These findings suggest that alcohol drinking and to a lesser extent occupational adjustment are related to angina directly and not through their association with other factors such as age, genetic background, smoking, physical exercise and early environment.
The relation of the ACE and AT1R gene polymorphisms to coronary heart disease and the severity of coronary artery stenosis has now been investigated in 133 patients with myocardial infarction (MI) or angina pectoris who underwent coronary angiography and in 258 control subjects.
A patient with this condition developed angina and therefore offered a unique opportunity to explore the differential expression of the defective myophosphorylase gene in skeletal and cardiac muscle.
The relation of the ACE and AT1R gene polymorphisms to coronary heart disease and the severity of coronary artery stenosis has now been investigated in 133 patients with myocardial infarction (MI) or angina pectoris who underwent coronary angiography and in 258 control subjects.
In summary, the II genotype of the ACE gene was associated with a longer period of time between the first anginal pain and the onset of myocardial infarction than the ID and DD genotypes of the ACE gene.
Prospective cohort studies of patients with previous myocardial infarction or angina pectoris have underlined the association between increased plasma PAI-1 levels and the risk of coronary events, but the predictive capacity of PAI-1 disappears after insulin resistance marker adjustments.
We assessed the 4G/5G polymorphism of the PAI-I gene in 500 subjects including 148 normal controls, 23 subjects with normal coronary arteries, 28 subjects with a paradoxical acetylcholine response, 97 subjects with angina pectoris (AP) and 204 subjects with myocardial infarction (MI).
We determined the frequency of the Pla2 allele in 589 prospectively recruited subjects aged <50 years presenting with symptomatic CAD with or without myocardial infarction and documented by coronary angiography (group I), 207 subjects investigated prospectively for restenosis 6 months after coronary balloon angioplasty (group II), and 570 control subjects without a history of angina or myocardial infarction, randomly selected from the community.
We determined the frequency of the Pla2 allele in 589 prospectively recruited subjects aged <50 years presenting with symptomatic CAD with or without myocardial infarction and documented by coronary angiography (group I), 207 subjects investigated prospectively for restenosis 6 months after coronary balloon angioplasty (group II), and 570 control subjects without a history of angina or myocardial infarction, randomly selected from the community.