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Myocardial infarct
Myocardial Infarction
| Question | Answer |
|---|---|
| Myocardial ischemia definition | Condition of reversible inadequate blood supply to the heart due to fixed coronary stenosis, increased myocardial demand, coronary vasospasm, intraplaque hemorrhage, superimposed thrombosis, or any combination of these |
| What is acute ischemia? | Ischemia that has only lasted minutes to hours, or at the most a few days |
| How long does it take for ischemia to cause loss of glycogen, mitochondrial swelling, cellular swelling, and loss of contractility? | One minute |
| Are manifestations of acute myocardial ischemia visible? | In general, acutely ischemic cardiac myocytes look normal under light microscopy; need electron microscopy to see changes; most changes are FUNCTIONAL, not STRUCTURAL |
| What is the prognosis for cardiac myocytes after acute ischemia once blood flow is returned? | Cardiac myocytes only gradually recover their contractile function; may take several hours, days, or weeks depending on level of ischemia |
| What causes myocardium to become "stunned myocardium" after an acute ischemic event? | Accumulated excess calcium, O2 derived radicals, and damage to cytoplasmic proteins and organelles; takes time to reverse |
| What is chronic ischemia? | ischemia that lasts weeks, months, or years |
| What do cardiac myocytes do to protect themselves during sublethal chronic ischemia? | hunker down metabolically, catabolize contractile proteins, and revert to primitive state limited to survival functions; clearing (vacuolization) of myocyte cytoplasm under light microscopy--myocytolysis |
| What is myocytolysis? | clearing (vacuolization) of myocyte cytoplasm under light microscopy due to myocytes catabolizing contractile proteins |
| What happens if you return blood flow to cardiac myocytes if they have been in a sate of chronic ischemia? | Function of chronically ischemic myocytes can return with regeneration of all normal cytoplasmic proteins, BUT return is GRADUAL |
| What changes do you see in the coronary circulation in a state of chronic ischemia? | Collateral coronary arteries develop when chronic myocardial ischemia causes growth or enlargement of arteries into ischemic areas, provided ischemia develops slowly enough |
| What is ischemic preconditioning? | Brief episodes of myocardial ischemic insult may render myocytes less vulnerable to infarction with subsequent episodes |
| Myocardial infarction: definition | irreversible necrosis of heart muscle due to prolonged ischemia (20 minutes +) |
| When should thrombolytic therapy or angioplasty be provided for ischemia? | Myocardial infarction through to be wavefront in nature, starting with subendocardial region-->not complete until 6 hours after start; Tx worth it between 20 minutes and 6 hours after ischemia onset |
| How can chronic ischemia not automatically lead to infarction? | Can be either 1) repeated episodes of ischemia too brief to cause infarction or 2) inadequate perfusion low enough to injure but not kill myocytes |
| What are the major causes of myocardial infarctions? | 90%: Coronary atherosclerosis, 10% other causes (including coronary vasculitis), emboli from endocarditis, vasospasm, hypercoaguable states (e.g. after surgery), blood hyperviscosity, congenital abnormalities |
| Transmural infarction | involves full thickening of the heart wall; associated with occlusive thrombosis superimposed on atherosclerotic plaque that undergoes an acute change (typically disruption of unstable plaque by ulceration or rupture) |
| Subendocardial infarctions | Involve inner portion of heart wall; more likely to be patchy and have episodes of extensions with additional infarction at the periphery; becoming more common than transmural |
| What gross pathological changes do you expect in your average classic unreperfused myocardial infarction (finding and time) | Acute: none (0-12 hrs); progressive pallor (12-24 hours), yellow and softened (2-3 days). Subacute: red (granulation tissue) border (4-7 days), gradual replacement of yellow infarct by red (1-6 weeks); gradual white scarring (6-12 wks) |
| What is the earliest light microscopic finding after a myocardial infract? | Thin wavy myocytes (dead); 1-3 hours; at the periphery of the infarct |
| What microscopic pathological findings do you see in the ACUTE phase of myocardial infarction (1-3 days)? | Thin wavy myocytes (1-3 hours); coagulation necrosis; neutrophilic infiltration; contraction band necrosis in periphery of infarct; myocytolysis in viable myocytes around infarct |
