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. 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 de...

12 patients who had atrial flutter without clinical, echocardiographic or angiographic evidence of aortic insufficiency were studied with simultaneous echo- and phonocardiograms. In patients with high-grade atrioventricular (AV) block, the mitral valve opened and closed with each flutter wave. Of seven patients, two had persistent and five had intermittent early mitral valve closure before QRS inscription. In five patients (three with 2:1 AV block) the mitral valve closed on time. In one patient with a mitral valve prosthesis, echocardiography and cinefluorography demonstrated closure during mid-diastole, with reopening in late diastole after a flutter wave. Final valve closure occurred before the onset of the QRS, and each closure was associated with a click. Simultaneous phonocardiographic analysis in these patients demonstrated that the first heart sound intensity was inversely related to the degree of mitral valve preclosure. This relationship was independent of the length of the RR interval. Thus, atrial flutter independent of any other cause of abnormal hemodynamics may produce early mitral valve closure. The echocardiographic finding of premature mitral arrhythmias, may not have the same diagnostic or prognostic significance previously described in patients with sinus rhythm and normal AV conduction.

EXPERIMENTAL AND CLINICAL cardiomyopathies are characteristically associated with progressive cardiac failure and death.' Cardiac function is often impaired long before clinical symptoms occur. In congestive cardiomyopathy hemodynamic and angiographic evaluations reveal elevated enddiastolic pressures, abnormal ventricular function curves, and diffuse hypokinetic contraction patterns.2 However, idiopathic hypertrophic subaortic stenosis (IHSS), a primary cardiac myopathic disorder, is paradoxically associated with increased myocardial contractility. The left ventricle in this entity is hyperdynamic and angiographic ejection fractions are frequently in excess of 0.70.3 Histologic studies of the myocardial cells in IHSS have shown them to be multinucleated, bizarre, and misaligned," 5 thus confirming that this is a myopathic disease. These abnormalities are restricted most often to the interventricular septum." Furthermore, disproportionate

Background: Right ventricular (RV) dysfunction after left ventricular assist device (LVAD) implantation significantly complicates post-device management and has been shown to be associated with increased mortality. Pre-operative identification of patients who may develop post-LVAD RV dysfunction is challenging. This study was designed to evaluate pre-operative echocardiographic speckle tracking imaging as a predictor of post operative RV dysfunction. Methods: Thirty-nine patients who underwent Heartmate II LVAD placement in a single center were studied. Pre-and post-operative clinical, hemodynamic, laboratory, and echocardiographic data were prospectively collected as part of an ongoing institutional LVAD database. RV strain parameters were measured retrospectively using off-line speckletracking analysis software. Results: Twenty five of 39 LVAD recipients developed acute RV failure during the early post-operative period. RV function in 14 of these recipients improved with inotropes and judicious adjustment of LVAD parameters. Eleven patients, however, expired despite aggressive medical therapy including 7 patients who underwent placement of an RVAD. These 11 individuals were identified as having significantly lower global RV strain prior to device placement (p<0.05). Seventy two percent of the patients with a peak longitudinal systolic RV strain higher than-3%, expired. Twenty-four of 27 (88%) patients with a global RV strain of-3% or lower survived without need for an RVAD (p<0.001). Hemodynamic, laboratory and traditional echocardiographic data were not predictive of post-LVAD RV dysfunction or survival. Multivariate analysis showed RV longitudinal strain, especially global strain, to be the only significant predictor of severe RV dysfunction. Conclusion: Poor intrinsic RV myocardial function is associated with a higher mortality in LVAD patients. Speckle-tracking echocardiography imaging, particularly, peak systolic global RV strain appears to be promising in predicting LVAD patients who require RVAD.

SUMMARY To determine the causes of cardiac failure during cardiac tamponade in man, we studied left ventricular volume and function in eight patients during pericardiocentesis using gated equilibrium radionuclide ventriculography. In the seven patients with clinical and hemodynamic evidence of cardiac tamponade, end-diastolic and end-systolic volumes increased progressively as the initial 500 ml offluid were removed; the most marked increase occurred during the removal of the first 200 ml of pericardial fluid. After removal of 500 ml of pericardial fluid, end-diastolic volume increased from 52 ± 8 ml to 111 ± 13 ml (p < 0.05) and end-systolic volume from 17 ± 5 ml to 34 ± 7 ml (p < 0.05). Right-heart catheterization was performed at the bedside using a #7F triple-lumen thermodilution balloon catheter. Arterial pressure was obtained with a #18 or #20 Teflon catheter inserted percutaneously into a radial or brachial artery. Percutaneous pericardiocentesis was performed by puncturing the pericardial sac with a stainless-steel needle. The needle was used as an exploring electrode to achieve continuous electrocardiographic monitoring by connecting it to the V lead of a standard electrocardiograph. A 5.5-inch #19 Teflon catheter with four side holes was then advanced over the rigid needle so that all side holes were within the pericardial cavity and no damage was done to the cardiac structures. The needle was then withdrawn. There were no complications of the pericardiocentesis, and the initial insertion was performed with a single puncture in all cases. In patient 6, mechanical problems with the catheter necessitated repeat puncture after 200 ml of pericardial fluid had been withdrawn. In patient 5, withdrawal of pericardial fluid was halted after 500 ml because of unsustained ventricular tachycardia related to negative pressure applied to the pericardial catheter.Pressures were measured with Statham P231D transducers and recorded along with a bipolar electrocardiographic lead on an Electronics for Medicine VR6 recorder. To ensure precise linearity of response, the transducers were connected to a single manifold, which allowed them to be calibrated simultaneously. Thermodilution cardiac output was calculated by a computer from the curve generated by hand injection of 10 ml of room temperature 5% dextrose solution.