Survival after an experimental myocardial infarction: beneficial effects of long-term therapy with captopril.

Pfeffer, Marc A.; Pfeffer, Janice M.; Steinberg, Christian; Finn, Peter

doi:10.1161/01.cir.72.2.406

Cited by 678 publications

(319 citation statements)

References 23 publications

(5 reference statements)

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“…These effects are not only mediated by circulating components, but also by paracrine effects of components of the cascade in several organs and tissues, including the heart, blood vessels, kidneys, and central nervous system. It has been described that infarcted rats treated long-term with captopril show hemodynamic preservation and improved survival (26). This classic study highlights the participation of the RAAS cascade in cardiac remodeling.…”

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 71%

Remodeling in the ischemic heart: the stepwise progression for heart

Mill¹,

Stefanon

Santos

et al. 2011

Braz J Med Biol Res

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Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.

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Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 71%

Remodeling in the ischemic heart: the stepwise progression for heart

Mill¹,

Stefanon

Santos

et al. 2011

Braz J Med Biol Res

View full text Add to dashboard Cite

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“…13 The investigation conformed to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health. Adenoviral vector harboring the human kallistatin cDNA under the control of the cytomegalovirus enhancer/ promoter (Ad.HKS) or adenoviral vector alone (Ad.Null) (1 Â 10 10 plaque-forming units) was injected intramyocardially at six different sites along the border of infarcted area and noninfarcted area at 20 min after ligation.…”

Section: Materials and Methods MI Surgery In Rats And Adenoviral Vectmentioning

confidence: 99%

Role of kallistatin in prevention of cardiac remodeling after chronic myocardial infarction

Gao

Yin

Smith

et al. 2008

Laboratory Investigation

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Oxidative stress causes cardiomyocyte death and subsequent ventricular dysfunction and cardiac remodeling after myocardial infarction (MI), thus contributing to high mortality in chronic heart failure patients. We investigated the effects of kallistatin in cardiac remodeling in a chronic MI rat model and in primary cardiac cells. Human kallistatin gene was injected intramyocardially 20 min after ligation of the left coronary artery. At 4 weeks after MI, expression of human kallistatin in rat hearts was identified by reverse transcription-polymerase chain reaction, immunohistochemistry and ELISA. Kallistatin administration improved cardiac performance, increased mean arterial pressure, decreased myocardial infarct size and restored left ventricular wall thickness. Kallistatin treatment significantly attenuated cardiomyocyte size and atrial natriuretic peptide expression. Kallistatin also reduced collagen accumulation, collagen fraction volume and expression of collagen types I and III, transforming growth factor-b1 (TGF-b1) and plasminogen activator inhibitor-1 in the myocardium. Inhibition of cardiac hypertrophy and fibrosis by kallistatin was associated with increased cardiac nitric oxide (NO) levels and decreased superoxide formation, NADH oxidase activity and p22-phox expression. Moreover, in both primary cultured rat cardiomyocytes and myofibroblasts, recombinant kallistatin inhibited intracellular superoxide formation induced by H 2 O 2 , and the antioxidant effect of kallistatin was abolished by No-nitro-L-arginine methyl ester (L-NAME), indicating a NO-mediated event. Kallistatin promoted survival of cardiomyocytes subjected to H 2 O 2 treatment, and inhibited H 2 O 2 -induced Akt and ERK phosphorylation, as well as NF-kB activation. Furthermore, kallistatin abrogated TGF-b-induced collagen synthesis and secretion in cultured myofibroblasts. This is the first study to demonstrate that kallistatin improves cardiac performance and prevents post-MI-induced cardiac hypertrophy and fibrosis through its antioxidant action. Myocardial infarction (MI) leads to cardiac remodeling with complex structural alterations. After an ischemic insult, left ventricle (LV) enlargement is followed by progressive diastolic stiffness, enhanced wall stress and oxygen consumption, thus resulting in cardiomyocyte hypertrophy, interstitial fibrosis and decreased cardiac output. Increased reactive oxygen species (ROS) levels are recognized to be involved in ischemic heart failure and considered to be a major cause of cardiomyocyte death, ventricular dysfunction and heart failure progress. 1 Under pathological conditions, increased oxidative stress damages DNA and mitochondrial function, activates proapoptotic signaling kinases and leads to myocyte apoptosis or necrosis. 2,3 Elevation of ROS activates a series of hypertrophic signaling kinases and transcription factors to stimulate cardiac hypertrophy. 3,4 Moreover, ROS stimulate fibroblast proliferation and activate the expression of profibrotic factors, including transforming growth...

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“…of other experimental models, where a decrease in mortality with the use of ACEIs after acute myocardial infarction was observed 26,27 . This difference could be explained by the duration of the study as those authors observed their animals for a period of one year but our follow-up lasted only three months.…”

Section: Referencesmentioning

confidence: 87%

“…Pfeffer et al 26 showed that the administration of captopril to rats reduces mortality in an observational period of one year after coronary artery occlusion only in animals with infarcts that occupied from 20% to 40% of the left ventricle (moderate infarct). Animals with small (<20% of the left ventricle) and large (>40% of the left ventricle) infarcts did not benefit from the treatment in regard to survival.…”

Section: Referencesmentioning

confidence: 99%