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Old Myocardial Infarction
Myocardial infarction (MI) is characterized by acute ischemia caused by occlusion of an epicardial coronary artery causing irreversible cardiomyocyte death and subsequent cell necrosis, which results in a localized inflammatory response with recruitment and migration of macrophages, monocytes, neutrophils, and fibroblasts into the infarcted zone and eventual discrete collagen scar formation. , Within hours of the initial insult, acute dilatation and thinning of the area of infarction, also termed infarct expansion, occurs because of slippage between muscle bundles in the infarcted zone and stretching of the underlying collagen scaffold of the extracellular matrix (ECM). , As a consequence of this early remodeling caused by infarct expansion and decrease in ventricular contractility, the remote myocardium is asked to work harder, with neurohormonal-induced tachycardia and gradual left ventricular (LV) dilatation to increase preload and therefore preserve stroke volume. As an adaptive response over the following days to weeks, the noninfarcted remote myocardium undergoes compensatory hypertrophy to decrease the augmented wall stress caused by this early LV dilation. This adaptive stress response is mediated by multiple factors, including mechanical deformation from increased myocardial stretch, neurohormonal activation with increased norepinephrine producing direct and indirect activation of hypertrophic response, and renin–angiotensin–aldosterone system (RAAS) upregulation.
Despite advances in coronary reperfusion and evidence-based pharmacotherapy, approximately 30% of patients with anterior acute MI and 17% of patients with nonanterior acute MIs still experience adverse postinfarct remodeling. Current estimates suggest that for patients aged 45 years or older who experience their first MI, 16% of men and 22% of women will progress to develop heart failure (HF) within 5 years post-infarct. Furthermore, development of HF among patients with ST-elevation myocardial infarction (STEMI) confers a poor prognosis, with much higher long-term mortality rates compared with patients who do not develop HF. Use of guideline directed medical therapy including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, β-blockers, mineralocorticoid receptor antagonists, and neprilysin inhibitors all demonstrated potential for reverse remodeling and additionally have shown mortality benefit among patients with heart failure with reduced ejection fraction (EF). As such, ventricular remodeling is an important prognostic factor after acute MI and a clear target for therapeutic intervention.
The diagnosis of remodeling after infarction involves detection of morphologic changes, including LV size and shape, LV mass, LV volumes and indexes of function, extent and transmurality of scar, myocardial strain, fibrosis, and inflammatory infiltrates. Current clinical practice employs a combination of imaging modalities (echocardiography, radionuclide imaging, and cardiac magnetic resonance imaging [CMRI]) for diagnostic and prognostic assessment after MI.
Timing of Imaging
Data from the National Cardiovascular Data Registry (NCDR) Acute Coronary Treatment and Intervention Outcomes Network Registry—Get with the Guidelines (ACTION Registry-GWTG) showed that among 128,845 patients at 383 treatment centers with non–ST-segment elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI) between 2007 and 2009, 93% had in-hospital assessment of LVEF, a marked improvement compared with approximately 80% at the beginning of the decade. Importantly, patients that received in-hospital LVEF assessment were more likely to be discharged on secondary prevention medical therapies compared with those that did not undergo LVEF assessment. Present guidelines provide a strong recommendation for evaluation of LVEF, with preference for echocardiography rather than ventriculography given that valvular disease may influence revascularization strategy; assessment is recommended within 24-48 hours post-MI. , Follow-up postinfarct echocardiography is further recommended within the first 3 months after infarction.
For CMRI, no guideline recommendations currently exist for exact timing postinfarct. Notably, clinical studies appear to demonstrate variability in CMRI quantification of infarct size, LV function, and LV volume during the first week after acute MI. In a study from 2011 evaluating 57 patients with first STEMI who underwent percutaneous coronary intervention (PCI) within 12 hours of symptom onset, they found that CMRI imaging at 1 week was an independent predictor of LVEF and infarct size at 3 months, whereas imaging within the first 72 hours was not.
Risk Factors for Chronic Remodeling
As our understanding of the mechanism leading to and propagating chronic remodeling has improved, our identification of potential risk factors for development of adverse remodeling has expanded. Well-validated determinants of LV remodeling include large infarct size, anterior location, transmurality, lack of patency of the infarct vessels, and lack of use of thrombolytic agents. Fig. 45.1 illustrates a patient with a large acute infarct in the territory of the left anterior descending (LAD) coronary artery who underwent PCI; however, the presence of no-reflow phenomenon was revealed by microvascular obstruction seen on the CMRI. Consequently, this patient is likely to have acute and delayed complications from MI.
Video 45.1. Apical four-chamber ( A ), three-chamber ( B ), two-chamber ( C ), parasternal long-axis ( D ), and parasternal short-axis ( E ) transthoracic echocardiography views show large area of akinesis in the acute left descending coronary territory.
Infarct size may be the most important predictor of adverse LV remodeling and notably is linearly dependent on myocardial salvage by coronary reperfusion in the acute peri-infarct setting. Success of reperfusion is suggested by late patency of the infarct-related artery. Additionally, the presence of collateral circulation is associated with survival benefit and may confer better prediction of LV volume change than with infarct size.
More recently, introduction of CMRI and contrast-enhanced echocardiography have elucidated a better understanding of additional biological factors affecting remodeling, particularly markers of myocardial and microvascular damage such as microvascular obstruction, myocardial salvage, intramyocardial hemorrhage, and late gadolinium enhancement.
Chronic Remodeling
Left Ventricular Size, Shape, and Function
A consensus international forum has defined cardiac remodeling as a “genome expression resulting in molecular, cellular, and interstitial changes and manifested clinically as changes in size, shape, and function of the heart resulting from cardiac load or injury,” with clear delineation of two types of cardiac remodeling: physiologic (adaptive) and pathologic (maladaptive or adverse) remodeling. Quantitatively, adverse LV remodeling has been defined as an increase in LV end-diastolic volume (LVEDV) or LV end-systolic volume (LVESV) of 20% from baseline at 6 months after MI. Importantly, this definition was derived using two-dimensional (2D) echocardiography.
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