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A CUTE DECOMPENSATED HEART failure (ADHF) remains a common cause of hospitalization worldwide but it is not clear how patients admitted for clinical deterioration should be managed. Patients are generally treated with diuretics and vasodilators, while patients with evidence of peripheral hypoperfusion also may receive positive inotropes, usually dobutamine or milrinone. These positive inotropic agents improve hemodynamics and symptoms by increasing intracellular cyclic adenosine monophosphate within the failing heart but have been associated with an increased risk of death and other cardiovascular events. 1,2 Levosimendan is a pharmacological agent that exerts positive inotropic effects by binding to cardiac troponin C in a calcium-dependent manner, sensitizing myofilaments to calcium.3,4 Levosimendan also has vasodilatory proper- Context Because acute decompensated heart failure causes substantial morbidity and mortality, there is a need for agents that at least improve hemodynamics and relieve symptoms without adversely affecting survival.Objective To assess the effect of a short-term intravenous infusion of levosimendan or dobutamine on long-term survival. Design, Setting, and PatientsThe Survival of Patients With Acute Heart Failure in Need of Intravenous Inotropic Support (SURVIVE) study was a randomized, doubleblind trial comparing the efficacy and safety of intravenous levosimendan or dobutamine in 1327 patients hospitalized with acute decompensated heart failure who required inotropic support. The trial was conducted at 75 centers in 9 countries and patients were randomized between March 2003 and December 2004. Interventions Intravenous levosimendan (n = 664) or intravenous dobutamine (n=663).Main Outcome Measure All-cause mortality at 180 days.Results All-cause mortality at 180 days occurred in 173 (26%) patients in the levosimendan group and 185 (28%) patients in the dobutamine group (hazard ratio, 0.91; 95% confidence interval, 0.74-1.13; P=.40). The levosimendan group had greater decreases in B-type natriuretic peptide level at 24 hours that persisted through 5 days compared with the dobutamine group (PϽ.001 for all time points). There were no statistical differences between treatment groups for the other secondary end points (all-cause mortality at 31 days, number of days alive and out of the hospital, patient global assessment, patient assessment of dyspnea at 24 hours, and cardiovascular mortality at 180 days). There was a higher incidence of cardiac failure in the dobutamine group. There were higher incidences of atrial fibrillation, hypokalemia, and headache in the levosimendan group. ConclusionDespite an initial reduction in plasma B-type natriuretic peptide level in patients in the levosimendan group compared with patients in the dobutamine group, levosimendan did not significantly reduce all-cause mortality at 180 days or affect any secondary clinical outcomes. Trial Registration clinicaltrials.gov Identifier: NCT00348504

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AbbVie.

Abstract-Recent reports suggesting that the prevalence of primary hyperaldosteronism may be higher than historically thought have relied on an elevated plasma aldosterone concentration/plasma renin activity ratio to either diagnose or identify subjects at high risk of having primary hyperaldosteronism and have not included suppression testing of all evaluated subjects. In this prospective study of 88 consecutive patients referred to a university clinic for resistant hypertension, we determined the 24-hour urinary aldosterone excretion during high dietary salt ingestion, baseline plasma renin activity, and plasma aldosterone in all subjects. Primary hyperaldosteronism was confirmed if plasma renin activity was Ͻ1.0 ng/mL per hour and urinary aldosterone was Ͼ12 g/24-hour during high urinary sodium excretion (Ͼ200 mEq/24-hour). Eighteen subjects (20%) were confirmed to have primary hyperaldosteronism. The prevalence of hyperaldosteronism was similar in black and white subjects. Of the 14 subjects with confirmed hyperaldosteronism who have been treated with spironolactone, all have manifested a significant reduction in blood pressure. In this population, an elevated plasma aldosterone/plasma renin activity ratio (Ͼ20) had a sensitivity of 89% and a specificity of 71% with a corresponding positive predictive value of 44% and a negative predictive value of 96%. These data provide strong evidence that hyperaldosteronism is a common cause of resistant hypertension in black and white subjects. Key Words: hyperaldosteronism Ⅲ hypertension, essential Ⅲ blacks Ⅲ diuretics Ⅲ renin P rimary hyperaldosteronism (PA) has historically been thought to be an uncommon cause of hypertension, with an estimated prevalence of Ͻ2% among the general hypertensive population. Recent studies, however, have suggested that the prevalence of PA may be as high as 8% to 30% in selected hypertensive populations. 1-10 These reports have been based on either a high plasma aldosterone/plasma renin activity ratio (ARR) or a lack of suppression of plasma or urinary aldosterone in patients identified by an elevated ARR. As PA is generally remediable by treatment with an aldosterone antagonist or, in the case of adrenal adenoma, by adrenalectomy, knowing the true prevalence of PA in selected hypertension populations is clinically important for maximizing diagnosis and treatment.Prior studies determining the prevalence of PA have been based on an elevated ARR or confirmatory suppression testing in subjects preselected for a high ARR. The former approach would tend to overestimate the prevalence of PA, because patients with a falsely elevated ARR would be included, whereas the latter approach would underestimate the prevalence of PA because of the exclusion of patients with a falsely low ARR. Diagnosis of PA by confirmatory suppression testing of all evaluated patients would be necessary to overcome these limitations.The prevalence of PA has not been systematically determined in a population that has included a large proportion of African American subject...