VALVUIAR HEART DISEASE Pulmonary arterial V waves in mitral regurgitation : clinical and experimental observations

Pulmonary arterial early diastolic waves (V waves) were investigated in patients and experimental animals with mitral regurgitation. V waves exceeding systolic pressure in the pulmonary artery were recorded in the main pulmonary artery with micromanometer catheters both in patients and animals, eliminating the possibility of catheter artifact. In experimental animals, aortic closure preceded pulmonic closure by 33 + 12 msec at baseline. With the creation of acute mitral insufficiency, a pulmonary arterial V wave occurred in six of eight animals. Early pulmonic valve closure occurred only in the six animals with a pulmonary arterial V wave. In these animals, pulmonic closure preceded aortic closure by 28 + 7 msec during mitral insufficiency (p < .05). Of 70 patients with severe mitral regurgitation at cardiac catheterization, 14 had a pulmonary arterial V wave. In five patients recordings with micromanometer catheters were made and early pulmonic closure was also observed in four of these patients who had pulmonary arterial V waves at rest or upon provocation. Patients with pulmonary arterial V waves had a more acute onset of symptoms, shorter duration of mitral regurgitation, higher pulmonary capillary wedge V waves, and lower pulmonary arterial resistances than patients without them and were more likely to have nonrheumatic mitral regurgitation. Circulation 69, No. 2, 214-222, 1984. EARLY DIASTOLIC PRESSURE waves (V waves) have been recorded in the pulmonary artery during mitral regurgitation with fluid-filled catheters.14 Spring and Row' demonstrated that the magnitude of this early diastolic pressure wave could exceed that of pulmonary arterial systolic pressure. In addition, they found indirect evidence that the pulmonary arterial early diastolic pressure wave could cause premature pulmonic valve closure. However, a direct association between the early diastolic pressure wave and pulmonic valve closure was never confirmed. In this study, data obtained with micromanometer catheters during acute mitral regurgitation in dogs were used to further investigate pulmonary arterial diastolic pressure waves and their relationship to pulmonic valve closure. Concurrently, the clinical occurrence of this phenomenon was reviewed from catheterization laboratory data, and its pathophysiologic characteristics were further investigated with the use of micromanometer recordings from patients. From the Department of Medicine and Division of Cardiology, Montefiore Medical Center and Albert Einstein College of Medicine, New York. Address for correspondence: Richard Grose, M.D., Division of Cardiology, Montefiore Medical Center, 1 1 1 East 2 10th St., Bronx, NY 10467. Received Aug. 15, 1983; revision accepted Oct. 13, 1983. Methods Patients. Cardiac catheterization was performed on 2590 adults at Montefiore Medical Center over a 3 year period from January 1980 to December 1982. Right heart catheterization was performed in 648 patients with suspected valvular heart disease or with elevations in pulmonary arterial pressure and was performed with either a No. 7 thermodilution balloon catheter or No. 7 Cournand catheter. Mitral regurgitation was assessed angiographically during left ventriculography and classified as 1 + (left atrial contrast clearing with each diastole), 2 + (opacified blood not clearing with each beat, but with the left atrium less densely opacified than the left ventricle), 3 + (the left atrium filling as densely as the left ventricle), or 4 + (opacification of the left atrium usually during a single left ventricular systole and more densely than the left ventricle or aorta with contrast refluxing into the pulmonary veins).' Severe regurgitation was defined as either 3 + or 4 +. Of the patients in whom a right heart catheterization was performed, 70 had angiographically proven severe mitral regurgitation and form the basis of this report. The pulmonary arterial and wedge pressure tracings of these 70 patients with severe mitral regurgitation were then reviewed. In the pulmonary wedge trace, a V wave was defined as large if the peak pressure exceeded the mean by at least 10 mm Hg.6 A pulmonary arterial early diastolic pressure wave (which for simplicity will be called a pulmonary arterial V wave) was defined as a wave in the pulmonary arterial tracing that: (1) peaked in early diastole, (2) equalled or exceeded pulmonary arterial systolic pressure, (3) had a contour and timing similar to the pulmonary wedge V wave, and (4) could be recorded in the main pulmonary artery just above the pulmonic valve (to preclude mixed pulmonary arterial-pulmonary wedge tracings). In each of five patients (three with and two without pulmoCIRCULATION 214 by gest on N ovem er 7, 2017 http://ciajournals.org/ D ow nladed from PATHOPHYSIOLOGY AND NATURAL HISTORY-VALVULAR HEART DISEASE nary arterial V waves at rest) a micromanometer-tipped catheter (Millar microtip PC484A) was