The relationship of pulmonary valve motion to the motion of surrounding cardiac structures: a two-dimensional and dual M-mode echocardiographic study.

Abstract

SUMMARY To assess the relationship of late diastolic pulmonary valve motion to motion of adjacent cardiac structures, we performed two-dimensional and dual M-mode echocardiography on 15 pulmonary normotensive (group A) and nine pulmonary hypertensive subjects (group B). Simultaneous pulmonary valve and posterior aortic wall a-waves were less prominent in group B than in group A (p < 0.001), and their amplitudes were linearly related within each group (r = 0.83). Analysis of two-dimensional studies confirmed a relationship between pulmonary valve and posterior aortic wall late diastolic motion. No subject had independent presystolic motion of the pulmonary valve within the pulmonary artery. Subjects with shallow a-waves had impaired left atrial emptying compared with those with normal a-wave amplitudes (p < 0.01). We conclude that the pulmonary valve a-wave does not represent independent valvular displacement, but rather, reflects motion of the entire cardiac base. Variations in a-wave morphology may result, at least in part, from the effects of altered ventricular geometry and compliance on left atrial emptying.THE DIASTOLIC WAVE FORM of the pulmonary valve echocardiogram includes a presystolic a-wave of uncertain origin and physiologic significance. Investigators disagree as to the relative contributions of transvalvular pressure gradients,'-5 transducer position" and left atrial emptying7 to the a-wave and its variations in disease states. The presence of nearly identical a-waves in the echocardiograms of the atriopulmonary sulcus,' aortic valve, and posterior aortic wall7 suggests a common a-wave origin. We used twodimensional and dual M-mode echocardiography to assess the relationship of late diastolic pulmonary valve motion to events in adjacent structures. MethodsTwo-dimensional and dual pulmonary and aortic valve M-mode echocardiographic examinations were performed on 24 adult subjects in sinus rhythm. The control group (group A) consisted of 15 subjects. tension was defined as a pulmonary artery diastolic pressure greater than 15 mm Hg with a mean pressure of 22 mm Hg or more. The pulmonary artery pressure was confirmed by cardiac catheterization in the two group A subjects with coronary artery disease and in all group B subjects. Hemodynamic measurements were obtained within 2 days of echocardiographic examination except in subject 23, who was catheterized 21 days before study. Her clinical status did not change between the time of hemodynamic study and echocardiography. The study group's characteristics are summarized in table 1.Echocardiograms were obtained with a commercially available phased-array sector scanner (Toshiba Sonolayergraph, Model SSH-1OA) with dual M-mode capabilities in a single transducer. The transducer was held in the third or fourth left intercostal space while real-time, two-dimensional, short-axis views of the heart were obtained at the level of the semilunar valves8 ( fig. 1)

Anatomical Considerations for the Development of a New Transcatheter Aortopulmonary Shunt Device in Patients with Severe Pulmonary Arterial Hypertension

“…However, it has been shown that the vertical and anteroposterior movement of the aorta and pulmonary artery is small and is further attenuated in patients with PAH. 18,19 CONCLUSION This study shows that the LPA and dAO have a close and describable relationship in patients with PAH. Information obtained in this study regarding the landing zone area, left pulmonary artery and descending aorta diameters, and distance from the main pulmonary artery bifurcation to the left pulmonary artery at the contact point are essential toward development of a TAPS device and its delivery system.…”

“…However, it has been shown that the vertical and anteroposterior movement of the aorta and pulmonary artery is small and is further attenuated in patients with PAH. 18,19…”

A prominent ‘A’ notch in the pulmonary valve M mode-one more cause of the same

“…Green and Popp13 have given another explanation for the ‘a’ dip in normals and in pulmonary hypertension. Green and Popp examined the relationship of pulmonary valve motion and ‘a’ wave depth to posterior aortic wall motion and ‘a’–wave depth and to left atrial events by linear regression analysis.…”