Ultrafiltration versus intravenous loop diuretics in patients with acute decompensated heart failure: a meta-analysis of clinical trials.

Background Intravenous loop diuretics are the first-line therapy for acute decompensated heart failure (ADHF) but many patients are discharged with unresolved congestion resulting in higher re-hospitalization and mortality rates. Ultrafiltration (UF) is a promising intervention for ADHF. However, studies comparing UF to diuretics have been inconsistent in their clinical outcomes. Methods A comprehensive literature search was performed. Trials were included if they met the following criteria: (1) randomization with a control group, (2) comparison of UF with a loop diuretic, and (3) a diagnosis of ADHF. Results When compared to diuretics, UF was associated with a reduced risk of clinical worsening (odds ratio (OR) 0.57, 95% CI: 0.38-0.86, P-value 0.007), increased likelihood for clinical decongestion (OR 2.32, 95% CI: 1.09-4.91, P-value 0.03) with greater weight (0.97 Kg, 95% CI: 0.52-1.42, P-value <0.0001) and volume reduction (1.11 L, 95% CI: 0.68-1.54, P-value <0.0001). The overall risk of re-hospitalization (OR 0.92, 95% CI: 0.62-1.38, P-value 0.70), return to emergency department (OR 0.69, 95% CI: 0.44-1.08, P-value 0.10) and mortality (OR 0.99, 95% CI: 0.60-1.62, P-value 0.97) were not significantly improved by UF treatment. Conclusions UF is associated with significant improvements in clinical decongestion but not in rates of re-hospitalization or mortality.

Use of apixaban after development of suspected rivaroxaban-induced hepatic steatosis; a case report.

Postmarketing reports have emerged associating rivaroxaban with drug-induced liver injury (DILI); however, management strategies of patients with suspected rivaroxaban-induced liver injury requiring continued anticoagulation have not been published. The present report describes a 67-year-old male with atrial fibrillation receiving rivaroxaban who developed a 16-fold elevation in alanine transaminase, a nearly two-fold elevation in total bilirubin, and ultrasound confirmed hepatic steatosis. The patient was switched from rivaroxaban to apixaban with subsequent rapid resolution of laboratory abnormalities. Rapid improvement in liver function tests despite use of an alternative factor Xa inhibitor suggests that rivaroxaban's mechanism of hepatotoxicity may be unrelated to its pharmacologic action. When using rivaroxaban, clinicians should be aware of the small but potentially serious risk of DILI. Because most anticoagulants have been associated with DILI, selection of an alternative anticoagulant may be challenging; however, the use of apixaban in this case suggests it may be a reasonable alternative.

Acute myocardial infarction during regadenoson myocardial perfusion imaging.

Pharmacologic stress testing uses vasodilators to provide objective evidence of myocardial ischemia. Adenosine and dipyridamole are nonselective adenosine receptor agonists that have been associated with myocardial infarction (MI) during intravenous infusion. Mechanisms postulated for this effect include coronary steal, transmural steal, global hypotension, and direct vasoconstriction. Regadenoson, a direct A2A agonist, was approved for use in stress testing in 2008. We describe a 68-year-old man who presented to our institution with typical angina, relieved by nitroglycerin. He did not have electrocardiogram (ECG) changes suggestive of myocardial pathology, and laboratory testing did not reveal a significant rise in troponin-I levels. To further assess the etiology of his symptoms, he underwent a pharmacologic stress test with regadenoson followed by technetium 99 m sestamibi. Six minutes after regadenoson infusion, the patient developed severe retrosternal chest pain accompanied by ST elevations on ECG. Sublingual nitroglycerin was administered that resolved both the pain and ECG changes. The patient subsequently underwent urgent coronary angiography and was found to have a 95% critical stenosis involving the left anterior descending artery. We conclude this case represents a MI secondary to coronary steal phenomenon induced by regadenoson infusion. Clinicians should be aware this adverse effect can occur despite the improved side-effect profile of regadenoson. Continuous monitoring of vital signs and the ECG with regular assessment of symptoms is imperative to identify this rare but potentially devastating adverse event.