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Ischemic Heart Disease, ISCHEMIC HEART DISEASE Acute Coronary Syndromes MI Complications-3/4 of acute MI followed by 1 or more Contractile Dysfcn-LV dysfcn ->PV congestion, pulm edema -severe pump failure=cardio shock 10-15% of acute MI pts-LARGE -70% mortality Arrhythmias-conduction disturbances or myocardial irritability->sudden death -sinus brady/tachy, PVC/tachy, V.fib, asystole -inferoseptal MI->heart block Rupture-1)Free Wall-MOST COMMON->tamp, death 2)Vent. Septum-L->R shunt 3)Pap mm.-least common->severe mitral regurg -usually 3-7 days after MI Pericarditis-fibrinous or fibrohemorrhagic -day 2-3 after transmural-resolves over time RV infarction-isolated rare, but follows often Infarct Extension-new necrosis adjacent to existing Infarct Expansion-weak necrotic mm->stretching, dilating, thinning of infarct w/ transmural -esp w/ anteroseptal defects Mural Thrombus-from stasis->thromboembolism Ventricular Aneurysm-late-paradoxical systolic BULGE -w/ transmural lesion and thin scar ->mural thrombus, arrhythmias, failure, NOT rupture Papillary Mm Dysfcn->postinfarct mitral regurg -regurg MOSTLY due to ischemic dysfcn,, not rupture ->then shortens Progressive Late Heart Failure-chronic IHD, MI Complications-3/4 of acute MI followed by 1 or more Contractile Dysfcn-LV dysfcn ->PV congestion, pulm edema -severe pump failure=cardio shock 10-15% of acute MI pts-LARGE -70% mortality Arrhythmias-conduction disturbances or myocardial irritability->sudden death -sinus brady/tachy, PVC/tachy, V.fib, asystole -inferoseptal MI->heart block Rupture-1)Free Wall-MOST COMMON->tamp, death 2)Vent. Septum-L->R shunt 3)Pap mm.-least common->severe mitral regurg -usually 3-7 days after MI Pericarditis-fibrinous or fibrohemorrhagic -day 2-3 after transmural-resolves over time RV infarction-isolated rare, but follows often Infarct Extension-new necrosis adjacent to existing Infarct Expansion-weak necrotic mm->stretching, dilating, thinning of infarct w/ transmural -esp w/ anteroseptal defects Mural Thrombus-from stasis->thromboembolism Ventricular Aneurysm-late-paradoxical systolic BULGE -w/ transmural lesion and thin scar ->mural thrombus, arrhythmias, failure, NOT rupture Papillary Mm Dysfcn->postinfarct mitral regurg -regurg MOSTLY due to ischemic dysfcn,, not rupture ->then shortens Progressive Late Heart Failure-chronic IHD Post-MI Reperfusion Injury-restore flow w/in 3-4 hrs Thrombolytics-streptokinase, tissue-type plasminogen activator PCTA-angioplasty-eliminate occlusion and relieve some of original obstruction w/in 15-20 min may prevent all necrosis Later-can salvage some myocytes, some die Some of injured vasculature can ->leaks w/ new flow Injured Myocytes w/ CONTRACTION BANDS -closely-packed hypercontracted sarcomeres -b/c of exaggerated contraction w/ new blood -from lots of Ca++ inot dmged cells -and necrosis -for salvaged cells-'stunned,' recovering in fcn -repetitively stunned-HIBERNATING PRECONDITIONING MIGHT HELP PARADOXICALLY -via repetitive angina, silent ischemia, MI Complications-3/4 of acute MI followed by 1 or more Contractile Dysfcn-LV dysfcn ->PV congestion, pulm edema -severe pump failure=cardio shock 10-15% of acute MI pts-LARGE -70% mortality Arrhythmias-conduction disturbances or myocardial irritability->sudden death -sinus brady/tachy, PVC/tachy, V.fib, asystole -inferoseptal MI->heart block Rupture-1)Free Wall-MOST COMMON->tamp, death 2)Vent. Septum-L->R shunt 3)Pap mm.