AimsHeart failure (HF) with normal or preserved left ventricular (LV) ejection fraction (HFPEF) has been reported to be associated with similar outcome as HF with reduced EF (HFREF) in registry-based and epidemiological analyses, but many of these studies excluded patients who did not have EF measurements. Conversely, prior prospective studies have reported better outcome for patients with HFPEF. We performed a meta-analysis of prospective observational studies comparing all-cause mortality in patients with HFREF and HFPEF. Methods and resultsWe searched several online databases for studies comparing outcome in HFREF and HFPEF, published before 2007. Inclusion criteria: prospective, clinical HF, near complete EF data, and mortality outcome. Review Manager version 4.2.3 software was used for the analysis. Overall, 24 501 patients [9299 deaths (38%)] from 17 studies are included. Average follow-up was 47 months; the HFPEF group was older (69 vs. 66 years) and more likely to be female (44% vs. 26%). Of the 7688 patients with HFPEF 2468 died (32.1%), compared with 6831 of the 16 813 patients with HFREF (40.6%): odds ratio 0.51 (95% CI: 0.48, 0.55). ConclusionThis literature-based meta-analysis demonstrates that mortality among patients with HFPEF was half that observed in those with HFREF, in contrast to previous reports suggesting that mortality may be similar between both groups.--
BackgroundLeft ventricular hypertrophy (LVH) is a strong predictor of cardiovascular disease and is common among patients with type 2 diabetes. However, no systematic screening for LVH is currently recommended for patients with type 2 diabetes. The purpose of this study was to determine whether NT-proBNP was superior to 12-lead electrocardiography (ECG) for detection of LVH in patients with type 2 diabetes.MethodsProspective cross-sectional study comparing diagnostic accuracy of ECG and NT-proBNP for the detection of LVH among patients with type 2 diabetes. Inclusion criteria included having been diagnosed for > 5 years and/or on treatment for type 2 diabetes; patients with Stage 3/4 chronic kidney disease and known cardiovascular disease were excluded. ECG LVH was defined as either the Sokolow-Lyon or Cornell voltage criteria. NT-proBNP level was measured using the Roche Diagnostics Elecsys assay. Left ventricular mass was assessed from echocardiography. Receiver operating characteristic curve analysis was carried out and area under the curve (AUC) was calculated.Results294 patients with type 2 diabetes were recruited, mean age 58 (SD 11) years, BP 134/81 ± 18/11 mmHg, HbA1c 7.3 ± 1.5%. LVH was present in 164 patients (56%). In a logistic regression model age, gender, BMI and a history of hypertension were important determinants of LVH (p < 0.05). Only 5 patients with LVH were detected by either ECG voltage criteria. The AUC for NT-proBNP in detecting LVH was 0.68.ConclusionsLVH was highly prevalent in asymptomatic patients with type 2 diabetes. ECG was an inadequate test to identify LVH and while NT-proBNP was superior to ECG it remained unsuitable for detecting LVH. Thus, there remains a need for a screening tool to detect LVH in primary care patients with type 2 diabetes to enhance risk stratification and management.
