Alcohol consumption and cardiovascular risk in hypertensives with left ventricular hypertrophy: the LIFE study.

The Losartan Intervention For End point reduction in hypertension (LIFE) study showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke, and myocardial infarction in hypertensives with left ventricular hypertrophy. We compared hazard ratios (HR) in 4287 and 685 participants who reported intakes of 1-7 and >8 drinks/week at baseline, respectively, with those in 4216 abstainers, adjusting for gender, age, smoking, exercise, and race. Within categories, clinical baseline characteristics, numbers randomized to losartan and atenolol, and blood pressure (BP) lowering were similar on the drug regimens. Overall BP control (<140/90 mmHg) at end of follow-up was similar in the categories. Composite end point rate was lower with 1-7 (24/1000 years; HR 0.87, P<0.05) and >8 drinks/week (26/1000 years; HR 0.80, NS) than in abstainers (27/1000 years). Myocardial infarction risk was reduced in both drinking categories (HR 0.76, P<0.05 and HR 0.29, P<0.001, respectively), while stroke risk tended to increase with >8 drinks/week (HR 1.21, NS). Composite risk was significantly reduced with losartan compared to atenolol only in abstainers (HR 0.81 95% confidence interval, CI (0.68, 0.96), P<0.05), while benefits for stroke risk reduction were similar among participants consuming 1-7 drinks/week (HR 0.73, P<0.05) and abstainers (HR 0.72, P<0.01). Despite different treatment benefits, alcohol-treatment interactions were nonsignificant. In conclusion, moderate alcohol consumption does not change the marked stroke risk reduction with losartan compared to atenolol in high-risk hypertensives. Alcohol reduces the risk of myocardial infarction, while the risk of stroke tends to increase with high intake.

How smoking affects blood pressure.

The addictive effects of smoking are only partly known, but it is likely that hemodynamic effects of tobacco smoking may contribute to the habituation. It has since long been known that blood pressure and heart rate increase during smoking. These effects are specifically associated with nicotine while the other components of which more than a thousand have been isolated seem to be of minor importance. The rise in blood pressure is due both to an increase in cardiac output and total peripheral vascular resistance. The blood pressure rise appears immediately and occurs before any increase in circulating catecholamines. In hypertensive patients the blood pressure lowering effect of beta-blockers may be partly abolished by tobacco smoking whereas alpha-receptor blockers seem to maintain the antihypertensive efficacy in smokers. It is a paradox that while smoking acutely increases blood pressure, a slightly lower blood pressure level has been found among smokers than nonsmokers in larger epidemiological studies. Because blood pressure may increase after cessation of smoking, a smoke quitting program should not postpone initiation of antihypertensive treatment in patients otherwise in need of such treatment.

[How does smoking affect blood pressure?]. / Hvordan påvirker røyking blodtrykket?

It has been known for a long time that blood pressure and heart rate increase during smoking. These effects are associated specifically with nicotine. The rise in blood pressure is due both to an increase in cardiac output and in total peripheral vascular resistance. The rise in blood pressure occurs immediately, before any increase in circulating catecholamines. In hypertensives the blood pressure lowering effect of beta-blockers may be diminished by tobacco smoking whereas alpha-receptor blockers on the other hand seem to maintain their antihypertensive efficacy. It is a paradox that while smoking acutely increases blood pressure, some extensive epidemiological studies have shown a slightly lower blood pressure level among smokers than among non-smokers. Because blood pressure may rise after discontinuation of smoking, a smoking cessation programme should not postpone initiation of antihypertensive drug therapy in patients otherwise in need of such treatment.

The Bergen blood pressure study: sodium intake and ambulatory blood pressure in offspring of hypertensive and normotensive families.

Sodium intake, estimated by the 24-h urine sodium excretion, was assessed in 39 offspring of hypertensive families and 37 offspring of normotensive families. The family history of hypertension or normotension was defined according to parental BP data from two surveys conducted 27 years apart. Urine-sodium excretion was similar in offspring of hypertensive and normotensive families, averaging 136 and 137 mmol/24 h, respectively. Monitored by non-invasive methodology in the urine sampling period, the average 24-h ambulatory blood pressure (BP) was approximately 10/10 mmHg higher in offspring of hypertensive than normotensive families. The clinically and statistically significant differences in BP between groups could not be explained by differences in sodium intake. After adjustment for confounding variables, the BP was not associated with the sodium excretion in the material as a whole or in either offspring group.

The Bergen Blood Pressure Study: definition of hypertensive and normotensive families based on 27 years' follow-up.

The familial aggregation of hypertension is well documented. However, many studies on the familial predisposition have suffered from insufficient knowledge of parental blood pressure (BP). In the present study, the family history is defined according to parental data from two BP surveys conducted almost 30 years apart. Data from a population screening in Bergen in 1963-64 were linked with information on marital status to define couples with or without a history of hypertension. Within the screened population a total of 344 married couples, 688 individuals, matched defined age and BP criteria. Four hundred and thirty individuals, representing 270 of the 344 families initial included (79%), attended a follow-up examination in 1990. Six hundred and ninety-one offspring were registered. In all families represented at follow-up, parental BP data from the 1963-64 screening were available. In 160 families (noffspring = 393), both parents also attended the follow-up examination in 1990. In 23 families (noffspring = 54) both parents were hypertensive in 1963-64 as well as in 1990. In 22 families (noffspring = 55) both parents were normotensive at both examinations. Thus, a family data base which is assumed to be useful for studies on offspring with or without a family history of hypertension, has been established. The offspring studies include BP, 24-h ambulatory BP, electrocardiography, echocardiography, endocrine parameters, electrolytes and anthropometric variables.