Trends in the risk of mortality due to cardiovascular diseases in five Brazilian geographic regions from 1979 to 1996.

OBJECTIVE - To analyze the trends in risk of death due to cardiovascular diseases in the northern, northeastern, southern, southeastern, and central western Brazilian geographic regions from 1979 to 1996. METHODS - Data on mortality due to cardiovascular, cardiac ischemic, and cerebrovascular diseases in 5 Brazilian geographic regions were obtained from the Ministry of Health. Population estimates for the time period from 1978 to 1996 in the 5 Brazilian geographic regions were calculated by interpolation with the Lagrange method, based on the census data from 1970, 1980, 1991, and the population count of 1996, for each age bracket and sex. Trends were analyzed with the multiple linear regression model. RESULTS - Cardiovascular diseases showed a declining trend in the southern, southeastern, and northern Brazilian geographic regions in all age brackets and for both sexes. In the northeastern and central western regions, an increasing trend in the risk of death due to cardiovascular diseases occurred, except for the age bracket from 30 to 39 years, which showed a slight reduction. This resulted from the trends of cardiac ischemic and cerebrovascular diseases. The analysis of the trend in the northeastern and northern regions was impaired by the great proportion of poorly defined causes of death. CONCLUSION - The risk of death due to cardiovascular, cerebrovascular, and cardiac ischemic diseases decreased in the southern and southeastern regions, which are the most developed regions in the country, and increased in the least developed regions, mainly in the central western region.

Effect of Controlling Hypercholesterolemia on Myocardial Ischemia.

Hypercholesterolemia causes myocardial ischemia, even in the absence of obstructive coronary artery lesions. Reductions in cholesterol are associated with improved clinical outcomes that may reflect reversal of endothelial dysfunction, lesion regression, or both. This review explores experimental and clinical evidence that supports these observations. These include: 1) mechanisms by which hypercholesterolemia (and other risk factors for coronary artery disease) causes endothelial dysfunction; 2) the role that hypercholesterolemia and endothelial dysfunction play in atherogenesis, lesion complications, and clinical ischemic syndromes; and 3) compelling data that illustrate the benefits of cholesterol control. The latter include transformation of the plaque lipid composition to a more favorable profile, improved blood pressure control, normalization of exercise test results, improved exercise tolerance, and reversal or prevention of myocardial perfusion abnormalities. Collectively, these data support the notion that control of cholesterol is important to both the prevention and treatment of cardiac disease.) (c)2001 CHF, Inc.

Angiotensin-converting enzyme and apolipoprotein B polymorphisms in coronary artery disease.

The association between angiotensin-converting enzyme (ACE) as well as apolipoprotein B polymorphisms and dyslipidemia and coronary artery disease (CAD) is controversial. We assessed the distribution of ACE insertion and/or deletion, apolipoprotein B signal peptide insertion and/or deletion, and apolipoprotein B XbaI restriction fragment length polymorphisms in 388 nondiabetic patients. We studied 112 patients with angiographically defined asymptomatic CAD or with stable functional classes I and II angina and 139 patients with acute myocardial infarction who were age matched to 137 control subjects. Univariate analysis showed higher prevalence of Xba50% reduction of lumen diameter. Overall, multivariable regression disclosed traditional risk factors and elevated levels of apolipoprotein B for men and reduced levels of apolipoprotein AI for women as independent variables for CAD. After adjustment for the most important subset of risk factors (age, hypertension, hypercholesterolemia, and smoking), apolipoprotein B XbaI polymorphism was disclosed as an independent variable for CAD. Apolipoprotein B XbaI was also selected as an independent variable for acute myocardial infarction after adjusting for age, hypertension, hypercholesterolemia, and smoking. Thus, in addition to traditional coronary risk factors, apolipoproteins B and AI, and apolipoprotein B XbaI polymorphism could be considered predictors of CAD.

Smoking and lipoprotein abnormalities on platelet aggregation in coronary heart disease.

This study aimed to clarify whether smoking had any influence on platelet aggregability in coronary patients with different lipoprotein abnormalities. We studied 297 non-diabetic patients with coronary heart disease, 40 to 85 years of age, 223 (75%) male, 167 smokers and 130 never smokers. After 3 months on Step-One diet, without any regular medication, patients had fasting plasma total cholesterol levels > or = 6.2 mmol/L; low-density lipoprotein > or = 4.14 mmol/L; and different levels of high-density lipoprotein and triglycerides. Platelet aggregation was analyzed by turbidometric method of Born. Patients were classified in groups of smokers and non-smokers. Results showed that platelet hyperaggregability was more prevalent in smokers with lower levels of high-density lipoprotein (47% vs. 20%; P=0.004 for spontaneous platelet aggregation, 56% vs. 33%; P=0.02 for adenosine diphosphate induced platelet aggregation), and in smokers with hypertrygliceridemia (64% vs. 29%; P=0.004 for spontaneous, 81% vs. 43%; P<0.0001 for adenosine diphosphate induced, and 87% vs. 46%; P<0.0001 for adrenaline induced platelet aggregation). Platelet hypoaggregability was greater in non-smokers with normal high-density lipoprotein and triglycerides plasma levels when compared to non-smokers with the same lipid profile (39% vs. 12%; P=0.004). In conclusion, smoking increased platelet reactivity in hypercholesterolemic patients with low high-density lipoprotein levels or high triglycerides levels.