PCI rather than fibrinolysis in most cases, similar to patients without COVID-19.
(See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy",
section on 'Primary PCI preferred to fibrinolysis'.)
In some circumstances, available local resources and the ability to protect the staff
from infection also need to be taken into account. Some centers have chosen to
administer fibrinolytic therapy in eligible patients [24]. 
●Irrespective of COVID-19 status, we mask all patients and we use personal
protective equipment for all staff.

Diagnosis and differential diagnosis — The diagnosis of STEMI is normally not

difficult. However, during the pandemic, alternative causes of myocardial injury (such
as stress [Takotsubo] cardiomyopathy or myocarditis) are important to consider (table
1). 

STEMI usually requires that the patient have chest pain or anginal equivalent
symptomatology and ECG characteristics that include ST-segment elevation in at least
two contiguous leads (see "Diagnosis of acute myocardial infarction", section on 'ST-
elevation'):

●New ST-segment elevation at the J-point in two contiguous leads with the cut-
points: ≥0.1 mV in all leads other than leads V2 to V3. 
●For leads V2 to V3: ≥2 mm in men ≥40 years of age, ≥2.5 mm in men <40 years
of age, or ≥1.5 mm in women regardless of age.
●In the absence of ST elevation on ECG, new left bundle branch block with
anginal symptoms is considered to be a STEMI equivalent.

However, ECG criteria are not specific for coronary artery thrombosis, particularly in
COVID-19 patients in whom ST elevation may occur with stress cardiomyopathy or
possibly myocarditis. Thus, noncoronary artery COVID-19-associated myocardial
injury needs to be carefully considered as a diagnostic possibility before reperfusion
therapy is considered. In most patients with ST elevation, the diagnosis will be
thrombotic occlusion of a coronary artery. (See "Coronavirus disease 2019 (COVID-
19): Myocardial injury".) 

For patients with an elevated troponin and suspected STEMI, echocardiography is not
generally used to identify which patients need emergent angiography since we believe
the vast majority of patients require angiography regardless of echocardiographic
findings. (See 'Echocardiography' below.)

Management — For STEMI patients who are known to not be infected with the virus,
we manage them with the usual approach of primary PCI except that we mask all
patients. If myocarditis seems more likely than STEMI (see 'Diagnosis and differential
diagnosis' above), we suggest a conservative approach with aspirin and heparin
administration until the diagnosis becomes clearer. 
For confirmed cases or COVID-19 status under investigation in patients with STEMI,
there are two important early management questions: 

●Does the patient have a life-threatening (critical) illness, such as respiratory

failure from COVID-19, that makes them a less-than-ideal candidate for
reperfusion? Practitioners typically asked this question before revascularization in
all patients prior to the pandemic. During the pandemic, it is an essential question.
●During the pandemic, should fibrinolytic therapy be used more liberally as the
choice for early reperfusion? 

With regard to the first issue, the harm associated with pursuing reperfusion therapy
may exceed the anticipated gain in some COVID-19 patients, particularly if the primary
competing illness portends a poor outcome. As is true for all patients with STEMI,
comorbidities, size of infarction, delay to presentation, and hemodynamic status must be
considered when determining if reperfusion therapy will be employed.

Regarding the second issue, and with the understanding that PCI is generally preferred
to fibrinolytic therapy, some experts have raised the possibility that a more liberal use of
fibrinolytic therapy (than what is normally recommended) may be necessary in some
settings due to resource utilization and risk of viral exposure for health care providers.
(See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy",
section on 'Summary and recommendations'.)

The argument, in part, is that there will be less viral exposure to the catheterization
laboratory staff. It should be recognized, however, that fibrinolysis may not reduce
resource utilization during the pandemic since the majority of patients receiving
fibrinolytic therapy will still require coronary angiography at some point during
hospitalization, usually within 3 to 24 hours as part of a pharmacoinvasive or rescue
strategy for fibrinolysis failure. These patients will require monitoring in an intensive
care unit, thereby utilizing a scarce resource and prolonging length of stay. Furthermore,
there are some patients who may be exposed to the risk of bleeding from fibrinolysis,
specifically intracranial hemorrhage, in the setting of myocarditis, and some may not
realize the benefit of myocardial salvage in the context of a competing life-threatening
illness or small territory at risk. As such, we continue to prefer PCI as the reperfusion
strategy during the COVID-19 pandemic. Nevertheless, the decision must be considered
in the larger context of the availability of resources within the system, as well as
important patient factors including age, infarct location, and duration of symptoms that
influence fibrinolysis efficacy, bleeding risk, and the chances of substantial myocardial
salvage.

