Low Diastolic Blood Pressure and Mortality in Older Women. Results From the Women's Health Initiative Long Life Study.

BACKGROUND: Recommended systolic blood pressure targets often do not consider the relationship of low diastolic blood pressure (DBP) levels with cardiovascular disease (CVD) and all-cause mortality risk, which is especially relevant for older people with concurrent comorbidities. We examined the relationship of DBP levels to CVD and all-cause mortality in older women in the Women's Health Initiative Long Life Study (WHI-LLS). METHODS: The study sample included 7,875 women (mean age: 79 years) who underwent a blood pressure measurement at an in-person home visit conducted in 2012-2013. CVD and all-cause mortality were centrally adjudicated. Hazard ratios (HRs) were obtained from adjusted Cox proportional hazards models. RESULTS: After 5 years follow-up, all-cause mortality occurred in 18.4% of women. Compared with a DBP of 80 mm Hg, the fully adjusted HR for mortality was 1.33 (95% confidence interval [CI]: 1.04-1.71) for a DBP of 50 mm Hg and 1.67 (95% CI: 1.29-2.16) for a DBP of 100 mm Hg. The HRs for CVD were 1.14 (95% CI: 0.78-1.67) for a DBP of 50 mm Hg and HR 1.50 (95% CI: 1.03-2.17) for a DBP of 100 mm Hg. The nadir DBP associated with lowest mortality risk was 72 mm Hg overall. CONCLUSIONS: In older women, consideration should be given to the potential adverse effects of low and high DBP. Low DBP may serve as a risk marker. DBP target levels between 68 and 75 mm Hg may avoid higher mortality risk.

Salt and cardiovascular disease: insufficient evidence to recommend low sodium intake.

Several blood pressure guidelines recommend low sodium intake (<2.3 g/day, 100 mmol, 5.8 g/day of salt) for the entire population, on the premise that reductions in sodium intake, irrespective of the levels, will lower blood pressure, and, in turn, reduce cardiovascular disease occurrence. These guidelines have been developed without effective interventions to achieve sustained low sodium intake in free-living individuals, without a feasible method to estimate sodium intake reliably in individuals, and without high-quality evidence that low sodium intake reduces cardiovascular events (compared with moderate intake). In this review, we examine whether the recommendation for low sodium intake, reached by current guideline panels, is supported by robust evidence. Our review provides a counterpoint to the current recommendation for low sodium intake and suggests that a specific low sodium intake target (e.g. <2.3 g/day) for individuals may be unfeasible, of uncertain effect on other dietary factors and of unproven effectiveness in reducing cardiovascular disease. We contend that current evidence, despite methodological limitations, suggests that most of the world's population consume a moderate range of dietary sodium (2.3-4.6g/day; 1-2 teaspoons of salt) that is not associated with increased cardiovascular risk, and that the risk of cardiovascular disease increases when sodium intakes exceed 5 g/day. While current evidence has limitations, and there are differences of opinion in interpretation of existing evidence, it is reasonable, based upon observational studies, to suggest a population-level mean target of <5 g/day in populations with mean sodium intake of >5 g/day, while awaiting the results of large randomized controlled trials of sodium reduction on incidence of cardiovascular events and mortality.

Hypertension: evolving from standardized to individualized care.

: The hypertension paradigm has contributed to a dramatic reduction in CVD mortality. This has been achieved by applying average results of population studies to identify a target population and design a common intervention to achieve a BP goal. Progressive lowering of the BP threshold has expanded the fraction of persons at risk who have access to treatment. Meanwhile, falling risk reduces potential benefit, while treatment-induced adverse events increase - making further expansion of the treatment pool no longer tenable. Still, CVD remains the leading cause of death. Fortunately, new science reveals opportunities to enhance CVD prevention when BP management is based upon individual characteristics. Treatment can be directed at those most likely to benefit, while sparing others the hazards of unnecessary therapy. Treatment can be designed to achieve a variety of physiological objectives that influence cardiovascular outcomes. This new strategy should improve both the efficacy and efficiency of BP-related CVD prevention.

Should Antihypertensive Treatment Recommendations Differ in Patients With and Without Coronary Heart Disease? (from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]).

