Persistent Proarrhythmic Neural Remodeling Despite Recovery From Premature Ventricular Contraction-Induced Cardiomyopathy.

Background: The presence and significance of neural remodeling in premature ventricular contraction-induced cardiomyopathy (PVC-CM) remain unknown.

Objectives: This study aimed to characterize cardiac sympathovagal balance and proarrhythmia in a canine model of PVC-CM.

Methods: In 12 canines, the investigators implanted epicardial pacemakers and radiotelemetry units to record cardiac rhythm and nerve activity (NA) from the left stellate ganglion (SNA), left cardiac vagus (VNA), and arterial blood pressure.

Left ventricular systolic dysfunction induced by ventricular ectopy: a novel model for premature ventricular contraction-induced cardiomyopathy.

Background: Premature ventricular contractions (PVCs) commonly coexist with cardiomyopathy. Recently, PVCs have been identified as a possible cause of cardiomyopathy. We developed a PVC-induced cardiomyopathy animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this cardiomyopathy and examine the associated histopathologic abnormalities.

Aspirin desensitization/challenge in 3 patients with unstable angina.

Aspirin sensitivity is relatively frequent and can be a major problem in patients who need percutaneous coronary intervention and stenting with subsequent dual antiplatelet therapy. Desensitization is often the therapy in these patients, but this can prolong the time to revascularization significantly. Rapid oral aspirin desensitization protocols have been described since 2000.

Aortic baroreceptor function and depressed baroreflex sensitivity following myocardial infarction.

Depressed sinoaortic baroreflex control of heart rate following myocardial infarction (MI) is associated with increased morbidity and mortality. The etiology of this autonomic disturbance is unknown but could potentially occur at several levels of the reflex arc. The purpose of this study was to assess whether depressed baroreflex sensitivity (BRS) post-MI is associated with aortic baroreceptor dysfunction.