When deciding between primary PCI and fibrinolytic therapy, factors such as significant
associated comorbidities and hospital resource limitations should be taken into account.
For example, a patient with COVID-19 pneumonia with respiratory failure may not be
an optimal candidate to reap the benefit of myocardial reperfusion, while a patient with
suspected COVID-19 and mild or moderate infection is likely to benefit from
myocardial salvage, and if the resources are available, then reperfusion should be
performed despite the risk to providers and the resources required.

Irrespective of the initial reperfusion strategy, we treat all STEMI patients with
early aspirin, P2Y12inhibitor, and anticoagulation. High-dose statin is started as soon as
possible after the diagnosis.
Non-ST-elevation myocardial infarction — NSTEMI patients require urgent
management but generally do not require a catheterization laboratory emergently
(see "Non-ST elevation acute coronary syndromes: Revascularization", section on
'Timing'). In the face of resource limitation during the COVID-19 pandemic, any
decision to proceed with an invasive strategy should take into account current health
care resources. In some geographies, cardiac catheterization laboratories have been
converted to intensive care units.

For patients in whom medical therapy is likely to lead to a worse outcome (ie, higher-
risk patients) (see "Risk stratification after non-ST elevation acute coronary syndrome",
section on 'Very high-risk patients' and "Risk stratification after non-ST elevation acute
coronary syndrome", section on 'Early risk stratification tools'), we attempt to utilize the
catheterization laboratory. 

We perform urgent catheterization on NSTEMI patients for reasons such as ongoing

evidence of myocardial ischemia (eg, repetitive episodes of angina or dynamic ECG
changes, ventricular arrhythmias, or heart failure). 

Other complications have included arrhythmias and shock. In one study, these were
reported in 17, 7, and 9 percent of patients, respectively [1]. In a series of 21 severely ill
patients admitted to the intensive care unit in the United States, one-third developed
cardiomyopathy [27]. 

Diagnosis uncertain — Where there is uncertainty as to whether the individual has an

ACS due to plaque rupture, combined use of clinical evaluation and ECG is usually
sufficient to make a decision. (See "Evaluation of emergency department patients with
chest pain at low or intermediate risk for acute coronary syndrome" and "Initial
evaluation and management of suspected acute coronary syndrome (myocardial
infarction, unstable angina) in the emergency department".) 

Consultation with a cardiologist is suggested for cases where the diagnosis remains
uncertain.

Echocardiography — Among patients with COVID-19 with suspected ACS, the role

of echocardiography in altering the pretest probability of CAD is limited to low- or
intermediate-risk patients. In patients with COVID-19, an echocardiogram may be
performed if requested by a consulting cardiologist and if it is expected to have a
significant impact on management or is likely to change the patient's prognosis.
(See "Noninvasive testing and imaging for diagnosis in patients at low to intermediate
risk for acute coronary syndrome" and "Evaluation of emergency department patients
with chest pain at low or intermediate risk for acute coronary syndrome".)

Findings on an echocardiogram that favor a condition other than ACS (eg, stress
cardiomyopathy, myocarditis, pericarditis, or noncardiac cause of chest pain) include:

●No wall motion abnormalities during chest pain

●Wall motion abnormalities not supportive of regional injury suggested by the
ECG
●Wall motion abnormalities in a noncoronary distribution
●Less specific findings, such as small pericardial effusion
It is recognized that focal wall motion abnormalities may be present in patients with
noncoronary myocardial injury and conversely that global dysfunction may accompany
ACS, and so the echocardiography cannot be the sole determinant of whether
reperfusion therapy is pursued. 

