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BackgroundSeveral studies have shown an independent relationship between body mass index (BMI) and the incidence of atrial fibrillation (AF). However, little is known about the influence of BMI on AF recurrence after electrical cardioversion (ECV).MethodsWe selected 1121 patients who reverted to sinus rhythm after scheduled ECV and were included in three prospective Spanish registries of ECV in persistent AF. The patients were classified according to baseline BMI into three categories (normal weight, overweight, obesity). We assessed the influence of BMI on the rate of AF recurrence at 3 months.ResultsWe identified 538 patients (48%) who had AF recurrence in the first 3 months after successful ECV. The patients who suffered AF recurrence had a higher BMI than those who remained in sinus rhythm (29.66±4.57 vs. 28.87±4.64 Kg/m2, respectively; p = 0.004). We observed a higher incidence of AF recurrence in the overweight and obese patients (BMI ≥25 kg/m2) than in those classified as normal weight (50.5% vs. 35.6%, respectively; pConclusionsIncreased BMI is independently related to AF recurrence after ECV. BMI should also be taken into account when making decisions about the indication for ECV in persistent AF.

In Brugada syndrome, even within the same family where all affected individuals share the same mutation, phenotypic variation is prominent, with variable penetrance and expressivity, presenting different degrees of involvement. It is difficult to establish a direct correlation between genotype and phenotype to predict prognosis in complications and risk of sudden death. The factors that modulate this inter- and intra-familial phenotypic variability remain to be determined. With the intention of testing whether other genetic factors, in addition to the causal mutation in SCN5A, may have a modulating effect on the Brugada phenotype and the risk of sudden death, we have studied 8 families with a causal variant in SCN5A with at least two affected individuals, one of whom has suffered cardiac arrest or sudden death. Whole exome sequencing was performed looking for additional variants that modify the phenotype and allow us to predict a better or worse prognosis for the evolution of the disease. The results did not show any clear genetic modifier; nevertheless, highlight the possible implication of the cholesterol and fibrosis pathways, as well as the circadian rhythm, as possible modulators of Brugada syndrome phenotype.

In Brugada syndrome, even within the same family where all affected individuals share the same mutation, phenotypic variation is prominent, with variable penetrance and expressivity, presenting different degrees of involvement. It is difficult to establish a direct correlation between genotype and phenotype to predict prognosis in complications and risk of sudden death. The factors that modulate this inter- and intra-familial phenotypic variability remain to be determined. With the intention of testing whether other genetic factors, in addition to the causal mutation in SCN5A, may have a modulating effect on the Brugada phenotype and the risk of sudden death, we have studied 8 families with a causal variant in SCN5A with at least two affected individuals, one of whom has suffered cardiac arrest or sudden death. Whole exome sequencing was performed looking for additional variants that modify the phenotype and allow us to predict a better or worse prognosis for the evolution of the disease. The results did not show any clear genetic modifier; nevertheless, highlight the possible implication of the cholesterol and fibrosis pathways, as well as the circadian rhythm, as possible modulators of Brugada syndrome phenotype.

BackgroundAssociation between obesity and cardiovascular diseases is well known, however increased susceptibility of obese patients to develop several cancer types is not so commonly known. Current data suggest that poorer overall survival in cancer patients might be associated to non-cancer-related causes such as higher risk of cardiotoxicity in obese patients treated with chemotherapeutic agents. Omentin, a novel adipokine decreased in obesity, is actually in the spotlight due to its favourable effects on inflammation, glucose homeostasis and cardiovascular diseases. Also, recent data showed that in vitro anthracycline-induced cardiomyocyte apoptosis is counteracted by omentin suggesting its cardioprotective role.ObjectiveOur aim was to evaluate omentin effects against docetaxel toxicity.ResultsOur data indicate that omentin inhibits docetaxel-induced viability loss and that increased viability is associated to decreased caspase-3 expression and cell death. Although omentin reduces NOX4 expression, it failed to reduce docetaxel-induced reactive oxygen species production. Our results indicate that omentin decreases docetaxel-induced endoplasmic reticulum stress, suggesting that cardioprotective role might be associated to ERS inhibition.ConclusionThese data suggest that omentin treatment may contribute to decrease susceptibility to DTX-induced cardiotoxicity.

BackgroundAlthough the assessment of diastolic dysfunction (DD) is an integral part of routine cardiologic examinations, little is known about associated electrocardiographic (ECG) changes. Our aim was to investigate a potential role of ECG indices for the recognition of patients with DD.Methods and resultsECG parameters correlating with echocardiographic findings of DD were retrospectively assessed in a derivation group of 172 individuals (83 controls with normal diastolic function, 89 patients with DD) and their diagnostic performance was tested in a validation group of 50 controls and 50 patients. The patient group with a DD Grade 1 and 2 showed longer QTc (422 ± 24 ms and 434 ± 32 ms vs. 409 ± 25ms, pConclusionsA novel electrocardiographic index Tend-P/(PQxAge) demonstrates a high diagnostic accuracy for the diagnosis of DD and yields a substantial added value when combined with the LAESVI.