Infarct expansion: Pathologic analysis of 204 patients with a single myocardial infarct

Pirolo, John S.; Hutchins, Grover M.; Moore, Gary

doi:10.1016/s0735-1097(86)80504-6

Cited by 171 publications

(58 citation statements)

References 11 publications

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“…The increase in %AWM observed for this subgroup was accounted for by increases in the extension subgroup. While the %AWM for the dilatation group did not significantly change (34.4±12.4% at entry versus 31.5±14.2% at 3 months), the %AWM for the extension group increased from 24 involved by AWM or enlargement of the total left ventricular surface area. Thus, to fully understand the natural history of these variables, it is necessary to quantitate their absolute and relative changes with a three-dimensional model of the ventricle.…”

Section: Infarct Groupsmentioning

confidence: 78%

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

et al. 1990

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To investigate the natural history of regional dyssynergy and left ventricular size after myocardial infarction, 57 patients with a first Q wave myocardial infarction (18 anterior, 35 inferior, and four apical by echocardiography) were studied by two-dimensional echocardiography and compared with 30 control patients. Measurements from the echocardiograms were used to construct maps of the left ventricular endocardial surface from which the endocardial surface area index (ESAi) and the percent of the endocardial surface area involved by abnormal wall motion (%AvAWM) were calculated. The maps from entry and 3-month echocardiograms were used to classify patients based on changes in ESAi and abnormal wall motion. Two subgroups of patients were identified at entry -those with a normal ESAi (group 1, n =50) and those with an increased ESAi (group 2, n =7 (Circulation 1990;82:484-494) T wo-dimensional echocardiography is an ideal noninvasive method for visualizing the changes in left ventricular structure and function that occur during myocardial ischemia and after infarction.1-10 Clinical studies with this technique have demonstrated a clear relation between the location and extent of echocardiographically defined regional dysfunction and electrocardiographic infarct location,1-3,5-8 pathological size of infarction,,'9 clinical status of the patient,2,6,7 occurrence of complications,2,3 and survival

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Section: Infarct Groupsmentioning

confidence: 78%

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

et al. 1990

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“…A large autopsy series confirmed the association of infarct expansion with large transmural infarcts. 35 Infarct expansion occurred more frequently in the left anterior descending coronary artery than in the right coronary artery, and increased heart weight correlated inversely with expansion. Differences in regional wall thickness, the radius of curvature, and intramural tension also influence infarct expansion and remodeling.…”

Section: Infarct Artery Patencymentioning

confidence: 94%

Left Ventricular Remodeling After Myocardial Infarction

2000

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L eft ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. 1,2 Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease ( Figure 1). This article will review postinfarction remodeling, pathophysiological mechanisms, and therapeutic intervention. Pathophysiology Postinfarction Left Ventricular RemodelingThe acute loss of myocardium results in an abrupt increase in loading conditions that induces a unique pattern of remodeling involving the infarcted border zone and remote noninfarcted myocardium. Myocyte necrosis and the resultant increase in load trigger a cascade of biochemical intracellular signaling processes that initiates and subsequently modulates reparative changes, which include dilatation, hypertrophy, and the formation of a discrete collagen scar. Ventricular remodeling may continue for weeks or months until the distending forces are counterbalanced by the tensile strength of the collagen scar. This balance is determined by the size, location, and transmurality of the infarct, the extent of myocardial stunning, the patency of the infarct-related artery, and local tropic factors. 1,3 The myocardium consists of 3 integrated components: myocytes, extracellular matrix, and the capillary microcirculation that services the contractile unit assembly. Consideration of all 3 components provides important insights into the remodeling process and a rationale for future therapeutic strategies. The cardiomyocyte is terminally differentiated and develops tension by shortening. The extracellular matrix provides a stress-tolerant, viscoelastic scaffold consisting of type I and type III collagen that couples myocytes and maintains the spatial relations between the myofilaments and their capillary microcirculation. 4,5 The collagen framework couples adjacent myocytes by intercellular struts that align myofilaments to optimize force development, distribute force evenly to the ventricular walls, and prevent sarcomeric deformation. 5 Myocardial infarction results in the migration of macrophages, monocytes, and neutrophils into the infarct zone; this initiates intracellular signaling and neurohormonal activation, which localizes the inflammatory response. Changes in circulatory hemodynamics are determined primarily by the magnitude of myocyte loss, the stimulation of the sympathetic nervous system and renin-angiotensin-aldosterone system, and the release of natriuretic peptides.Postinfarction remodeling has been arbitrarily divided into an early phase (within 72 hours) and a late phase (beyond 72 hours). The early phase involves expansion of the infarct zone, 5 which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. The failure to normalize increa...

