"

•MV ,
Diseases of Cardiovascular System 191 X: '

=*> t Q . Describe the etiopathogenesis , clinical infarction . Initially subendocardium is affected because
‘ features , diagnosis and management of this is the least supplied area. With continued ischemia
J acute myocardial infarction (STEMI) . the infarct zone extends through the subepicardial
V
myocardium , producing a transmural Q wave myocardial
• Myocardial infarction ( MI) (i.e. heart attack ) is the infarction. Areas of myocardium which are ischemic but
irreversible necrosis of heart muscle secondary to not yet undergone infarction can be salvaged by early
prolonged ischemia . This usually results from an reperfusion therapy.
imbalance in oxygen supply and demand, which is most • Microscopy shows coagulative necrosis of myocardial
often caused by plaque rupture with thrombus formation fibers that is ultimately followed by myocardial fibrosis.
in a coronary vessel, resulting in an acute reduction of
blood supply to a portion of the myocardium. Clinical Features
• Myocardial injury is reflected by elevated cardiac • In up to one-half of cases, a precipitating factor appears
1
enzymes troponin I and T, CK-MB. Two patterns of MI to be present before MI , such as vigorous physical
can be recognized based on ECG findings. exercise, emotional stress, or a medical or surgical illness.
t
• Non-STsegment elevation Ml ( NSTEMI ) : This is unstable • Patient usually presents with chest pain, located in the .

angina accompanied by elevated markers of myocardial
injury, such as troponins and CK-MB , but no ST segment
elevation in ECG.
• ST segment elevation Ml ( STEMI ): When myocardial
B injury is accompanied by both enzyme and ST segment
substernal region which frequently radiates to the neck,
left shoulder, and left arm. Chest pain of MI is more
severe than angina and lasts for more than 20 minutes.
Patient may also have dizziness, syncope, dyspnea, and
fatigue.

I elevation it is reffered to as ST segment elevation Ml • Anginal “equivalents” such as dyspnea and epigastric
( STEMI ).
.
discomfort may also occur.

I It is important to differentiate between non-ST segment

elevation MI and ST segment elevation MI because early
* recanalization therapy improves the outcome in ST
elevation MI but not in non-ST segment elevation MI.
le NSTEMI has been described along with unstable angina.
\ The following description is about STEMI.
‘g; Etiology
ro • Atherosclerosis is the disease responsible for most acute Electrocardiogram
coronary syndrome (ACS) cases including myocardial
at infarction. Approximately 90% of myocardial infarctions *
result from an acute thrombus that obstructs an
Examination may reveal diaphoresis, pale cool skin ,
tachycardia, a third and/or fourth heart sound, bilateral
basal crepitations (due to pulmonary edema) , and some-
times hypotension. A transient systolic murmur may be
heard over the apex due to ischemic dysfunction of the
mitral valve apparatus.
Investigations
EGG may be normal. If normal, it should be
rePeated every 15 minutes ECG shows ST elevation in
'

atherosclerotic coronajry artery. MI. Complete heart block, bundle branch block and
ig
• Non-atherosclerotic causes of myocardial infarction
' arrhythmias may be seen. ECG changes are seen in leads
include: Coronary occlusion secondary to vasculitis ; which correspond to the infarcted region of myocardium.
ventricular hypertrophy (e.g. idiopathic hypertrophic The presence of new ST elevation >2 mm in chest leads
1 and >1 mm in other leads suggests MI.
:or subaortic stenosis , underlying valve disease); coronary
:t artery emboli , secondary to cholesterol , air, or the
products of sepsis; congenital coronary anomalies ;
coronary trauma; coronary vasospasm; drug use (e.g .
Sr
cocaine, ephedrine) , increased oxygen requirement (such segment
^f as heavy exertion, fever, or hyperthyroidism); decreased si I :4 4H: 4-
sebment rnrr ±
rrir oxygen delivery (severe anemia, carbon monoxide ' ; : 4
i
I
posoning) ; aortic dissection, with retrograde involvement
4
- ; :
7
i5 r of the coronary arteries.

m4
.

