Evidence of a Dominant Backward-Propagating “Suction” Wave Responsible for Diastolic Coronary Filling in Humans, Attenuated in Left Ventricular Hypertrophy

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 approach—using wave intensity analysis—to 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 ejection—the dominant forward-traveling pushing wave; and later a suction wave caused by relief of myocardial microcirculatory compression—the dominant backward-traveling suction wave. The dominant backward-traveling suction wave (18.2±13.7×103 W m−2 s−1, 30%) was larger than the dominant forward-traveling pushing wave (14.3±17.6×103 W m−2 s−1, 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.

[1]  K. Parker,et al.  Nonlinearity of human arterial pulse wave transmission. , 1992, Journal of biomechanical engineering.

[2]  M. Frank,et al.  Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease. , 1990, Journal of the American College of Cardiology.

[3]  M. Noble,et al.  The Contribution of Blood Momentum to Left Ventricular Ejection in the Dog , 1968, Circulation research.

[4]  J. A. E. Spaan,et al.  Mechanical determinants of myocardial perfusion , 1995, Basic Research in Cardiology.

[5]  A. Savitzky,et al.  Smoothing and Differentiation of Data by Simplified Least Squares Procedures. , 1964 .

[6]  B. De Bruyne,et al.  Experimental Basis of Determining Maximum Coronary, Myocardial, and Collateral Blood Flow by Pressure Measurements for Assessing Functional Stenosis Severity Before and After Percutaneous Transluminal Coronary Angioplasty , 1993, Circulation.

[7]  B. Strauer,et al.  Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension. , 1993, Circulation.

[8]  K. Parker,et al.  Forward and backward running waves in the arteries: analysis using the method of characteristics. , 1990, Journal of biomechanical engineering.

[9]  Motoaki Sugawara,et al.  Compression and expansion wavefront travel in canine ascending aortic flow: wave intensity analysis , 2002, Heart and Vessels.

[10]  M. Frank,et al.  Relation among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease☆ , 1990 .

[11]  K. Parker,et al.  Wave-intensity analysis: a new approach to coronary hemodynamics. , 2000, Journal of applied physiology.

[12]  D. Sabiston,et al.  Effect of Cardiac Contraction on Coronary Blood Flow , 1957, Circulation.

[13]  J D Laird,et al.  Diastolic‐Systolic Coronary Flow Differences are Caused by Intramyocardial Pump Action in the Anesthetized Dog , 1981, Circulation research.

[14]  E S Kirk,et al.  Inhibition of Coronary Blood Flow by a Vascular Waterfall Mechanism , 1975, Circulation research.

[15]  A W Khir,et al.  Arterial waves in humans during peripheral vascular surgery. , 2001, Clinical science.

[16]  J. Downey,et al.  Effects of Myocardial Strains on Coronary Blood Flow , 1974, Circulation research.

[17]  Jamil Mayet,et al.  Use of simultaneous pressure and velocity measurements to estimate arterial wave speed at a single site in humans. , 2006, American journal of physiology. Heart and circulatory physiology.

[18]  M Sugawara,et al.  "Wavefronts" in the aorta--implications for the mechanisms of left ventricular ejection and aortic valve closure. , 1993, Cardiovascular research.

[19]  M. Sugawara,et al.  Aortic blood momentum--the more the better for the ejecting heart in vivo? , 1997, Cardiovascular research.

[20]  Carl J. Wiggers,et al.  STUDIES ON THE CONSECUTIVE PHASES OF THE CARDIAC CYCLE , 1921 .

[21]  Motoaki Sugawara,et al.  A new noninvasive measurement system for wave intensity: evaluation of carotid arterial wave intensity and reproducibility , 2002, Heart and Vessels.

[22]  R Krams,et al.  Varying elastance concept may explain coronary systolic flow impediment. , 1989, The American journal of physiology.

[23]  Junichiro Hayano,et al.  Clinical usefulness of carotid arterial wave intensity in assessing left ventricular systolic and early diastolic performance , 2003, Heart and Vessels.

[24]  B. G. Brown Effect of lovastatin or niacin combined with colestipol and regression of coronary atherosclerosis. , 1992, European heart journal.

[25]  B. Strauer,et al.  Morphometric investigation of human myocardium in arterial hypertension and valvular aortic stenosis. , 1992, European heart journal.