Why the study?
Do patients with refractory angina have altered aortic wave reflection characteristics and increased wasted left ventricular pressure energy compared to treated hypertensive patients?
Do patients with refractory angina have altered aortic wave reflection characteristics and increased wasted left ventricular pressure energy compared to treated hypertensive patients?
Patients with refractory angina exhibit adverse changes in systolic wave reflections and diastolic timing that increase left ventricular afterload and wasted energy, potentially exacerbating ischemia.
Altered wave reflections may exacerbate ischemia in refractory angina; leaves open causal role and need for prospective trials.
Background: Early return of reflected blood pressure (BP) waves from the lower body augments central systolic BP and increases systolic pressure-time index (SPTI) and wasted left ventricular (LV) pressure energy, which increase afterload and myocardial oxygen (MVO 2 ) demand.Accordingly, we sought to determine wave reflection characteristics and diastolic timing in a group of patients with chronic stable angina resistant to anti-anginal therapy.Methods: Radial artery BP waveforms were recorded non-invasively by applanation tonometry in 36 patients with refractory angina (RA) and a reference control (CON) group of 36 successfully treated hypertensive patients without angina matched for age, gender, height, BMI, and mean BP.Pulse wave analysis (PWA) of the ascending aortic BP waveform was used to determine central hemodynamics, diastolic timing, wave reflection characteristics and wasted LV pressure energy (LVEw).Results: Compared to the CON group, RA patients had higher central aortic augmented BP, augmentation index (Alx) and reflected pressure wave systolic duration (SDR).These modifications in wave reflection characteristics were associated with an increase in SPTI and LVEw and a decrease in pulse BP amplification and the diastolic pressure time fraction.Conclusions: RA patients have changes in systolic wave reflections and diastolic timing that increase LV afterload, MVO 2 demand and wasted LV energy and reduce coronary artery perfusion.These alterations in cardiovascular function contribute to an undesirable mismatch in the MVO 2 supply/demand ratio that favors ischemia and angina pectoris and may precipitate future adverse cardiovascular events.
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Gurovich et al. (2014) studied this question.
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