<
Pathogenesis ;
i
• Rupture or erosion of an atherosclerotic plaque in the 4 ill
•
:::: - Ft-T tfT; it•
.

jl coronary artery induces local thrombus formation which Fig. 3.7: Normal ECG ( left ) and abnormal ECG with ST
occludes coronary artery leading to myocardial elevation ( right)

3
Diseases of Cardiovascular System

i
 0
Manipal Prep Manual of Medicine

• ECG may show pathological Q waves after a few hours Management of Myocardial Infarction
when the MI has evolved fully. Some patients may have Immediate
Measures
O
only ST elevation and may not develop Q waves ( non -Q
wave MI). Presence of Q waves suggests that Ml has • Note that time is muscle and treatment should be initiated ’erf
fully evolved and there is full thickness infarct. as early as possible. More delay means more myocardial
* New onset LBBB also suggests MI.
damage. Q'
• Oxygen by nasal prongs or face mask (2-4 liters/ min
ECG leads showing ST-T
changes
Correspond to for 6-12 hours after infarction ) .
C
• Aspirin 300 mg oral and clopidogrel 300 mg oral loading
n
• V3, V4, V5, V6
• V2, V 3
• Anterior wall Ml
• Septal Ml
dose should be given and continued at lower doses
thereafter.
o
• II, III, aVF » Inferior wall Ml
• Sublingual glyceryl trinitrate 0.4 mg. Repeat at 5 - min
intervals up to 3 doses. This relieves chest pain and
O
• I, aVL, V5, V6 • Lateral wall Ml improves coronary circulation.
• Intravenous heparin is given for all patients unless there
Biochemical Markers
is a contraindication.
• CK-MB , troponin-I and troponin-T levels are elevated • Injection morphine 2-5 mg intravenously, improves chest O
whenever there is myocardial injury (in STEM) and
NSTEMI). Troponins are more specific for myocardial
pain and controls anxiety.
• Intravenous beta blocker, e.g. metoprolol, 5 mg every ©
injury because elevated CK-MB levels may be found in B
2 to 5 mins for a total of three doses . Beta blockers
skeletal muscle damage also. New markers are becoming
decrease heart rate and sympathetic overactivity and 0
available such as myeloperoxidase and glutathione
hence reduce myocardial oxygen demand. Beta blockers
peroxidase-1.
should be avoided if PR interval is >0.24 s, 2nd or 3rd O
degree atrioventricular block is present, heart rate is
Echocardiogram
<60 beats/min, systolic blood pressure <90 mm Hg,
• Hypokinesia or akinesia of ventricular wall may be
present due to ischemia or infarction. Echocardiogram
history of asthma or COPD is present and severe left
ventricular failure is present. q
o
can assess left ventricular (LV ) function and also identify

ventricular aneurysm, pericardial effusion , and LV

thrombus. VSD and mitral regurgitation may develop in
.
the presence of right ventricular ( RV ) infarction , Reperfusion Therapy
Coronary reperfusion can be established by two ways ;
( 1 ) percutaneous coronary intervention ( PCI ) and
MI, which can be identified by echocardiogram . (2) thrombolytic therapy.

Coronary Angiography (CAG )

