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Nighttime Blood Pressure Linked to Congestive Heart Failure


UPPSALA, Sweden - A nighttime increase in diastolic blood pressure, or blood pressure that fails to dip at night, are significant independent predictors of congestive heart failure, researchers here reported.

UPPSALA, Sweden, June 28 - A nighttime increase in diastolic blood pressure, or blood pressure that fails to dip at night, are significant independent predictors of congestive heart failure, researchers here found.

In a prospective observational study of 951 men 70 or older, non-dipping nighttime pressure was associated with more than a twofold increase in risk of congestive heart failure, Erik Ingelsson, M.D., Ph.D., and colleagues, of Uppsala University reported in the June 28 issue of the Journal of the American Medical Association.

After adjusting for antihypertensive medication as well as established risk factors for congestive heart failure, including prior acute myocardial infarction, diabetes, smoking, body mass index, and serum cholesterol, as well as office blood pressure, non-dipping was associated with a hazard ratio of 2.21 (95% CI 1.12-4.36) versus men whose blood pressure dropped during nighttime hours (P<0.05).

When 24-hour ambulatory monitoring data were included in the analysis the hazard ratio for nondippers was 2.19 (95% CI 1.06-4.53 P<0.05).

"After adjusting for potential confounders in four different models, a 5-mm Hg increase in nighttime ambulatory [diastolic blood pressure] was associated with a 13% to 25% increased risk of congestive heart failure," the authors wrote.

When patients who with a history of myocardial infarctions were excluded from the analysis, the hazard ratio for nondipping was 2.58 (95% CI 1.09-6.12) after adjusting for antihypertensive medications, traditional congestive heart failure risks and office blood pressure and 2.73 (95% CI 1.10-6.76) when 24-hour monitoring was factored into the analysis, both of which were significant (P<0.05).

The men were recruited between 1990 and 1995 and followed through 2002. The men were age 70 at baseline and were free of congestive heart failure, valvular heart disease, and left ventricular hypertrophy at baseline.

Seventy men developed congestive heart failure during follow-up, with an incidence rate of 8.6 per 1,000 person-years at risk.

The authors noted that earlier studies have linked endothelial dysfunction and hemostasis to nondipping and other studies have suggested that endothelial dysfunction is "an important component of the pathophysiological mechanisms of congestive heart failure, and it has been associated with the progression and prognosis of congestive heart failure. Thus, it is possible that endothelial dysfunction could be a link between increased nocturnal blood pressure and congestive heart failure."

Increased sympathetic activity, they added, has also been associated with both nondipping and as a "presumed causal factor in congestive heart failure."

The authors cited an ongoing controversy about "whether the absence of a nighttime blood pressure decrease per se or an increased 24-hour blood pressure load causes damage."

To address this issue they included 24-hour monitoring data in one of the analysis models and in those analyses "nondipping and nighttime diastolic blood pressure remained significant predictors of congestive heart failure, indicating that nondipping blood pressure pattern per se is important-or is an indicator of an important trait." One such trait, they wrote, is sleep apnea, a trait that will require additional study since this study was not designed to address its possible importance.

Since the study only included elderly, Swedish men, it is unknown if its findings are generalizable to women or to other ethnic groups or other ages. And since men taking antihypertensive medications were permitted in the study the results could reflect residual confounding "despite adjustment for specific antihypertensive treatment."

The authors concluded that nighttime blood pressure "appears to convey additive risk information about congestive heart failure, but its clinical value remains to be established in future studies."

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