Mutations in APOA5 or LDLR increase risk of myocardial infarction

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Multiple rare alleles at LDLR and APOA5 confer risk for early- onset myocardial infarction

Myocardial infarction (MI), a leading cause of death around the world, displays a complex pattern of inheritance1,2. When MI occurs early in life, the role of inheritance is substantially greater1. Previously, rare mutations in low-density lipoprotein (LDL) genes have been shown to contribute to MI risk in individual families3–8 whereas common variants at more than 45 loci have been associated ...

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Multiple rare alleles at LDLR and APOA5 confer risk for early-onset myocardial infarction

Myocardial infarction (MI), a leading cause of death around the world, displays a complex pattern of inheritance1,2. When MI occurs early in life, the role of inheritance is substantially greater1. Previously, rare mutations in low-density lipoprotein (LDL) genes have been shown to contribute to MI risk in individual families3–8 whereas common variants at more than 45 loci have been associated ...

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Thrombin inhibitor reduces myocardial infarction in apoE-/- x LDLR-/- mice.

We have previously shown that atherosclerotic apolipoprotein E-deficient (apoE(-/-)) x LDL receptor-deficient (LDLR(-/-)) mice develop myocardial infarction when exposed to hypoxic stress. This study was performed to assess the role of thrombin and thrombosis in this process. ApoE(-/-) x LDLR(-/-) mice were fed a cholesterol-rich diet for 8 mo and were then subjected to hypoxic stress while rec...

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Angiotensin receptor blockers do not increase risk of myocardial infarction.

The efficacy and safety of angiotensin-converting enzyme (ACE) inhibitors has been well established; these agents have shown an overwhelming and unequivocal benefit in placebo-controlled trials across a spectrum of patients at risk for cardiovascular events.1–9 What has been less clear, however, is whether inhibition of the renin-angiotensin-aldosterone system with angiotensin receptor blockers...

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ژورنال

عنوان ژورنال: Nature Reviews Cardiology

سال: 2014

ISSN: 1759-5002,1759-5010

DOI: 10.1038/nrcardio.2014.213