Long-term left ventricular pacing: assessment and comparison with biventricular pacing in patients with severe congestive heart failure.
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OBJECTIVE: The purpose of this study is to report prospectively the results of six-month follow-up of permanent left ventricular (LV) based pacing in patients with severe congestive heart failure (CHF) and left bundle branch block (LBBB). BACKGROUND: Left ventricular pacing alone has been demonstrated to result in identical improvement compared to biventricular pacing (BiV) during acute hemodynamic evaluation in patients with advanced CHF and LBBB. However, to our knowledge, the clinical outcome during permanent LV pacing alone versus BiV pacing mode has not been evaluated. METHODS: Pacing configuration (LV or BiV) was selected according to the physician's preference. Patient evaluation was performed at baseline and at six months. RESULTS: Thirty-three patients with advanced CHF and LBBB were included. Baseline characteristics of LV (18 patients) and BiV (15 patients) pacing groups were similar. During the six-month follow-up period, seven patients died three BiV and four LV). In the surviving patients at 6 months, 8 of 14 patients in the LV group and 9 of 12 in the BiV group were in New York Heart Association class I or II (p = 0.39). No significant difference was observed between the two groups in terms of objective parameters except for LV end-diastolic diameter decrease (-4.4 mm in BiV group vs. -0.7 mm in LV group; p = 0.04). CONCLUSION: At six-month follow-up, a trend toward improvement was observed in objective parameters in patients with severe CHF and LBBB following LV-based pacing. The two pacing modes (LV and BiV) were associated with almost equivalent improvement of subjective and objective parameters. (+info)
Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3.
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BACKGROUND: The electrocardiographic pattern of right bundle-branch block with ST-segment elevation in leads V1 to V3 is increasingly recognized among patients who have aborted sudden cardiac death, but also in asymptomatic individuals, raising questions about its prognostic significance. METHODS AND RESULTS: The clinical, electrophysiological, and follow-up data of 334 patients with the Brugada phenotype were analyzed. A total of 79 women and 255 men with a mean age at diagnosis of 42+/-16 years were studied. The abnormal ECG was recognized after a resuscitated cardiac arrest in 71 patients (group A), after a syncopal episode in 73 patients (group B), and in 190 asymptomatic individuals (group C). Sustained ventricular arrhythmias were inducible in 83%, 63%, and 33% of patients in group A, group B, and group C, respectively. During 54+/-54 and 26+/-36 months of follow-up, respectively, 62% of patients in group A and 19% of group B patients had a new arrhythmic event. Inducibility of ventricular arrhythmias was the only predictor of arrhythmia occurrence in both groups. During a mean follow-up of 27+/-29 months, 8% of group C individuals had a first arrhythmic event. In these individuals, inducibility of ventricular arrhythmias and a basal abnormal ECG were predictors of arrhythmia occurrence. CONCLUSIONS: An ECG showing right bundle-branch block and ST-segment elevation in the right precordial leads is a marker of malignant ventricular arrhythmias and sudden death. Recurrence of malignant arrhythmias is high after the occurrence of symptoms. Among asymptomatic individuals, those with a spontaneously abnormal ECG and inducible to ventricular arrhythmias have the poorer prognosis. (+info)
Doppler myocardial imaging to evaluate the effectiveness of pacing sites in patients receiving biventricular pacing.
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OBJECTIVES: The goal of this study was to compare the efficacy of biventricular pacing (BIV) at the most delayed wall of the left ventricle (LV) and at other LV walls. BACKGROUND: Biventricular pacing could provide additional benefit when it is applied at the most delayed site. METHODS: In 31 patients with advanced nonischemic heart failure, the activation delay was defined, in blind before BIV, by regional noninvasive Tissue Doppler Imaging as the time interval between the end of the A-wave (C point) and the beginning of the E-wave (O point) from the basal level of each wall. The left pacing site was considered concordant with the most delayed site when the lead was inserted at the wall with the greatest regional interval between C and O points (CO(R)). After BIV, patients were divided into group A (13/31) (i.e., paced at the most delayed site) and group B (18/31) (i.e., paced at any other site). RESULTS: After BIV, in all patients LV end-diastolic (LVEDV) and end-systolic (LVESV) volumes decreased (p = 0.025 and 0.001), LV ejection fraction (LVEF) increased (p = 0.002), QRS narrowed (p = 0.000), New York Heart Association class decreased (p = 0.006), 6-min walked distance (WD) increased (p = 0.046), the interval between closure and opening of mitral valve (CO) and isovolumic contraction time (ICT) decreased (p = 0.001 and 0.000), diastolic time (EA) and Q-P(2) interval increased (p = 0.003 and 0.000), while Q-A(2) interval and mean performance index (MPI) did not change. Group A showed greater improvement over group B in LVESV (p = 0.04), LVEF (p = 0.04), bicycle stress testing work (p = 0.03) and time (p = 0.08) capacity, CO (p = 0.04) and ICT (p = 0.02). CONCLUSIONS: After BIV, LV performance improved significantly in all patients; however, the greatest improvement was found in patients paced at the most delayed site. (+info)
Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation.
