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Increased wave reflection and ejection duration in women with chest pain and nonobstructive coronary artery disease: ancillary study from the Women's Ischemia Syndrome Evaluation

Nichols, Wilmer W.a; Denardo, Scott J.b; Johnson, B. Deliac; Sharaf, Barry L.d; Bairey Merz, C. Noele; Pepine, Carl J.a

doi: 10.1097/HJH.0b013e3283611bac
ORIGINAL PAPERS: Blood vessels

Objective: Wave reflections augment central aortic SBP and increase systolic pressure time integral (SPTI) thereby increasing left ventricular (LV) afterload and myocardial oxygen (MVO2) demand. When increased, such changes may contribute to myocardial ischemia and angina pectoris, especially when aortic diastolic time is decreased and myocardial perfusion pressure jeopardized. Accordingly, we examined pulse wave reflection characteristics and diastolic timing in a subgroup of women with chest pain (Women's Ischemia Syndrome Evaluation, WISE) and no obstructive coronary artery disease (CAD).

Methods: Radial artery BP waveforms were recorded by applanation tonometry, and aortic BP waveforms derived. Data from WISE participants were compared with data from asymptomatic women (reference group) without chest pain matched for age, height, BMI, mean arterial BP, and heart rate.

Results: Compared with the reference group, WISE participants had higher aortic SBP and pulse BP and ejection duration. These differences were associated with increased augmentation index and reflected pressure wave systolic duration. These modifications in wave reflection characteristics were associated with increased SPTI and wasted LV energy (Ew) and a decrease in pulse pressure amplification, myocardial viability ratio, and diastolic pressure time fraction.

Conclusion: WISE participants with no obstructive CAD have changes in systolic wave reflections and diastolic timing that increase LV afterload, MVO2 demand, and Ew with the potential to reduce coronary artery perfusion. These alterations in cardiovascular function contribute to an undesirable mismatch in the MVO2 supply/demand that promotes ischemia and chest pain and may contribute to, or increase the severity of, future adverse cardiovascular events.

aDivision of Cardiovascular Medicine, University of Florida College of Medicine, Gainesville, Florida

bDivision of Cardiovascular Medicine, Duke University Medical Center, Durham, North Carolina

cDepartment of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania

dDivision of Cardiology, Rhode Island Hospital, Providence, Rhode Island

eHeart Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA

Correspondence to Carl J. Pepine, MD, Division of Cardiovascular Medicine, Box 100277, University of Florida, Gainesville, FL 32601, USA. Tel: +1 352 273 9082; fax: +1 352 371 0370; e-mail: carl.pepine@medicine.ufl.edu

Abbreviations: AIx, aortic augmentation index; BP, blood pressure; CAD, coronary artery disease; CFR, coronary flow reserve; DPTF, diastolic pressure time fraction; DPTI, diastolic pressure time index; F, fraction of time during cardiac cycle; HRT, hormone replacement therapy; LV, left ventricular; LVH, left ventricular hypertrophy; MVO2, myocardial oxygen; Pi, inflection point; PP, pulse pressure; PWA, pulse wave analysis; SDR, systolic duration of reflected wave; SPTF, systolic pressure time fraction; SPTI, systolic pressure time index

Received 12 September, 2012

Revised 11 February, 2013

Accepted 11 March, 2013

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins