Angiotensin-converting enzyme DD genotype in patients with ischaemic or idiopathic dilated cardiomyopathy

Raynolds, Mary V.; Bristow, Michael R.; Bush, Erik W.; Abraham, William T.; Lowes, Brian D.; Zisman, Lawrence S.; Taft, Charles; Perryman, M. Benjamin

doi:10.1016/0140-6736(93)92061-w

Cited by 385 publications

(158 citation statements)

References 12 publications

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“…The frequency of ACE DD genotype has been reported to be increased in patients with MI [38], dilated cardiomyopathy, and SCD [38][39][40]. Although one recent study showed that HF patients carrying the DD genotype were more likely to die from progressive pump failure rather than SCD, the differential use of ACE inhibitors in the two groups (i.…”

Section: Renin-angiotensin-aldosterone (Raas) Cascadementioning

confidence: 99%

Genomics, heart failure and sudden cardiac death

Darbar

2008

Heart Fail Rev

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Sudden cardiac death (SCD) is among the most common causes of death in developed countries throughout the world. Despite decreased overall cardiac mortality, SCD vrates appear to be increasing in concert with escalating global prevalence of coronary disease and heart failure, the two major conditions predisposing to SCD. This unfavorable trend is a consequence of our inability to identify those who will die suddenly from lethal ventricular arrhythmias and to develop effective therapies for all populations at risk. The known risk factors for SCD lack the predictive power needed to generate preventive strategies for the large number of fatal arrhythmic events that occur among lowerrisk subsets of the population. Even among recognized high-risk subsets, prediction of SCD remains challenging. With the exception of the implantable cardioverter defibrillator (ICD) there are few effective strategies for the prevention and treatment of SCD. This article discusses the prospect of genomic science as an approach to the identification of patients at high-risk for SCD. While the final common pathway for SCD is malignant ventricular arrhythmias, there are many potential contributors, pathways, and mechanisms by which common genetic variants (polymorphisms) could affect initiation and propagation of life-threatening cardiac arrhythmias. Recent advances in genomic medicine now provide us with novel approaches to both identify candidate genes/pathways and relatively common polymorphisms which may predispose patients to increased risk for SCD. Improved understanding of the relationship between common polymorphisms and SCD will not only improve risk stratification such that ICDs can be targeted to those patients most likely to benefit from them but also provide new insight into the pathophysiology of SCD. KeywordsSudden cardiac death; Genomics; Heart failure; Single nucleotide polymorphisms Heart failure and SCD Heart failure (HF) afflicts approximately 5 million people in the United States, with 550,000 new cases reported annually, but as the population ages both the incidence and prevalence is expected to rise [1]. HF is associated with high mortality and is reportedly responsible for 300,000 deaths annually in the US [1]. Prior to advent of neuro-hormonal antagonists, the mean duration of survival after onset of HF was 1.7 years for men and 3.2 years for women, with only half of patients still alive after 5 years of onset [2]. The two modes of death in patients with HF are circulatory failure due to progressive left ventricular (LV) dysfunction associated with gradual worsening of symptoms, or sudden cardiac death (SCD) in relatively clinically stable patients [3].Although the proportion of sudden deaths in published trials varies significantly, probably due to varying interpretations of reported modes of death, clinical trials data suggests that SCD accounts for approximately one-third of all HF deaths [4]. Epidemiologic evidence from the Framingham heart study suggests that about one-half of all deaths due to HF occur...