The role of echocardiography in patients with COVID-19 without suspected ACS is

discussed separately. (See "Coronavirus disease 2019 (COVID-19): Myocardial
injury".)

Cardiogenic shock — The primary disorder in the majority of patients with severe

COVID-19 infection is hypoxia-related respiratory failure. A proportion develop
systemic hyperinflammatory response and vasodilatory shock as the viremia clears. This
phase of illness may be accompanied by concomitant myocardial suppression and
cardiogenic shock. This mixed etiology of shock can be difficult to manage, particularly
if the patient has preexisting cardiovascular dysfunction. It has been observed
infrequently that more severe cardiovascular dysfunction occurs with mild respiratory
compromise and inflammation. It is possible that these patients are suffering from
myocardial injury as a manifestation of or response to the infection [28].
(See "Coronavirus disease 2019 (COVID-19): Myocardial injury" and "Definition,
classification, etiology, and pathophysiology of shock in adults", section on 'Systemic
inflammatory response syndrome (SIRS)' and "Coronavirus disease 2019 (COVID-19):
Critical care and airway management issues".)

There are anecdotal reports of patients recovering from the respiratory illness with
subsequent abrupt cardiovascular collapse. Whether this is related to an inflammatory or
some other process remains uncertain. It remains to be described whether an unchecked
inflammatory response results in these late hemodynamic sequelae. 

Other issues

Issues facing catheterization laboratory personnel — We generally agree with

approaches outlined in a report from the American College of Cardiology's
Interventional Council and the Society of Cardiovascular Angiography and Intervention
[29]. Similar protocols have been created, including one from the Interventional
Cardiology Association and Heart Rhythm Association of the Spanish Society of
Cardiology [30]. 

Efforts should be made to avoid the patient remaining in waiting areas and halls,
particularly in which staff will be directly interacting with the patient. Equipment for
PCI (eg, sheath, guiding catheter, and possibly a workhorse wire and balloon) should be
placed in the room prior to patient arrival to avoid repeated entry and exit of the staff.

We encourage training and simulation in donning and doffing personal protective

equipment (PPE), observing to monitor adherence to best practices, and reading the
proper sequences (figure 1 and figure 2) [31] (see "Coronavirus disease 2019 (COVID-
19): Critical care and airway management issues", section on 'Precautions' and 'Donning
and doffing personal protective equipment' below). We recommend daily checks to
ensure adequate PPE is available and standard checks of the "code" or "crash" cart.
There is no consensus as to whether positive-pressure catheterization rooms should be
converted to no-pressure or negative-pressure rooms. 
If resources allow, it appears prudent to designate one room for suspected/confirmed
COVID-19-positive patients, recognizing this may not be possible in some situations.
Equipment in closed cabinets is not thought to require disinfectant after a procedure that
involves a patient with established or suspected COVID-19, but only a minimal amount
of supplies and equipment should be kept in this room. Unused equipment that is not
covered, especially if the procedure involved aerosolization (eg, intubation,
transesophageal echocardiography, cardiopulmonary resuscitation [CPR]), should be
discarded or the packaging should be disinfected before additional use. The minimal
number of personnel should enter the room, with at least the operator or a nurse in the
room and a technologist in the control booth. 

Donning and doffing personal protective equipment — A reasonable sequence for

donning and doffing PPE is as follows (see "Coronavirus disease 2019 (COVID-19):
Infection control in health care and home settings"):

●Remove any personal items.

●Put on the lead apron.
●Put on a disposable gown.
●Gather the necessary PPE and check for its integrity.
●Perform hand hygiene with alcohol hand gel/rub.
●Put on the proper disposable respirator (N95 or FFP2 standard; FFP3 is available
for anesthesiologists and nurses helping with airway maneuvers).
●Put on hair cover.
●Put on shoe covers.
●Put on goggles and/or face shield, avoiding any interference with the respirator.
●Perform hand hygiene. 
●Put on the first pair of gloves.
●Put on a second gown (sterile or not, according to your role in catheterization
laboratory), not using the inside tie. 
●Put on a second pair of gloves (over cuff) (sterile if needed).

