Effect of an intensive lifestyle intervention on the structural and functional substrate for atrial fibrillation in people with metabolic syndrome.

AIMS: To evaluate the effect of an intensive lifestyle intervention (ILI) on the structural and functional cardiac substrate of atrial fibrillation (AF) in overweight or obese people with metabolic syndrome (Mets). METHODS AND RESULTS: Participants of the PREvención con DIeta MEDiterranea-Plus trial (n = 6874) were randomized 1:1 to an ILI programme based on an energy-reduced Mediterranean diet, increased physical activity, and cognitive-behavioural weight management or to a control intervention of low-intensity dietary advice. A core echocardiography lab evaluated left atrial (LA) strain, function, and volumes in 534 participants at baseline, 3-year, and 5-year follow-ups. Mixed models were used to evaluate the effect of the ILI on LA structure and function. In the subsample, the baseline mean age was 65 years [standard deviation (SD) 5 years], and 40% of the participants were women. The mean weight change after 5 years was -3.9 kg (SD 5.3 kg) in the ILI group and -0.3 kg (SD 5.1 kg) in the control group. Over the 5-year period, both groups experienced a worsening of LA structure and function, with increases in LA volumes and stiffness index and decreases in LA longitudinal strain, LA function index, and LA emptying fraction over time. Changes in the ILI and control groups were not significantly different for any of the primary outcomes {LA emptying fraction: -0.95% [95% confidence interval (CI) -0.93, -0.98] in the control group, -0.97% [95% CI -0.94, -1.00] in the ILI group, Pbetween groups = 0.80; LA longitudinal strain: 0.82% [95% CI 0.79, 0.85] in the control group, 0.85% [95% CI 0.82, 0.89] in the ILI group, Pbetween groups = 0.24} or any of the secondary outcomes. CONCLUSION: In overweight or obese people with Mets, an ILI had no impact on the underlying structural and functional LA substrate measurements associated with AF risk.

This study evaluated whether an intervention-modifying lifestyle had an effect on the parts of the heart involved in the development of atrial fibrillation (AF), a common problem of the heart rhythm. This intervention was implemented in people who had excessive body weight and the metabolic syndrome (Mets), which is a combination of several cardiovascular risk factors. The lifestyle intervention included promoting a Mediterranean diet low in calories and increasing exercise to facilitate weight loss, and this intervention was compared with a control intervention to follow a healthy diet. We performed repeated studies of the heart structure and function with imaging over a period of 5 years. During the 5 years of the study, both study groups (intervention and control) showed changes in their heart consistent with ageing. However, these changes were not different in those who were receiving the lifestyle intervention. Also, participants who lost more weight, adhered better to the study diet, or did more physical activity, overall did not show any differences in their heart compared with those who did not achieve their lifestyle goals.In conclusion, a lifestyle intervention focusing on weight loss, better diet, and more exercise was not effective in improving parts of the heart potentially involved with the risk of AF.In people with metabolic syndrome, a weight control lifestyle intervention, based on an energy-reduced Mediterranean diet and physical activity, had no effect on the structural and functional cardiac substrate of atrial fibrillation.

Effect of an intensive lifestyle intervention on the structural and functional substrate for atrial fibrillation in people with metabolic syndrome.

Aims: To evaluate the effect of an intensive lifestyle intervention (ILI) on the structural and functional cardiac substrate of atrial fibrillation (AF) in overweight or obese people with metabolic syndrome (MetS). Methods: Participants of the PREDIMED-PLUS trial (n=6874) were randomised 1:1 to an ILI program based on an energy-reduced Mediterranean diet, increased physical activity, and cognitive-behavioural weight management, or to a control intervention of low-intensity dietary advice. Left atrial (LA) strain, function, and volumes were evaluated by a core echocardiography lab in 534 participants at baseline, 3-year and 5-year follow-up. Mixed models were used to evaluate the effect of the ILI on LA structure and function. Results: In the subsample, baseline mean age was 65 years (SD 5 years), and 40% of the participants were women. Over the 5-year period, both groups experienced worsening of LA structure and function, with increases in LA volumes and stiffness index and decreases in LA longitudinal strain, LA function index and LA emptying fraction over time. Changes in the ILI and control group were not significantly different for any of the primary outcomes (LA emptying fraction: -0.95% (95%CI -0.93, -0.98) in control group, -0.97% (95%CI -0.94, -1.00) in ILI group, p between groups =0.80; LA longitudinal strain: 0.82% (95%CI 0.79, 0.85) in control group, 0.85% (95%CI 0.82, 0.89) in ILI group, p between groups =0.24) or any of the secondary outcomes. Conclusions: In overweight or obese people with MetS, an ILI had no impact on the underlying structural and functional left atrial substrate measurements associated with AF risk.

