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Flashcards in Ischemic heart disease Deck (10)
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Clinical presentation of angina pectoris

-Paroxysmal and recurrent attacks of substernal or precordial chest discomfort
-Silent ischemia is common in geriatrics or diabetics
-Stable: deep, poorly localized pressure, squeezing or burning sensation that is relieved by rest or vasodilators
-Prinzmetal: unrelated to physical activity, heart rate or BP. Responds to vasodilators


Pathogenesis of angina pectoris

-Caused by transient myocardial ischemia that is insufficient to induce myocyte necrosis

-Pain is a consequence of ischemia induced release of adenosine, bradykinin and other molecules
-Caused by decreased perfusion, increased demand, and coronary arterial pathology

-Stable: imbalance of coronary perfusion relative to myocardial demand. Triggers are physical activity, emotional excitement or psychological stress.

-Prinzmetal: uncommon. From coronary artery spasm

-Unstable: increasingly frequent, prolonged or severe angina precipitated by lower levels of physical activity or at rest. Caused by the disruption of an atherosclerotic plaque. Half have myocardial necrosis


Clinical course of MI

-Reversible injury within 20-30 minutes of onset
Contractile dysfunction: some type of left ventricular failure
-Arrhythmias: myocardial irritability that cause sinus brady, a fib, heart block, tachy, ventricular premature contractions, ventricular tachy, v fib
-Myocardial rupture: transmural necrosis weakens the wall and happens within 2 to 4 days
-Risk factors for rupture: over 60, first MI, transmural and anterior MI, absence of LVH, preexisting HTN
-Ventricular aneurysm: late complication of transmural infarcts when the myocardium has become scarred
-pericarditis: 2 to 3 days after: Dressler syndrome
-Infarct expansion
-Mural thrombosis
-Papillary muscle dysfunction
-Progressive late heart failure
-Postinfarct complications depend on size, location and fraction of wall
-Non-infarcted segments undergo ventricular remodeling of hypertrophy and dilation


Diagnosis of MI

-Diagnosed by clinical symptoms, lab tests, and EKG changes
-Chest pain, sweating, nausea and vomiting, dyspnea from pulmonary congestion
-Blood levels of cTnT and cTnI and CK-MB are diagnostic markers
-Troponins I and T are not normally found in circulation but begin to rise at 3-12 hours. Troponin T peaks at 12-48. Troponin I max at 24 hours.
-Creatine kinase: brain, myocardium and skeletal muscle. MB is specific for the heart
-CK-MB rises within 3-12 hours and peaks at 24. Returns to normal at 48 to 72


Treatment of MI

Therapy: morphine, reperfusion, aspirin, heparin, nitrates, beta blockeers, antiarrhythmics, ACE inhibitors, oxygen


Pathogenesis of MI

-Coronary arterial occlusion: plaque undergoes hemorrhage or rupture, platelets adhere and form a microthrombi, vasospasm, tissue factor starts coagulation cascade, thrombus expands to occlude the vessel
-This sequence is why coronary revascularization and clot busting works

-Other mechanisms: vasospasm due to drugs, emboli from left atrium, ischemia without detectable or significant coronary atherosclerosis and thrombosis

-With prolonged vascular compromise, there is myocardial death

-Area at risk: the region of the heart supplied by occluded artery
-Severity and duration
-Myocardial contractility ceases within a minute
-Reversible ultrastructural changes: myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling
-Earliest detectable feature is disruption of the sarcolemmal membrane (what allows the blood testing for injury)
-Transmural: occlusion of an epicardial vessel. Chronic atherosclerosis, acute plaque change, superimposed thrombis
-Subendocardial: most vulnerable area. Inner third of the ventricular wall. If the clot is lysed before full thickness. From global hypotension, this is circumferential
-Multifocal microinfarction: involves small intramural vessels. Microemboli, vasculitis, or vascular spasm. Epi or drugs. Can cause sudden cardiac death


Morphology of MI

-Ischemia is the worst in the subendocardium
-“wavefront” of cell death that progressively goes more towards transmural
-Morphology depends on: location severity and rate of obstruction, size of the vascular bed, duration of occlusion, metabolic needs, collateral circulation, vasospasm, HR, rhythm, O2 sat
-Half thickness in 2 to 3 hours. Full thickness in 6 hours
-Patterns: transmural, subendocardial (most vulnerable), Multifocal (microthrombi)
-Nearly all contain a portion of the left ventricle
-Entire zone of the occluded coronary artery
-Left anterior descending: anterior wall of the left ventricle near septum
-Right coronary: inferior/posterior wall of left ventricle
-Left circumflex: lateral wall of left ventricle
-Irreversibly injured cells have contraction bands
-Early: Usually are not apparent grossly. Stained w/ triphenyltetrazolium chloride
-12 to 24 hrs: reddish-blue area of discoloration
-10 dayrs to 2 weeks: Vascularized granulation tissue
-Weeks: covered by a fibrous scar
-Wavy fibers develop at the edge of the infarct
-Myocytolysis occurs at the edge of the infarcts
-Macrophages remove the necrotic myocytes in 3 to 7 days
-Highly vascularized granulation tissue is there from 1 to 2 weeks and then is replaced by fibrous tissue after
-Scarring is advanced by week 6
-Heal from the margins towards the center


Reperfusion after MI

restoration of blood flow. Salvages cardiac muscle and limits infarct size. Preeminent objective. Thrombolysis, angioplasty, stent, CABG.
-Reperfusion benefits depend on: rapidity of resolution, extent of restoration
-Reperfused infarcts are usually hemorrhagic
-Reperfusion can trigger arrhythmias and damage on the original ischemia
-Oxidative stress, calcium overload and inflammatory cells
-Reperfusion causes hemorrhage, endothelial swelling, and damage to cells. Up to 50% of infarct size can be due to reperfusion
-Stunned myocardium: prolonged cardiac failure from short-term ischemia that lasts days
-Hibernation: decreased metabolism and function following ischemia


Pathogenesis of chronic ischemic heart disease

-Progressive congestive heart failure due to accumulated ischemic myocardial damage
-Usually from prior MI
-Due to functional decompensation of hypertrophied non-infarcted myocardium
-Severe obstructive coronary artery disease may cause this as well


Morphology of chronic ischemic heart disease

Cardiomegaly w/ LVH and dilation
-stenotic coronary atherosclerosis is usually present
-Healed infarcts generally seen
-patchy fibrous thickening and mural thrombi present
-Myocardial hypertrophy, diffuse subendocaridal vacuolization and fibrosis