| What is the nature of coagulation necrosis? When is it first visible? | 4-12 hours; characteristic microscopic pathology of unreperfused myocardial infarct: 1) hypereosinophilia, 2) loss of striations, 3) nuclear changes (pyknosis, karyorrhexis, karyolysis, and disappearance) |
| What is the cause of edema and (sometimes) hemorrhage seen 6-12 hours after the onset of myocardial infarct? | neutrophilic infiltration; usually peaks in third day |
| What is contraction band necrosis? What causes it? | dense hypereosinophilic transverse bands of hypercontracted sarcomeres in dead myocytes; sometimes seen in periphery of an infarct; results from influx of Ca++ through damaged cell membranes-->Exagerated contraction of myofibrils |
| What pathologic findings do you see i within the early subacute phase of myocardial infarction (days 4-10)? | Characterized by infiltration of infarct by lymphocytes (by day 2), macrophages (by day 3), and fibroblast (by day 4). Eosinophils and plasma cells may join, but role unclear. Process begins in periphery of unreperfused infarct --> spreads to infarct |
| What pathologic findings do you see by the late subactue phase (day 11 - week 12)? | Ingrowth of capillaries (angiogensis) and proliferation of fibroblasts --> converts tissue cleared of dead myocytes into granulation tissue. Fibroblasts gradually replace granulation tissue by acellular fibrous collage scar. |
| What is the best way to prevent or minimize the effects of myocardial infarction? | Reperfusion of blood flow to ischemic cardiac myocytes by ANGIOPLASTY, THROMBOLYTIC THERAPY, or CORONARY BYPASS |
| What happens when you reperfuse the heart at the start of myocardial infraction? What if it's too late? | Reperfusing heart after start of myocardial infarction can salvage reversibley injured myocytes; restoring the blood supply too late to irreversibly fatally injured (dead) heart muscle does NOT save it, but alters appearance of infarct |
| Reperfusion of a myocardial infarction causes it to be... (9): | 1) smaller, 2) patchier, 3) hemorrhage into it, 4) more contraction band necrosis, 5) accelerated inflammation and repair, 6) diffusion of inflammation and repair, 7) fewer neutrophiles, 8 and 9) more macrophages and interstitial fibrosis |
| The gross pathology of a reperfused myocardial infarction is ... (acute, days 1-3) | Days 1-3: dark mottling and hemorrhage immediately following reperfusion |
| The gross pathology of a reperfused myocardial infarction is ... (earliest subacute, days 4-5) | Dark mottled red and brown (no change) |
| The gross pathology of a reperfused myocardial infarction is ... (early subacute, days 6-10) | shrunken red and brown and bits of gray-white |
| The gross pathology of a reperfused myocardial infarction is ... (mid-subacute, days 11-14) | brown and intermingled with gray white |
| The gross pathology of a reperfused myocardial infarction is ... (late subacute, weeks 2-7) | progressive white, intermingled normal |
| The microscopic pathology of the average reperfused myocardial infarction in the acute phase (days 1-3) is... | Contraction band necrosis and hemorrhage; no reflow phenomenon; edema and neutrophilic infiltration; myocytolosis around infarct; macrophages and fibroblasts arrive earlier |
| The microscopic pathology of the average reperfused myocardial infarction in the early subacute phase (days 4-10) is.... | Lymphocytes and sometimes eosinophils + plasma cells-->formation of granulation tissue and then collagen; acceleration of inflammation and repair makes it seem older |
| The microscopic pathology of the average reperfused myocardial infarction in the late subacute phase (days 11-the end) is... | Large infarct healed from 12 to 7 weeks; small within 2; reperfusion accelerates healing by about 40%; patches of preserved myocardium commonly interspersed with scar; scar more interstitial rather than confluent |
| The hemorrhage and the no-reflow phenomenon associated with restoring myocardial blood flow are exampes of ____ injury. | Reperfusion |
| Reperfusion injury refers to what type of damage? | The damage to tissue when blood supply is restored after a brief period of ischemia; cell membranes are rendered abnormally permeable by ischemia-->higher Ca++ inflow + O2 can give rise to free radicals and ROS + overzealous inflammatory cells |
| What complications can arise from myocardial infarction reperfusion injury? | Scar formation --> re-entrant ventricular cardiac arrhythmias due to irregular and circuitous routes for cardiac rhythm conduction |
| What accounts for the no-reflow phenomenon seen when reperfusing myocardial tissue in the acute phase? What about the hemorrhage? | Capillary endothelial swelling, capillary plugging by neutrophils, microthrombosis, and microembolism. Hemorrhage: due to microvascular injury |
Created by:
karkis77
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