A Fibrosis Biomarker Early Predicts Cardiotoxicity Due to Anthracycline-Based Breast Cancer Chemotherapy.

Anthracycline-based cancer chemotherapy (ACC) causes myocardial fibrosis, a lesion contributing to left ventricular dysfunction (LVD). We investigated whether the procollagen-derived type-I C-terminal-propeptide (PICP): (1) associates with subclinical LVD (sLVD) at 3-months after ACC (3m-post-ACC); (2) predicts cardiotoxicity 1-year after ACC (12m-post-ACC) in breast cancer patients (BC-patients); and (3) associates with LVD in ACC-induced heart failure patients (ACC-HF-patients). Echocardiography, serum PICP and biomarkers of cardiomyocyte damage were assessed in two independent cohorts of BC-patients: CUN (n = 87) at baseline, post-ACC, and 3m and 12m (n = 65)-post-ACC; and HULAFE (n = 70) at baseline, 3m and 12m-post-ACC. Thirty-seven ACC-HF-patients were also studied. Global longitudinal strain (GLS)-based sLVD (3m-post-ACC) and LV ejection fraction (LVEF)-based cardiotoxicity (12m-post-ACC) were defined according to guidelines. BC-patients: all biomarkers increased at 3m-post-ACC versus baseline. PICP was particularly increased in patients with sLVD (interaction-p < 0.001) and was associated with GLS (p < 0.001). PICP increase at 3m-post-ACC predicted cardiotoxicity at 12m-post-ACC (odds-ratio ≥ 2.95 per doubling PICP, p ≤ 0.025) in both BC-cohorts, adding prognostic value to the early assessment of GLS and LVEF. ACC-HF-patients: PICP was inversely associated with LVEF (p = 0.004). In ACC-treated BC-patients, an early increase in PICP is associated with early sLVD and predicts cardiotoxicity 1 year after ACC. PICP is also associated with LVD in ACC-HF-patients.

Is plasma cardiotrophin-1 a marker of hypertensive heart disease?

OBJECTIVE: This study was designed to investigate whether plasma concentration of cardiotrophin-1 (CT-1), a cytokine that induces cardiomyocyte hypertrophy and stimulates cardiac fibroblasts, is related to hypertensive heart disease, as defined by the presence of echocardiographically assessed left ventricular hypertrophy (LVH). METHODS: The study was performed in 31 normotensive subjects and 111 patients with never-treated essential hypertension (54 without LVH and 57 with LVH). Causes of LVH other than hypertension were excluded after a complete medical workup. A novel enzyme-linked immunosorbent assay was developed to measure plasma CT-1. RESULTS: Plasma CT-1 was increased (P < 0.001) in hypertensives compared with normotensives. The value of CT-1 was higher (P < 0.001) in hypertensives with LVH than in hypertensives without LVH. Some 31% of patients without LVH exhibited values of CT-1 above the upper normal limit in normotensives. A direct correlation was found between CT-1 and left ventricular mass index (r = 0.319, P < 0.001) in all subjects. Receiver operating characteristic curves showed that a cutoff of 39 fmol/ml for CT-1 provided 75% specificity and 70% sensitivity for predicting LVH with a relative risk of 6.21 (95% confidence interval, 2.95 to 13.09). CONCLUSIONS: These results show an association between LVH and the plasma concentration of CT-1 in essential hypertension. Although preliminary, these findings suggest that the determination of CT-1 may be an easy and reliable method for the initial screening and diagnosis of hypertensive heart disease.