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“…Furthermore, LV volumes were more increased in LAD MI group, indicating more severe post-MI LV remodeling than in the LCx MI group. It has been shown that infarct expansion occurs predominantly in MI associated with the LAD (28). Therefore, the remodeling process is more intensified after LAD MI and thus recapitulates important characteristic of clinical HF development.…”

Section: Discussionmentioning

confidence: 95%

Characterizing preclinical models of ischemic heart failure: differences between LAD and LCx infarctions

Ishikawa

Agüero

Hammoudi

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Large animal studies are an important step toward clinical translation of novel therapeutic approaches. We aimed to establish an ischemic heart failure (HF) model with a larger myocardial infarction (MI) relative to previous studies, and characterize the functional and structural features of this model. An MI was induced by occluding the proximal left anterior descending artery (LAD; n ϭ 15) or the proximal left circumflex artery (LCx; n ϭ 6) in Yorkshire pigs. Three pigs with sham procedures were also included. All pigs underwent hemodynamic and echocardiographic assessments before MI, at 1 mo, and 3 mo after MI. Analyses of left ventricular (LV) myocardial mechanics by means of strains and torsion were performed using speckle-tracking echocardiography and compared between the groups. The proximal LAD MI approach induced larger infarct sizes (14.2 Ϯ 3.2% vs. 10.6 Ϯ 1.9%, P ϭ 0.03), depressed systolic function (LV ejection fraction; 39.8 Ϯ 7.5% vs. 54.1 Ϯ 4.6%, P Ͻ 0.001), and more LV remodeling (end-systolic volume index; 82 Ϯ 25 ml/m 2 vs. 51 Ϯ 18 ml/m 2 , P ϭ 0.02, LAD vs. LCx, respectively) compared with the LCx MI approach without compromising the survival rate. At the papillary muscle level, echocardiographic strain analysis revealed no differences in radial and circumferential strain between LAD and LCx MIs. However, in contrast with the LCx MI, the LAD MI resulted in significantly decreased longitudinal strain. The proximal LAD MI model induces more LV remodeling and depressed LV function relative to the LCx MI model. Location of MI significantly impacts the severity of HF, thus careful consideration is required when choosing an MI model for preclinical HF studies.anterior; posterior; remodeling; torsion; sphericity THE STATISTICAL REPORT FROM the American Heart Association revealed a decline in mortality attributable to cardiovascular diseases by 30.6% in the last decade. However, one out of three patients still die from cardiovascular diseases in the US and the mortality in heart failure (HF) patients remains high (31). Significant progresses in treatment devices as well as modern pharmacotherapy have improved prognoses, while efforts on greater improvements continue. Several novel treatments for HF including gene therapy and cell therapy, and novel pharmaceuticals show promising results in small animal experimental studies. However, structural and physiological differences between human and small animals (27) continue to limit their clinically relevant predictive value for translating to humans. Hence, the need for large animal studies is still required to validate the efficacy and safety of these novel treatments in more clinically relevant models of HF.There are several large animal models of HF using diverse species. Pigs, dogs, and sheep are frequently used animals in translational experimental studies of cardiovascular diseases (18). Among them, the pig is most common due to similar coronary anatomies to humans, lack of inherent coronary collaterals, and ease of handling (14). HF can be induced b...

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Infarct expansion: Pathologic analysis of 204 patients with a single myocardial infarct

Cited by 171 publications

References 11 publications

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

Left Ventricular Remodeling After Myocardial Infarction

Characterizing preclinical models of ischemic heart failure: differences between LAD and LCx infarctions

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