positioned with the micromanometer in the main pulmonary artery just above the pulmonic valve and in the aorta just above the aortic valve. In these patients, simultaneous aortic and pulmonary arterial pressures were recorded at baseline and with various physiologic maneuvers at a paper speed 100 or 150 mm/sec on an Electronics for Medicine VR12 physiologic recorder. All patients had standard M mode echocardiographic examinations before undergoing cardiac catheterization. These studies were reviewed for measurements of left atrial size and mitral valve motion abnormalities. Statistical analysis. Patients with severe mitral regurgitation were separated into two groups based on the presence or absence of pulmonary arterial V waves at rest. Clinical, hemodynamic, angiographic, and echocardiographic parameters were analyzed and comparisons made between the two groups with chi-squared or Student's unpaired t tests or a rank-sum analysis. Differences were considered significant if the p was less than .05. Values are expressed as mean + SD. Animals. Greyhound dogs were sedated with morphine sulfate (1 mg/kg) and anesthetized with intravenous sodium pentobarbital (25 mg/kg). After left thoracotomy, micromanometertipped catheters (Millar microtip No. 471) were inserted into (1) the right ventricle via the right internal jugular vein, (2) the main pulmonary artery by direct puncture and positioned immediately above the pulmonic valve, and (3) the aorta via the right femoral artery and positioned just above the aortic valve. Great care was taken to ensure that the micromanometer-tipped catheters in the pulmonary artery and right ventricle were equisensitive. In addition, zero baseline drift was checked frequently and corrected by superimposing the micromanometer pressure tracings on tracings of pressures from the fluid-filled lumens of the micromanometer catheters. The left atrial pressure was measured with a short No. 8F fluid-filled catheter inserted through the left atrial appendage. Pressures from the fluid-filled lumens were measured with Statham P23Db transducers. In three animals M mode echocardiograms of the pulmonic and aortic valves were obtained by placing a 2.25 MHz echocardiographic transducer directly on the pulmonary artery and aorta, respectively, using a commercially available ultrasonic gel for coupling. To confirm which valve was being echoed, saline was injected sequentially into the right ventricle and left atrium and the passage of microbubbles across the valve was observed. The echocardiograms were recorded with simultaneous pulmonary arterial and aortic micromanometer pressures to determine the relationship of aortic and pulmonic valve closure to the aortic and pulmonary arterial dicrotic notches, respectively. In two animals, an electromagnetic flowmeter was positioned around the main pulmonary artery just distal to the pulmonic valve, and the flow signal was recorded along with the other hemodynamic parameters. Initial right ventricular, pulmonary arterial, left atrial, and aortic pressures, echocardiograms, and pulmonary artery flow signals were recorded with the electrocardiogram at a paper speed of 100 mm/sec on an Electronics for Medicine VR6 physiologic recorder. After completion of all baseline recordings, acute mitral regurgitation was created by inserting a hook with an inside cutting edge through a small incision in the anterior wall of the left ventricle just below the mitral anulus.7 With the aid of a finger inserted into the left ventricular cavity via the left atrial appendage, the hook was manipulated to sever chordae tendineae. Individual chordae were severed until a thrill was felt in the left atrium and a large V wave appeared in the left atrial tracing. It was usually necessary to cut three to five chordae to produce severe mitral regurgitation. The hook and finger were then removed and hemostasis was obtained. Normal saline (up to 500 ml) was given as volume replacement, and intravenous lidocaine was used to control ventricular irritability during the creation of mitral regurgitation. Recordings of all parameters were then repeated. All measurements were made on 5 consecutive sinus beats and averaged. Heart rate and pressures were determined in the standard fashion. The pulmonary arterial V wave was defined as above. The intervals from the onset of the QRS complex to the incisura of the aortic dicrotic notch (QADN) and from the onset of the QRS complex to the incisura of the pulmonic dicrotic notch (Q-PDN) were measured. The difference between these intervals [(Q-ADN) (Q-PDN)] represents the delay between closure of the two semilunar valves. In addition, the interval from the onset of the QRS to the onset of right ventricular negative dP/dt (Q-O) was used as a measure of the duration of right ventricular electromechanical systole.8 Statistical analysis. Student's paired t test was used to determine statistical significance. Differences were considered significant if the p value was less than .05. Values are expressed as mean + SD.