ABSTRACT
Ventricular arrhythmias are frequent in patients with systemic sclerosis and may result in sudden cardiac death. We report the case of a patient with systemic sclerosis and recent syncopes in whom induction of unstable sustained ventricular tachycardia of 2 different morphologies accompanied by syncopal event was demonstrated at the electrophysiological study. He was then implanted a 3rd generation implantable cardioverter defibrillator and remained thereafter asymptomatic. We suggest that aggressive testing is warranted in systemic sclerosis patients with suspected malignant arrhythmias to identify candidates for defibrillator implantation and prevent sudden deaths.
ABSTRACT
We observed a patient with syncope, who implanted a pacemaker with advanced algorithms such as "atrial-tachy response" and "dynamic atrio-ventricular delay". After one year, conventional ECG Holter showed pacemaker malfunction, wrongly attributed to exposure to electromagnetic field. In fact, telemetry revealed an inappropriate programming and solved our case. Holter monitoring is commonly performed in the evaluation of pacemaker malfunction, albeit it remains a quite shallow diagnostic method especially to detect electromagnetic interferences. New algorithms seem important, but it is reasonable to obtain more suitable analytical tools, too.
Subject(s)
Algorithms , Electrocardiography, Ambulatory , Pacemaker, Artificial , Aged , Female , Humans , TelemetryABSTRACT
AIMS: Recent data from the COMPANION trial have documented that cardiac resynchronization therapy (CRT) with biventricular (BiV) pacing reduces mortality and hospitalization in patients with advanced CHF, but little is known regarding the cellular and molecular mechanisms of CRT. Our aim is to evaluate interstitial remodelling, tumor necrosis factor-alpha (TNF-alpha) expression, and apoptosis in patients with advanced CHF treated with CRT. METHODS AND RESULTS: We performed endomyocardial biopsies in 10 patients, aged 62, with dilated cardiomyopathy before and 6 months after the implantation of a BiV pacing device. Clinical status and left ventricular (LV) architecture and function were assessed as well as myocardial histology, TNF-alpha expression, and apoptotic index. CRT improved clinical status, as shown by a significant reduction of the Minnesota living with heart failure questionnaire (MLHFQ) score (from 53 to 40) and 6-min walked distance (from 290 to 330 m) (all P<0.05 vs. baseline). This was associated with reverse LV remodelling substantiated by significant reductions of LV volumes and end-systolic circumferential wall stress. Examination of myocardial tissue revealed a significant decrease of collagen volume fraction (CVF) (from 25.16 to 18.0%), TNF-alpha expression (from 9.5 to 3.6 pixel x 10(3)), and apoptotic index (from 2030 to 1408 apoptotic nuclei/10(6)), with increased capillary density (from 1801 to 2011 capillary/mm(2)) after 6 months of CRT (all P<0.05 vs. baseline). Moreover, changes in TNF-alpha expression were positively correlated with both CVF and end-systolic circumferential wall stress (r=0.80 and 0.70, respectively). CONCLUSION: We provide the first evidence that CRT reduces interstitial remodelling, TNF-alpha expression, and apoptosis. The data may explain the beneficial effects of CRT on CHF progression and survival.
