Ischemic Heart Disease Flashcards
Systolic Heart Failure
Deterioration of myocardial contraction
Diastolic Heart Failure
Inability of heart chamber to relax, expand, and adequately fill during diastole
Left-Sided Heart Failure
Damming of blood in pulmonary circulation, diminished peripheral blood flow
Orthopenia, pulmonary problems, have to sit upright
Right-Sided Heart Failure
Engorgement of systemic and portal venous circulation
Peripheral edema, acites, systemic/portal venous hypertension
Ischemic Heart Disease
Caused by decreased perfusion/coronary blood flow or increased myocardial demand
Leads to Angina pectoris, AMI, chronic heart failure, sudden cardiac death
Stable Angina Pectoris
Chronic stenosing coronary atherosclerosis (>74%)
Substernal chest pressure on physical activity or emotional excitement
Relieved with rest, vasodilator (NO)
Unstable Angina Pectoris
aka Crescendo angina, preinfarction angina
Atherosclerotic plaque disruption (platelets activate/aggretate, vasospasm, create partially occluding thrombus)
Pain happen even in patient at rest
Vulnerable plaques (lipid rich atheromas, thin fibrous caps, inflammation)
Pain is frequent, upon less effort, at rest, of longer duration
Prinzmetal Variant Angina
Coronary artery spasm
unrelated to physical activity, HR, BP
Responds to vasodilators
Myocardial Infarction
“Heart attach”
Pathogenesis: plaque disruption, platelet adhesion, occlusive thrombus formation or embolization to distal heart)
Transmural infarct
Completely through the wall, usually from occlusive thrombus
Non-transmural infarct
Usually subendocardial layer infarcts
Can be from occlusive thrombus that is treated immediately
Small intramural vessel infarct
Microinfarcts in the center of the heart muscle
Usually from cocaine or vasculitis
Myocardial Infarction Morphology
1/2 - 4 hours
No gross or light microscopic changes
If sudden death occurs, pathologists might not be able to detect anything
Myocardial Infarction Morphology
4-12 hours
Beginning of coagulation necrosis
Myocardial Infarction Morphology
12-24 hours
Gross: Dark mottling (hemorrhaging in myocardium)
ongoing coagulation necrosis
Pyknosis of nuclei
Myocardial Infarction Morphology
1-3 days
Gross: Mottled
Loss of nuclei and myocytes
Neutrophil infiltrate
Myocardial Infarction Morphology
3-7 days
Myocytes disintegration, phagocytosis of dead cells
Lots of neutrophils
Shadows of myocytes
Myocardium appears yellow (from infiltration of neutrophils)
Myocardial Infarction Morphology
7-10 days
Well-developed phagocytosis and early granulation tissue
Scar formation
Myocytes do not regrow
Myocardial Infarction Morphology
10-14 days
Granulation tissue
Whisps of mature collagen (stain blue)
Myocardial Infarction Morphology
2-8 weeks
Scar formation
Well-developed scar
Lots of collagen
Laboratory Evaluation
Measure troponin and creatinine kinase enzyme
Myoglobin is an insensitive test because other muscle in the body can release myoglobin
Treatment of MI
ASA and other antiplatelet agents heparin thrombolytic therapy (drug vs interventional) B-Blockers ACE inhibitors Nitrates Oxygen
Reperfusion injury
Free radical production
Myocyte hypercontracture, increased Ca
Leukocyte aggregation (proteases, elastases)
Mitochondrial dysfunction (apoptosis)
MI Complications
Cardiogenic shock (severe pump failure) Arrhythmia (conduction disturbance, myocardial irritability) Myocardial rupture (3-7 days, free wall/ventricular septum/papillary muscle. Occurs because wall is composed of dead myocytes and neutrophils and is not very strong) Acute pericarditis (2-3 days, nonspecific chest pain following MI) Ventricular aneurysm (late complication, dead part can outpouch, thrombi can form and embolize to other parts of the body) Progressive heart failure (living myocytes hypertrophy and become ischemic, fetal genes expressed, heart can no longer compensate)
Sudden Cardiac Death
Lethal arrhythmia
Underlying structural heart disease (ie chronic severe atherosclerotic heart disease)
Usually not from acute infarction
Electrical irritability of myocardium
Hypertensive Heart Disease
Left-sided
Hypertrophy of left ventricle
Mild blood pressure elevation can induce LVH
Asymptomatic, CHF, arrhythmias (afib)
Cardiac Hypertrophy
Systemic hypertension
Increases LV wall thickness
Weight >500 gram
Can be caused by aortic stenosis
Pulmonary Hypertensive Heart Disease
Cor pulmonale
Pulmonary HTN due to pathology of lung vasculature
From COPD, pulmonary fibrosis, chronic PE, primary pulmonary HTN
Right ventricular hypertrophy and dilation
