Pulmonary valve echo motion in pulmonary regurgitation.

Four cases are presented to illustrate the echo patterns of pulmonary valve motion in patients with pulmonary regurgitation caused by pulmonary hypertension, idiopathic dilatation of the pulmonary artery, or congenital absence of the pulmonary valve or in association with pulmonary stenosis. Absence of the pulmonary 'a' wave, fluttering of the e-f slope, and midsystolic closure or 'notching' of the valve were noted with pulmonary hypertension. In the case with idiopathic dilatation of the pulmonary artery a normal echo pattern of pulmonary valve motion along with distinct dilatation of the pulmonary artery at the valvular level were present. Pronounced dilatation and systolic expansion of the pulmonary artery along with dilatation of the right ventricle were seen with congenital absence of the pulmonary valve. No pulmonary valve could be demonstrated on multiple scans from the right ventricle to pulmonary artery. In Case 4 large 'a' waves (14 mm) were noted, indicating a reversal of the normal end-diastolic gradient across the valve and suggesting that pulmonary regurgitation in this case was associated with right ventricular outflow obstruction. Study of the echo pattern of pulmonary valve motion may therefore provide useful information in establishing the cause of pulmonary regurgitation.     

Pulmonary valve echo motion in clinical practice

Examination of the pattern of pulmonary valve echo motion provides useful diagnostic information in a variety of clinical situations. This report describes the normal patterns and variations in pulmonary valve echo motion. It further discusses the applications and limitations of M-mode and cross-sectional echocardiography in detecting obstruction to right ventricular outflow at both the valvular and infundibular level; the wide ranging effects of increases in pulmonary artery pressure on the pulmonary valve echogram; and alterations in right ventricular compliance and volume which may combine to produce diastolic opening of the pulmonary valve. It is emphasized that the thin pliable pulmonary leaflets move in response to local alterations in pressure and flow. The patterns of pulmonary valve echo motion, therefore, although not specific for any particular clinical disorder, may provide valuable, indirect information concerning local pressure and flow characteristics and, as such, may prove extremely helpful when applied to a specific clinical situation.     

Assessing prosthetic mitral valve regurgitation by transoesophageal echo/Doppler

Transoesophageal echocardiography has greatly improved our ability to detect structural and regurgitant abnormalities associated with prosthetic mitral valves.     

Isolated acquired pulmonary valve regurgitation. Report of long-term follow-up

A patient is reported with isolated pulmonary valvular regurgitation acquired probably as a result of endocarditis at age 22 years. The patents remained essentially asymptomatic with physical findings compatible with haemodynamically significant pulmonary regurgitation until death at age 85 years. A necropsy confirmed the presence of isolated severe pulmonary valvular destruction. This long-term follow-up lends further support to the concept that significant volume overload of the right ventricle from pulmonary regurgitation is well tolerated and usually does not require surgical intervention.     

Isolated acquired pulmonary valve regurgitation. Report of long-term follow-up.

A patient is reported with isolated pulmonary valvular regurgitation acquired probably as a result of endocarditis at age 22 years. The patents remained essentially asymptomatic with physical findings compatible with haemodynamically significant pulmonary regurgitation until death at age 85 years. A necropsy confirmed the presence of isolated severe pulmonary valvular destruction. This long-term follow-up lends further support to the concept that significant volume overload of the right ventricle from pulmonary regurgitation is well tolerated and usually does not require surgical intervention.     

Echocardiographic abnormalities of tricuspid valve motion in pulmonary embolism.

Echocardiographic findings in five patients with pulmonary embolism were studied. Tricuspid echocardiograms showed abnormalities in valve motion, that is a monophasic triangular wave during diastole in all the patients as well as an increased dimension of the right ventricle. An "a' dip of the pulmonary valve echocardiogram was also recognised in all five. Later tricuspid echocardiograms regained the normal M-shaped configuration. The monophasic triangular pattern of the tricuspid valve during diastole may be related to the shorter duration of tricuspid valve opening compared with that of the mitral valve. Tachycardia cannot explain this difference between tricuspid and mitral valve motion, which seems to be caused by a prolonged isovolumic relaxation time of the right ventricle resulting in a delayed opening of the tricuspid valve. These results were obtained by comparing these data with those of control subjects and patients with chronic right ventricular overloading resulting from atrial septal defect.     

