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Coronary Physiology During Exercise and Vasodilation in the Healthy Heart and in Severe Aortic Stenosis

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)688-697
Number of pages10
JournalJournal of the American College of Cardiology
Volume68
Issue number7
Early online date16 Aug 2016
DOIs
Publication statusE-pub ahead of print - 16 Aug 2016

King's Authors

Abstract

Background

Severe aortic stenosis (AS) can manifest as exertional angina even in the presence of unobstructed coronary arteries.
Objectives

The authors describe coronary physiological changes during exercise and hyperemia in the healthy heart and in patients with severe AS.
Methods

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 (CBF).
Results

Despite a greater myocardial workload in AS patients compared with 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), CBF was similar in both groups. Hyperemic CBF was less in AS compared with controls (2,170 vs. 2,716 cm/min−1; p = 0.05). Diastolic time fraction was greater in AS compared with 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. By contrast, in AS, perfusion efficiency decreased due to augmentation of early systolic deceleration and an attenuated rise in systolic acceleration waves.
Conclusions

Invasive coronary physiological evaluation can be safely performed during exercise and hyperemia in patients with severe aortic stenosis. Ischemia in AS is not related to microvascular disease; rather, it is driven by abnormal cardiac-coronary coupling.

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