• It can identify the site of block and allow percutaeous
coronary intervention.
Radionuclide Imaging
* These imaging techniques are not used commonly
because they lack sensitivity and specificity and are
available in a few centers. Myocardial perfusion imaging
with thallium-201 or technetium-99m sestamibi can show
uptake defects (cold spots) due to infarction . Perfusion
scanning cannot distinguish new infarcts from old Fibrinolysis
infarcts. Radionuclide ventriculography , with • Fibrinolytic therapy reduces infarct size, limits LV
technetium-99m-labeled red blood cells, can demonstrate
wall motion disorders and reduction in the ventricular
ejection fraction in MI.
• Highest benefit is obtained if fibrinolysis is done within
Other Investigations
• Full blood count, renal function tests, serum electrolytes,
glucose, and lipid profile should be done for all patients.
3
• PCI is the treatment of choice if facilities for PCI are
available. If there are no facilities for (PCI), the patient
0
is treated with fibrinolytic therapy. O
• Patients with continued chest pain or failure to resolve
ST segment elevation by about 90 min after fibrinolysis
should be referred for rescue PCI.
• Pre-hospital treatment, including thrombolysis, can be
given by trained personnel under strict guidelines if there
is going to be significant delay before reaching the
hospital .
V
k'
dysfunction, and reduces the incidence of complications 0
'
such as septal rupture, cardiogenic shock, and malignant
ventricular arrhythmias.
1 to 3 hours of the onset of symptoms. Modest benefit is
seen if given 3 to 6 hours after the onset of infarction .
Benefit may be seen up to 12 hours if chest pain is
(
n
 Diseases of Cardiovascular System
3 persisting and ST segment remains elevated without Q
waves . Fibrinolytic agents activate plasminogen to
plasmin which breaks down the thrombus . Currently
available fibrinolytic agents include streptokinase , tissue
plasminogen activator ( tPA ) , reteplase and tenecteplase.
• Streptokinase is given in a dose of 1.5 million units as
1) intravenous infusion over 1 hour. tPA is given as 15 mg
bolus IV followed by 0.75 mg/ kg IV over 30 minutes
1 followed by 0.5 mg/kg IV over the next 60 minutes .
Streptokinase is not fibrin specific where as tPa is fibrin
specific and hence associated with less chances of
hemorrhage.
• Trials have shown that tissue plasminogen activator (tPA)
plus heparin is better than streptokinase in improving
survival as well as patency of coronary artery. Longer-
acting variants of tPA, given by single (tenecteplase) or
double bolus ( reteplase) injections, have been developed
and are more convenient to give.
i 8
The major risk of thrombolytic therapy is bleeding.
Intracerebral hemorrhage is the most serious and
frequently fatal complication.
• Note that fibrinolysis is not useful in non -ST elevation ,
MI and may be harmful .
D torsemide or spironolactone) which reduce blood volume
Table 3.24 Contraindications to thrombolysis
Absolute contraindications
• Hemorrhagic stroke or stroke of unknown origin at any
-J time and ischemic stroke in preceding 6 months
• Intracranial or spinal cord neoplasms
• Active bleeding or bleeding diathesis
• Suspected or known aortic dissection
Relative contraindications
• Severe uncontrolled hypertension (systolic blood pressure
>180 mm Hg)
• Recent major trauma/surgery/head injury (within preceding
3 weeks)
• Anticoagulation with INR >2-3
8
Old ischemic stroke
8
Oral anticoagulant therapy
8 Pregnancy or within 1 week postpartum
8
Recent non-compressible vascular punctures
• Recent retinal laser therapy
Percutaneous coronary intervention (PCI)
8
PCI includes angioplasty and/or stenting. If PCI is done
without preceding fibrinolysis, it is referred to as primary Mitral Regurgitation
PCI. It is useful for patients who have contraindications * Severe mitral regurgitation can occur early in the course
to fibrinolytic therapy, when the diagnosis is in doubt,
cardiogenic shock is present, increased bleeding risk is
present, or symptoms have been present for at least 2 to
3 hours when the clot is more mature and fibrinolytics
are less effective. Even if there are no contraindications,
193 X > -
PCI can be a treatment option because it is more effective
than fibrinolysis in opening occluded coronary arteries
and has better short- and long- term clinical outcomes.
Disadvantages of PCI are increased cost , limited
availability and requirement of experts .
Coronary artery bypass grafting (CABG )
