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(Circulation. 2006;113:1768-1778.)
© 2006 American Heart Association, Inc.
Heart Failure |
From the International Centre for Circulatory Health, St Marys Hospital and Imperial College (J.E.D., Z.I.W., D.P.F., C.H.M., R.A.F., I.S.M., A.D.H., J.M.); the Department of Bioengineering, Physiological Flow Unit, Imperial College (J.A.-S., K.H.P.); and the Department of Clinical Engineering, Royal Brompton Hospital (K.W.), London, United Kingdom.
Correspondence to Dr Justin Davies, International Centre for Circulatory Health, St Marys Hospital and Imperial College, 59-61 North Wharf Road, Paddington, London W2 1LA, UK. E-mail coronarywia{at}heart123.com
Received August 15, 2005; de novo received November 21, 2005; accepted January 23, 2006.
Background Coronary blood flow peaks in diastole when aortic blood pressure has fallen. Current models fail to completely explain this phenomenon. We present a new approachusing wave intensity analysisto explain this phenomenon in normal subjects and to evaluate the effects of left ventricular hypertrophy (LVH).
Method and Results We measured simultaneous pressure and Doppler velocity with intracoronary wires in the left main stem, left anterior descending, and circumflex arteries of 20 subjects after a normal coronary arteriogram. Wave intensity analysis was used to identify and quantify individual pressure and velocity waves within the coronary artery circulation. A consistent pattern of 6 predominating waves was identified. Ninety-four percent of wave energy, accelerating blood forward along the coronary artery, came from 2 waves: first a pushing wave caused by left ventricular ejectionthe dominant forward-traveling pushing wave; and later a suction wave caused by relief of myocardial microcirculatory compressionthe dominant backward-traveling suction wave. The dominant backward-traveling suction wave (18.2±13.7x103 W m2s1, 30%) was larger than the dominant forward-traveling pushing wave (14.3±17.6x103 W m2 s1, 22.3%, P =0.001) and was associated with a substantially larger increment in coronary blood flow velocity (0.51 versus 0.14 m/s, P<0.001). In LVH, the dominant backward-traveling suction wave percentage was significantly decreased (33.1% versus 26.9%, P=0.01) and inversely correlated with left ventricular septal wall thickness (r=0.52, P<0.02).
Conclusions Six waves predominantly drive human coronary blood flow. Coronary flow peaks in diastole because of the dominance of a "suction" wave generated by myocardial microcirculatory decompression. This is significantly reduced in LVH.
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