-least common->severe mitral regurg -usually 3-7 days after MI Pericarditis-fibrinous or fibrohemorrhagic -day 2-3 after transmural-resolves over time RV infarction-isolated rare, but follows often Infarct Extension-new necrosis adjacent to existing Infarct Expansion-weak necrotic mm->stretching, dilating, thinning of infarct w/ transmural -esp w/ anteroseptal defects Mural Thrombus-from stasis->thromboembolism Ventricular Aneurysm-late-paradoxical systolic BULGE -w/ transmural lesion and thin scar ->mural thrombus, arrhythmias, failure, NOT rupture Papillary Mm Dysfcn->postinfarct mitral regurg -regurg MOSTLY due to ischemic dysfcn,, not rupture ->then shortens Progressive Late Heart Failure-chronic IHD Location, Timing->Complications Early-Cardiogenic Shock, V. Fib, extension 1 wk-Rupture of vent wall, pap. mm., septum Late-Thromboembolism to head, leg, vent. arrhythmia, ISCHEMIC HEART DISEASE Acute Coronary Syndromes Sudden Cardiac Death -don't develop acute MI 300-400K/yr in US -unexpected death from cardiac causes soon after (əhr) or w/out onset of Sx -majority of pts w/ this as first IHD Sx As age decrease, more likely due to: Congenital, Ao stenosis, MV prolapse, Myocarditis, DCM, HCM, pulm HTN, conduction, isolated hypertrophy Ultimate mech-ARRHYTHMIA -asystole, V fib -due to irritated electrical from ischemia MORPHOLOGY ᢃ% stenosis in at least 1 major vessel in 80-90% victims -high grade and acute plaque disruption 10-20% nonatherosclerotic Healed MI in 40% New MI found in 1/3 of resuscitated pts Subendocard vacuolization like CIHD, ISCHEMIC HEART DISEASE Pathogenesis Vasoconstriction -can also ->plaque fracture Occurs via: 1)adrenergic agonists 2)released platelet contents 3)impaired NO secretion due to atheroma 4)mast cell mediators and other inflam, MI Complications-3/4 of acute MI followed by 1 or more Contractile Dysfcn-LV dysfcn ->PV congestion, pulm edema -severe pump failure=cardio shock 10-15% of acute MI pts-LARGE -70% mortality Arrhythmias-conduction disturbances or myocardial irritability->sudden death -sinus brady/tachy, PVC/tachy, V.fib, asystole -inferoseptal MI->heart block Rupture-1)Free Wall-MOST COMMON->tamp, death 2)Vent. Septum-L->R shunt 3)Pap mm.-least common->severe mitral regurg -usually 3-7 days after MI Pericarditis-fibrinous or fibrohemorrhagic -day 2-3 after transmural-resolves over time RV infarction-isolated rare, but follows often Infarct Extension-new necrosis adjacent to existing Infarct Expansion-weak necrotic mm->stretching, dilating, thinning of infarct w/ transmural -esp w/ anteroseptal defects Mural Thrombus-from stasis->thromboembolism Ventricular Aneurysm-late-paradoxical systolic BULGE -w/ transmural lesion and thin scar ->mural thrombus, arrhythmias, failure, NOT rupture Papillary Mm Dysfcn->postinfarct mitral regurg -regurg MOSTLY due to ischemic dysfcn,, not rupture ->then shortens Progressive Late Heart Failure-chronic IHD Post-MI Ventricular Remodeling-change size, shape, thickness; thin, heal, hypertrophy, dilation -initially beneficial, but later impairment, ISCHEMIC HEART DISEASE Pathogenesis Acute Plaque Change-plaques are dynamic -ppts most acute cor syndromes -disrupt previous partial obstruction -most events from MODERATELY stenotic lesions -after plaque change... severe->collaterals Hemorrhage into atheroma Rupture/fissuring-thrombogenic plaque stuff -esp at shoulder Erosion/ulceration-thrombogenic subendoth -ppting factors-vasospasm, systemic HTN, awakening/emotional stress (adrenergic) Anatomy of plaque -large soft necrotic/lipid core, macs, fibrous cap -degradation of collagen (cap)->rupture -via metalloproteinases (from macs), MI Complications-3/4 of acute MI followed by 1 or more Contractile Dysfcn-LV dysfcn ->PV congestion, pulm edema -severe pump failure=cardio shock 10-15% of acute MI pts-LARGE -70% mortality Arrhythmias-conduction disturbances or myocardial irritability->sudden death -sinus brady/tachy, PVC/tachy, V.fib, asystole -inferoseptal MI->heart block Rupture-1)Free Wall-MOST COMMON->tamp, death 2)Vent. Septum-L->R shunt 3)Pap mm.