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.

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.

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.

Antiplatelet therapy in acute coronary syndromes: focus on ticagrelor.

The use of antiplatelet agents, specifically the thienopyridines, has become a standard of care in the approach to the patient presenting with an acute coronary syndrome. These drugs irreversibly inhibit the platelet by permanently binding to the surface P2Y12 receptor and blocking the downstream fibrinogen cross-linking between platelets, which leads to aggregation and thrombus. However, currently available therapeutic choices are limited by potential interaction with other medications, slow hepatic conversion to active metabolite, genetic resistance, and narrow therapeutic safety margin.