Evaluation of asynchronous left ventricular relaxation by Doppler echocardiography during ventricular pacing with AV synchrony (VDD): comparison with atrial pacing (AAI).

The effect of right ventricular pacing on left ventricular relaxation was studied in 13 patients (age 62 +/- 3 years), with the atrial sensing ventricular pacing mode (VDD). A control group of similar age (64 +/- 4 years) consisted of 11 patients with atrial pacing (AAI). The timing of events was determined in both groups at similar R-R intervals (921 +/- 77 ms vs 967 +/- 37 ms). The loading conditions as estimated by peak systolic wall stress (afterload) and end-diastolic left ventricular dimensions (preload) were approximately the same in both groups. The ratio of late to early filling velocities were similar in both groups. Dominant changes were: increased preejection period (142 +/- 13 ms vs 95 +/- 15 ms); and higher velocities of isovolumic relaxation flow (60 +/- 34 cm/s vs 25 +/- 4 cm/s) in patients with ventricular pacing. The isovolumic relaxation time was longer in patients with VDD pacing (127 +/- 14 ms vs 108 +/- 12 ms). Anterior systolic interventricular septal motion (paradoxal motion) was recorded in nine patients with VDD pacing and in none of the patients with AAI pacing. Isovolumic relaxation flow was detected during atrial pacing in five (45%) patients and in 13 (100%) patients during atrial sensing ventricular pacing, indicating asynchronous left ventricular relaxation. This data shows that VDD pacing compared to atrial pacing resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction with interventricular septal motion abnormalities and prolonged asynchronous left ventricular relaxation with abnormal motion manifested by the presence of isovolumic relaxation flow.

Pulmonary venous flow pattern studied by transoesophageal pulsed Doppler echocardiography in mitral stenosis in sinus rhythm: effect of atrial systole.

In 13 patients with isolated mitral stenosis in sinus rhythm the pulmonary venous flow was evaluated by transoesophageal pulsed Doppler echocardiography. The patients were divided into two groups according to their mitral valve area (MVA); Group I (MVA < 1.5 cm2, n = 7 patients); and Group II (MVA > 1.5 cm2, n = 6). The patients in group I with haemodynamically significant mitral stenosis had lower velocities of systolic (S), diastolic (D) and atrial retrograde (A) waves of pulmonary venous flow (PVF) compared to milder stenosis (P < 0.05). The peak velocity of pulmonary retrograde venous flow at atrial contraction (A) primarily depends on the relative amplitude of the atrial transmitral wave (RA), which is measured from the onset of atrial systole to its peak velocity. We found a highly positive correlation between RA of mitral valve flow (MVF) and A wave of PVF (r = 0.87, P < 0.0001). There was also a highly negative correlation (r = 0.80, P < 0.001) between A of PVF and ratio of early (PE) to late (PA) velocities of MVF. Therefore, the retrograde A wave of PVF is related to the pressure generated in the left atrium during atrial systole. Use of pulmonary vein velocities in conjunction with mitral flow velocities can increase our understanding of the haemodynamics of mitral stenosis and provide a new insight into left atrial performance.

Jugular venous 'a' wave in pulmonary hypertension: new insights from a Doppler echocardiographic study.

OBJECTIVE: To study the mechanisms underlying the dominant 'a' wave seen in patients with primary pulmonary hypertension. DESIGN: Retrospective and prospective examination of the jugular venous pulse recording, flow in the superior vena cava, and Doppler echocardiographic studies. SETTING: A tertiary referral centre for both cardiac and pulmonary disease, with facilities for invasive and non-invasive investigation, and assessment for heart and heart-lung transplantation. PATIENTS: 12 patients with primary pulmonary hypertension, most being considered for heart-lung transplantation. RESULTS: Two distinct patterns of venous pulse and superior vena caval flow were identified: a dominant 'a' wave with no 'v' wave, an absent or poorly developed 'y' descent, and exclusively systolic downward flow in the superior vena cava (group 1, n = 8), and a dominant 'v' wave, deep 'y' descent and exclusively diastolic downward flow in the superior vena cava (group 2, n = 4). A comparison between the two groups showed age (mean (SD)) 42 (18) v 36 (7) years, RR interval 700 (65) v 740 (240) ms, left ventricular end diastolic dimension 3.6 (0.8) v 3.2 (1.0) cm and end systolic dimension 2.1 (0.5) v 2.3 (0.3) cm, right ventricular end diastolic dimension 2.6 (0.5) v 2.8 (0.6) cm, and pressure drop between right ventricle and right atrium 60 (8) v 70 (34) mm Hg to be similar. Duration of tricuspid regurgitation 520 (30) v 420 (130) ms and the time interval of pulmonary closure to the end of the tricuspid regurgitant signal 140 (30) v 110 (40) ms were longer in group 1 compared with group 2, whereas right ventricular filling time was much shorter 180 (70) v 350 (130) ms. In seven patients from group 1, a single peak of forward tricuspid flow was present, but this pattern was seen in only one patient from group 2. CONCLUSION: In patients with primary pulmonary hypertension, the apparent 'a' wave seen in the venous pulse is, in fact, a summation wave. It is probably the result of large pressure changes that must underlie rapid acceleration and deceleration of blood across the tricuspid valve when the right ventricular filling time is short.

Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction.

OBJECTIVE: To examine the effects of pulmonary hypertension on left ventricular diastolic function and to relate the findings to possible mechanisms of interdependence between the right and left sides of the heart in ventricular disease. DESIGN: A retrospective and prospective analysis of echocardiographic and Doppler studies. SETTING: A tertiary referral centre for both cardiac and pulmonary disease. PATIENTS: 29 patients with pulmonary hypertension (12 primary pulmonary hypertension, 10 pulmonary fibrosis, five atrial septal defect (ASD), and two scleroderma) were compared with a control group of 10 patients with an enlarged right ventricle but normal pulmonary artery pressure (six ASD, one after ASD closure, one ASD and pulmonary valvotomy, one tricuspid valve endocarditis and repair, and one pulmonary fibrosis). None had clinical or echocardiographic evidence of intrinsic left ventricular disease. MAIN OUTCOME MEASURES: M mode echocardiographic measurements were made of septal thickness, and left and right ventricular internal cavity dimensions. Doppler derived right ventricular to right atrial pressure drop, and time intervals were measured, as were isovolumic relaxation time, and Doppler left ventricular filling characteristics. RESULTS: The peak right ventricular to right atrial pressure gradient was (mean (SD)) 60 (16) mm Hg in pulmonary hypertensive patients, and 18 (5) mm Hg in controls. The time intervals P2 to the end of the tricuspid regurgitation, and P2 to the start of tricuspid flow were both prolonged in patients with pulmonary hypertension compared with controls (115 (60) and 120 (40) v 40 (15) and 45 (10) ms, p values less than 0.001). Pulmonary hypertensive patients commonly had a dominant A wave on the transmitral Doppler (23/29); however, all the controls had a dominant E wave. Isovolumic relaxation time of the left ventricle was prolonged in pulmonary hypertensive patients compared with controls, measured as both A2 to mitral valve opening (80 (25) v 50 (15) ms) and as A2 to the start of mitral flow (105 (30) v 60 (15) ms, p values less than 0.001). The delay from mitral valve opening to the start of transmitral flow was longer in patients with pulmonary hypertension (30 (15) ms) compared with controls (10 (10) ms, p less than 0.001). At the time of mitral opening there was a right ventricular to right atrial gradient of 12 (10) mm Hg in pulmonary hypertensive patients, but this was negligible in controls (0.4 (0.3) mm Hg, p less than 0.001). CONCLUSIONS: Prolonged decline of right ventricular tension, the direct result of severe pulmonary hypertension, may appear as prolonged tricuspid regurgitation. It persists until after mitral valve opening on the left side of the heart, where events during isovolumic relaxation are disorganised, and subsequent filling is impaired. These effects are likely to be mediated through the interventricular septum, and this right-left ventricular asynchrony may represent a hitherto unrecognised mode of ventricular interaction.

Assessment of the peak tricuspid regurgitant velocity from the dynamics of retrograde flow.

We describe a simple, non-invasive and practical method to determine the peak velocity of tricuspid regurgitant flow (and hence derive systolic pulmonary artery pressure) from examination of the dynamics of retrograde tricuspid flow on Doppler. Based on a previously described relationship between right ventricular systolic pressure and the time interval between pulmonary valve closure and tricuspid valve opening, our technique does not require the peak tricuspid regurgitant velocity to be recorded; nor, as in previous studies does it rely upon recording the jugular venous pulse, right ventricular apexcardiogram or invasive pressure measurements. We have studied 65 patients with right ventricular disease (53 with pulmonary hypertension), and 24 with dilated cardiomyopathy, with M-mode, two-dimensional echocardiography, Doppler, and phonocardiography. The peak tricuspid regurgitant velocity could be predicted from the interval between pulmonary closure and the end of the tricuspid regurgitant signal on Doppler in patients with pulmonary hypertension and those with right ventricular disease with normal pulmonary artery pressure, but not in patients with dilated cardiomyopathy. In patients with pulmonary hypertension or right ventricular dilatation, this may be a useful alternative method in estimating pulmonary artery pressure from Doppler, in cases where it is not possible to record the peak tricuspid regurgitant velocity.