Echocardiographic patterns of pulmonary valve motion in valvular pulmonary stenosis

Echocardiographic tracings of the pulmonary valve were examined in 14 patients with isolated pulmonary stenosis, 20 normal subjects, 26 patients with pulmonary hypertension, 10 patients with a left to right shunt and 28 patients with various forms of heart disease other than pulmonary stenosis. Because of the plane of pulmonary valve motion and the angle of the ultrasonic beam, usually the echoes from only one posterior pulmonary leaflet were recorded. In normal patients atrial systole caused slight posterior motion of the pulmonary valve leaflet in late diastole (average 3, range 0 to 7 mm). The degree of valvular motion after atrial systole (the a wave) increased with inspiration. The position of the leaflet at the onset of ventricular systole varied with the depth of the a wave and the length of the P-R interval, but in the normal subjects the leaflet always returned to a base line or closed position at some time during the respiratory cycle. In 10 patients with moderate or severe pulmonary stenosis (gradient 50 to 142 mm Hg) the depth of the a wave increased markedly (average 10, range 8 to 13 mm). In patients with a gradient of more than 65 mm Hg (8 of 10) the leaflet never returned to a base line or closed position before ventricular systole. In three of four patients with mild pulmonary stenosis (gradient less than 50 mm Hg) and all patients with a left to right shunt or heart disease without pulmonary involvement the a wave was within the normal range. In 25 of 26 patients with pulmonary hypertension no a wave was present. In moderate to severe pulmonary stenosis, the exaggerated leaflet motion after atrial systole probably reflects increased right ventricular end-diastolic pressure and force of atrial contraction which, in the face of a normal or reduced pulmonary arterial pressure, produces a positive gradient across the valve in end-diastole.     

Mitral valve regurgitation causing right upper lobe pulmonary edema

When radiography is performed in patients with mitral regurgitation, cardiogenic pulmonary edema is a typical finding; however, asymmetric pulmonary edema has also been reported. We describe the case of a patient in whom mitral valve regurgitation caused isolated pulmonary edema in the right upper lung. We include a discussion of pulmonary edema in conjunction with mitral regurgitation.     

Pulmonary valve morphology after balloon dilatation of pulmonary valve stenosis

Percutaneous balloon valvuloplasty (BV) for pulmonic valve stenosis (PS) is increasingly becoming a nonsurgical alternative in patient management. However, the mechanism by which BV dilates the obstructive lesion has not been firmly established. We have had the opportunity to examine the effects of BV in the setting of PS and present two illustrative cases documenting the morphology after BV of the stenotic bicuspid and tricuspid pulmonary valve.     

Mitral valve regurgitation

The mitral apparatus is a complex structure composed of several components, each of which can be affected by a variety of diseases, resulting in mitral regurgitation. The physiologic consequences of mitral regurgitation include reduced forward stroke volume; increased left atrial volume and pressure; and reduced resistance to left ventricular ejection. The latter explains why indices of systolic left ventricular function (ejection fraction) are often increased early in the course of mitral regurgitation. With the insidious development of mitral regurgitation, the left atrium dilates to accommodate the increase in volume, thereby reducing the atrial pressure. However, with the acute development of mitral regurgitation into a nondilated left atrium, pressure rises rapidly, producing pulmonary edema. The predominant clinical symptoms in chronic mitral regurgitation of dyspnea and fatigue result from pulmonary venous hypertension and low cardiac output. The cardinal physical finding is a mitral systolic murmur. Since the murmur can assume various configurations, the most reliable way to establish its correct origin is by bedside physiologic maneuvers. Typically, in the beat following a premature contraction or after a long pause during atrial fibrillation, the murmur of mitral regurgitation is unchanged in intensity, but murmurs due to left ventricular outflow obstruction increase. Also, isometric handgrip exercise increases the intensity of the murmur and a Valsalva maneuver decreases it during the strain phase. Echocardiography is the most useful noninvasive technique for evaluating patients with mitral regurgitation. Visualization of the mitral apparatus may establish the etiology of regurgitation, and measurement of left atrial size and left ventricular size and performance is useful for assessing the functional significance of the lesion. Doppler echocardiography can establish the diagnosis of mitral regurgitation in difficult cases with multi valve disease and can estimate the severity of the regurgitation. Cardiac catheterization and angiography are usually reserved for the patient being considered for valvular surgery. The natural history of chronic mitral regurgitation is characterized by slowly progressive symptoms, and often the onset of disabling symptoms is the result of irreversible left ventricular dysfunction. Medical therapy consists of digitalis, diuretics, and vasodilators for symptomatic patients. When symptoms occur despite this therapy, valvular surgery should be considered before left ventricular function becomes abnormal.     

Anasarca due to pulmonic valve regurgitation with low pulmonary vascular resistance

A 57-year-old woman underwent pulmonic valvotomy for congenital pulmonic stenosis. She developed severe pulmonic insufficiency, secondary tricuspid regurgitation, and anasarca in spite of a normal pulmonary artery pressure. Insertion of a pulmonary valve prosthesis and tricuspid valve plication reversed all clinical symptoms and signs of this rare complication of pulmonary valvotomy.     

Transient mitral regurgitation due to mitral valve prolapse accompanied by systolic anterior motion of the mitral valve

A grade 4/6 systolic murmur, systolic anterior motion of the mitral valve (SAM), and severe mitral regurgitation (MR) documented by two-dimensional Doppler echocardiography developed suddenly on the structurally normal heart of a patient with idiopathic portal hypertension. The patient did not have signs of congestive heart failure and the aforementioned phenomenon disappeared completely when the patient was in hepatic failure. This could be explained by a change in circulating blood volume either by gastrointestinal hemorrhage or hepatic failure.