Lubomír Křivan

Right Ventricular Perforation with an ICD Defibrillation Lead Managed by Surgical Revision and Epicardial Leads—Case Reports

The authors present two cases of patients with perforation of the right ventricular wall by the implantable cardioverter defibrillator (ICD) lead. The complication was resolved by cardiosurgical revision and epicardial leads stitched onto the diaphragmatic wall of the heart. The perforation was identified by electrical parameter changes of the leads, echocardiography, and computed tomography. Both patients had satisfactory values of electrical parameters and ICD function with epicardial leads. The importance of regular follow‐up and a check of the lead parameters are emphasized.

Circadian variations in the occurrence of ventricular tachyarrhythmias in patients with implantable cardioverter defibrillators.

KOZÁK, M., et al.: Circadian Variations in the Occurrence of Ventricular Tachyarrhythmias in Patients with Implantable Cardioverter Defibrillators. A circadian distribution has been demonstrated in episodes of sudden cardiac death, acute myocardial infarction, ventricular premature complexes, heart rate variability, and ventricular tachyarrhythmias. The aim of this study was to evaluate the circadian distribution of ventricular tachyarrhythmia episodes in a population of ICD patients. Data were gathered from 72 patients (55 men, 17 women; mean age 62.7 ± 12.2 years, mean LVEF 0.0037 ± 0.0011 ) with ICDs implanted for standard indications. Patients were followed every 3 months over a mean period of 21 ± 12.8 months. At each examination, symptoms at arrhythmia onset and perception of ICD therapy were recorded, and the ICD memory was interrogated. During follow‐up, 1,023 episodes of malignant ventricular arrhythmias were detected and effectively terminated, 506 of which were fully analyzed. A morning peak in ventricular tachyarrhythmias was demonstrated between 7:00 and 11:00 am, and an afternoon peak between 6:00 and 7:00 pm. A significantly lower occurrence of VT was observed at 1:00 am and between 4:00 and 6:00 am. A circadian distribution in the occurrence of ventricular tachycardias was found. The three striking features of the data are: the early morning peak (about three hours after waking up), relatively stable incidence throughout waking hours, and decline in incidence in the previous period. (PACE 2003; 26:731–735)

Endothelin-1 gene polymorphism in patients with malignant arrhythmias.

The endothelins are peptides with vasoconstricting and growth-promoting properties. Endothelin-1 (ET-1) is known with its direct positive inotropic and chronotropic effects on isolated heart and with growth effects. The aim of this pilot study was to investigate the frequency distribution of the common polymorphism of the ET-1 gene and its possible relation with hemodynamic consequences of malignant ventricular arrhythmias in patients with structural heart disease. We studied 26 consecutive patients with malignant ventricular arrhythmias and implantable cardioverterdefibrillators with a mean age of 62.7 ± 12.2 years and a mean left ventricular ejection fraction of 0.37 ± 11.0. Taq polymorphism of ET-1 was detected using our original polymerase chain reaction method. The polymerase chain reaction product with a length of 358 basepairs (bp) (primers 5′-CAA ACC GAT GTC CTC TGT A-3′ and 5′-ACC AAA CAC ATT TCC CTA TT-3′) in its non-mutated form contains a target sequence for TaqI restrictive enzyme, while a mutated product loses this cleavage site. Of 26 patients, nine (34%) had recurrent palpitations and eight (30.8%) had syncopes during their malignant arrhythmias. Nineteen patients were given amiodarone after implantable cardioverter-defibrillator insertion and seven were not treated with amiodarone. Fifteen patients had (++), 11 (+-) and 0 (- -) ET-1 genotype. The risk for syncopes was associated with the (++) genotype of the ET-1 gene (P = 0.01). Patients receiving amiodarone had significantly higher frequency of the (++) genotype (P = 0.011). All our results indicate that the presence of the ET-1 genotype (++) in patients with structural heart disease, severe left ventricular dysfunction and malignant ventricular arrhythmias increases the risk for these patients of hemodynamic collapse during these arrhythmias.