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OBJECTIVES: We sought to investigate the electrocardiographic (ECG) characteristics for guiding catheter ablation in patients with repetitive monomorphic ventricular tachycardia (RMVT) originating from the aortic sinus cusp (ASC). BACKGROUND: Repetitive monomorphic ventricular tachycardia can originate from the right ventricular outflow tract (RVOT) and ASC in patients with a left bundle branch block (LBBB) morphology and an inferior axis. METHODS: Activation mapping and ECG analysis was performed in 15 patients with RMVT or ventricular premature contractions. The left main coronary artery (LMCA) was cannulated as a marker and for protection during radiofrequency delivery if RMVT originated from the left coronary ASC. RESULTS: During arrhythmia, the earliest ventricular activation was recorded from the superior septal RVOT in eight patients (group 1) and from the ASC in the remaining seven patients (group 2). The indexes of R-wave duration and R/S-wave amplitude were significantly lower in group 1 than in group 2 (31.8+/-13.5% vs. 58.3+/-12.1% and 14.9+/-9.9% vs. 56.7+/-29.5%, respectively; p < 0.01), despite similar QRS morphology. In five patients from group 2, RMVT originated from the left ASC, with a mean distance of 12.2+/-3.2 mm (range 7.3 to 16.1) below the ostium of the LMCA. In the remaining two patients, the RMVT origin was in the right ASC. All arrhythmias were successfully abolished. None of the patients had recurrence or complications during 9+/-3 months of follow-up. CONCLUSIONS: On the surface ECG, RMVT from the ASC has a QRS morphology similar to that of RVOT arrhythmias. The indexes of R-wave duration and R/S-wave amplitude can be used to differentiate between the two origins. Radiofrequency ablation can be safely performed within the left ASC with a catheter cannulating the LMCA. (+info)
Biventricular pacing improves clinical behavior and reduces prevalence of ventricular arrhythmia in patients with heart failure.
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PURPOSE: To analyze the influence of biventricular pacing (BP) on clinical behavior, ventricular arrhythmia (VA) prevalence, and left ventricular ejection fraction (LV EF) by gated ventriculography. METHODS: Twenty-four patients with left bundle branch block (LBBB) and NYHA class III and IV underwent pacemaker implantation and were randomized either to the conventional or BP group, all receiving BP after 6 months. RESULTS: Sixteen patients were in NYHA class IV (66.6%) and 8 were in class III (33.4%). After 1-year follow-up, 14 patients were in class II (70%) and 5 were in class III (25%). Two sudden cardiac deaths occurred. A significant reduction in QRS length was found with BP (p=0.006). A significant statistical increase, from a mean of 19.13 +/- 5.19% (at baseline) to 25.33 +/- 5.90% (with BP) was observed in LVEF Premature ventricular contraction prevalence decreased from a mean of 10,670.00 +/- 12,595.39 SD or to a mean of 3,007.00 +/- 3,216.63 SD PVC/24 h with BP (p<0.05). Regarding the hospital admission rate over 1 year, we observed a significant reduction from 60. To 16 admissions with BP (p<0.05). CONCLUSION: Patients with LBBB and severe heart failure experienced, with BP, a significant NYHA class and LVEF improvement. A reduction in the hospital admission rate and VA prevalence also occurred. (+info)
A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease.
