Ventricular arrhythmias in the acute and chronic phases after acute myocardial infarction. Effect of intervention with captopril.

Søgaard, Peter; Gøtzsche, Carl-Otto; Ravkilde, Jan; Nørgaard, Aage; Thygesen, Kristian

doi:10.1161/01.cir.90.1.101

Cited by 55 publications

(30 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Remodeling is linked to heart failure progression and is associated with poor prognosis following myocardial infarction. Ventricular dilation following myocardial infarction is an important predictor of mortality [6] and adverse cardiac events [7], including the development of heart failure and ventricular arrhythmias [8], [9]. The extent of adverse remodeling depends on the size of the infarct but is also directly affected by the pathologic and structural changes associated with infarct healing.…”

Section: Introductionmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

571

499

View full text Add to dashboard Cite

Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

show abstract

Section: Introductionmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

571

499

View full text Add to dashboard Cite

show abstract

“…6, lead to worse arrhythmic outcomes because of increased wall strain and stress, which in turn trigger stretch-activated ion channels. 23,24 Also, LV remodeling is correlated with infarct size, 25,26 and so are arrhythmic events. 27 The increased wall stress caused by LV dilation and thinning also elicit compensatory responses, and when these responses are inadequate, a vicious cycle of further dilation ensues, and the heart eventually fails.…”

Section: Discussionmentioning

confidence: 99%

Image-Based Left Ventricular Shape Analysis for Sudden Cardiac Death Risk Stratification

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Experimental and clinical studies have demonstrated that angiotensin-converting enzyme (ACE) inhibitors prevent ventricular arrhythmias following acute or chronic myocardial ischemia [1, 2, 3, 4, 5, 6]. This antiarrhythmic effect was generally considered to be the result of reduced severity of ischemia and the subsequent injury to the myocardium [6].…”

Section: Introductionmentioning

confidence: 99%

“…Recent animal studies have indicated that other factors, such as the remodelling of the left ventricle [1], the suppressed release of endothelin-1 [2]and noradrenaline [3], may be also responsible for the antiarrhythmic effect of ACE inhibitors. In patients with acute or chronic myocardial ischemia, the attenuation of sympathetic activation [4]and left ventricular dilatation [5]is particularly important in mediating the antiarrhythmic effect of ACE inhibitors.…”

Section: Introductionmentioning

confidence: 99%

ACE Inhibitors Suppress Ischemia-Induced Arrhythmias by Reducing the Spatial Dispersion of Ventricular Repolarization

Wang

1999

Cardiology

View full text Add to dashboard Cite

The effect of angiotensin-converting enzyme (ACE) inhibitors on ischemia-induced spatial dispersion of ventricular repolarization was investigated in 12 pentobarbitone-anesthetized sheep. The obtuse marginal coronary artery was occluded in the pretreated animals (enalapril maleate, 0.4 mg/kg, i.v., n = 6) and controls (normal saline, i.v., n = 6). The activation-recovery intervals were determined from the unipolar ECGs acquired from the ischemic region. There was a significant increase in the pooled activation-recovery interval dispersion in both groups at 30 min of coronary occlusion (p < 0.01), however, the increase in the treatment group was smaller than that of the controls (15.9 ± 9.7 vs. 43.6 ± 19.9 ms, p < 0.01). Ventricular ectopic beats were observed in the 6 controls and in only 1 pretreated animal. Conclusions: ACE inhibitors suppress the spatial dispersion of ventricular repolarization and this may be attributed to, at least in part, its antiarrhythmic effect.

show abstract

Ventricular arrhythmias in the acute and chronic phases after acute myocardial infarction. Effect of intervention with captopril.

Cited by 55 publications

References 29 publications

The immune system and cardiac repair

The immune system and cardiac repair

Image-Based Left Ventricular Shape Analysis for Sudden Cardiac Death Risk Stratification

ACE Inhibitors Suppress Ischemia-Induced Arrhythmias by Reducing the Spatial Dispersion of Ventricular Repolarization

Contact Info

Product

Resources

About