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Right ventricle free wall mechanics in metabolic syndrome without type-2 diabetes: effects of a 3-month lifestyle intervention program.
Serrano-Ferrer, J, Walther, G, Crendal, E, Vinet, A, Dutheil, F, Naughton, G, Lesourd, B, Chapier, R, Courteix, D, Obert, P
Cardiovascular diabetology. 2014;:116
Abstract
BACKGROUND Growing evidence demonstrates subtle left ventricular myocardial dysfunction in patients with metabolic syndrome (MetS), with central obesity, glucose intolerance and inflammation emerging as important contributors. Whether these results can be translated to the right ventricle (RV) is not yet fully elucidated. Furthermore, although lifestyle intervention favorably impacts MetS components and inflammatory biomarkers, its effect on RV myocardial function remains unknown today. METHODS Thirty-nine MetS adults free of diabetes were enrolled in a three month lifestyle intervention program including diet and physical exercise, and compared with forty healthy controls. Blood biochemistry, echocardiography including tissue Doppler imaging (TDI), and vector velocity imaging of the RV free wall to assess global longitudinal strain (GLS) and strain rates (SR) were obtained at baseline and after the intervention. RESULTS Compared with controls, MetS patients presented similar right atrial and RV morphology but reduced systolic (P = 0.04) and early diastolic (P = 0.02) velocities of the tricuspid annulus. They showed attenuated RV GLS (-21.4 ± 4.5 vs -25.7 ± 4.9%, P < 0.001) as well as early diastolic (P = 0.003) and systolic (P < 0.001) SR. Multiple regression analyses revealed log PAI-1 active, (P < 0.001), log adiponectin, (P = 0.01), LV mass indexed (P = 0.004) and central fat (P = 0.03) as independent predictors of RV GLS (R2 = 0.46, P < 0.001). Biological markers of MetS and inflammation as well as RV GLS (-21.8 ± 3.8 vs -24.3 ± 3.0%, P = 0.009) and systolic (P = 0.003) and early diastolic (P = 0.01) SR, but not TDI indexes, significantly improved after diet and exercise training, and vector velocity imaging data in MetS following the lifestyle intervention no longer differed from controls. CONCLUSIONS MetS is associated with subtle impairments in both RV free wall diastolic and systolic myocardial function which could be partly related to central-obesity induced changes in pro- and anti-inflammatory cytokines and left ventricular remodeling. The favorable impact of healthy dieting and physical activity on RV free wall mechanics indicates that cellular and sub-cellular alterations responsible for the RV myocardial abnormalities are probably not permanent and modifiable throughout adequate interventional strategies. TRIAL REGISTRATION American National Institutes of Health database NCT00917917.
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[Vitamin D deficiency, left ventricular dysfunction and heart failure].
Cioffi, G, Gatti, D, Adami, S
Giornale italiano di cardiologia (2006). 2010;(9):645-53
Abstract
Epidemiologic data indicate that about one million people worldwide suffer from and should be treated for vitamin D deficiency. The clinical impact of vitamin D deficiency is very high if we consider the pivotal role that this condition plays in determining osteoporosis, fractures, cancers, diabetes, vascular inflammation, which can severely reduce functional capacity, quality of life and may often lead to disability. Vitamin D deficiency is a widely underdiagnosed pathological condition. Although many cardiovascular diseases such as arterial hypertension, myocardial ischemia, diabetic cardiomyopathy and heart failure, may arise from a low vitamin D status, cardiologists do not routinely search for this disease in clinical practice. Vitamin D, indeed, stimulates the synthesis of various contractile proteins and activates crucial intracellular mechanisms that manage calcium metabolism and energy production. These functions can be altered once vitamin D deficiency develops. This review focuses on the relationship between vitamin D deficiency, asymptomatic changes in left ventricular geometry and function, and heart failure syndrome through a recall of the myocardial metabolic processes regulated by vitamin D. The analysis of the available data from the literature leads to raise some questions that, at present, have no answer. Future prospective studies are needed to assess the effect of treatment of vitamin D deficiency on cardiac function.
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[Microalbuminuria, a marker of artery rigidity and cardiac dysfunction].
