Key result
Coronary vascular dysfunction linked to impaired LV filling and increased LVEDP during handgrip stress.
Why the study?
Coronary vascular dysfunction often causes angina with no obstructive coronary arteries and is increasingly described as a contributor and predictor of heart failure with preserved ejection fraction. This study tested the hypothesis that coronary vascular dysfunction contributes to cardiac dysfunction.
Does coronary vascular dysfunction impair left ventricular filling adaptation during isometric handgrip stress in patients with angina and no obstructive coronary arteries?
Observational (n=68)
Does coronary vascular dysfunction impair left ventricular filling adaptation during isometric handgrip stress in patients with angina and no obstructive coronary arteries?
In patients with angina and no obstructive coronary arteries, coronary vascular dysfunction is associated with impaired left ventricular diastolic filling adaptation and elevated filling pressures during isometric handgrip stress.
Supports mechanistic link in suspected cases; leaves open whether targeting coronary vascular dysfunction alters HFpEF outcomes.
Angina with no obstructive coronary arteries is often due to coronary vascular dysfunction, which is increasingly described as a contributor and predictor of heart failure with preserved ejection fraction. We tested the hypothesis that coronary vascular dysfunction contributes to cardiac dysfunction. Sixty-eight participants with suspected coronary vascular dysfunction underwent LV pressure-volume assessment at rest and during isometric handgrip stress. Coronary function testing was performed by infusing standard doses of adenosine, acetylcholine, and nitroglycerine through a guiding catheter placed in the left main coronary artery, per established protocols. Of the participants studied, 12 had normal coronary vascular function while 56 had coronary vascular dysfunction. At rest, there were no differences between groups in any invasive pressure or volumetric measurement. With isometric handgrip, peak filling rate increased significantly in participants with normal coronary vascular function (0.56 ± 0.31 vs. 0.85 ± 0.68 1/s/mmHg) but remained unchanged in participants with coronary vascular dysfunction (0.51 ± 0.22 vs. 0.55 ± 0.43 1/s/mmHg; group x time interaction, p = 0.04). Moreover, left ventricular end-diastolic pressure decreased significantly with isometric handgrip in participants with normal coronary vascular function (12 ± 3 vs. 9 ± 4 mmHg) but increased in participants with coronary vascular dysfunction (14 ± 4 vs. 15 ± 6 mmHg; group x time interaction, p = 0.03). Coronary vascular dysfunction was associated with an impaired ability of the LV to adapt its filling during stress. Further work is needed to assess potential clinical significance.
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Oneglia et al. (2026) conducted an observational in Angina with no obstructive coronary arteries (suspected coronary vascular dysfunction) (n=68). Coronary vascular dysfunction vs. Normal coronary vascular function was evaluated on Peak LV filling rate (1/s/mmHg) and LV end-diastolic pressure (mmHg) during isometric handgrip stress (p=0.04). Coronary vascular dysfunction impaired LV filling adaptation during handgrip stress, with unchanged peak filling rate (p=0.04) and increased LVEDP (14 to 15 vs 12 to 9 mmHg, p=0.03).
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