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Aims To assess the cost-effectiveness and the cost utility of remote patient monitoring (RPM) when compared with the usual care approach based upon differences in the number of hospitalizations, estimated from a meta-analysis of randomized clinical trials (RCTs). Methods and results We reviewed the literature published between January 2000 and September 2009 on multidisciplinary heart failure (HF) management, either by usual care or RPM to retrieve the number of hospitalizations and length of stay (LOS) for HF and for any cause. We performed a meta-analysis of 21 RCTs (5715 patients). Remote patient monitoring was associated with a significantly lower number of hospitalizations for HF [incidence rate ratio (IRR): 0.77, 95% CI 0.65–0.91, P < 0.001] and for any cause (IRR: 0.87, 95% CI: 0.79–0.96, P = 0.003), while LOS was not different. Direct costs for hospitalization for HF were approximated by diagnosis-related group (DRG) tariffs in Europe and North America and were used to populate an economic model. The difference in costs between RPM and usual care ranged from €300 to €1000, favouring RPM. These cost savings combined with a quality-adjusted life years (QALYs) gain of 0.06 suggest that RPM is a ‘dominant’ technology over existing standard care. In a budget impact analysis, the adoption of an RPM strategy entailed a progressive and linear increase in costs saved. Conclusions The novel cost-effectiveness data coupled with the demonstrated clinical efficacy of RPM should encourage its acceptance amongst clinicians and its consideration by third-party payers. At the same time, the scientific community should acknowledge the lack of prospectively and uniformly collected economic data and should request that future studies incorporate economic analyses. [ABSTRACT FROM PUBLISHER]

Aims: Hypertrophic cardiomyopathy (HCM) is a genetic disease histologically characterized by a profound disarray of myocardial fibres and by local fibrosis. We sought to characterize regional left ventricular contractility in HCM patients using deformation analysis and to compare it with the presence or absence of delayed enhancement in cardiac magnetic resonance (CMR). [ABSTRACT FROM PUBLISHER]

Barth syndrome is an X-linked recessive disorder caused by the tafazzin (TAZ) gene mutations and includes dilated cardiomyopathy (DCM) with left ventricular non-compaction, neutropenia, skeletal myopathy, abnormal mitochondria and 3-methylglutaconic aciduria. Dilated cardiomyopathy with left ventricular non-compaction transmitted as an autosomal dominant condition has also been associated with LIM domain-binding 3 (LDB3) gene defects. We describe a family in which the 12-year-old proband had left ventricular non-compaction and DCM. His mother had five miscarriages, two other sons who died in infancy, and a healthy son and daughter. The proband showed left ventricular non-compaction-DCM, skeletal myopathy, recurrent oral aphthous ulcers and cyclic neutropenia. The DCM progressively improved with age; medical therapy was discontinued at 5 years of age. At present, left ventricular function is normal and arrhythmias are absent. Magnetic resonance imaging documented left ventricular non-compaction. However, oral aphthous ulcers and cyclic neutropenia have recurred. In the proband we identified two novel mutations, one of maternal origin in the TAZ gene (p.[Glu202ValfsX15]) and one of paternal origin in the LDB3 gene (p.[Thr350Ile]). The mother, brother and father are healthy; although the latter two show prominent left ventricle trabeculation without dysfunction. Expression studies of TAZ and LDB3 genes were conducted in family members and controls. In the proband, brother and father, LDB3 expression was similar to control cases. TAZ and LDB3 expression progressively declined with age in control both blood and myocardial samples. However, an endomyocardial biopsy performed in the proband at 6 months of age, showed significantly lower TAZ and LDB3 expression than in age-matched myocardial controls. We believe that the clinical, genetic and expression data support the hypothesis that tafazzins are essential during fetal and early post-natal life.