Thiazide-type diuretics have been recommended for initial treatment of hypertension in most patients, but should this recommendation differ for patients with and without coronary heart disease (CHD)? The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) was a randomized, double-blind hypertension treatment trial in 42,418 participants with high risk of combined cardiovascular disease (CVD) (25% with preexisting CHD). This post hoc analysis compares long-term major clinical outcomes in those assigned amlodipine (n = 9048) or lisinopril (n = 9,054) with those assigned chlorthalidone (n = 15,255), stratified by CHD status. After 4 to 8 years, randomized treatment was discontinued. Total follow-up (active treatment + passive surveillance using national databases for deaths and hospitalizations) was 8 to 13 years. For most CVD outcomes, end-stage renal disease, and total mortality, there were no differences across randomized treatment arms regardless of baseline CHD status. In-trial rates of CVD were significantly higher for lisinopril compared with chlorthalidone, and rates of heart failure were significantly higher for amlodipine compared with chlorthalidone in those with and without CHD (overall hazard ratios [HRs] 1.10, p <0.001, and 1.38, p <0.001, respectively). During extended follow-up, significant outcomes according to CHD status interactions (p = 0.012) were noted in amlodipine versus chlorthalidone comparison for CVD and CHD mortality (HR 0.88, p = 0.04, and 0.84, p = 0.04, respectively) in those with CHD at baseline (HR 1.06, p = 0.15, and 1.08, p = 0.17) and in those without. The results of the overall increased stroke mortality in lisinopril compared with chlorthalidone (HR 1.2; p = 0.03) and hospitalized heart failure in amlodipine compared with chlorthalidone (HR 1.12; p = 0.01) during extended follow-up did not differ by baseline CHD status. In conclusion, these results provide no reason to alter our previous recommendation to include a properly dosed diuretic (such as chlorthalidone 12.5 to 25 mg/day) in the initial antihypertensive regimen for most hypertensive patients.

Pressor response to initial blood pressure monotherapy is associated with cardiovascular mortality.

BACKGROUND: A paradoxical pressor systolic response to initial antihypertensive monotherapy has been observed in 8% of hypertensive patients. The long-term consequences of this finding are unknown. METHODS: We included 945 hypertensive patients with baseline systolic blood pressure (SBP) ≥140mm Hg. A 4-week washout period free of antihypertensive drugs was allowed for those already on treatment at entry. Mortality outcomes were ascertained from the National Death Index. Subjects were categorized by SBP response into depressor (≥10mm Hg fall), nonresponder, and pressor (≥10mm Hg rise) categories. RESULTS: There were 268 fatalities. Of these, 100 (37%) were from cardiovascular disease (CVD), of which 70 (70%) were due to coronary artery disease (CAD). A pressor response was associated with higher SBP at 1 year compared with the nonresponder or depressor response (141 vs. 136 vs. 136mm Hg). CVD mortality was greater in pressors than depressors (hazard ratio (HR) = 3.0; 95% confidence interval (CI) = 1.4-6.4; P = 0.004], as was CAD (HR = 3.1; 95% CI = 1.4-6.8; P < 0.01) and all-cause mortality (HR = 1.7; 95% CI = 1.1-2.6; P = 0.02), after adjusting for 1-year SBP and other possible confounders. CONCLUSIONS: We found the incidence of a pressor response to monotherapy at 3 months was significantly, specifically, and independently associated with higher subsequent cardiovascular mortality.

Water and sodium in heart failure: a spotlight on congestion.

Despite all available therapies, the rates of hospitalization and death from heart failure (HF) remain unacceptably high. The most common reasons for hospital admission are symptoms related to congestion. During hospitalization, most patients respond well to standard therapy and are discharged with significantly improved symptoms. Post-discharge, many patients receive diligent and frequent follow-up. However, rehospitalization rates remain high. One potential explanation is a persistent failure by clinicians to adequately manage congestion in the outpatient setting. The failure to successfully manage these patients post-discharge may represent an unmet need to improve the way congestion is both recognized and treated. A primary aim of future HF management may be to improve clinical surveillance to prevent and manage chronic fluid overload while simultaneously maximizing the use of evidence-based therapies with proven long-term benefit. Improvement in cardiac function is the ultimate goal and maintenance of a "dry" clinical profile is important to prevent hospital admission and improve prognosis. This paper focuses on methods for monitoring congestion, and strategies for water and sodium management in the context of the complex interplay between the cardiac and renal systems. A rationale for improving recognition and treatment of congestion is also proposed.