Anti-Heart Antibodies in the Postpericardiotomy and the Postmyocardial-Infarction Syndromes

Geld, H. van der; D'Ailly, Thea

doi:10.1016/s0140-6736(64)90512-4

Cited by 135 publications

(22 citation statements)

References 19 publications

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“…Almost 50 years ago, detection of anticardiac antibodies suggested an immunological mechanism in the pathogenesis of the postmyocardial infarction syndrome (373). However, specific immune pathways mediating pericardial inflammation following myocardial infarction have not been identified.…”

Section: Pericardial Disease Following Myocardial Infarctionmentioning

confidence: 99%

Pathophysiology of Myocardial Infarction

Frangogiannis

2015

Comprehensive Physiology

500

391

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Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction.

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Section: Pericardial Disease Following Myocardial Infarctionmentioning

confidence: 99%

Pathophysiology of Myocardial Infarction

Frangogiannis

2015

Comprehensive Physiology

500

391

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“…Anti-heart antibodies have been described in a var iety of human cardiac disorders [6][7][8], including the postcardiotomy syndrome [9], the post-myocardial in farction syndrome [10] and rheumatic heart disease [11], Two types of anti-heart antibodies have been de scribed: heart/skeletal-muscle-specific and non-tis sue-specific antibodies [12], The former consists main ly of antibodies reactive with sarcolemmal, sarcoplas mic or striational components of muscle, while the non-tissue-specific antibodies can be of the anti-in terstitial (heterophile) type or react with cardiac mito chondria [12].…”

Section: Discussionmentioning

confidence: 99%

Anti-Heart Antibodies in Cardiac Allograft Recipients

Cave

et al. 1984

Int Arch Allergy Immunol

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Serum antibodies reactive with rat cardiac and skeletal muscle were found by indirect immunofluorescence in 11 of 16 heart transplant patients receiving heterologous antithymocyte globulin and 1 of 5 patients receiving cyclosporin A. These antibodies appeared de novo following transplantation and were present for variable lengths of time. Antibodies reactive with rat liver, stomach and kidney were also found in several patients. 9 out of 16 patients receiving equine globulin had antibodies directed against components of the microvasculature, including endothelial, smooth muscle and vessel wall connective tissue. Analysis of antibody kinetics and acute cardiac rejection did not reveal any well-defined associations, though anti-heart antibodies were present in 4 of 6 patients who died from acute rejection.

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“…He presumes that the ability to distinguish antigenic exchanged tissue as 'not self' can be genetically proved. H. van Geld [9] has found antibodies against myocardium in 8 of 14 patients after myocardial infarction by means of the indirect fluorescence method and antiglobulin consumption test. Duheille and Petetier [10] have examined 184 patients with various rheumatic ischaemic cardiopathies and post-myocardial infarction states.…”

Section: Discussionmentioning

confidence: 99%