Ischemic Heart Disease

Question 1

what is the leading cause of death and disability

Answer 1

Heart Disease

Question 2

Heart Failure

Answer 2

Heart unable to pump blood sufficiently to meet needs of tissue
- Ventricle unable to fill with or eject blood
“Congestive Heart Failure”

Usually progressive condition with poor prognosis

Question 3

systolic heart failure

Answer 3

deterioration of myocardial contraction leading to an inability to pump blood (thin, weakened heart muscle)

Question 4

Diastolic heart failure

Answer 4

Inability of heart chamber to relax, expand, and adequately fill during diastole (thick hypertrophied ventricles usually due to hypertension)

Question 5

what is the #1 cause of right sided heart failure

Answer 5

left sided heart failure

Question 6

Cor pulmonale

Answer 6

right sided heart failure without left sided

Question 7

right sided heart failure causes

Answer 7

Engorgement of systemic and portal venous circulation (edema)

Question 8

left sided heart failure causes

Answer 8

Damning of blood in pulmonary circulation
Diminished peripheral blood flow

Ischemia
HTN
Aortic/mitral valve disease
Nonichemic myocardial diseases

Question 9

Symptoms of left sided heart failure

Answer 9

shortness of breath, worse when laying down

Question 10

risk factors for Ischemic heart disease

Answer 10

atherosclerosis risk factors

Question 11

how does ischemic heart failure happen

Answer 11

Decreased perfusion (coronary blood flow)
 and Increased myocardial demand lead to: 

Angina Pectoris
Acute Myocardial Infarction
Chronic Ischemic Heart Disease/ Heart Failure
Sudden Cardiac Death

Question 12

Stable (Typical) Angina Pectoris

Answer 12

Chronic stenosing coronary atherosclerosis (>75% reduction of lumen area) (happens over years)

Increased cardiac demand and workload needs unmet
Substernal chest pressure
- Physical activity, emotional excitement
- Relieved with rest (Vasodilator, nitroglycerin)

Question 13

what are the 3 types of angina

Answer 13

stable, unstable, and Prinzmetal Variant Angina

Question 14

Unstable Angina Pectoris

Answer 14

(aka Crescendo angina, preinfarction angina)
Atherosclerotic plaque disruption (abrupt)
• Thrombogenic plaque components, subendothelial basement membrane exposed
• Platelets activation, aggregation
• Vasospasm
• **Partially occluding thrombus

Anginal symptoms
frequent, less effort, at rest, longer duration

Question 15

stable vs vulnerable plaques

Answer 15

Vulnerable plaques
Lipid rich atheromas
Thin fibrous caps
Inflammation
Moderately stenotic - 50-75%

stable plaques
smaller core
thicker cap
less inflammation
may be more stenotic

Question 16

Prinzmetal Variant Angina

Answer 16

Coronary artery spasm
Unrelated to physical activity, heart rate, blood pressure
Responds to vasodilators

• You will usually make sure to rule out other causes of chest pain before making this diagnosis

Question 17

MI pathogenesis/mechanisms

Answer 17

Pathogenesis

• Plaque disruption (Hemorrhage, ulceration, rupture, fissuring)
• Platelet adhesion, aggregation, activation
• Vasospasm
• Coagulation
• OCCLUSIVE THROMBUS FORMATION

Question 18

for how long is ischemia reversible

Answer 18

30minutes - irreversible, coagulative necrosis

Question 19

transmural vs. nontransmural infarcts

Answer 19

transmural affect the full thickness of the wall - due to permanent obstruction of an arterial branch

while non-transmural are often subendocardial, can be due to a transient /partial obstruction, hypotension, or microinfarcts(spasms from cocaine use)

Question 20

when a coronary artery becomes obstructed what part of the muscle is affected first

