Effect of nesiritide in patients with acute decompensated heart failure.

BACKGROUND: Nesiritide is approved in the United States for early relief of dyspnea in patients with acute heart failure. Previous meta-analyses have raised questions regarding renal toxicity and the mortality associated with this agent. METHODS: We randomly assigned 7141 patients who were hospitalized with acute heart failure to receive either nesiritide or placebo for 24 to 168 hours in addition to standard care. Coprimary end points were the change in dyspnea at 6 and 24 hours, as measured on a 7-point Likert scale, and the composite end point of rehospitalization for heart failure or death within 30 days. RESULTS: Patients randomly assigned to nesiritide, as compared with those assigned to placebo, more frequently reported markedly or moderately improved dyspnea at 6 hours (44.5% vs. 42.1%, P=0.03) and 24 hours (68.2% vs. 66.1%, P=0.007), but the prespecified level for significance (P≤0.005 for both assessments or P≤0.0025 for either) was not met. The rate of rehospitalization for heart failure or death from any cause within 30 days was 9.4% in the nesiritide group versus 10.1% in the placebo group (absolute difference, -0.7 percentage points; 95% confidence interval [CI], -2.1 to 0.7; P=0.31). There were no significant differences in rates of death from any cause at 30 days (3.6% with nesiritide vs. 4.0% with placebo; absolute difference, -0.4 percentage points; 95% CI, -1.3 to 0.5) or rates of worsening renal function, defined by more than a 25% decrease in the estimated glomerular filtration rate (31.4% vs. 29.5%; odds ratio, 1.09; 95% CI, 0.98 to 1.21; P=0.11). CONCLUSIONS: Nesiritide was not associated with an increase or a decrease in the rate of death and rehospitalization and had a small, nonsignificant effect on dyspnea when used in combination with other therapies. It was not associated with a worsening of renal function, but it was associated with an increase in rates of hypotension. On the basis of these results, nesiritide cannot be recommended for routine use in the broad population of patients with acute heart failure. (Funded by Scios; ClinicalTrials.gov number, NCT00475852.).

Traumatic coronary artery fistula management.

Traumatic coronary artery-cameral fistulas (TCAF) are uncommon sequelae of trauma that require early surgical intervention to prevent complications. The etiology of traumatic coronary artery-cameral fistulas may be classified as accidental or iatrogenic and have distinctly different courses depending on the etiology. The two operations described for definitive surgical closure of a traumatic coronary-cameral fistula are external ligation/obliteration of the fistula (with or without bypass grafting to the coronary artery distal to the fistula) and direct repair of the fistula from within the recipient chamber. The technique of fistula closure from within the recipient chamber is associated with a reduced incidence of fistula recurrence. A case report and a collective literature review are presented.

Spontaneous pericardial tamponade during PTCA.

A case of acute hemorrhagic pericardial tamponade complicating a successful percutaneous transluminal coronary angioplasty (PTCA) is described, in the setting of rheumatoid arthritis (with no evidence of prior or concomitant pericarditis), large doses of intravenous heparin administration and a relatively high activated clotting time. There was no evidence of coronary artery rupture and there was no recent use of other anticoagulants or thrombolytic agents. Successful treatment comprised emergency pericardial drainage and intravenous protamine sulphate. The authors believe this to be the first reported case of acute hemorrhagic pericardial tamponade due solely to heparin administration. The possibility of acute hemorrhage of a rheumatoid nodule was considered but subsequent magnetic resonance imaging scan with contrast gadolinium was normal.

Pulmonary 'mainline' granulomatosis: talcosis of intravenous methadone abuse.

Seventeen intravenous abusers of methadone underwent clinical, roentgenologic and physiologic assessment. Two complained of dyspnea on exertion and two had cor pulmonale. Of 15 patients whose fundi were examined, nine had talc particles in their retinal vessels. The chest roentgenograms of seven showed a diffuse pin-point micronodular pattern and two of the seven also manifested volume loss, one with coalescence of opacities simulating progressive massive fibrosis. Twelve patients had some degree of pulmonary dysfunction, 10 with lowered steady state diffusing capacity and 11 with decreased flow rates (FEV1 and MMF). There was no hyperinflation, but two showed an increase in residual volume. Corticosteroid therapy was attempted on two and was ineffective. Necropsy on the one patient who died revealed severe pulmonary fibrosis and talc granulomas in lungs, liver, kidneys and lymph nodes.