RIGHT-VENTRICULAR STIFFNESS MEASURED BY A NEW METHOD WITHOUT VOLUME ESTIMATION IN CORONARY-ARTERY DISEASE

This study was designed to measure the right ventricular (RV) stiffnes s (Delta P/Delta V) with a new method without estimating the RV volume itself. RV stiffness has rarely been measured due to the difficulty i n estimating the RV volume. Without measuring RV volume itself, stiffn ess can be determined by measuring its volume change (Delta V). Tricus pid filling flow volume, which is the diastolic RV Delta V, is measura ble by using Doppler echocardiography. Thus, Delta V stiffness may pos sibly be obtained from Doppler echocardiography combined with high-fid elity RV pressure. Subjects consisted of 8 controls, 8 patients with a ngina pectoris, 8 with anterior, 8 with posterior, and 8 with inferior prior myocardial infarction. Tricuspid annular dimension was measured by 2-dimensional echocardiography and the tricuspid annular area was calculated. Velocity-time integral of the tricuspid filling flow durin g the late diastole was measured by pulsed Doppler echocardiography. T hen, the late diastolic RV Delta V was obtained as the product of the tricuspid annular area and the integral. The late diastolic RV pressur e rise (Delta P) was also measured with a micromanometer catheter. The RV elastic chamber stiffness constant ([Delta P/Delta V]/P) was obtai ned by dividing simple stiffness by the mean RV pressure during late d iastole. The RV elastic chamber stiffness constant did not significant ly differ among controls, patients with angina pectoris, and those wit h anterior and posterior myocardial infarction (0.0054 +/- 0.0009 vs 0 .0057 +/- 0.0018 vs 0.0064 +/- 0.002 vs 0.0052 +/- 0.0019 ml(-1)). How ever, it was significantly increased in patients with inferior myocard ial infarction (0.010 +/- 0.004 ml(-1), p <0.01 or 0.05) compared with those in the other 4 groups. These results suggest (1) that RV stiffn ess can be measured with a new method without RV volume estimation, an d (2) that this new method is useful in evaluating RV diastolic pathop hysiology in patients with coronary artery disease.