Beneficial effects of angiotensin-converting enzyme inhibitor and nitrate association on left ventricular remodeling in patients with large acute myocardial infarction: the delapril remodeling after acute myocardial infarction (DRAMI) trial

Latini, Roberto; Staszewsky, Lidia; Maggioni, Aldo P.; Marino, Paolo; Hernández-Bernal, Francisco; Tognoni, Gianni; Labarta, Violeta; Gramenzi, Silvana; Bianchi, Federico; Sarcina, Giuseppe; Cremonesi, G; Nicolosi, Gian Luigi; Geraci, E

doi:10.1016/s0002-8703(02)94777-0

Cited by 9 publications

(4 citation statements)

References 19 publications

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“…Clinical trials of the TGF-β/SMADs pathway in MI The statin, angiotensin converting enzyme inhibitor (ACEI) and angiotensin receptor antagonist (ARB) mentioned above that may inhibit this pathway have been widely used in clinical practice and achieved good results in patients with MI 469,470 . Besides, N-acetylcysteine (NAC) can reduce serum TGF-β levels in Patients with ST-segment elevation MI 471 .…”

Section: Tgf-β/smads Signaling Pathway In MImentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

350

117

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Although the treatment of myocardial infarction (MI) has improved considerably, it is still a worldwide disease with high morbidity and high mortality. Whilst there is still a long way to go for discovering ideal treatments, therapeutic strategies committed to cardioprotection and cardiac repair following cardiac ischemia are emerging. Evidence of pathological characteristics in MI illustrates cell signaling pathways that participate in the survival, proliferation, apoptosis, autophagy of cardiomyocytes, endothelial cells, fibroblasts, monocytes, and stem cells. These signaling pathways include the key players in inflammation response, e.g., NLRP3/caspase-1 and TLR4/MyD88/NF-κB; the crucial mediators in oxidative stress and apoptosis, for instance, Notch, Hippo/YAP, RhoA/ROCK, Nrf2/HO-1, and Sonic hedgehog; the controller of myocardial fibrosis such as TGF-β/SMADs and Wnt/β-catenin; and the main regulator of angiogenesis, PI3K/Akt, MAPK, JAK/STAT, Sonic hedgehog, etc. Since signaling pathways play an important role in administering the process of MI, aiming at targeting these aberrant signaling pathways and improving the pathological manifestations in MI is indispensable and promising. Hence, drug therapy, gene therapy, protein therapy, cell therapy, and exosome therapy have been emerging and are known as novel therapies. In this review, we summarize the therapeutic strategies for MI by regulating these associated pathways, which contribute to inhibiting cardiomyocytes death, attenuating inflammation, enhancing angiogenesis, etc. so as to repair and re-functionalize damaged hearts.

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Section: Tgf-β/smads Signaling Pathway In MImentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

350

117

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“…The exact mechanism by which captopril exerts its action on nerve sprouting and nerve uniform regeneration after MI is not known. However, ACEI has proven effects in improving left ventricular remodeling after myocardial infarction 26,27 and in reducing infarct size in animal models. 28 In addition, previous studies have documented that ACEI promotes angiogenesis and increase capillary density in the infarct zone and border zone.…”

Section: Discussionmentioning

confidence: 99%

Effects of angiotensin converting enzyme inhibition on cardiac innervation and ventricular arrhythmias after myocardial infarction