A safe doffing area should be identified in each catheterization laboratory, in particular

if no anteroom exists. If no anteroom is available, doffing of PPE could be done inside
the laboratory, at the end of procedure, and when the patient has been transferred away.
Only the facial respirator must be removed outside the contaminated area. The
following are sequential steps:

●Avoid any contact with your face, hair, and eyes before completing the entire
doffing process.
●Place any disposable PPE in the clinical waste bin.
●Do not fill the clinical waste bin more than three-fourths full in order to be able to
close it safely without squeezing contaminated materials to avoid aerosolization.
●Reprocess the non-disposable PPE.

Inside the catheterization laboratory:

●Wait until the patient is out of the room; close the door.
●Perform hand hygiene over the gloves.
●Peel off gown and gloves together and roll inside, slowly and carefully, avoiding
aerosolization.
 ●If gloves are removed separately, touch only the external part (use glove-in-glove
or beak technique).
●Perform hand hygiene (over the internal gloves).
●Remove face shield and/or goggles, avoiding contact with face and eyes, and
dispose them safely or put into a separate container for reprocessing.
●Perform hand hygiene (over the internal gloves).
●Remove hair cover and dispose it safely.
●Remove shoe covers and dispose them safely.
●Perform hand hygiene (over the internal gloves).
●Remove internal gloves and dispose them safely.
●Perform hand hygiene.
●Step out of the catheterization laboratory and immediately close the door.

Outside the operating room:

●Put on another pair of gloves

●Remove facial respirator without touching the front side of the respirator
●Remove the gloves
●Remove lead apron
●Perform hand hygiene with soap, water, and alcohol gel/rub

No guidelines have been issued that address whether health care workers exposed to
blood of COVID-19 patients should be managed any differently than usual. 

Cardiopulmonary resuscitation — A discussion of cardiopulmonary resuscitation in

COVID-19 patients is presented separately. (See "Advanced cardiac life support
(ACLS) in adults", section on 'Resuscitation of patients with COVID-19'.) 

Prognosis — Prognosis for patients with COVID-19 is worse with comorbidities such

as cardiovascular disease. In an early report from China, mortality was 10.5 percent in
patients with cardiovascular disease [32].

Mortality rates appear to increase significantly with increasing age; case fatality rates
<1 percent have been reported for those under 50 years of age, with rates approaching
15 percent for patients 80 years of age or older [16]. Similarly, mortality increases with
disease severity, as there were no deaths reported among the mild or severe cases in the
Chinese cohort, but mortality approached 50 percent among critically-ill patients [16]. 

Underlying medical comorbidities appear to significantly impact COVID-19 severity

and mortality. Patients with underlying cardiovascular disease and hypertension have
been reported to have significantly high case fatality rates compared with patients
without these underlying comorbidities (10.5 and 6 percent mortality, respectively,
compared with 0.9 percent mortality without underlying comorbidities) [16,33].

In addition, reports have found that the higher the troponin level, the worse the
prognosis. This has been generally found in other situations. (See "Troponin testing:
Clinical use", section on 'Prognosis'and "Troponin testing: Clinical use", section on
'General population'.)
 STABLE CORONARY ARTERY DISEASE PATIENTS We do

not change our usual management of CAD in patients with COVID-19 infection, with
one exception: We attempt to delay elective revascularization procedures in patients for
whom the indication is relief of symptoms. Such an approach protects the patient and
health care workers from potential viral exposure. For patients who must have
revascularization for reasons such as extremely poor quality of life or prolongation of
life, as with significant left main CAD, we test the patient for COVID-19 infection.

Decisions regarding the type of revascularization (eg, coronary artery bypass graft
surgery versus percutaneous coronary intervention [PCI]) in these patients may be
altered during the pandemic, favoring PCI as a method to shorten the duration of
exposure of the patient to the hospital environment. We encourage heart team
discussion with inclusion of the patient regarding these issues. We do not routinely test
the patient for COVID-19 infection in this setting. 