Abstract-Women younger than 75 years with stable angina or acute coronary syndrome have higher cardiac mortality than similarly aged men, despite less obstructive coronary artery disease. To determine whether the myocardial structure and coronary microvasculature of women differs from that of men, we performed histological analysis of biopsies from nonischemic left ventricular myocardium from 46 men and 11 women undergoing coronary artery bypass graft surgery who did not have previous cardiac surgery, myocardial infarction, heart failure, atrial fibrillation, or furosemide therapy. The 2 patient groups had similar clinical characteristics, apart from a lower body surface area (BSA) in women (Pϭ0.0015). Women had less interstitial fibrosis than men (Pϭ0.019) but similar perivascular fibrosis. Arteriolar wall area/circumference ratio, a measure of arteriolar wall thickness, was 47% greater in women than men (Pϭ0.012).Cardiomyocyte width and diffusion radius were positively correlated, and capillary length density was negatively correlated with BSA (PϽ0.05). Whereas cardiomyocyte width, capillary length density, diffusion radius, and cardiomyocyte width/BSA ratio were similar for men and women, women had a greater diffusion radius/BSA ratio (Pϭ0.0038) and a greater diffusion radius/cardiomyocyte width ratio (Pϭ0.027). Women also had lower vascular endothelial growth factor (VEGF) receptor-1 levels (Pϭ0.048) and VEGF receptor-1/VEGF-A ratio (Pϭ0.024) in plasma. We conclude that women with extensive coronary artery disease have greater arteriolar wall thickness and diffusion radius relative to BSA and to cardiomyocyte width than men, which may predispose to myocardial ischemia. Additional studies of larger numbers of women with less extensive coronary artery disease are required to confirm these findings. Key Words: gender Ⅲ ischemic heart disease Ⅲ myocardial fibrosis Ⅲ coronary microvasculature I schemic heart disease of women is different from that of men. 1,2 Women with stable angina referred for angiographic evaluation are less likely to have significant coronary artery disease, 3 yet women younger than 75 years with stable angina have a higher coronary standardized mortality ratio than men. 4 Moreover, when women present with an acute coronary syndrome, they are less likely to have an STsegment elevation myocardial infarction and more likely to have unstable angina, 5 and although they are less likely to have significant coronary artery disease, 3,5 women less than 75 years of age with myocardial infarction have a higher risk of coronary death than men. 3,6 -8 Evidence for a greater role for coronary microvascular dysfunction in ischemic heart disease of women is the report that retinal arterial narrowing, a marker of lower hyperemic myocardial blood flow and perfusion reserve, 9 predicted coronary events in women, but not in men. 10 To investigate the possibility that the different characteristics of ischemic heart disease in men and women reflect differences in myocardial structure and coronary microvascula...
BackgroundType 2 diabetes and the metabolic syndrome are associated with impaired diastolic function and increased heart failure risk. Animal models and autopsy studies of diabetic patients implicate myocardial fibrosis, cardiomyocyte hypertrophy, altered myocardial microvascular structure and advanced glycation end-products (AGEs) in the pathogenesis of diabetic cardiomyopathy. We investigated whether type 2 diabetes and the metabolic syndrome are associated with altered myocardial structure, microvasculature, and expression of AGEs and receptor for AGEs (RAGE) in men with coronary artery disease.MethodsWe performed histological analysis of left ventricular biopsies from 13 control, 10 diabetic and 23 metabolic syndrome men undergoing coronary artery bypass graft surgery who did not have heart failure or atrial fibrillation, had not received loop diuretic therapy, and did not have evidence of previous myocardial infarction.ResultsAll three patient groups had similar extent of coronary artery disease and clinical characteristics, apart from differences in metabolic parameters. Diabetic and metabolic syndrome patients had higher pulmonary capillary wedge pressure than controls, and diabetic patients had reduced mitral diastolic peak velocity of the septal mitral annulus (E'), consistent with impaired diastolic function. Neither diabetic nor metabolic syndrome patients had increased myocardial interstitial fibrosis (picrosirius red), or increased immunostaining for collagen I and III, the AGE Nε-(carboxymethyl)lysine, or RAGE. Cardiomyocyte width, capillary length density, diffusion radius, and arteriolar dimensions did not differ between the three patient groups, whereas diabetic and metabolic syndrome patients had reduced perivascular fibrosis.ConclusionsImpaired diastolic function of type 2 diabetic and metabolic syndrome patients was not dependent on increased myocardial fibrosis, cardiomyocyte hypertrophy, alteration of the myocardial microvascular structure, or increased myocardial expression of Nε-(carboxymethyl)lysine or RAGE. These findings suggest that the increased myocardial fibrosis and AGE expression, cardiomyocyte hypertrophy, and altered microvasculature structure described in diabetic heart disease were a consequence, rather than an initiating cause, of cardiac dysfunction.
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