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Rigshospitalet - en del af Københavns Universitetshospital
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Overlap between angina without obstructive coronary artery disease and left ventricular diastolic dysfunction with preserved ejection fraction

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  • Marie Mide Michelsen
  • Adam Pena
  • Naja D Mygind
  • Nis Høst
  • Ida Gustafsson
  • Peter Riis Hansen
  • Henrik Steen Hansen
  • Jens Kastrup
  • Eva Prescott
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Background 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. Methods 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. Results 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/m2, 95% CI: 3.71; 7.75), left atrial volume index (2.34 ml/m2, 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. Conclusions 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.

OriginalsprogEngelsk
Artikelnummere0216240
TidsskriftPLoS One
Vol/bind14
Udgave nummer5
Sider (fra-til)e0216240
ISSN1932-6203
DOI
StatusUdgivet - 1 maj 2019

ID: 57230456