Brahimi, M, Le Clésiau, H, Ouazen, Z, Soufi, K, Michault, A, Pariès, J, Cosson, E, Valensi, P
Archives des maladies du coeur et des vaisseaux. 2007;(8):673-6
Abstract
INTRODUCTION Microalbuminuria is considered as a marker of endothelial dysfunction and is associated with an increase in cardiovascular risk. The aim of this study was to evaluate this parameter as a potential marker of artery rigidity and left ventricle (LV) function. SUBJECTS AND METHODS We included 375 subjects referred to a health assessment center. They were 228 men and 147 women aged in means of 52.7 and 53.1 years, respectively. Among this population, 57 had type 2 diabetes, 28 of them with hypertension, 65 were hypertensive but free of diabetes, and 39 were free of diabetes but exhibited a metabolic syndrome (NCEP-ATP III). Urinary albumin excretion rate (UAER) was determined. Artery rigidity was evaluated by pulse pressure of the brachial artery (plethysmographic method), pulse pressure of the radial artery and aorta and pulse wave velocity (PWV) measured by aplanation tonometry (SphygmoCor). LV afterload was appreciated by LV telesystolic pressure and coronary perfusion by the diastolic area/systolic area ratio for aortic pressure curve (Buckberg index). RESULTS UAER correlated with PWV in the overall population (p<0.0001) and in the diabetic sub-group (p<0.001). In the overall population UAER correlated with LV telesystolic pressure (p=0.006) but not with Buckberg index. In the overall population and the diabetic subgroup, the artery rigidity indexes correlated strongly with LV telesystolic pressure, and radial and aortic pulse pressure correlated negatively with Buckberg index. CONCLUSION These data suggest that 1) microalbuminuria may be considered as a marker of artery rigidity, in line with experimental data which indicate the deleterious role of endothelial dysfunction on artery compliance; 2) artery rigidity is a potent determinant of LV afterload and coronary perfusion, in particular in diabetic patients.
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Trimetazidine administration minimizes myocardial damage and improves left ventricular function after percutaneous coronary intervention.
Labrou, A, Giannoglou, G, Zioutas, D, Fragakis, N, Katsaris, G, Louridas, G
American journal of cardiovascular drugs : drugs, devices, and other interventions. 2007;(2):143-50
Abstract
BACKGROUND AND OBJECTIVE The aim of this study was to evaluate whether the administration of trimetazidine, a piperazine derivative, to patients before and after percutaneous coronary intervention (PCI) minimizes the PCI-induced myocardial damage and improves left ventricular function 1 and 3 months after the procedure. METHODS Fifty-two patients hospitalized for acute coronary syndromes (ACS) were included in this study. Patients were randomized into two groups: group A (trimetazidine group; n = 27) and group B (placebo group; n = 25). All patients received conventional antianginal therapy. In addition, group A patients received oral trimetazidine 20 mg every 8 hours, starting 15 days before PCI and continuing for 3 months after the procedure. For each patient, serum troponin I and creatinine kinase (CK)-MB levels were measured before PCI, then at 6, 24, and 48 hours after the procedure; a 2D cardiac echocardiogram was performed before PCI and at 1 and 3 months after the procedure. RESULTS Twenty-four hours after PCI, troponin I levels were >1 ng/mL in 7 of 27 patients (26%) of group A and 11 of 25 patients (44%) in group B. Fourty-eight hours after revascularization troponin levels remained elevated in 15% of patients in group A and in 32% of patients in group B. Twenty-two percent of patients in group A had CK-MB levels >5 ng/mL, 24 hours after PCI, compared with 40% of patients in group B; four patients of group A had high CK-MB levels prior to PCI procedure. Echocardiographic measurements before revascularization revealed that 11 of 27 patients (40%) in group A had an ejection fraction <50% versus 8 of 24 patients (33%) in group B . The number of patients with an ejection fraction <50% was significantly reduced in group A compared with group B at 1 and 3 months after PCI, i.e. 11% versus 16% (p = 0.046) at 1 month and 4% versus 16% (p = 0.017) at 3 months.A significant improvement in regional wall motion was noted after treatment with trimetazidine compared with placebo. One month after PCI, inferior left ventricular (LV) wall hypokinesia had improved in 4 of 6 trimetazidine recipients and in 4 of 14 placebo recipients (p = 0.014, group A vs group B). After 3 months inferior wall hypokinesia improved in four patients in group A versus six patients in group (p = 0.05). Similarly, anterior LV wall motion improved in 3 of 11 patients in group A and in 1 of 6 patients in group B at 1 month. After 3 months anterior wall hypokinesia had improved in eight patients in group A and in two patients in group B (p = 0.04, group A vs group B). CONCLUSION The metabolic agent trimetazidine appears to minimize myocardial reperfusion injury during PCI and improves global and regional wall motion at 1 and 3 months after PCI. This study was limited by small patient numbers and further studies are necessary to evaluate exact mechanisms of action and clinical implications of using trimetazidine in conjunction with PCI.