Exercise and Vasodilation Coronary Physiology in Aortic Stenosis
What are the coronary physiological changes during exercise and hyperemia in the healthy heart and in patients with severe aortic stenosis (AS)?
Simultaneous intracoronary pressure and flow velocity recordings were made in unobstructed coronary arteries of 22 patients with severe AS (mean effective orifice area, 0.7 cm2) and 38 controls; at rest, during supine bicycle exercise, and during hyperemia. Stress echocardiography was performed to estimate myocardial work. Wave intensity analysis was used to quantify waves that accelerate and decelerate coronary blood flow.
Despite greater myocardial workload in patients with AS compared to controls at rest (12,721 vs. 9,707 mm Hg/min–1, p = 0.003) and during exercise (27,467 vs. 20,841 mm Hg/min–1, p = 0.02), coronary blood flow was similar in both groups. Hyperemic coronary blood flow was less in AS compared to controls (2,170 vs. 2,716 cm/min–1, p = 0.05). Diastolic time fraction (the diastolic temporal fraction of the cardiac cycle) was greater in AS compared to controls, but minimum microvascular resistance was similar. With exercise and hyperemia, efficiency of perfusion improved in the healthy heart, demonstrated by an increase in the relative contribution of accelerating waves. In contrast, in AS, perfusion efficiency decreased due to augmentation of early systolic deceleration and an attenuated rise in systolic acceleration waves.
Invasive coronary physiological evaluation can be safely performed during exercise and hyperemia in patients with severe AS. Ischemia in AS is not related to microvascular disease; rather, it is driven by abnormal cardiac-coronary coupling.
Severe AS can manifest with exertional angina in the absence of obstructive coronary artery disease (CAD). These data suggest that the efficiency of the healthy heart improves during exercise and hyperemia due to an increase in the relative contribution of waves that accelerate flow, although the reverse was observed in AS due to an increase in the contribution of waves that decelerate flow. The inability to adequately augment coronary blood flow caused by a pathophysiological imbalance of forces accelerating and decelerating coronary blood flow in AS, and an impingement on diastolic perfusion time, presumably are responsible for ischemia in the absence of obstructive CAD among patients with AS.
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