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Yoshiyama, Minoru; Takeuchi, Kazuhide; Omura, Takashi; Izutani, Satoru; Nakamura, Yasuhiro; Akioka, Kaname; Kim, Shokei; Itoh, Hiroshi; Yoshikawa, Junichi

doi:10.1023/a:1007752310881

Cited by 9 publications

(1 citation statement)

References 30 publications

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“…However, it should be noted that a clinical trial of a dihydropyridine CCB (amlodipine) in chronic heart failure was neutral [63]. Furthermore, non-dihydropyridine CCBs to prevent ventricular remodelling after acute myocardial infarction in the context of LV impairment have been associated with harm [64], despite similarly promising pre-clinical evidence [65].…”

Section: Discussionmentioning

confidence: 99%

Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis

et al. 2019

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Current myocarditis guidelines do not advocate treatment to prevent myocardial injury and scar deposition in patients with myocarditis and normal left ventricular ejection fraction. We aimed to ascertain the utility of beta blockers, calcium channel blockers and antagonists of the renin–angiotensin system in ameliorating myocardial injury, scar formation and calcification in animal in vivo models of myocarditis. The project was prospectively registered with the PROSPERO database of systematic reviews (CRD42018089336). Primary outcomes (necrosis, fibrosis and calcification) were meta-analysed with random-effects modelling. 52 studies were systematically reviewed. Meta-analysis was performed compared with untreated controls. In each study, we identified all independent comparisons of treatment versus control groups. The pooled weighted mean difference (WMD) indicated treatment reduced necrosis by 16.9% (71 controlled analyses, 95% CI 13.2–20.7%; P < 0.001), however there was less evidence of an effect after accounting for publication bias. Treatment led to a 12.8% reduction in fibrosis (73 controlled analyses, 95% CI 7.6–18.0%; P < 0.001). After accounting for publication bias this was attenuated to 7.8% but remained significant. Treatment reduced calcification by 4.1% (28 controlled analyses, 95% CI 0.2–8.0%; P < 0.0395). We observed significant heterogeneity in effect size in all primary endpoints, which was predominantly driven by differences between drug categories. Beta blockers and angiotensin-converting enzyme (ACE) inhibitors were the only agents that were effective for both necrosis and fibrosis, while only ACE inhibitors had a significant effect on calcification. This study provides evidence for a role for ACE inhibitors and beta blockers to prevent myocardial injury and scar deposition in in vivo models of myocarditis. There is a need for further well-designed studies to assess the translational application of these treatments.Electronic supplementary materialThe online version of this article (10.1007/s00395-019-0754-x) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis

et al. 2019

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Compound Danshen Tablets ameliorate myocardial ischemia/reperfusion injury-induced ventricular remodeling by regulating autophagy via AMPK/mTOR signaling pathway

Li,

Luo,

Guo

et al. 2024

Chinese Herbal Medicines

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Scar and pulmonary expression and shedding of ACE in rat myocardial infarction

Gaertner

Prunier

Philippe

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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We examined the topology of angiotensin-converting enzyme (ACE) mRNA expression, activity, and shedding in myocardial infarction-induced heart failure and sought to elucidate the source of the increased plasma ACE activity in this model. Three months after coronary ligature, lung, scar, and remaining viable left ventricular tissues were analyzed for ACE mRNA expression as well as tissue and solubilized ACE activity. ACE mRNA expression increased in the scar with respect to infarct severity, decreased in the lung, and remained unchanged in the left ventricle. ACE activity decreased in the lung and increased in the scar tissue and plasma. Shedding of ACE remained constant in the lung and increased in the scar. This study shows that ACE expression and activity is shifted from the pulmonary endothelium to the infarct scar tissue and that constancy of shedding in the lung and its increase in the scar are the source of the increased plasma ACE in congestive heart failure.

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Untitled

Cited by 9 publications

References 30 publications

Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis

Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis

Compound Danshen Tablets ameliorate myocardial ischemia/reperfusion injury-induced ventricular remodeling by regulating autophagy via AMPK/mTOR signaling pathway

Scar and pulmonary expression and shedding of ACE in rat myocardial infarction

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