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Section: Renin-angiotensin-aldosterone (Raas) Cascadementioning

confidence: 99%

Genomics, heart failure and sudden cardiac death

Darbar

2008

Heart Fail Rev

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“…The ACE I/D polymorphism has been linked to various functional effects, for example the DD genotype being associated with high plasma ACE levels in addition to numerous diseases. One of the most extensively studied associations is with cardiovascular diseases, including myocardial infarction (Cambien et al, 1992 ;Nakai et al, 1994), left ventricular hypertrophy and dysfunction (Schunkert et al, 1994), dilated cardiomyopathy (Raynolds et al, 1993;Harn et al, 1995) hypertrophic cardiomyopathy (Marian et al, 1993), carotid thickening (Castellano et al, 1995;Kauma et al, 1996), venous thrombosis (Philipp et al, 1998), nephropathy (Schmidt & Ritz, 1997) and coronary restenosis after stent implantation (Amant et al, 1997). Currently, the best evidence for an association with the ACE I/D polymorphism is with arterial hypertension in men (Fornage et al, 1988 ;Higaki et al, 2000) ; one study of male carriers of the DD genotype showed a 1 .…”

Section: Introductionmentioning

confidence: 99%

The geographic distribution of the ACE II genotype: a novel finding

2007

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SummaryAngiotensin converting enzyme (ACE) gene polymorphism insertion (I) or deletion (D) has been widely studied in different populations, and linked to various functional effects and associated with common diseases. The purpose of the present study was to investigate the relationship between the ACE I/D frequency in different populations and geographic location; ACE I/D allele frequency in the Lebanese population and ACE II genotype contribution to the geographic trend were also identified. Five hundred and seventy healthy volunteers were recruited from the Lebanese population. Genomic DNA was extracted from buccal cells, and amplified by polymerase chain reaction; products were then identified by gel electrophoresis. The frequencies of the different ACE I/D genotypes were determined and tested for Hardy-Weinberg equilibrium (HWE). To assess the relationship between ACE I/D frequency and geographic location, and to identify how the Lebanese population contributes to the geographic trend in ACE I/D frequencies, Eurasian population samples and Asians were incorporated in the analyses from the literature. The frequency of the I allele in the Lebanese population was 27% and the corresponding II genotype was at a frequency of 7 . 37% (in HWE ; P=0 . 979). The ACE I allele and genotype frequencies show an association with longitude, with frequencies increasing eastwards and westwards from the Middle East.

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“…7 The ACE DD genotype is associated with highest circulating and cellular concentration of ACE. 7 Associations have been found between the DD genotype and various conditions, including idiopathic dilated cardiomyopathy, 8 myocardial infarction, 9 and renal diseases. 10,11 The local RAS inhibits penile erection by contracting penile smooth muscle.…”

Section: Introductionmentioning

confidence: 99%

Gene-polymorphisms of angiotensin converting enzyme and endothelial nitric oxide synthase in patients with erectile dysfunction

Jk¹,

Kim

Sw³

et al. 1999

Int J Impot Res

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Aims of the study: Regulation of the penile smooth muscle tone and contractility is closely related to the activity of vasoactive substances, angiotensin II or nitric oxide. We investigated the relationship between gene polymorphism in the angiotensin converting enzyme (ACE) or endothelial nitric oxide synthase (ecNOS) and development of erectile dysfunction. Methods: In 84 subjects with organic erectile dysfunction and 63 control subjects, gene polymorphisms in the ACE and ecNOS were determined by the polymerase chain reaction (PCR). Results: The DD genotype of ACE was signi®cantly (P`0.01) more frequent in subjects with organic erectile dysfunction (54%) than in control subjects (24%). There was no signi®cant difference in the distribution of the genotypes of ecNOS. Conclusion: The deletion polymorphism in the ACE gene, the DD genotype, as a marker of general vascular disease, may be seen more frequently in men with a diagnosis of vasculogenic erectile dysfunction.

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Angiotensin-converting enzyme DD genotype in patients with ischaemic or idiopathic dilated cardiomyopathy

Cited by 385 publications

References 12 publications

Genomics, heart failure and sudden cardiac death

Genomics, heart failure and sudden cardiac death

The geographic distribution of the ACE II genotype: a novel finding

Gene-polymorphisms of angiotensin converting enzyme and endothelial nitric oxide synthase in patients with erectile dysfunction

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