Left ventricular mechanical dyssynchrony (LVMD), left ventricular hypertrophy, and impaired cardiac sympathetic innervation are closely related to the development of heart failure (HF) and unfavorable outcomes.A total of 705 consecutive HF patients with reduced left ventricular ejection fraction (EF) < 50% were registered in our hospital HF database. LVMD and left ventricular mass index (LVMI) were evaluated three-dimensionally by gated myocardial perfusion SPECT. LVMD was measured as a heterogeneity index (phase SD) of the regional contraction phase angles calculated by Fourier analysis. Cardiac sympathetic innervation was quantified as a normalized heart-to-mediastinum ratio (HMR) of the 123I-metaiodobenzylguanidine (MIBG) activity. The patients were followed up with a primary end point of lethal cardiac events (CEs) for 42 months. CEs were documented in 246 of the HF patients who had a greater phase SD, greater LVMI, and lower MIBG HMR than those in HF patients without CEs. In the overall multivariate analysis, phase SD, LVMI, and MIBG HMR were identified as significant CE determinants. The three biomarkers were incrementally related to increases in CE risks.Assessment of cardiac sympathetic innervation can further stratify patients with systolic heart failure at increased cardiac risk identified by left ventricular hypertrophy and mechanical dyssynchrony.
Implantable cardioverter defibrillator (ICD) and cardiac resynchronization with a defibrillator (CRT-D) are established therapies for secondary prevention of sudden cardiac death (SCD) in patients with structural heart disease (SHD), but the rates of subsequent ICD/CRT-D therapy widely differ among patients with SHD. The aim of this study was to determine clinical factors associated with appropriate therapy for preventing SCD in patients with SHD.We enrolled 147 patients with SHD (mean age, 59 ± 15 years; mean ejection fraction [EF], 45 ± 15%) who underwent ICD/CRT-D implantation for secondary prevention of SCD (ischemic heart disease, n = 50; nonischemic heart disease, n = 97). ICD/CRT-D was implanted for aborted cardiopulmonary arrest (CPA, n = 65) or sustained ventricular tachycardia (VT, n = 82).During a follow-up period of 3.2 ± 3.6 years, 79 of the 147 patients had appropriate ICD/CRT-D therapies. A Kaplan-Meier survival curve showed that the rate of appropriate therapy was 54% at 5-year follow-up. Prior sustained VT, lower EF, and use of a class I antiarrhythmic drug were significantly more frequent in patients with appropriate therapy. In multivariate analysis, prior sustained VT (hazard ratio, 2.8; 95% CI, 1.60-4.46; P = .001) was the only independent predictor for appropriate ICD/CRT-D therapy. Kaplan-Meier survival curves showed that rates of appropriate therapy during a 5-year follow-up period were 70% and 34% in patients with sustained VT and those with CPA, respectively (P = .001).In SHD patients implanted with an ICD/CRT-D, prior sustained VT as an indication of ICD/CRT-D implantation, but not EF or an antiarrhythmic drug, predicts a high rate of appropriate therapy.
Sympathetic nerve activities have pivotal roles in pathophysiology and prognosis in patients with heart failure. Among the various available techniques for the analysis of sympathetic nerve function, cardiac neuroimaging with a norepinephrine analogue is a noninvasive, specific and powerful modality that enables in vivo assessment of cardiac sympathetic innervation and activity and has demonstrated pathophysiological alterations at pre-synaptic nerve terminals and their clinical implications. Impaired cardiac metaiodobenzylguanidine (MIBG) activity and, conversely, increased systemic sympathetic function drive closely correlate with clinical outcomes. Cardiac MIBG activities have independent but incremental prognostic values in combination with known clinical determinants in patients with heart failure. Systemic inhibition of sympathetic drive and the rennin-angiotension-aldosterone system can improve cardiac MIBG activity and kinetics together with functional improvement in heart failure patients. Prognostic efficacy of contemporary drug treatment is, however, likely to depend on the severity of the impairment of cardiac MIBG activity. Patients who have impaired cardiac MIBG activity with blunted heart rate variability, an elevated brain natriuretic peptide level or LV dysfunction are likely to have appropriate discharges of an implantable cardioverter defibrillator. Thus, cardiac neuroimaging could enable appropriate selection of patients at greater risk for lethal outcomes, who can probably benefit most from pharmacological and invasive strategies. Keywords: heart failure, sudden cardiac death, cardiac sympathetic innervation, scintigraphic imaging, drug treatment, prognosis
The effects of L-carnitine on the hemodynamic state of chronic hemodialysis patients have been debated. In order to clarify the effect of administered L-carnitine on cardiac function and hypotensive episodes during the hemodialysis procedure, a randomized double-blind placebo-controlled study was performed for 3 months.TWENTY STABLE OUTPATIENTS UNDERGOING HEMODIALYSIS TREATMENT WERE DIVIDED INTO TWO GROUPS: controls (placebo) and treated patients (L-carnitine 900 mg p.o. daily). After 3 months, cardiac function was reevaluated by echocardiography, and hypotensive episodes during hemodialysis were assessed. Free and acyl carnitine levels increased significantly from 22.3 ± 7.1 to 140.3 ± 57.5 μmol/l and from 15.8 ± 2.8 to 94.8 ± 50.4 μmol/l, respectively, in the treated group. The ejection fraction significantly increased from 61.8 ± 16.0 to 64.4 ± 13.8% (p < 0.05) in the treated group. However, there was no difference in other echocardiographic parameters between the two groups. Hypotensive episodes significantly decreased from 4.0 ± 1.7 to 1.3 ± 0.9 times per month (p < 0.05), although patients' body weight did not change significantly.Beneficial effects of L-carnitine on the hemodynamic state of chronic hemodialysis patients were observed. L-Carnitine supplementation might be considered especially for chronic hemodialysis patients with unstable hemodynamic conditions.
Introduction: In order to clarify the characteristics of different administration routes and to optimize the dosage, carnitine kinetics was investigated under oral and intravenous supplementation. Methods: L- carnitine was administered orally (900mg) for 12months, intravenously (1000 mg) for 3months and (500mg) for 3months sequentially in 18 chronic hemodialysis patients. Plasma free and acyl carnitine concentrations were assessed before and after hemodialysis procedure at the end of each administration protocol. The muscle carnitine content was calculated by active transport curve. Results: Plasma free carnitine concentration increased from 22.1±6.9 μM/L to 139.1±40.4 μM/L (900 mg p.o), 280.1±52.2μM/L (1000 mg i.v) and 169.7±25.9 μM/L (500mg i.v) before dialysis procedure. Although acyl/free carnitine ratio decreased significantly after each supplementation method (p<0.05), there was no difference of acyl/free carnitine ratio among each group. The simulation of muscle carnitine content indicated that the active transport is mainly depend on high affinity component, and oral 900mg daily supplementation and intravenous 500 mg administration after each hemodialysis procedure are enough dosage to achieve the normal carnitine content of muscle tissue in chronic hemodialysis patients. Conclusion: It would be suggested that oral 900 mg daily supplementation and intravenous 500 mg administration (10 mg/kg) after each hemodialysis procedure are reasonable dosage and have equal efficacy from the viewpoint of muscle carnitine content, although the plasma carnitine concentration curves were quite different.
Background:Complete left atrial posterior wall isolation (LAPI) is not always achieved. We examined whether incomplete LAPI has an effect on outcomes after catheter ablation (CA).
