1.This review argues that the deletion (D) allele of an insertion (I)/deletion polymorphism of the angiotensin I-converting enzyme (ACE) gene is a marker for a variant associated with increased ACE expression, as well as myocardial infarction (MI) and other life-threatening conditions.2.
ACE insertion/deletion gene polymorphism is associated neither with the prevalence nor the extent of coronary artery disease, nor with myocardial infarction in this relatively large sample of Caucasian men and women.
Angiotensin-converting enzyme (ACE) inhibitors reduce the progression of atherosclerosis in animal models and reinfarction rates after myocardial infarction in humans.
ACE genotype distributions were not different between the Caucasian community control group and the CHD or the MI subgroups; the odds ratios and 95% confidence limits for the CHD group were 0.96 (0.73-1.27) for the D allele and 1.02 (0.80-1.31) for D homozygotes; for the MI group these values were 1.00 (0.83-1.20) and 0.99 (0.74-1.32) respectively.
Angiotensin-converting enzyme gene polymorphism interacts with left ventricular ejection fraction and brain natriuretic peptide levels to predict mortality after myocardial infarction.
Angiotensin-converting enzyme (ACE) inhibitors improve the prognosis in mild, moderate and severe heart failure, as well as preventing the onset of heart failure in patients with chronic asymptomatic left-ventricular dysfunction and in those with reduced ejection fraction after myocardial infarction (MI).
ACE polymorphism is not associated with the development of premature MI and this might be due to the low prevalence of hypertension in young coronary patients.
Angiotensin converting enzyme inhibitors (ACE-I), are beneficial both in heart failure with reduced ejection fraction (HF-REF) and after myocardial infarction (MI).
Angiotensin-Converting Enzyme Inhibitors Provide Better Long-Term Survival Benefits to Patients With AMI Than Angiotensin II Receptor Blockers After Survival Hospital Discharge.
Angiotensin-converting enzyme inhibitors versus angiotensin receptor blockers in hypertensive patients with myocardial infarction or heart failure: a systematic review and meta-analysis.
ACE inhibitor suppresses cardiac remodeling after myocardial infarction by regulating dendritic cells and AT<sub>2</sub> receptor-mediated mechanism in mice.
Angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism has been shown to be an independent risk factor for myocardial infarction and other cardiovascular diseases.
A 287-bp insertion/deletion polymorphism in intron 16 of the ACE gene was examined by polymerase chain reaction in a cross-sectional study of 100 healthy subjects and 178 patients with coronary artery disease (CAD) (70 angina pectoris, 108 myocardial infarction), whose serum ACE levels were concomitantly measured.
A deletion polymorphism localized in intron 16 of the human angiotensin converting enzyme gene, corresponding to a 287 bp long Alu repetitive sequence, was found to be associated with increased risk of myocardial infarction in various subgroups, including European, French and Japanese coronary patients.