Risk of early mortality after placement of a temporary-permanent pacemaker.

BACKGROUND: Temporary-permanent pacemakers [TPPM] are externally placed permanent generators attached to active fixation transvenous leads. TPPM can be used as an alternative to standard temporary pacing leads when placement of a permanent pacemaker is contraindicated. We sought to determine the incidence and risk factors for early (within 6months) mortality after placement of a TPPM. METHODS: Electronic medical records were used to extract baseline characteristics for 152 patients from Wake Forest Baptist Medical Center who had a TPPM placed between the years 2007 and 2012. Multivariable adjusted Cox proportional hazard models were used to estimate hazard ratios [HR] and 95% confidence intervals [C]) for baseline characteristics [age, sex, race, hypertension, diabetes, heart failure, coronary artery disease, smoking, dyslipidemia, chronic kidney disease [CKD], and indication for pacemaker] on early mortality. RESULTS: Of the 152 patients [mean age 68.9years; 57.2% female; 86.8% white], 45 [29.6%] died within the first 6months after TPPM placement. No deaths occurred as a direct result of TPPM placement, and only 1 patient experienced documented non-fatal complications. Maximum time to PPM from the date of insertion of TPPM was 336days. Using a backward multivariable adjusted hazard regression model, independent risk factors for early mortality were pre-existing CKD [HR (95% CI): 2.240 (1.002-5.010) for eGFR 30-59 and 7.645 (3.594-16.263) for eGFR <30 compared to eGFR >60] and history of smoking [HR (95% CI): 2.015 (1.099-3.696)]. Surprisingly, dyslipidemia was protective of early mortality [HR (95%CI): 0.470 (0.240-0.924)]. CONCLUSION: TPPM placement is a safe procedure with rare direct complications. CKD and smoking are predictive of increased risk for early mortality in patients undergoing TPPM placement.

Inter-relationship between electrocardiographic left ventricular hypertrophy and QT prolongation as predictors of increased risk of mortality in the general population.

BACKGROUND: Prolonged-QT commonly coexists in the ECG with left ventricular hypertrophy (ECG-LVH). However, it is unclear whether to what extent QT prolongation coexisting with ECG-LVH can explain the prognostic significance of ECG-LVH, and whether prolonged-QT coexisting with ECG-LVH should be considered as an innocent consequence of ECG-LVH. METHODS AND RESULTS: The study population consisted of 7506 participants (mean age, 59.4±13.3 years; 49% whites; and 47% men) from the US Third National Health and Nutrition Examination Survey. ECG-LVH was defined by Cornell voltage criteria. Prolonged heart-rate-adjusted QT (prolonged-QTa) was defined as QTa≥460 ms in women or 450 ms in men. Cox proportional hazards analysis was used to calculate the hazard ratios with 95% confidence intervals for the risk of all-cause mortality for various combinations of ECG-LVH and prolonged-QTa. ECG-LVH was present in 4.2% (N=312) of the participants, of whom 16.4% had prolonged-QTa. In a multivariable-adjusted model and compared with the group without ECG-LVH or prolonged-QTa, mortality risk was highest in the group with concomitant ECG-LVH and prolonged-QTa (hazard ratio, 1.63; 95% confidence interval, 1.12-2.36), followed by isolated ECG-LVH (1.48; 1.24-1.77), and then isolated prolonged-QTa (1.27; 1.12-1.46). In models with similar adjustment where ECG-LVH and prolonged-QTa were entered as 2 separate variables and subsequently additionally adjusted for each other, the mortality risk was essentially unchanged for both variables. CONCLUSIONS: Although prolonged-QT commonly coexists with LVH, both are independent markers of poor prognosis. Concomitant presence of prolonged-QT and ECG-LVH carries a higher risk than either predictor alone.