Comprehensive mitral valve prolapse assessment by cardiovascular MRI.

Mitral valve (MV) prolapse (MVP) is a not fully understood common MV disorder. The development of sophisticated cardiovascular magnetic resonance imaging (CMRI) sequences over the last decades has allowed a more detailed assessment and provided better understanding of the pathophysiology of MVP to guide management, interventions, and risk stratification of patients affected. This review provides an overview of the most recent insights about this multifaceted pathology, particularly regarding the emerging concepts of mitral annular disjunction (MAD), and risk of arrhythmia and sudden death associated with myocardial fibrosis. We describe the emerging role of CMRI in both diagnosis and, more importantly, risk assessment of this disease, aiming to provide a comprehensive protocol for the assessment of MVP, which could represent a practical guide to clinicians and MRI practitioners working in the field.

From the BMI paradox to the obesity paradox: the obesity-mortality association in coronary heart disease.

Despite a strong association between body weight and mortality in the general population, clinical evidence suggests better clinical outcome of overweight or obese individuals with established coronary heart disease. This finding has been termed the 'obesity paradox', but its existence remains a point of debate, because it is mostly observed when body mass index (BMI) is used to define obesity. Inherent limitations of BMI as an index of adiposity, as well as methodological biases and the presence of confounding factors, may account for the observed findings of clinical studies. In this review, our aim is to present the data that support the presence of a BMI paradox in coronary heart disease and then explore whether next to a BMI paradox a true obesity paradox exists as well. We conclude by attempting to link the obesity paradox notion to available translational research data supporting a 'healthy', protective adipose tissue phenotype. © 2016 World Obesity.

Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta.

OBJECTIVE: To investigate the effects of atorvastatin on endothelial function and low-grade systemic inflammation in subjects with successful surgery for aortic coarctation repair (SCR). DESIGN: Open-label study. SETTING: Outpatients visiting the adult congenital heart disease department of our hospital. PATIENTS: 34 young people with SCR. INTERVENTIONS: Patients with SCR received atorvastatin 10 mg/day (n=17) or no treatment (n=17) for 4 weeks. At baseline and at 4 weeks, endothelial function was assessed by flow-mediated dilatation (FMD) of the right brachial artery, and blood samples were obtained. Serum levels of interleukin (IL) 1b, IL-6 and soluble vascular cell adhesion molecule-1 (sVCAM-1) were determined by ELISA. MAIN OUTCOME MEASURES: Effects of treatment on FMD and serum levels of IL-1b, IL-6 and sVCAM-1. RESULTS: FMD in the atorvastatin group was significantly improved after 4 weeks (from 6.46±0.95% to 11.24±1.38%, p<0.01), while remaining unchanged in the control group (from 6.74±0.58% to 6.95±0.53%, p=NS). Even though atorvastatin had no effect on serum IL-6 levels (0.62 (0.37-0.88) pg/ml to 0.53 (0.28-0.73) pg/ml, p=NS), it significantly reduced circulating levels of IL-1b (from 1.17 (0.92-1.77) pg/ml to 1.02 (0.75-1.55) pg/ml, p<0.05) and sVCAM-1 (from 883.4 (660.3-1093.1) ng/ml to 801.4 (566.7-1030.2) ng/ml, p<0.05). No changes were seen in serum levels of IL-6, IL-1b and sVCAM-1 in the control group after 4 weeks compared with baseline (p=NS for all). CONCLUSIONS: Atorvastatin treatment for 4 weeks in subjects with SCR significantly improved endothelial function and suppressed systemic inflammatory status by decreasing circulating levels of IL-1b and sVCAM-1.

Exercise duration as a determinant of vascular function and antioxidant balance in patients with coronary artery disease.

BACKGROUND: Exercise improves the clinical outcome of patients with coronary artery disease (CAD); however, the ideal exercise duration for each patient remains unclear. OBJECTIVE: To investigate the effects of exercise duration on arterial elastic properties and antioxidant/pro-oxidant mechanisms in patients with CAD. DESIGN, SETTING, PATIENTS, INTERVENTIONS: Sixty male patients with CAD were randomised into two groups, and underwent exercise for 30 min or 60 min in a crossover design with 2 weeks' wash-out period. In all participants aortic and radial blood pressures (BP) and arterial elastic properties (augmentation index (AIx)/pulse wave velocity (PWV)) were determined at baseline and 24 h after exercise. Plasma malonyldialdehyde (MDA) and superoxide dismutase (SOD)1 and SOD2 levels were also measured. RESULTS: Exercise had no effect on aortic and radial BP (p=NS for all). Walking for 30 min improved AIx (from 33.79 ± 0.91% to 31.73 ± 0.86%, p<0.001) and PWV (from 9.26 ± 0.95 m/s to 9.06 ± 0.21 m/s, p<0.001), while exercise for 60 min had adverse effects on vascular stiffness (for AIx: from 33.37 ± 0.93% to 33.73 ± 1.05%, p=NS and for PWV: from 9.25 ± 0.19 m/s to 9.37 ± 0.21 m/s, p < 0.05 mainly in older patients). Exercise for 60 min was associated with a significant 20% increase in MDA levels (p<0.05). Exercise had no effects on SOD1 levels, however it significantly increased SOD2 levels after 30 min (from 2.26 ± 0.22 ng/mL to 2.36 ± 0.18 ng/mL, p < 0.05) but not after 60 min (p=NS). Conclusion Shorter exercise duration was associated with favourable antioxidant and vascular effects, while longer exercise blunted these beneficial effects and was accompanied by adverse effects on vascular function, mainly in older coronary patients. Further studies are required to explore the hypothesis that a more individualised approach to the selection of the appropriate exercise programme should be considered for patients with CAD.

Adiponectin: from obesity to cardiovascular disease.

Adiponectin is an adipokine whose biosynthesis is deranged in obesity and diabetes mellitus, predisposing to atherosclerosis. Evidence suggests that adiponectin has anti-atherogenic properties by improving endothelial function and having anti-inflammatory effects in the vascular wall. In addition, adiponectin modifies vascular intracellular redox signalling and exerts indirect antioxidant effects on human myocardium. However, its clinical role in cardiovascular disease is obscure. Adiponectin's positive prognostic value in coronary artery disease had been widely supported over the last years, but this view has been questioned recently. High adiponectin levels are paradoxically associated with poorer prognosis in heart failure syndrome. These controversial findings seem surprising as adiponectin has been viewed overall as an anti-atherogenic molecule. Therefore, any certain conclusion about adiponectin's role in cardiovascular disease seems premature. Despite the rapidly accumulating literature on this adipokine, it is still unclear whether adiponectin is a key mediator or a bystander in cardiovascular disease. It is still uncertain whether adiponectin levels have any clinical significance for risk stratification in cardiovascular disease or they just reflect the activation of complex and opposing underlying mechanisms. Circulating adiponectin levels should be interpreted with caution, as they may have completely different prognostic value, depending on the underlying disease state.