Incidence of ineffective safety margin testing (<10 J) and efficacy of routine subcutaneous array insertion during implantable cardioverter defibrillator implantation.

The purpose of this study was to assess (1) the incidence of safety margin testing <10 J (SMT) and (2) the efficacy/safety of routinely adding a subcutaneous array (SQA) (Medtronic 6996SQ) for these patients. Patients with SMT smaller than a 10-J safety margin from maximum output were considered to have very high readings and underwent SQA insertion. These patients were compared with the rest of the patients who had acceptable SMT (≥10 J). A total of 616 patients underwent ICD implantation during the analysis period. Of those, 16 (2.6%) had SMT <10 J. By univariate analysis, younger age, and non-ischemic cardiomyopathy, were all significant predictors of SMT <10 J (p < 0.05). In all 16 cases, other methods to improve SMT prior to array insertion were attempted but failed for all patients: reversing shock polarity (n = 15), removing the superior vena cava coil (n = 14), reprogramming shock waveform (n = 9), and repositioning right ventricular lead (n = 9). Addition of the SQA successfully increased SMT to within safety margin for all patients (32 ± 2 versus 21 ± 3 J; p < 0.001). Follow-up (mean 48.1 ± 21 months) was available for all patients with SQA, only 2 cases with inappropriate shocks due to atrial fibrillation had to be noted. None of the patients experienced complications due to SQA implantation. SMT <10 J occur in about 2.6% of patients undergoing ICD implantation. SQA insertion corrects this problem without procedural/mid-term complications.

Incidence, predictors, and outcome of inadvertent malposition of transvenous pacing or defibrillation lead in the left heart.

AIMS: Inadvertent lead malposition (ILM) in the left heart is a potential cause of thromboembolism and, therefore, a complication of heart rhythm device implantation [HRDI: pacemaker, implantable cardioverter defibrillator (ICD), cardiac resynchronization therapy (CRT)]. The aim of the study was to report the incidence and clinical outcome of ILM. METHODS AND RESULTS: Postoperative lateral and posterior-anterior chest X-rays of all consecutive patients undergoing HRDI from 2007 through 2012 were retrospectively analysed. During the study period, 2579 patients underwent HRDI at our institution. ILM was present in six patients (0.34%, 50% male, mean age 71.5 ± 9.4 years). In one and four patients, malposition was in the left atrium and ventricle, respectively. In one case, the RV-lead was placed in a coronary sinus branch. In four patients, ILM was detected intra-operatively or in the early postoperative period. In the remaining two patients, malposition was not recognized and they suffered cerebral embolism 4 months and 1 year after implantation. ILM was corrected during the same hospital stay (four cases), or during follow-up by percutaneous extraction (two cases). Patients with ILM had significantly more scoliosis (16.7 vs. 0.17%; P = 0.01), congenital heart disease (CHD: 33.3 vs. 0.4%; P = 0.003), or prior surgery for CHD (16.7 vs. 0.5%; P = 0.03). The likelihood of ILM was also increased when HRDI was performed by an inexperienced operator (<100 HRDI; P < 0.01). CONCLUSION: The incidence of ILM was 0.34% in our series. Scoliosis, CHD, prior correction of CHD, and limited operator experience were identified as risk factors.

Utility of a bedside acoustic cardiographic model to predict elevated left ventricular filling pressure.

BACKGROUND: The authors previously described an acoustic cardiographic model that predicted echocardiographic correlates of elevated left ventricular (LV) filling pressure. This study evaluated this bedside acoustic cardiographic model against invasive measurements of LV filling pressure. METHODS AND RESULTS: Data were prospectively obtained from 68 adults referred for right heart catheterisation. Acoustic cardiographic measurements were obtained during right heart catheterisation. Elevated LV filling pressure was defined as a pulmonary capillary wedge pressure (PCWP) > or =15 mm Hg. Parameters generated from a previous dataset used for the current analysis were measures of LV systolic time, maximum negative area of the P wave, QTc interval and third heart sound (S3) score. Logistic regression was used to calculate area under the curve (AUC). Of the 66 patients included, 39 had elevated PCWP. Estimating the probability of an elevated PCWP from the derived model resulted in an AUC of 0.72 (95% CI 0.60 to 0.85). When the regression model's parameters were held constant but the parameter estimates were allowed to vary, the AUC in the validated model was 0.76 (95% CI 0.64 to 0.88). At a specificity of 90% the positive likelihood ratio (LR+) was 5.0 (1.7 to 15.3) and the negative likelihood ratio was 0.49 (0.34 to 0.71). CONCLUSION: These data demonstrate that the four-variable model predicts elevated filling pressure at the bedside with high specificity and an intermediate LR+. With improvements in sensitivity and further prospective validation of this model in a cohort of emergency department patients with undifferentiated dyspnoea this may be a useful bedside diagnostic modality.

Inferior and lateral electrocardiographic repolarization abnormalities in Brugada syndrome.

BACKGROUND: Repolarization abnormalities in the inferior-lateral leads in Brugada syndrome (BS) have not been systematically investigated. METHODS AND RESULTS: 280 patients (age, 41+/-18 years; 168 males) with BS were screened for inferior-lateral repolarization abnormalities. The repolarization abnormalities were classified either as early repolarization pattern or coved > or = 2-mm Brugada pattern and as spontaneous or class I antiarrhythmic drug (AAD) induced. Thirty-two patients (11%) had inferior-lateral spontaneous early repolarization pattern. These patients were less likely to be asymptomatic at first presentation (13 of 32 versus 156 of 248 patients, P=0.02), and spontaneous type I ECG was more frequent among them (38% versus 21%, P=0.05). The spontaneous early repolarization pattern occurred more frequently among patients with BS than in 283 family members not having BS (11% versus 6%, P=0.03). Class I AAD administration provoked inferior-lateral coved Brugada pattern in 13 patients with BS. These patients had longer baseline PR intervals (206+/-48 versus 172+/-31 ms, P<0.001) and class I AAD-induced QRS interval prolongation (108 to 178 versus 102 ms to 131 ms, P<0.001). In 3 patients, the class I AAD-provoked coved Brugada pattern was only present in the inferior leads. CONCLUSIONS: Inferior-lateral early repolarization pattern occurs spontaneously relatively frequently in BS. These patients have a more severe phenotype. Class I AAD administration provokes inferior-lateral coved Brugada pattern in 4.6% of patients. We report for the first time 3 patients in whom the class I AAD-provoked coved Brugada pattern was only observed in the inferior leads.