Safety and efficacy of external electrical cardioversion in patients with left ventricular leads.

BACKGROUND: Atrial arrhythmias lower the biventricular pacing percentage in cardiac resynchronization therapy (CRT) treated patients (pts) and have a high prevalence in this population. External electrical cardioversion (ECV) is commonly performed to restore sinus rhythm. There is a paucity of data on the safety and efficacy of ECV in pts with CRT devices. METHODS: Forty-three pts with CRT devices undergoing ECV at two centers were included prospectively. Devices were interrogated immediately prior to and after ECV, as well as after 4 weeks. RESULTS: Devices (CRT-D in 38 and CRT-P in 5) were all implanted in left pectoral position, with predominantly bipolar left ventricular (LV) leads. Sixty-one shocks were delivered, all biphasic. Arrhythmia had recurred in 36 % of pts at follow-up (FU). There was a significant increase in LV lead threshold voltage and drop in bipolar LV lead impedance after ECV, which returned to normal at FU. An at least twofold increase in pacing threshold voltage at FU was seen in 2 LV leads and a 0.5 V increase in threshold in 3 LV leads. Overall, biventricular pacing significantly increased during FU. CONCLUSION: ECV in CRT pts was safe and effective in this two-center study. A transient increase in LV lead pacing threshold was observed. Relevant changes in pacing threshold at FU occurred in five LV leads-identification and regular FU of these pts are necessary. Restoring SR through ECV significantly increased the biventricular pacing percentage but arrhythmia recurrence was frequent. CRT pts with atrial arrhythmias require close FU after ECV.

Noncompaction of the ventricular myocardium is associated with a de novo mutation in the beta-myosin heavy chain gene.

Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM. Twenty four family members were clinically assessed using advanced imaging techniques. For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12. Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the alpha- and beta-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7. The mutation affects a highly conserved amino acid in the myosin subfragment-1 (R281T). In silico simulations suggest that the mutation R281T prevents the formation of a salt bridge between residues R281 and D325, thereby destabilizing the myosin head. The mutation was exclusively present in morphologically affected family members. A few members of the family displayed NVM in combination with other heart defects, such as dislocation of the tricuspid valve (Ebstein's anomaly, EA) and atrial septal defect (ASD). A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life. The data presented in this report provide first evidence that a mutation in a sarcomeric protein can cause noncompaction of the ventricular myocardium.

Evidence of left ventricular dyssynchrony resulting from right ventricular pacing in patients with severely depressed left ventricular ejection fraction.

AIMS: Cardiac resynchronization therapy (CRT) has recently emerged as an effective treatment for patients with moderate-to-severe systolic heart failure and left bundle branch block (LBBB). Right ventricular pacing (RVP) leads to an LBBB-like pattern in the electrocardiogram. The aim of this study was to evaluate the frequency of ventricular mechanical dyssynchrony in patients induced by RVP. METHODS AND RESULTS: The study included 33 patients with a conventional single or dual chamber pacemaker, 18 with ejection fraction (EF) > 35% and 15 with EF < or = 35%. In all patients, an intrinsic rhythm without intraventricular conduction delay (QRS < or = 120 ms) was present without RVP. Two-dimensional and Doppler echocardiographic criteria for mechanical dyssynchrony [aortic pre-ejection delay (APE), interventricular mechanical delay (IVMD), delayed activation of the posterior left ventricular wall (PD), septal-to-posterior wall motion delay (SPWMD)] were evaluated in all patients with and without RVP. QRS duration showed no difference between the two EF-groups without RVP (93 +/- 10 vs. 96 +/- 9 ms), but was significantly longer in patients with low EF with RVP (152 +/- 18 vs. 181 +/- 18 ms; P < 0.001). In patients with EF > 35%, only APE was slightly prolonged by RVP (111 +/- 20 vs. 129 +/- 17 ms; P = 0.03), whereas in patients with EF < or = 35% marked pathological differences in APE (118 +/- 29 vs. 169 +/- 24 ms; P < 0.001), IVMD (22 +/- 17 vs. 58 +/- 14 ms; P < 0.001), SPWMD (103 +/- 28 vs. 125 +/- 29 ms; P = 0.004), and PD (-21 +/- 25 vs. - 39 +/- 25 ms; P = 0.005) were found. A significant correlation between QRS duration and mechanical ventricular dyssynchrony was only found for two echocardiographic parameters (IVMD, APE) with RVP. CONCLUSION: In patients with a conventional pacemaker, mechanical dyssynchrony with RVP was shown exceptionally in patients with preserved or moderately depressed systolic left ventricular (LV) function, but in nearly all patients with severely depressed systolic LV function. These patients might benefit from CRT when frequent RVP is required.

[Infection of ICD: prevention and therapy]. / ICD-Infektionen: Prävention und Therapie.

Infections of implantable cardioverter defibrillators (ICD) are severe, potentially life-threatening complications of ICD therapy. In the majority these infections are nosocomial by staphylococci, which become apparent within 0.5 years after implantation. Prophylaxis requires a strictly sterile environment during implantation and perioperative antibiotics. While infection of the ICD pocket is diagnosed clinically, infection of the electrodes must be proven by transesophageal echocardiography and positive blood cultures. Therapeutically, the complete ICD system has to be removed to avoid relapses of infection. Beyond 6 months after implantation, lead extraction might become technically demanding and should be done with a standby of cardiac surgery. Antibiotic treatment has to be started before removal of the system, continued for at least 2 weeks before reimplantation and for another 10 days thereafter. Reimplantation should be done outside the originally infected area.