CAD and CMD common in HFpEF patients and may serve as therapeutic targets: JAMA

Written By :  Medha Baranwal
Medically Reviewed By :  Dr. Kamal Kant Kohli
Published On 2021-10-15 05:00 GMT   |   Update On 2021-10-15 06:34 GMT
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UK: A recent study in the journal JAMA Cardiology has shed light on the prevalence of coronary artery disease (CAD) and coronary microvascular dysfunction (CMD) in patients with heart failure with preserved ejection fraction (HFpEF). 91% of HFpEF patients were found to have evidence of epicardial CAD, CMD, or both. Of the people without obstructive CAD, 81% had CMD. 

Obstructive epicardial CAD and CMD are common and often unrecognized in hospitalized patients with HFpEF and may be therapeutic targets, wrote the lead author Christopher J. Rush, University of Glasgow, Glasgow, United Kingdom, and colleagues. 

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Myocardial ischemia due to epicardial CAD, CMD, or both may be a disease mechanism and therapeutic target in some patients with heart failure with HFpEF. Myocardial ischemia can result in left-ventricular (LV) diastolic and systolic dysfunction -- both of which are common in HFpEF. Inflammation-associated CMD may also contribute to pathophysiologic characteristics of HFpEF as supported by noninvasive studies, an autopsy series, and small invasive studies.

However, according to Rush and the team, the prevalence of epicardial CAD, CMD, and coronary endothelial dysfunction have not been systematically studied in HFpEF patients. Considering this they aimed to examine the prevalence of CAD and CMD in hospitalized patients with HFpEF in a prospective, multicenter, cohort study conducted between January 2, 2017, and August 1, 2018. 

A total of 106 consecutive patients hospitalized with HFpEF were evaluated. Participants underwent coronary angiography with guidewire-based assessment of coronary flow reserve, index of microvascular resistance, and fractional flow reserve, followed by coronary vasoreactivity testing.

Cardiac magnetic resonance imaging was performed with late gadolinium enhancement and assessment of extracellular volume. Myocardial perfusion was assessed qualitatively and semiquantitatively using the myocardial-perfusion reserve index.

Main outcomes included the prevalence of obstructive epicardial CAD, CMD, and myocardial ischemia, infarction, and fibrosis.

Of 106 participants enrolled, 75 had coronary angiography, 62 had assessment of coronary microvascular function, 41 underwent coronary vasoreactivity testing, and 52 received cardiac magnetic resonance imaging. 

The research revealed the following findings:

  • Obstructive epicardial CAD was present in 38 of 75 participants (51%); 19 of 38 (50%) had no history of CAD.
  • Endothelium-independent CMD (ie, coronary flow reserve <2.0 and/or index of microvascular resistance ≥25) was identified in 41 of 62 participants (66%).
  • Endothelium-dependent CMD (ie, abnormal coronary vasoreactivity) was identified in 10 of 41 participants (24%).
  • 45 of 53 participants (85%) had evidence of CMD and 29 of 36 (81%) of those without obstructive epicardial CAD had CMD.
  • Cardiac magnetic resonance imaging findings included myocardial-perfusion reserve index less than or equal to 1.84 (ie, impaired global myocardial perfusion) in 29 of 41 patients (71%), visual perfusion defect in 14 of 46 patients (30%), ischemic late gadolinium enhancement (ie, myocardial infarction) in 14 of 52 patients (27%), and extracellular volume greater than 30% (ie, diffuse myocardial fibrosis) in 20 of 48 patients (42%).
  • Patients with obstructive CAD had more adverse events during follow-up (28 [74%]) than those without obstructive CAD (17 [46%]).

"In this cohort study, epicardial CAD and CMD were common in the patients analyzed," the authors concldued. "These conditions might be unrecognized in hospitalized patients with HFpEF and may be therapeutic targets."

Reference:

Rush CJ, Berry C, Oldroyd KG, et al. Prevalence of Coronary Artery Disease and Coronary Microvascular Dysfunction in Patients With Heart Failure With Preserved Ejection Fraction. JAMA Cardiol. 2021;6(10):1130–1143. doi:10.1001/jamacardio.2021.1825

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Article Source : JAMA Cardiology

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