Safety of expedited anticoagulation in patients undergoing transesophageal echocardiographic-guided cardioversion.

Background: In patients undergoing transesophageal echocardiography-guided cardioversion, we evaluated the use and safety of an expedited in-hospital anticoagulation regimen that incorporates shorter-than-standard durations of precardioversion intravenous unfractionated heparin and postcardioversion bridging therapy with a low-molecular-weight heparin.

Methods: Adult patients who underwent successful transesophageal echocardiography-guided cardioversion for atrial fibrillation or atrial flutter between May 2000 and August 2003 were classified into 2 groups by duration of intravenous unfractionated heparin therapy (<24 h or > or =24 h) before transesophageal echocardiography and cardioversion. Safety end points evaluated included all-cause death, stroke or other thromboembolic events, and major bleeding complications within 1 month after successful cardioversion.

Ventricular structure and function in aged dogs with renal hypertension: a model of experimental diastolic heart failure.

Background: Heart failure (HF) with normal ejection fraction (diastolic HF [DHF]) usually occurs in elderly patients with hypertension. The presence and significance of altered systolic and diastolic ventricular function in DHF is increasingly controversial. Our objective was to develop a clinically relevant large-animal model to better understand the pathophysiology of DHF.

Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability.

The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined.