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Aims Hypertrophic cardiomyopathy is one of the main causes of sudden death in young people. Recent clinical practice guidelines include a risk prediction model for sudden death (HCM Risk-SCD), which facilitates the decision of whether to implant a defibrillator. The aim of our study was to ascertain the percentage of events in our series of primary prevention implantable cardioverter-defibrillator recipients with hypertrophic cardiomyopathy and whether HCM Risk-SCD predicts the onset of arrhythmic events. Methods and results This was an observational, retrospective cohort study, which included 48 primary prevention defibrillator recipient patients with HCM. We compiled their demographic and clinical characteristics, estimated 5-year risk using HCM Risk-SCD, and collected the documentation on arrhythmias during follow-up. The majority was male (66.7%) and mean age at implantation was 44.44 ± 14.46 years. Non-sustained ventricular tachycardia was the most prevalent risk factor (66.67%), followed by a family history of sudden death (47.92%). Mean HCM Risk-SCD was 6.15 ± 5.01%. HCM Risk-SCD was the only factor independently associated with the onset of ventricular tachyarrhythmia, above any other classic risk factor or association [odds ratio = 1.46 (95% confidence interval 1.051–2.013); P = 0.02]. None of the 11 patients estimated as low risk using HCM Risk-SCD suffered any appropriate events ( P < 0.05). Conclusions During an average follow-up of 4 years, 16.67% presented appropriate events (4.16%/year). HCM Risk-SCD predicted the onset of events more suitably than classic risk factors.

Aims Cardiac resynchronization therapy (CRT) improves survival and quality of life in advanced heart failure (HF). Although mitral regurgitation (MR) reduction has been reported, its presence has been associated with non-response to CRT. This study was undertaken to assess the potential role of significant mitral regurgitation (SMR) persistence after CRT on clinical outcome, major arrhythmic events, and echocardiographic response in the mid-long term. Methods and results Seventy-six patients (28.9% women, 63 ± 11 years) with dilated cardiomyopathy in advanced HF were included. SMR, defined as regurgitant orifice area ≥0.20 cm2, was assessed at baseline and its evolution 6 months after CRT. Clinical outcome (cardiovascular death/HF readmission), major arrhythmic events, and echocardiographic response (reverse remodelling) were recorded on follow-up. Thirty-two patients (42.1%) presented baseline SMR, becoming non-significant in 11 of the 32 patients (34.3%) 6 months after CRT. Its persistence was associated with higher rates of clinical events (46.4 vs. 18.7%, P = 0.011), arrhythmic events (35.7 vs. 14.5%, P = 0.034), and less reverse remodelling (28.5 vs. 83.3%, P < 0.001). Conclusion CRT can reduce moderate or severe baseline MR to non-significant in one-third of patients. However, its persistence was associated with worse clinical evolution, greater incidence of arrhythmic events, and less reverse remodelling.

The aim of this study was to compare the effects of cardiac resynchronization therapy on left ventricular function and reverse remodeling in patients in sinus rhythm with the effects in patients with atrial fibrillation who have not undergone atrioventricular node ablation. Echocardiographic and clinical parameters were evaluated at baseline and after 6 months of cardiac resynchronization therapy in 55 patients: 15 had atrial fibrillation and 40 were in sinus rhythm. Device programming was similar in the 2 groups, as were the reductions in QRS interval and echocardiographic measures of asynchrony observed after implantation. However, although significant improvements in end-systolic volume and ejection fraction were seen in both groups, reverse remodeling was greater in patients in sinus rhythm (reduction in end-systolic volume 30.9%+/-24.6% vs 12.5%+/-18.6%; P=.024), as was the relative increase in ejection fraction (15.4%+/-12.6% vs 5.0%+/-7.2%; P=.010). Cardiac resynchronization therapy in patients with atrial fibrillation who had not undergone atrioventricular node ablation resulted in significant improvements in ejection fraction and reverse remodeling, but these were less than those observed in patients in sinus rhythm.

Unexplained cardiac arrest (UCA) can be caused by low-penetrance genetic disorders. The aim of this cross-sectional study is to assess the usefulness of a new diagnostic protocol: Thirty-five patients were recruited from 9 Spanish centers. Electrocardiogram, echocardiogram, and coronary catheterization were used to rule out electrical or structural heart disease in all subjects. Patients underwent pharmacologic tests with epinephrine and flecainide, followed by assessment of family members using electrocardiogram and echocardiogram, and next-generation genetic sequencing to analyze 126 genes if all the other test results were negative. A firm diagnosis of channelopathy required phenotypic proof of the condition in unmasking tests, the presence of a pathogenic variant consistent with the phenotype observed, and/or co-segregation of the mutation found in a family member's phenotype. A firm diagnosis was made in 18 cases. The diagnoses were 7 Brugada syndrome, 5 catecholaminergic polymorphic ventricular tachycardia, 3 long QT syndrome, 2 early repolarization syndrome, and 1 short QT syndrome. Pharmacologic testing was the most frequent method of diagnosis. In 5 cases, the diagnosis was made based on positive genetic testing without phenotypic alterations. In conclusion, this sequential diagnostic protocol allows diagnoses to be made in approximately half of the UCA cases. These diagnoses are low clinical penetrance channelopathies. If interpreted carefully, genetic tests can be a useful tool for diagnosing UCA without a phenotype. (C) 2015 Elsevier Inc. All rights reserved.

reference group. They also found that normotensive individuals with preserved eGFR (≥90 ml/min/1.73 m) and moderately high ACR (30 to 299 mg/g) have an elevated risk of all-cause death [5]. The results are very similar to the results of our study. Therefore, to conclude that our results are inconsistent with the results of the previous studies may be the result of an incorrect interpretation of the results from the previous studies. Dr. Kawada requested the authors to add medication profiles for hypertension and diabetes mellitus [1]. We added the prevalence of hypertensive subjects on medication and diabetic subjects on medication in Table 2 of this paper. We are confident that the high risks of outcomes in individuals with preserved eGFR and albuminuria observed in our study reflect a true relationship. However, we agree with some of the comments by Dr. Kawada. We used too many explanatory variables in the multivariate-adjusted Poisson model and we share Dr. Kawada's concerns about type I error (overfitting) [6]. We hope the analyses were performed in the spirit of Dr. Kawada's intent. Finally, we strongly agree with the phrase “keeping a satisfactory number of events for the epidemiological study to keep the validity of the outcome” provided by Dr. Kawada. We appreciate having the opportunity to discuss the problem and we express our deepest gratitude to Dr. Kawada.

Background: Clinical practice guidelines recommend ad hoc screening of diabetes in patients admitted for macrovascular disease; however, these recommendations are rarely followed in real practice. This study was undertaken to assess whether impaired glucose metabolism, newly diagnosed after percutaneous coronary intervention (PCI) or known diabetes, provides prognostic information. Methods : We studied 374 patients who underwent PCI. An oral glucose tolerance test was carried out in the known non-diabetic patients with fasting glucose < 7 mmol/L. Results : Eighty-one percent of the patients presented impaired glucose metabolism, from which 35.3% were previously diagnosed with diabetics, 21.4% were newly detected diabetics, and 24.3% were pre-diabetics. After a mean follow-up of 35.8 ± 13.4 months, only a known history of diabetes was an independent predictor of revascularization (OR = 2.03, p = 0.025), non-fatal acute myocardial infarction (OR = 2.70, p = 0.029) and readmission due to heart failure during the follow-up (OR = 3.82, p = 0.022). Conclusions: Screening for impaired glucose metabolism after PCI permits the detection of a high proportion of patients with abnormal glucose regulations. However, previously known diabetes remains the only independent predictor of cardiovascular events in the follow-up.

Aims The combined use of an automatic defibrillator in resynchronization therapy for primary prevention in patients with idiopathic dilated cardiomyopathy is controversial. Methods and results We assessed a series of 46 patients (61 ± 10 years, 64% male) with idiopathic dilated cardiomyopathy undergoing resynchronization therapy combined with a defibrillator in primary prevention and the potential relationship between baseline characteristics and the onset of ventricular arrhythmic events. Of the 46 patients included, eight (17%) presented episodes of ventricular tachycardia/fibrillation during follow-up (19 ± 12 months). There were no baseline differences among these patients, except the proportion of males (57.9 vs. 100%, P = 0.02) and QRS width (162 ± 24 vs. 189 ± 26 ms, P = 0.008), which was the only independent predictor of arrhythmic events (OR 1.42, 95% CI 1.12–1.68; P = 0.03). Conclusion In patients with idiopathic dilated cardiomyopathy undergoing resynchronization therapy combined with a defibrillator, baseline QRS is an independent predictor of arrhythmic events.