Worsening thoracic impedance as a ventricular tachyarrhythmia risk.

The use of heart failure classification to identify patients with systolic dysfunction who are at risk for ventricular tachyarrhythmias (VAs), sudden cardiac death, and shocks from implantable cardioverter defibrillators (ICDs) is limited by its subjectivity. Measurement of thoracic impedance offers a more objective tool for assessing worsening of heart failure. We sought to look at the correlation between ventricular arrhythmia and heart failure as assessed objectively by thoracic impedance. We reviewed device interrogation data on thoracic impedance from ICD with Medtronic's OptiVol® feature (Medtronic Inc., Minneapolis, MN) at two medical centers. Data from the last two interrogations of the same device separated by at least 2 months were included. An OptiVol fluid index threshold of 60 represented early heart failure prior to appearance of symptoms. VAs included were ventricular fibrillation and/or ventricular tachycardia lasting more than 16 beats. Chi square distribution test was used in statistical data analysis. There were 24 VAs identified among the 322 interrogations reviewed (7.5%). Elevated OptiVol fluid index was seen in 71% (17/24), whereas normal OptiVol index was seen in the remaining 29% (7/24) of these interrogations with VA (P < .05). Our review shows that heart failure patients who have VA are approximately 2.5 times as likely to have worsening thoracic impedance as assessed objectively by the OptiVol fluid index. Careful monitoring of the OptiVol fluid index may identify a population at high risk of VA that merits more intense attention.

Cardiac amyloidosis responding to bortezomib: case report and review of literature.

We report a case of a 53-year old patient with symptoms of congestive heart failure in whom a restrictive cardiomyopathy and a kappa-chain monoclonal gammopahty were diagnosed. Treatment with eight cycles of Bortezomib, a proteasome inhibitor, resulted in a significant regression of myocardial amyloid deposition and a notable clinical and hemodynamic improvement. Over the last few years, the management of cardiac amyloidosis has taken advantage of many of the advances of the chemotherapeutic regimens, as well as the wider availability of stem cell transplantation. The management of cardiac amyloidosis is also expected to evolve and improve with the better understanding of the specific mechanisms of amyloidogenesis and myocardial deposition. This will probably make certain molecules targeting specific sites in this process, as potentially effective and minimally toxic compared therapy with the currently used ones. In this article, we describe one of the first reported cases of cardiac amyloidosis, successfully treated with Bortezomib. We describe and discuss the mechanisms of action of Bortezomib and provide a detailed review of cardiac amyloidosis, from pathophysiology to diagnosis and treatment.