L42 Ischemic Heart Disease Flashcards
What is the leading cause of mortality worldwide?
Cardiovascular disease (25% of US deaths)
What happens in heart failure (also known as congestive heart failure)?
The heart is unable to pump blood sufficiently to meet the needs of the tissue
What are the two types of heart failure?
Diastolic (inability of the heart chamber to relax, expand, and adequately fill during diastole; ventricle is unable to fill with blood)
Systolic (inadequate myocardial contractile function; the ventricle is unable to eject blood)
In which type of heart failure does the ejection fraction decrease?
Systolic heart failure
What increases in heart failure?
End diastolic ventricular volume, end diastolic pressures, venous pressure
What happens in right sided heart failure?
Engorgement of the systemic and portal venous circulation
What happens in left sided heart failure?
Damming of blood in the pulmonary circulation and diminished peripheral blood flow
What are some causes of left sided heart failure?
Ischemia, hypertension, aortic and mitral valve diseases, and non-ischemic myocardial diseases
What are the causes of right sided heart failure?
Left sided heart failure, cor pulmonale
What are some signs and symptoms of right sided heart failure?
Edema, dark purple legs (blood pooling), ascites, hepato/splenomegaly
What are some signs and symptoms of left sided heart failure?
Dyspnea, orthopnea, no edema, no ascites
What causes ischemic heart disease?
Decreased perfusion (coronary blood flow) and increased myocardial demand
What are four syndromes caused by ischemic heart disease?
- Angina pectoris
- Acute myocardial infarction
- Chronic ischemic heart disease/heart failure
- Sudden cardiac death
What are the three types of angina pectoris?
- Stable
- Unstable
- Prinzmetal
Describe stable angina pectoris.
Result of chronic stenosing coronary atherosclerosis; leads to increased cardiac demand and workload needs unmet
Describe the lumenal obstruction in stable angina pectoris.
> 75% reduction of lumen area
What are the symptoms of stable angina pectoris?
Substernal chest pressure during physical activity and emotional excitement that is relieved with rest
Describe unstable angina pectoris (aka crescendo agina, pre-infarction angina)
Caused by atherosclerotic plaque disruption; atheroma cap is breached, exposing the core, leading to platelet activation and aggregation; vasospasm may also occur. Eventually, there is a partially occluding thrombus formed.
Describe the lumenal obstruction of unstable angina pectoris.
50-75% (less than stable)
What are the symptoms of unstable angina pectoris?
Anginal symptoms, but they occur frequently with less effort/at rest for a longer duration
What types of plaques are vulnerable?
Lipid rich atheromas with thin fibrous caps and lots of inflammation
Describe Prinzmetal variant angina.
Caused by a coronary artery spasm unrelated to physical activity, heart rate, and blood pressure
Describe the pathogenesis of myocardial infarction.
Plaques are disrupted. Platelets adhere/aggregate/activate. Vasospasms occur. Coagulation is activated. Ultimately, an occlusive thrombus forms.
(There are other possible mechanisms).
Describe the development of acute coronary syndromes.
Atherosclerosis causes a fixed coronary obstruction (typical angina). This plaque can be disrupted/healed, leading to severe fixed coronary obstruction (chronic ischemic heart disease) or to thrombus formation.
What are the acute coronary syndromes?
Unstable angina, acute myocardial infarction
When does reversible ischemia become irreversible and progress to coagulative necrosis?
After 30 minutes
What is the difference between a transmural and nontransmural infarction?
Transmural: entire thickness of the wall is infarcted
Non-transmural: only a portion of the myocardium is infarcted
When a coronary artery is obstructed, which part of the heart infarcts first?
The part of the heart furthest from it (except a thin portion of the lumenal myocardium that is spared)
Describe the morphology of the myocardium after 0.5-4 hours.
No gross or light microscopic changes
Describe the morphology of the myocardium after 4-12 hours.
Beginning of coagulative necrosis, hemorrhage (eosinophilia of cytoplasm, loss of some nuclei, some hemorrhage)
Describe the morphology of the myocardium after 12-24 hours.
Gross: dark mottling (hemorrhage)
Histology: Ongoing coagulative necrosis, pyknosis of nuclei (very pink fibers, RBCs)
Describe the morphology of the myocardium after 1-3 days.
Gross: mottled myocardium
Histology: loss of nuclei and myocytes, neutrophil infiltrate
Describe the morphology of the myocardium after 3-7 days.
Myocyte disintegration, dying neutrophils, phagocytosis of dead cells
Describe the morphology of the myocardium after 7-10 days.
Well-developed phagocytosis and early granulation tissue
Describe the morphology of the myocardium after 10-14 days.
Granulation tissue
Describe the morphology of the myocardium after 2-8 weeks.
Scar formation
What are the symptoms of MI?
Crushing substernal chest pain, dyspnea, diaphoresis, tachycardia, pulmonary congestion, edema
What laboratory evaluations can be done to look for an MI?
Myoglobin (first), creatinine kinase (second), and troponin (third) all increase
What is a triphenyletrozolium chloride stain used for?
Stains LDH red (yellow when it isn’t there); this enzyme is depleted in MI
How can MI’s be treated?
- Aspirin/anti-platelet agents (counteract thrombus formation)
- Heparin (counteract coagulation cascade)
- Thrombolytic therapy (counteract thrombus formation)
- Beta blockers (slow heart rate/contractility, decrease demand of heart)
- ACE inhibitors (decrease remodeling)
- Nitrates (vasodilation)
- Oxygen (decrease demand)
What is the goal of therapy in the setting of an MI?
Myocardial salvage
What is reperfusion injury?
Restoration of blood flow leads to local myocardial damage (free radical production, hypercontracture due to increased intracellular calcium, leukocyte aggregation, and mitochondrial dysfunction)
What are 5 serious MI complications?
- Cardiogenic shock
- Arrhythmia
- Rupture
- Acute pericarditis
- Ventricular aneurysm
What happens in cardiogenic shock?
Severe pump failure in 10-15% of patients who have very large infarctions
Why does arrhythmia occur in the setting of an MI?
Myocardial irritability, conduction disturbances
When does myocardial rupture typically happen after MI?
After 3-7 days
Where can the myocardial rupture occur?
Free wall (leading to hemopericardium or cardiac tamponade), ventricular septum, or papillary muscle
Ventricular aneurysm is a late complication of MI. What is a complication of the aneurysm?
Mural thrombus
What is remodeling?
Alteration in the structure of the heart in response to hemodynamic load and/or cardiac injury in association with neurohormonal activation
Describe the process of remodeling.
Hypertension (pressure overload), valvular disease (pressure/volume overload), and MI (regional dysfunction with volume overload) all increase cardiac work. This increases wall stress. Cells stretch and hypertrophy and/or dilate.
What is the mechanism of sudden cardiac death in ischemic heart disease?
Lethal arrhythmia caused by myocardial irritability from ischemia or fibrosis
What are the effects of hypertension/left-sided hypertensive heart disease?
Hypertrophy of the left ventricle (can even be caused by mild BP elevation)
Compare a normal heart weight/LV wall thickness to that of someone with systemic hypertension and aortic stenosis.
Normal: 250-350 gm, 1.5cm thick
HTN: 500+ gm, 2+cm thick
Aortic stenosis: 800 gm
What can happen to someone with left-sided hypertensive heart disease?
- Asymptomatic
- CHF
- Arrhythmias/A Fib
What causes cor pulmonale (pulmonary hypertensive heart disease)?
Pulmonary HTN (caused by COPD, pulmonary fibrosis, chronic pulmonary thromboembolism, primary pulmonary HTN, increased resistance)
