15 research outputs found

    Overlap between angina without obstructive coronary artery disease and left ventricular diastolic dysfunction with preserved ejection fraction

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    <div><p>Background</p><p>A link between angina with no obstructive coronary artery disease (CAD) and heart failure with preserved left ventricular ejection fraction has been proposed, but evidence in support of this is lacking. In a cross-sectional study, we investigated whether left ventricular diastolic function in women with angina pectoris and no obstructive CAD differed from a reference population.</p><p>Methods</p><p>We included 956 women with angina and <50% coronary artery stenosis at invasive coronary angiography. Women with cardiovascular risk factors, but no history of chest pain or cardiac disease served as controls (n = 214). Left ventricular diastolic function was assessed by transthoracic echocardiography.</p><p>Results</p><p>The women with angina were slightly older, had higher body mass index, higher heart rate, and more had diabetes compared with controls while systolic blood pressure was lower. In age-adjusted analyses, angina patients had significantly lower E/A (Estimated difference -0.13, 95% CI: -0.17; -0.08), higher left ventricular mass index (5.73 g/m<sup>2</sup>, 95% CI: 3.71; 7.75), left atrial volume index (2.34 ml/m<sup>2</sup>, 95% CI: 1.23; 3.45) and E/e’ (0.68, 95% CI: 0.30; 1.05) and a larger proportion had higher estimated left ventricular filling pressure (17% versus 6%, p = 0.001). No between group differences were seen for e’ or deceleration time. After adjustment for known cardiovascular risk factors, between group differences for echocardiographic parameters remained statistically significant.</p><p>Conclusions</p><p>Patients with angina and no obstructive CAD had a more impaired left ventricular diastolic function compared with an asymptomatic reference population. This suggests some common pathophysiological pathway between the two syndromes.</p></div

    Inflammation, non-endothelial dependent coronary microvascular function and diastolic function-Are they linked?

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    PurposeSystemic inflammation and coronary microvascular dysfunction (CMD) may be causal drivers of heart failure with preserved ejection fraction (HFpEF). We tested the hypothesis that subclinical inflammation is associated with non-endothelial dependent CMD and diastolic dysfunction.MethodsIn a cross-sectional study of 336 women with angina but no flow limiting coronary artery stenosis (180 with diabetes) and 95 asymptomatic controls, blood samples were analysed for 90 biomarkers of which 34 were part of inflammatory pathways. CMD was assessed as coronary flow velocity reserve (CFVR) by transthoracic Doppler echocardiography and defined as CFVRResultsCMD was found in 59% of participants whereas only 4% fulfilled strict criteria for diastolic dysfunction. Thirty-five biomarkers, 17 of them inflammatory, were negatively correlated with CFVR and 25, 15 inflammatory, were positively correlated with E/e'. A total of 13 biomarkers, 9 inflammatory, were associated with both CFVR and E/e'. CFVR and E/e' were only correlated in the subgroup of patients with CMD and signs of increased filling pressure (E/e'>10) (p = 0.012).ConclusionThis is the first study to link a large number of mainly inflammatory biomarkers to both CMD and E/e', thus confirming a role of inflammation in both conditions. However, despite a high prevalence of CMD, few patients had diastolic dysfunction and the data do not support a major pathophysiologic role of non-endothelial dependent CMD in diastolic dysfunction

    Effect of the glucagon-like peptide-1 analogue liraglutide on coronary microvascular function in patients with type 2 diabetes – a randomized, single-blinded, cross-over pilot study

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    BACKGROUND: Impaired coronary microcirculation is associated with a poor prognosis in patients with type 2 diabetes. In the absence of stenosis of major coronary arteries, coronary flow reserve (CFR) reflects coronary microcirculation. Studies have shown beneficial effects of glucagon-like peptide-1 (GLP-1) on the cardiovascular system. The aim of the study was to explore the short-term effect of GLP-1 treatment on coronary microcirculation estimated by CFR in patients with type 2 diabetes. METHODS: Patients with type 2 diabetes and no history of coronary artery disease were treated with either the GLP-1 analogue liraglutide or received no treatment for 10 weeks, in a randomized, single-blinded, cross-over setup with a 2 weeks wash-out period. The effect of liraglutide on coronary microcirculation was evaluated using non-invasive trans-thoracic Doppler-flow echocardiography during dipyridamole induced stress. Peripheral microvascular endothelial function was assessed by Endo-PAT2000®. Interventions were compared by two-sample t-test after ensuring no carry over effect. RESULTS: A total of 24 patients were included. Twenty patients completed the study (15 male; mean age 57 ± 9; mean BMI 33.1 ± 4.4, mean baseline CFR 2.35 ± 0.45). There was a small increase in CFR following liraglutide treatment (change 0.18, CI95% [-0.01; 0.36], p = 0.06) but no difference in effect in comparison with no treatment (difference between treatment allocation 0.16, CI95% [-0.08; 0.40], p = 0.18). Liraglutide significantly reduced glycated haemoglobin (HbA1c) (-10.1 mmol/mol CI95% [-13.9; -6.4], p = 0.01), systolic blood pressure (-10 mmHg CI95% [-17; -3], p = 0.01) and weight (-1.9 kg CI95% [-3.6; -0.2], p = 0.03) compared to no treatment. There was no effect on peripheral microvascular endothelial function after either intervention. CONCLUSIONS: In this short-term treatment study, 10 weeks of liraglutide treatment had no significant effect on neither coronary nor peripheral microvascular function in patients with type 2 diabetes. Further long-term studies, preferably in patients with more impaired microvascular function and using a higher dosage of GLP-1 analogues, are needed to confirm these findings. TRIAL REGISTRATION: ClinicalTrials.gov: NCT01931982. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12933-015-0206-3) contains supplementary material, which is available to authorized users
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