Yan¹,

Hu²,

Wang³

et al. 2008

CIM

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Purpose: To investigate the influence of angiotensin-converting enzyme inhibitor (ACEI) on cardiac innervation and inducible ventricular arrhythmias (VAs) in healed myocardial infarction (MI). Methods: Left anterior descending coronary artery was ligated to induce MI in 30 rabbits. After oral captopril (10mg/kg/d) for 8 weeks, electrophysiological study was performed to evaluate the incidence of inducible VAs. RT-PCR and immunohistochemistry were used to measure the cardiac innervation. Results: Eight weeks after the operation, the incidence of inducible VAs in the MI-placebo group was higher (58.3%, 7/12) than in the sham operation group (16.7%, 2/12, P < 0.05). However, the incidence of inducible VAs in the MI-captopril group was lower (27.2%, 3/11) than in the MI-placebo group (P < 0.05). Proliferation and growth of nerve fibres in the MI-placebo group were mainly distributed at the periphery of the infarcted and perivascular regions of the myocardium. The density of nerve fibres increased in the MI-placebo group (3889±521 ?m2/mm2) compared with the sham group (1727±304 ?m2/mm2, P < 0.01) at the infarct border. In the MI-captopril group, the density of nerve fibres (3507±433 ?m2/mm2) at the infarct border did not differ from that in the MI-placebo group (P=0.07). MI-induced abnormal nerve fibre distribution was partly restored by captopril treatment. Conclusion: In this study, prolonged captopril treatment was effective in preventing VAs in healed MI, partly by attenuating the spatial heterogeneity of cardiac innervation.

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“…The use of oral ISMN plus an ACE inhibitor for 3 months was evaluated in 177 patients with a large acute myocardial infarction [83] . Patients were treated with one of two ACE-inhibitors plus ISMN or placebo.…”

Section: Acute Myocardial Infarctionmentioning

confidence: 99%

Side effects of using nitrates to treat heart failure and the acute coronary syndromes, unstable angina and acute myocardial infarction

Thadani¹,

Ripley²

2007

Expert Opinion on Drug Safety

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Nitrates are potent venous dilators and anti-ischemic agents. They are widely used for the relief of chest pain and pulmonary congestion in patients with acute coronary syndromes and heart failure. Nitrates, however, do not reduce mortality in patients with acute coronary syndromes. Combination of nitrates and hydralazine when given in addition to beta-blockers and angiotensin-converting enzyme (ACE) inhibitors reduce mortality and heart failure hospitalizations in patients with heart failure due to left ventricular systolic dysfunction who are of African-American origin. Side effects during nitrate therapy are common but are less well described in the literature compared with the reported side effects in patients with stable angina pectoris. The reported incidence of side effects varies highly among different studies and among various disease states. Headache is the most commonly reported side effect with an incidence of 12% in acute heart failure, 41-73% in chronic heart failure, 3-19% in unstable angina and 2-26% in acute myocardial infarction. The reported incidence of hypotension also differs: 5-10% in acute heart failure, 20% in chronic heart failure, 9% in unstable angina and < 1-48% in acute myocardial infarction, with the incidence being much higher with concomitant nitrate therapy plus angiotensin-converting enzyme inhibitors. Reported incidence of dizziness is as low as 1% in patients with acute myocardial infarction to as high as 29% in patients with heart failure. Severe headaches and/or symptomatic hypotension may necessitate discontinuation of nitrate therapy. Severe life threatening hypotension or even death may occur when nitrates are used in patients with acute inferior myocardial infarction associated with right ventricular dysfunction or infarction, or with concomitant use of phosphodiesterase-5 inhibitors or N-acetylcysteine. Despite the disturbing observational reports in the literature that continuous and prolonged use of nitrates may lead to increased mortality and recurrent myocardial infarction in patients with stable coronary artery disease, no such adverse effects of nitrates have been reported in the large randomized trials in patients with acute myocardial infarction or chronic heart failure.

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Beneficial effects of angiotensin-converting enzyme inhibitor and nitrate association on left ventricular remodeling in patients with large acute myocardial infarction: the delapril remodeling after acute myocardial infarction (DRAMI) trial

Cited by 9 publications

References 19 publications

Signaling pathways and targeted therapy for myocardial infarction

Signaling pathways and targeted therapy for myocardial infarction

Effects of angiotensin converting enzyme inhibition on cardiac innervation and ventricular arrhythmias after myocardial infarction

Side effects of using nitrates to treat heart failure and the acute coronary syndromes, unstable angina and acute myocardial infarction

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