-least common->severe mitral regurg -usually 3-7 days after MI Pericarditis-fibrinous or fibrohemorrhagic -day 2-3 after transmural-resolves over time RV infarction-isolated rare, but follows often Infarct Extension-new necrosis adjacent to existing Infarct Expansion-weak necrotic mm->stretching, dilating, thinning of infarct w/ transmural -esp w/ anteroseptal defects Mural Thrombus-from stasis->thromboembolism Ventricular Aneurysm-late-paradoxical systolic BULGE -w/ transmural lesion and thin scar ->mural thrombus, arrhythmias, failure, NOT rupture Papillary Mm Dysfcn->postinfarct mitral regurg -regurg MOSTLY due to ischemic dysfcn,, not rupture ->then shortens Progressive Late Heart Failure-chronic IHD Post-MI Damage Timing 0-30 min-no dmg 1/2-4 hr-no dmg seen-some WAVINESS at borders 4-12 hr-begin coag necrosis, edema, hemorr 12-24 hr-dark mottling-coag nec, pyknotic nuc, myocyte hypereosinophilia, PMNs begin, CONTRACTION BAND NECROSIS 1-3 days-mottling w/ yellow-tan-coag nec, lose striations, nuclei; PMNs 3-7 days-hyperemic border, central yellow-tan -myocyte disintegration, PMN death, macs at border 7-10 days-phagos of dead cells, fibrotic at margins 10-14 days-well-formed gran tissue, new vessels, collagen 2-8 wk-scar from border to core-more collagen deposition ɮ mo-scarring complete-can't tell age after complete scar, MI Complications-3/4 of acute MI followed by 1 or more Contractile Dysfcn-LV dysfcn ->PV congestion, pulm edema -severe pump failure=cardio shock 10-15% of acute MI pts-LARGE -70% mortality Arrhythmias-conduction disturbances or myocardial irritability->sudden death -sinus brady/tachy, PVC/tachy, V.fib, asystole -inferoseptal MI->heart block Rupture-1)Free Wall-MOST COMMON->tamp, death 2)Vent. Septum-L->R shunt 3)Pap mm.-least common->severe mitral regurg -usually 3-7 days after MI Pericarditis-fibrinous or fibrohemorrhagic -day 2-3 after transmural-resolves over time RV infarction-isolated rare, but follows often Infarct Extension-new necrosis adjacent to existing Infarct Expansion-weak necrotic mm->stretching, dilating, thinning of infarct w/ transmural -esp w/ anteroseptal defects Mural Thrombus-from stasis->thromboembolism Ventricular Aneurysm-late-paradoxical systolic BULGE -w/ transmural lesion and thin scar ->mural thrombus, arrhythmias, failure, NOT rupture Papillary Mm Dysfcn->postinfarct mitral regurg -regurg MOSTLY due to ischemic dysfcn,, not rupture ->then shortens Progressive Late Heart Failure-chronic IHD Location, Timing->Complications Distribution in right-dominant heart -LAD (40-50%)-ant wall of LV near apex -ant. septum, apex circumferentially -RCA (30-40%)-inf-post wall of LV, -post. septum, inf-post RV free wall -LCX (15-20%)-Lateral wall LV, not apex Can have severe stenosis (-)Sx-collaterals, ISCHEMIC HEART DISEASE Pathogenesis Coronary Thrombus -critical to pathogenesis of acute Acute Transmural MI-thrombus occludes Acute subendo, angina, sudden death -incomplete thrombus Thrombotic Potential increased via: -inc. blood fibrinogen, low PAF inhibitor, high lipoprotein (a)