None of the usual medications for the management of CAD, such as aspirin, beta
blockers, statins, and nitrates, have been associated with worse outcomes in the setting
of COVID-19 infection. We continue angiotensin-converting enzyme inhibitors and
angiotensin II receptor blockers. This issue is discussed in detail elsewhere.
(See "Coronavirus disease 2019 (COVID-19): Management in hospitalized adults",
section on 'ACE inhibitors/ARBs'.)

Patients admitted for management of COVID-19 — Many patients admitted for

management of COVID-19 will have stable CAD. (See 'Epidemiology' above
and "Coronavirus disease 2019 (COVID-19): Management in hospitalized adults",
section on 'General management issues'.)

Electrocardiogram — All patients in whom COVID-19 is suspected should have a

baseline ECG performed at the time of entry into the hospital. Ideally, this would be a
12-lead ECG, but a single- or multi-lead ECG from telemetry monitoring may be
adequate in this situation to minimize staff exposure to the patient. This will allow for
documenting baseline QRS-T morphology should the patient develop signs/symptoms
suggestive of myocarditis or an acute coronary syndrome (ACS). Additionally, the
baseline ECG allows for documentation of the QT (and corrected QTc) interval.
Importantly, QTc will need to be monitored if QT-prolonging therapies are initiated
(eg, azithromycin, chloroquine, etc) to reduce the risk of acquired long QT syndrome.
(See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and
management" and "Coronavirus disease 2019 (COVID-19): Arrhythmias and
conduction system disease", section on 'Patients receiving QT-prolonging treatments
(eg, hydroxychloroquine, chloroquine, azithromycin)'.)

Troponin — Cardiac troponin elevation is seen in about 10 to 30 percent of

hospitalized COVID-19 patients and is associated with a higher mortality [3,21,33].
Most patients with troponin elevation and COVID-19 do not have a clinical presentation
suggestive of an ACS. (See 'Association between baseline CVD and COVID-19' above.)

The optimal use of troponin testing in hospitalized COVID-19 patients without

suspected ACS is not known. Many centers obtain a troponin soon after admission in all
patients, as it may have prognostic value and may serve as a useful baseline for
comparison in patients who subsequently develop manifestations of possible myocardial
injury (such as heart failure or arrhythmia) [34]. Other centers limit troponin testing in
this setting to patients with a specific indication (such as suspected ACS based on
clinical presentation or new onset heart failure), as the clinical value of troponin levels
has not been established, and results may lead to unnecessary use of medical resources
(eg, serial troponins, ECGs, and cardiology consultations for elevated troponin) [35].
(See "Coronavirus disease 2019 (COVID-19): Myocardial injury".)

SUMMARY AND RECOMMENDATIONS

●A relatively high percent of patients admitted with COVID-19 will have

underlying coronary artery disease (CAD). For most, symptoms of CAD will not
be present on admission. (See 'Epidemiology' above.)
●It is likely that COVID-19 directly and indirectly affects the cardiovascular
system, causing or contributing to acute coronary syndrome (ACS), myocarditis,
and electrical heart disease. (See 'Impact on the cardiovascular system' above.)
●Health care providers should make every effort to persuade patients to seek
proper evaluation if the diagnosis of ACS is considered. (See 'Acute coronary
syndrome patients' above.)
●In patients with known or suspected COVID-19, we approach the diagnosis and
management of ST-elevation myocardial infarction (MI) similar to those without.
On occasion, it is reasonable to liberalize the use of fibrinolytic therapy relative to
primary percutaneous coronary intervention. (See 'ST-elevation myocardial
infarction' above.)
●In patients with known or suspected COVID-19, we approach the diagnosis and
management of non-ST-elevation MI similar to those without. (See 'Non-ST-
elevation myocardial infarction'above.)
●We do not change our usual management of CAD in patients with COVID-19
infection with one exception: We attempt to delay elective revascularization
procedures in patients for whom the indication is relief of symptoms. (See 'Stable
coronary artery disease patients' above.)
●For hospitalized COVID-19 patients with stable CAD, some centers routinely
obtain a baseline cardiac troponin while others do not. (See 'Troponin' above.)