• CABG is indicated for patients with left main stem or
triple vessel disease with impaired left ventricular
function .
Complications of Myocardial Infarction
Heart Failure
• Cardiac failure can happen after MI if significant
myocardium is damaged. The Killip classification is used
to assess patients with heart failure post - MI.
- Killip I : No crackles and no third heart sound
- Killip II : Crackles in <50% of the lung fields or a
third heart sound
- Killip III : Crackles in >50% of the lung fields
- Killip IV : Cardiogenic shock.
• Heart failure is treated with diuretics (furosemide or
and preload . Nitrates also reduce preload by venodilata-
tion without reducing blood volume. Digoxin is a positive
inotropic agent and helpful in severe heart failure.
Myocardial Rupture and Aneurysmal Dilatation
• Infarcted myocardium is weak and cannot tolerate the
pressure inside the ventricular chamber. This may lead
to rupture of the free wall of the left ventricle or
aneurysmal dilatation . Rupture is usually an early,
catastrophic and fatal event.
8
Ventricular aneurysm impairs cardiac output because
of paradoxical motion of its wall. Double, diffuse, or
displaced apical impulse is noted on physical
examination.
Ventricular Septal Defect (VSD )
8
Infarcted septum may perforate and lead to VSD. It is
common in elderly and hypertensive patients and after
delayed thrombolysis. It requires emergency surgical
repair.
of MI. Three mechanisms are responsible for mitral
regurgitation in MI, which are as follows:
- Left ventricular dysfunction and dilatation , causing
'
annular dilatation of the valve and subsequent
regurgitation.
3
Diseases of Cardiovascular System
 Manipal Prep Manual of Medicine
1 o
• Infarction of the inferior wall , producing dysfunction of • Aspirin and clopidogrel : Should be given to all patients
the papillary muscle. lifelong. Aspirin is given at a dose of 75-150 mg/day
and clopidogrel at 75 mg/day.
e
• Infarction and rupture of the papillary muscles, producing
sudden severe mitral regurgitation , pulmonary edema and • Beta blocker , e.g . metoprolol , carvedilol , atenolol . They
cardiogenic shock. decrease myocardial oxygen demand and should be given
• If there is rupture of papillary muscles emergency
surgery should be undertaken.
, to all patients with MI unless there is a contraindication
like asthma or severe LV dysfunction.
0
Cardiac Arrhythmias
• Oral nitrates , e.g. isosorbide dinitrate or mononitrate. o
o
They improve the symptoms of angina and heart failure
• Ventricular tachycardia and ventricularfibrillation ( VT and should be considered for all patients.
• ACE inhibitors , e.g . enalapril , ramipril , lisinopril,
o
and VF ) : Both are common after MI, especially after
reperfusion therapy. VF is a common cause of death after perindopril. They prevent adverse myocardial remodeling
MI in first 24 hours . Hemodynamically unstable after acute MI and reduce heart failure and death . They
( hypotension, cyanosis) VT and VF should be treated also reduce atherosclerosis progression and acute MI
with DC shock. Hemodynamically stable VT should be recurrence. All patients should be given ACE inhibitor
treated with intravenous beta blockers ( metoprolol ,
esmolol ), IV lidocaine, or IV amiodarone. Refractory
unless there is a contraindication like renal failure and
hypotension .
G
VT and VF may respond to IV magnesium sulphate. • Statins , e.g . atorvastatin , rosuvastatin , etc . LDL
• Atrial fibrillation: It is common after MI and can be cholesterol should be brought down to less than 100 mg/
treated with beta blockers and digoxin. DC shock may
also be given provided there is no clot in the heart.
dl. In addition to cholesterol lowering effect , statins also
help in plaque stabilization and regression of athero-
0
Intravenous diltiazem or verapamil can be used if there
is any contraindication to P blocker use. Amiodarone
sclerosis. Recent data show statins are effective in
secondary prevention regardless of age or baseline lipid
0
can be used daily to prevent recurrence. levels, even when the LDL is less than 100. (
• Bradyarrhythmias : These are common following MI and • Control of comorbid conditions: Like diabetes and
may be due to sinus node dysfunction and conduction hypertension help in reducing recurrent MI. For HTN,
disturbances . AV block may occur during acute MI, ACE inhibitors or p blockers are the first choice because
vr\
especially after inferior wall MI (the right coronary artery they also reduce cardiovascular mortality and morbidity
.,
!

