Acta Radiológica Portuguesa, Vol.XIX, nº 74, pág. 45-51, Abr.-Jun., 2007 Imaging of Coronary Artery Disease: II Jean Jeudy University of Maryland School of Medicine Department of Diagnostic Radiology Armed Forces Institute of Pathology Necrosis starts to develop in the subendocardium, about 15 30 min after coronary occlusion The necrotic region grows outward towards the epicardium over the next 3 6 h, eventually spanning the entire ventricular wall. Coronary thrombosis is the critical event resulting in infarction If occlusion occurs >30min, damage is irreversible Overview Some portions of the myocardium are reversibly damaged (stunned) and will eventually recover if blood flow is restored Contractility in the remaining viable myocardium become hyperkinetic The pathological hallmark of myocardial infarction is coagulative necrosis of the myocardium Ischemia causes immediate loss of contractility Between 4-12 h after cell death starts, the infarcted myocardium begins to undergo coagulation necrosis cell swelling, organelle breakdown and protein denaturation After about 18 h, neutrophils enter the infarct numbers reach a peak after about 5 days, and then decline ARP 45
After 3 4 days, granulation tissue appears at the edges of the infarct zone macrophages, fibroblasts, which lay down scar tissue, and new capillaries The infarcted myocardium is especially soft between 4 and 7 days, and is therefore maximally prone to rupturing may occur at any time during the first 2 weeks and is responsible for about 10% of MI mortality Abnormalities of perfusion have been well described on MDCT. Perfusion As the granulation tissue migrates inward toward the centre of the infarct over several weeks, the necrotic tissue is engulfed and digested by the macrophages granulation tissue progressively matures, with an increase in scar tissue and loss of capillaries Etiology of ischemia Role of imaging Identify viable vs nonviable myocardium Evaluate for complications associated with infarction Perfusion First pass MRI perfusion is emerging as a very capable alternative for non invasive assessment Excellent spatial resolution allows for detection of subendocardial ischemia 46 ARP
Viability Hypoperfused, but viable myocardium should be revascularized whereas nonviable myocardium should not Delay in restoring perfusion to at-risk myocardium increases mortality Accurate and reproducible noninvasive method of evaluating cardiac function. Excellent depiction of endocardial and epicardial borders allows accurate assessment of wall thickness and wall thickening. Global Function Cardiac MR Assessment Anatomic Assessment Chamber size Cardiac Wall motion Myocardial wall thickness Functional Assessment LV Ejection Fraction Myocardial Perfusion Viability Sequences Global Function Limitations Cannot determine precise size of myocardial infarction Discrimination between transmural and nontransmural infarct cannot be assessed. ARP 47
Delayed Enhancement Fast gradient echo MR sequences Imaging performed after rapid intravenous injection at a rate of 4-5 ml/sec Hypoperfusedareas will be hypointense 1 st Pass Perfusion Myocardial Ischemia ACUTE PHASE First few weeks after infarction extensive capillary damage resulting in microvascular obstruction LATE PHASE replacement of infarcted myocardium by scar Delayed Enhancement MR Inversion recovery Performed 10 to 30 minutes after administration of gadolinium Both acute and chronic infarct demonstrate hyperintense signal Vogel-Claussen et al, 2006 Myocardial Ischemia Delayed enhancement due to loss of cellular wall integrity and edema Size of acute infarct correlates with peak levels of creatine kinase Large q wave acute MI leads to microvascular obstruction Myocardial Ischemia Serial evaluation shows infarct size gradually decreases over time Overestimation of infarct size because of associated edema without myonecrosis Compensatory hypertrophy of noninfarcted myocardium during recovery phase Vogel-Claussen et al, 2006 48 ARP
Microvascular Obstruction Severely injured myocardium Occlusion of capillaries in association with recent myocardial infarction denotes poor prognosis Kim et al, 2001 Late (viability): Hyper-enhancement indicates scar/fibrosis in association with chronic MI Functional recovery inversely related to transmural extent of hyper-enhancement Early (perfusion): acute MI myocardial necrosis and microvascular obstruction, edema chronic MI corresponds to poorly perfused myocardial scar In both cases abnormalities depict most severely damaged myocardial tissue which is infarct core Late (viability): 90% of patients with transmural hyperenhancement >50% showed no improvement in wall motionafter revascularization. Kim et al 2000 Microvascular Obstruction Severely injured myocardium Viability using MDCT Occlusion of capillaries in association with recent myocardial infarction denotes poor prognosis Mahnken et al, 2005 ARP 49
Complications of Myocardial Infarction Cardiac rupture LV aneurysm Ventricular pseudoaneurysm Mitral regurgitation Pericarditis Cardiogenic shock Pulmonary hemorrhage Pulmonary edema Arrhythmia LV DILATION AND APICAL THROMBUS LEFT VENTRICULAR ANEURYSM Usually occurs in left anterior distribution in association with LAD occlusion Often denotes a wide infarcted area Complications VENTRICULAR PSEUDOANEURYSM Rare complication Occurs due to rupture of ventricular free wall which subsuquently becomes contained by overlying pericardium Most occur within 7 days after the acute event and have increased risk of rupture Complications 50 ARP
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