Peripheral arterial diseases (PAD) is an atherosclerotic occlusive disease in the periphery affecting 8-12 million U.S.adults. It has been reported that the PAD patients have attenuated coronary blood flow response to stress, however how the diseases influence aortic arterial pulse wave properties during exercise, and its relationship with coronary perfusion in this patient population is unknown. Accordingly, the primary aim of this study was to examine myocardial supply and demand relationship by investigating aortic pulse wave properties and their relationship with coronary perfusion during exercise in PAD. Methods: 13 PADpatients and 13 healthy (age, sex, BMI-matched) control subjects performed rhythmic plantar flexion for 14 minutes or until fatigue (30 contractions per minute). The workload started at 2 kg and increased by 1 kg every minute up to12 kg. Brachial (oscillometric cuff) and aortic (SphygmoCor, utilizing transfer function and brachial blood pressures) blood pressures were measured during supine rest and plantar flexion exercise as well as aortic pulse wave properties from derived-aortic pulse waveforms. On a separate visit, coronary blood flow velocity was measured non-invasively during rest and exercise. Results: Due to earlier arrival of reflected wave (140.9± 2.3 vs. 150.5± 3.4 ms; P =0.0289), baseline augmented pressure (15.9± 2.4 vs. 9.3± 1.7 mmHg; AP, P =0.0380), augmentation index (27.2± 2.7 vs. 19.1± 2.2 %; AI, P =0.0263), and cardiac wasted energy (4625± 590 vs. 2875± 491 s· dyne· cm 2 ; E w , P =0.0321) were greater compared to healthy control. During exercise, changes in aortic mean arterial pressure(21.90± 5.04 vs. 9.36± 2.20 mmHg; ΔaMAP, P =0.0041), end-systolic pressure (133.38± 4.85 vs. 111.46± 4.97 mmHg; ΔESP, P =0.0043), and the tension time index (1027± 216 vs. 504± 117 mmHg· S -1 · min -1 ; ΔTTI, P =0.0035) were significantly greater in PAD while ΔAI was not different. Intriguingly, despite the augmented TTI, the first and second peaks of CBV during exercise were not different between the groups leading to significantly attenuated subendocardial viability ratio responses to exercise (-34.66± 4.19 vs. -23.03± 3.37 %; ΔSEVR, P =0.0164). Conclusions: At this peak workload for PAD patients, the patients had a greater myocardial demand compared to healthy control. However, despite the increase in the myocardial demand and the accompanying increase in initial coronary perfusion pressure (ESP), CBV of PAD patients was not different from that seen in healthy control indicating limited myocardial supply during exercise in PAD. Consequently, PAD exhibited a greater mismatch of myocardial demand and supply at the peak workload. This suggests that, in PAD patients, there are mechanisms aside from changes in coronary perfusion pressure that limit myocardial supply during exercise (i.e. a greater coronary vascular tone and diastolic dysfunction).
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