usually supplies the S A and AV nodes). Heart block , with as described above. Angiotensin receptor blockers .

hemodynamic compromise ( hypotension ) requires
treatment with atropine or a temporary pacemaker. AV
blocks are usually transient and recover later. Permanent
pacemaker may be needed if they persist even after 2
weeks.
(ARBs) can be considered when ACE inhibitors are not
tolerated. ACE inhibitors and ARBs also reduce the long-
term complications of diabetes. Diabetes should be
strictly controlled by oral drugs or insulin or both. (

Acute Pericarditis
• Calcium channel blockers: They have negative inotropic
• It happens with large, “transmural” infarctions causing
pericardial inflammation and presents on days 2 to 4 after
MI. pericardial effusion may dev lop and cause tampo-
nade. Pericarditis developing later (2 to 10 weeks) after
acute MI may represent Dressier Is syndrome , which is
effect and are not routinely given. They may be given to
selected patients without LV dysfunction ( ejection
o
fraction greater than 40% ) who are intolerant of P V
blockers. Short acting nifedipine should be avoided as it
cause reflex tachycardia has been shown to increase
mortality rate.
* Smoking cessation : Continued smoking doubles

immune- mediated. Treatment includes aspirin or other subsequent mortality risk after acute MI and cessation
NSAIDs ( indomethacin ). Corticosteroids may be reduces risk of reinfarction and death.
required for severe pericarditis.

Post-MI Drug Therapy

Post-MI assessment o
• Extensive clinical trials have shown that many drugs
taken indefinitely by MI patients reduce the incidence
• Patients, in whom primary angioplasty has not been
performed , need to undergo exercise test to identify
residual ischemia and to determine the need for coronary
c- V

of recurrent MI and cardiovascular death. Therefore, all angiography. This can be done prior to discharge in
post-MI patients should be taking the following patients without angina or 6 weeks later. A positive test G
medications unless there are contraindications. requires diagnostic/ therapeutic coronary angiography / i

3
f

G
n
Restrictive Cardiomyopathy
Restrictive Cardiomyopathy versus Constructive Pericarditis
Dilated Cardiomyopathy
Myocarditis
Peripartum Cardiomyopathy
Drug induced cardiomyopathy

Alcohol induced cardiomyopathy

Hypertrophic cardiomyopathy
Takotsubo Cardiomyopathy
DCM Vs RCM Vs HCM
Hypotension
=
Acute renal failure
-

:-.
-

j ltydralajine
-

Large effusions comp ruin the bronchi e.

Lungs { produce dyspnea Ewart 's sign
PR
segment depression
- is characteristic of Acute pericarditis .

Normal, unless /
a w myocarditis .

Pear shaped
Cardiomegaly
for confirmation of Pericardial effusion pericarditis c- Effusion .

reserved for pt who don't respond to NSAID's .

 Transudate Hydro pericardium
Pericardial Effusion Maybe Exudate Pyopericardium
Blood Hemopericardium
 Jvp during Inspiration
.

Hallmark of cardiac Tamponade

when there is suspicion of TB .

 Tram cutaneous conventional tx
ly Approach
.

Intrapericardial
chemotherapeutic agent Effusion
in
malignant
.

Cardiac Tamponade Acute HF that Occurs as a result of Large

pericardial effusion ,
which compresses
the heart { impairs diastolic filling .

For cardiac tamponade to develop there must be

About 250mL of Fluid in rapidly developing effueiooy

More than 2000mL Fluid in slow
developing effusions

4F ,
Inu, My Same as pericardial effusion .
 Is End
stage inflammatory process involving pericardium
.

an

dlt rapid ventricular

filling
Heard in Early diastole, at lower

lateral sternal border

Pericavdectomy

Avoid p Blockers { Calcium channel Blockers

- .
 Pathology

.,-,..,., ., .,,,,Q, qb-,4?(qa,S q. 8- * r.

Hypertensive retinopathy affects precapillary arterioles and capiltaries

Vbsoconstrictive - initial response -

Classification and Clinical Features

KETTH-WAGNER.BARKER
Narrowing of retinal arterioles - arteriolar attenuation
light reflex
INormal AV diameter ratio 2:3, in Hypertensive retinopa thv
-1:3la
Grade ll Salus sign - deflection of veins at AV crossing
Grade lll Bonnet sign - banking of veins at AV crossing
Gunn signa -
tapering of veins at AV crossing
Cotton wool spotsa aqd flame shaped hemorrhagesa are
also seen
Grade lll changes (+) Papilledemaa
Malignant Hypertension - presents with retinal edemaa, cotton-wool spots, hard exudates in a macular stara configuratio:

s
&
C I4[nemonic
H Salman Khan
Kept his Gun
- nickname is Salu ) 5alus sign
-) Gunn's sign
On the Bonnet of his car

@
--) Bonnett sign