Efficacy of multidisciplinary outpatient management (MOM) program in long term heart failure care.

BACKGROUND: Heart failure (HF) management programs worldwide have reported conflicting outcomes in the past. OBJECTIVES: We sought to determine retrospectively whether the multidisciplinary outpatient management (MOM) program [heart failure clinic (HFC)], decreased readmission rates (RR), duration of hospital stay, and/or mortality in HF patients. METHODS: Records of 138 HF patients who had their first encounter either as admission for HF at St. Agnes Hospital or visit to HFC during the period June 2005 through June 2006 were evaluated for outcomes through September 2007. Twenty-seven patients were followed in the HFC and 111 were in the non-HFC group. During follow up, 39 of the non-HFC group patients crossed over to the HFC group. All baseline parameters, except age (P = 0.006), were similar in both groups. RESULTS: In the HFC group 4 patients had a total of 5 readmissions, whereas 85 patients had a total of 187 readmissions (P < 0.001) in the non-HFC group. Average lengths of hospitalization were 5.2 +/- 4.8 days and 4.2 +/- 3.2 days (P = 0.18) and the number of readmissions/patient/year was 0.3 and 1.45 (P < 0.001) in the HFC and non-HFC groups, respectively. In the subgroup analysis of cross overs (n = 39), there was a 60% reduction in the readmission rate after crossing over to the HFC group. The significance of decreased mortality in the HFC group could not be assessed due to the small sample size. CONCLUSION: The study suggests that the MOM program can significantly reduce RR secondary to HF.

Electrocardiographic features of arrhythmogenic right ventricular dysplasia.

BACKGROUND: The purpose of this study was to reevaluate the ECG features of arrhythmogenic right ventricular dysplasia (ARVD). The second objective was to evaluate the sensitivity and specificity of the standard and newly proposed diagnostic ECG markers in the presence of a right bundle-branch block (RBBB). METHODS AND RESULTS: One hundred patients with ARVD (57 men; aged 39+/-15 years) and 57 controls (21 men; aged 40+/-17 years) were included. Among the 100 patients with ARVD, a complete RBBB was present in 17 patients, and 15 patients had an incomplete RBBB. T-wave inversion through V(3) demonstrated optimal sensitivity and specificity in both ARVD patients without a complete RBBB or incomplete RBBB (71% [95% confidence interval, 58% to 81%] and 96% [95% confidence interval, 81% to 100%], respectively) and in ARVD patients with incomplete RBBB (73% [95% confidence interval, 45% to 92%] and 95% [95% confidence interval, 77% to 100%], respectively). Between ARVD patients and controls with a complete RBBB, the only 2 parameters that differed were the prevalence of T-wave inversion through V(4) (59% versus 12%, respectively; P<0.05) and an r'/s ratio in V(1) <1 (88% versus 14%, respectively; P<0.005). In ARVD patients with complete RBBB, the most sensitive and specific parameter was an r'/s ratio <1. CONCLUSIONS: We evaluated comprehensively the diagnostic value of ECG markers for ARVD. On the basis of the findings, we propose an algorithm, with examination of QRS morphology being the first step, for ECG evaluation of ARVD patients. Definite criteria are then applied on the basis of the presence of no RBBB, incomplete RBBB, and complete RBBB to obtain the best diagnostic utility of the ECG.

Overexpression of glial cell line-derived neurotrophic factor in the CNS rescues motoneurons from programmed cell death and promotes their long-term survival following axotomy.

To study the role of one of the most potent motoneuron (MN) survival factors, glial cell line-derived neurotrophic factor (GDNF) derived from the CNS, we generated transgenic animals overexpressing GDNF under the control of an astrocyte-specific GFAP promoter. In situ hybridization revealed that GDNF was expressed at high levels in astrocytes throughout the brain and spinal cord. We analyzed the effects of CNS-derived GDNF on MN survival during the period of programmed cell death (PCD) and after nerve axotomy. In GFAP-GDNF mice at E15, E18, and P1, the survival of brachial MNs was increased on average by 30%, lumbar MNs by 20%, and thoracic MNs at P1 by 33%. GDNF also prevented MN PCD in several cranial motor nuclei. We demonstrated for the first time that the number of MNs in the mouse abducens nucleus was also increased by 40%, thus extending known MN populations that are responsive to GDNF. Next, we tested if GDNF could support complete and relatively long-term survival of MNs following neonatal facial nerve axotomy. We found that virtually all MNs (91%) in GFAP-GDNF mice survived for up to 18 weeks post-axotomy. This is the longest GDNF-mediated survival of neonatal MNs reported following axotomy. Most of surviving MNs were not atrophic, and MN-specific ChAT and neurofilament immunoreactivity (IR) were preserved. Furthermore, GDNF attenuated axotomy-induced astroglial activation. These data demonstrate that overexpression of GDNF in the CNS has very profound effects on MN survival both during the PCD period and after neuronal injury. GFAP-GDNF mice will be valuable to study the effects of CNS-derived GDNF in mouse models of MN degenerative diseases and axonal regeneration in vivo.