Cardiovascular risk factors in South America and the Caribbean.

Facing the conclusion of the twentieth century, cardiovascular disease (CVD) remains a major cause of morbidity and a leading contributor to mortality worldwide. Developing countries, including those in South America and the Caribbean, contribute substantially to the global burden of CVD. Indeed, 8 to 9 million deaths attributable to CVD (63% of world total) occurred in developing countries in 1990, compared to 5.3 million deaths in developed nations. Over the next 25 years, it is projected that there will be a rise in CVD mortality rates in the developing countries, linked not only to demographic changes (expansion and aging of the population), but also to progressive urbanization and lifestyle modifications. As such, the ratio of deaths from CVD to deaths from infectious disease is likely to triple during the next 20 years in South America and the Caribbean. The identification of major risk factors and the implementation of control strategies (eg, community education and target of high risk individuals) have contributed to the fall in CVD mortality rates observed in industrialized nations. Most countries of South America and the Caribbean lack an efficient health care system, and the medical and socio-economic consequences of the projected rise in CVD will further strain financial resources. Therefore, appropriate strategies based on knowledge extrapolated from research among other populations should be initiated. The agenda of any lifestyle-related disease control program should include the promotion of healthy diet, exercise, and should encourage decreasing tobacco and alcohol usage.

Quinapril reduces microalbuminuria in essential hypertensive and in diabetic hypertensive subjects.

To investigate the metabolic and renal effects of the nonsulfhydryl, tissue-active ACE inhibitor quinapril in diabetes and in hypertension, we studied 30 essential hypertensives and 24 non-insulin-dependent (type II) diabetic (NIDDM) subjects with hypertension. Systolic and diastolic blood pressures, plasma glucose, and insulin responses to an oral glucose load (75 g), lipid profile, and urinary albumin excretion were evaluated before and after 8 weeks' administration of quinapril (10 to 40 mg/day). Quinapril produced a significant and comparable reduction of arterial blood pressure in both groups. Mean arterial pressure decreased from 114.8 +/- 0.9 to 94.2 +/- 1.1 (-17.9 +/- 1.5%) in the essential hypertensive group and from 118.4 +/- 1.6 to 96.2 +/- 1.4 (-18.4 +/- 1.6%) in the diabetic hypertensive group. In both essential hypertensives and diabetic-hypertensive subjects with microalbuminuria, quinapril significantly and comparably reduced the urinary albumin excretion rate (UAE); UAE decreased from 32.5 +/- 5.5 micrograms/min to 14.7 +/- 3.7 micrograms/min (P < .05 v baseline) in the diabetic-hypertensive group and from 27.5 +/- 3.0 micrograms/min to 11.6 +/- 2.7 micrograms/min (P < .05 v baseline) in the essential hypertensives. Altogether, a direct correlation was found between the initial level of UAE and the UAE reduction after quinapril (delta UAE) (r = 0.706, p < .05). Insulin and glucose responses to an oral glucose tolerance test and the lipid profiles were not modified by quinapril treatment. The results confirm that quinapril is an effective antihypertensive agent that additionally reduces microalbuminuria in both hypertensive diabetics and in patients with essential hypertension, without altering insulin sensitivity and lipid profiles.