Answer 20

subendocardial (furthest from the vessel

Question 21

Myocardial Infarction Morphology: 1/2 to 4 hours

Answer 21

No gross or light microscopic changes

Question 22

Myocardial Infarction Morphology: 4 to 12 hours

Answer 22

Beginning coagulation necrosis

Question 23

Myocardial Infarction Morphology: 12 to 24 hours

Answer 23

Gross - Dark mottling
Ongoing coagulation necrosis
Pyknosis of nuclei

Question 24

Myocardial Infarction Morphology: 1-3 days

Answer 24

Gross - mottled
Loss of nuclei and myocytes
Neutrophil infiltrate

Question 25

Myocardial Infarction Morphology: 3-7 days

Answer 25

Myocyte disintegration, phagocytosis of dead cells

Gross- yellow-tan softening

Question 26

Myocardial Infarction Morphology: 7- 10 days

Answer 26

Well-developed phagocytosis and early granulation tissue

Question 27

Myocardial Infarction Morphology: 10-14 days

Answer 27

Granulation tissue

Question 28

Myocardial Infarction Morphology: 2-8 weeks

Answer 28

scar formation

Question 29

symptoms of a MI

Answer 29

Crushing substernal chest pain, dyspnea, diaphoresis
Tachycardia, pulmonary congestion, edema

10-15% of patients – “silent”

Question 30

Laboratory Evaluation of an MI

Answer 30

troponin (peak 24hrs after)
CK-MB (peaks 18hrs)
Myoglobin (peak 2 hrs) - not specific to cardiac injury

Question 31

Triphenyltetrozolium chloride stain (LDH substrate)

Answer 31

stains myocardium but not the infarcted myocardium due to enzyme depletion

Question 32

MI treatment

Answer 32

Aspirin and other antiplatelet agents
Heparin
Thrombolytic therapy (Drug vs interventional)
Beta blockers
ACE inhibitors
Nitrates
Oxygen

Question 33

Reperfusion INJURY

Answer 33

Restoration of blood flow leads to local myocardial damage
• Free radical production
• Myocyte hypercontracture, increased Ca
• Leukocyte aggregation leads to proteases, elastases
• Mitochondrial dysfunction leads to apoptosis (caspase release)

Question 34

MI complications

Answer 34

1. Cardiogenic shock
   Severe pump failure
   10-15% patients
   Large infarcts (>40% ventricle)
2. Arrhythmia
   Conduction disturbances
   Myocardial irritability

3. Myocardial rupture
3-7 days
Free wall (Hemopericardium, Cardiac tamponade) 
Ventricular septum
Papillary muscle

4. Acute Pericarditis
   2-3 days
   Transmural MI
5. Ventricular aneurysm
   late complication
   mural thrombus
6. Progressive heart failure

Question 35

describe Progressive heart failure

Answer 35

when part of the heart has been previously infarcted, scar tissue forms in that area and is not contractile. The function of the heart then depends on the healthy tissue, which begins to hypertrophy to compensate. The increased size, mass, and protein synthesis requires more oxygen and nutrients than the arteries can supply. As a result small ischemic areas develop and extracellular matrix formation. eventually will lead to ischemic heart failure

Question 36

Sudden Cardiac Death mechanism

Answer 36

lethal arrhythmia

Underlying structural heart disease

Severe chronic coronary atherosclerosis with an associated
lethal arrhythmia is the etiology in 80-90% of cases
-At autopsy findings of acute plaque disruption are not
found in most cases -Usually NOT acute infarction
-Irritability of myocardium triggers arrhythmia

Question 37

Hypertension can lead to what affects on the heart

Answer 37

Hypertrophy of left ventricle

Mild blood pressure elevation can induce LVH

Question 38

“Cor Pulmonale”

Answer 38

Pulmonary HTN
Pathology of lung and/or lung vasculature
COPD, Pulmonary fibrosis, chronic pulmonary thromboembolism, primary pulmonary HTN
Increased pulmonary vascular resistance

leads to Right ventricular hypertrophy
Dilatation

Question 39

what commonly leads to cardiac hypertrophy

Answer 39

Systemic hypertension
LV wall thickness > 2cm
Weight > 500 gm

Aortic stenosis
800 gm

Normal heart 250 - 350 gm
Normal LV wall thickness ~1.5cm