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OBJECTIVE: Loss of Na(+) channel function has been implicated in idiopathic ventricular fibrillation (IVF) and Brugada syndrome. We have studied the biophysical properties of an IVF mutation (S1710L) that exhibited an unusual clinical phenotype: rate-dependent bundle branch block without manifestation of Brugada-type ECG pattern. METHODS: The mutant S1710L channels were expressed in mammalian cells and their gating properties, studied using whole-cell patch clamp techniques, were compared with wild-type (WT) and a Brugada syndrome mutant channel T1620M. RESULTS: The S1710L channel exhibited significantly faster macroscopic current decay than WT or T1620M. In addition, S1710L showed a negative shift in the voltage-dependence of fast inactivation and slower recovery from fast inactivation than in WT or T1620M. In addition to the alterations in fast inactivation most commonly observed in Brugada syndrome mutations, S1710L exhibited marked enhancement in slow inactivation and a large positive shift of activation that potentially decreases conduction velocity. CONCLUSIONS: These functional abnormalities may be responsible for the overlapping clinical phenotypes associated with Brugada syndrome and the cardiac conduction defect, a novel cardiac Na(+) channelopathy. (+info)
Cardiac autonomic dysfunction in Brugada syndrome.
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BACKGROUND: Patients with Brugada syndrome present with characteristic ECG abnormalities (atypical right bundle-branch block and ST-segment elevation) and life-threatening ventricular tachyarrhythmias despite structurally normal hearts. Involvement of the autonomic nervous system is suggested by the occurrence of ventricular tachyarrhythmias and sudden death at rest or during sleep and by changes of typical ECG signs under pharmacological modulation of the myocardial autonomic tone. METHODS AND RESULTS: This study investigated the presynaptic cardiac neuronal reuptake of norepinephrine (uptake 1) in 17 patients with Brugada syndrome and 10 age-matched control subjects with the use of the norepinephrine analogue [123I]m-iodobenzylguanidine (123I-MIBG), single-photon emission CT (SPECT), and quantitative 33-segment bull's-eye analysis. Regionally reduced 123I-MIBG uptake was present in 8 (47%) of 17 patients with Brugada syndrome but in none of the control subjects. Quantitative analysis showed segmental reduction of 123I-MIBG uptake in the inferior and septal left ventricular wall in patients with Brugada syndrome compared with control subjects (P<0.05). No correlation was found between the findings of 123I-MIBG-SPECT and clinical characteristics of the study patients. CONCLUSIONS: The present study demonstrated an abnormal 123I-MIBG uptake in patients with Brugada syndrome, indicating presynaptic sympathetic dysfunction of the heart. These findings may have potential impact on the pathophysiology and arrhythmogenesis in patients with Brugada syndrome. Future quantitative investigations of the presynaptic and postsynaptic sympathetic and parasympathetic branches of the cardiac autonomic nervous system may clarify whether these observations represent a primary adrenergic dysfunction or an imbalance between sympathetic and parasympathetic innervation of the heart. (+info)
Clinical and molecular heterogeneity in the Brugada syndrome: a novel gene locus on chromosome 3.
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BACKGROUND: Brugada syndrome is a form of idiopathic ventricular fibrillation characterized by a right bundle-branch block pattern and ST elevation (STE) in the right precordial leads of the ECG. Sodium channel blockers increase STE. Mutations of the cardiac sodium channel SCN5A cause the disorder, and an implantable cardioverter-defibrillator is often recommended for affected individuals. Mutations in other genes have not been identified, and it is not known if the efficacy of drug testing or the malignancy of arrhythmias correlates to the gene defect. METHODS AND RESULTS: We performed histories, physical examinations, ECGs, and drug testing on a large multigenerational family with Brugada syndrome. DNA isolated from blood samples, polymorphic genomic markers, and polymorphisms within candidate sodium channels were used for a genome-wide screen, fine mapping, and linkage analysis. We identified 12 affected individuals (right bundle-branch block, > or =1-mm STE) with an autosomal dominant inheritance pattern characterized by incomplete penetrance that appeared to be dependent on age and sex. Four affected individuals had syncope and 2 had documented ventricular arrhythmias, but there was minimal family history of sudden death. Procainamide infusions did not identify additional affected individuals. Linkage was present to an approximately equal 15-cM region on chromosome 3p22-25 (maximum LOD score=4.00). The sodium channel genes SCN5A, SCN10A, and SCN12A on chromosome 3 were excluded as candidates (LOD scores < or =-2). CONCLUSIONS: A Brugada syndrome locus distinct from SCN5A is associated with progressive conduction disease, a low sensitivity to procainamide testing, and a relatively good prognosis in a single large pedigree. (+info)