Clinical Usefulness of a Mobile Application for the Appropriate Selection of the Antiarrhythmic Device in Heart Failure.

BACKGROUND: Appropriate selection of implantable cardioverter defibrillator (ICD) or cardiac resynchronization therapy (CRT) device can be challenging in patients with left ventricular (LV) dysfunction. In this setting, limited information exists about the role of medical applications in helping physicians to choose the most useful device. METHODS: We developed a medical application that provides guidelines-based algorithms for helping doctors in decision process using the Apache Cordova application programming interface. e-CRTD App was tested in 36 consecutive patients (age 66.4 ± 8.5 years, 31 males) with diagnosis of heart failure (HF) addressed to electrophysiology laboratory for evaluation of ICD (N = 18) or CRT with defibrillator device (CRT-D; N = 18) implantation. Two separate teams evaluated each patient independently: expert electrophysiologists (Group A); cardiologists in training using the App (Group B). RESULTS: The outcomes of the clinical evaluation performed by Groups A and B were similar in 100% of patients in terms of classes of recommendations to device (Class I in eight cases, Class IIa in seven cases, Class III in the remaining 21). Surprisingly, the majority of indications from the general practitioners to cardiac device were inappropriate (N = 17 ICD, and N = 4 CRT-D, Class III); nevertheless, e-CRTD App helped Group B (nonexpert cardiologists) in excluding all these cases. CONCLUSIONS: This study describes and validates a mobile application realized to help the decision-making process in HF patients candidate to ICD/CRT-D. This application supports physicians to assess the eligibility for ICD or CRT-D according to current guidelines in patients with LV dysfunction.

MicroRNA-133 controls vascular smooth muscle cell phenotypic switch in vitro and vascular remodeling in vivo.

RATIONALE: MicroRNA (miR)-1 and -133 play a crucial role in skeletal and cardiac muscle biology and pathophysiology. However, their expression and regulation in vascular cell physiology and disease is currently unknown. OBJECTIVE: The aim of the present study was to evaluate the role, if any, of miR-1 and miR-133 in vascular smooth muscle cell (VSMC) phenotypic switch in vitro and in vivo. METHODS AND RESULTS: We demonstrate here that miR-133 is robustly expressed in vascular smooth muscle cells (VSMCs) in vitro and in vivo, whereas miR-1 vascular levels are negligible. miR-133 has a potent inhibitory role on VSMC phenotypic switch in vitro and in vivo, whereas miR-1 does not have any relevant effect per se. miR-133 expression is regulated by extracellular signal-regulated kinase 1/2 activation and is inversely correlated with VSMC growth. Indeed, miR-133 decreases when VSMCs are primed to proliferate in vitro and following vascular injury in vivo, whereas it increases when VSMCs are coaxed back to quiescence in vitro and in vivo. miR-133 loss- and gain-of-function experiments show that miR-133 plays a mechanistic role in VSMC growth. Accordingly, adeno-miR-133 reduces but anti-miR-133 exacerbates VSMC proliferation and migration in vitro and in vivo. miR-133 specifically suppresses the transcription factor Sp-1 expression in vitro and in vivo and through Sp-1 repression regulates smooth muscle gene expression. CONCLUSIONS: Our data show that miR-133 is a key regulator of vascular smooth muscle cell phenotypic switch in vitro and in vivo, suggesting its potential therapeutic application for vascular diseases.

High sensitive troponin T in individuals with chest pain of presumed ischemic origin.

This study was aimed at assessing the bias of high sensitive cardiac troponin T vs. the standard cardiac troponin T in a selected population with chest pain of presumed cardiac origin. Serum cTnT was determined in 132 patients and in 106 apparently healthy controls by both assays. The hs-cTnT outperformed the standard generation assay by: i) allowing a larger and earlier diagnosis of AMI (74.2 percent vs. 64.3 percent patients resulted positive at the final diagnosis of AMI when tested with the hs-cTnT or the std-cTnT assay, respectively); ii) showing a better time-dependent dynamics in patients with AMI due to a higher precision at low concentrations; iii) identifying, within the controls, 6 subjects in whom a further examination revealed the presence of chronic asymptomatic cardiac ischemia. The results underscore the excellent performance of the hs-cTnT assay in our population. The use of this test can thus be strongly recommended in subjects presenting to the emergency unit with chest pain of presumed ischemic origin in order to increase the probability of earlier diagnosis of AMI, especially in non-STEMI.