Tricuspid stenosis. Atrial systolic murmur, tricuspid opening snap, and right atrial pressure pulse

Observations on the atrial systolic murmur, the tricuspid opening snap, and the right atrial pressure pulse of tricuspid stenosis are presented, based on catheter manometer intracardiac sound and pressure recordings in five patients with hemodynamically significant tricuspid stenosis. The manometer-recorded right atrial pressure pulse of tricuspid stenosis differed from the normal, with (1) elevation of right atrial pressure, (2) different morphologic features (tall, spiky A wave complete before C; small V wave with an interruption, the tricuspid opening snap notch at termination of the gradual Y descent; a diastolic plateau, the relatively flat diastolic segment of the right atrial pressure pulse following the tricuspid opening snap notch prior to the next A wave), and (3) the relative lack of right atrial pressure and right atrial pressure pulse response with normal respiration. The atrial systolic murmur, recorded in the right ventricular inflow tract, was complete by S1; the crescendo-decrescendo atrial systolic murmur configuration paralleled the right ventricular-right atrial diastolic pressure gradient at the time of the atrial A wave. The right atrial contraction-relaxation process, as reflected by the right atrial A wave ascent and descent, was complete at the onset of ventricular systole with P-R intervals of 170 to 200 msec. Thus, the timing and configuration of the atrial systolic murmur reflected the timing and completion of the right atrial contraction-relaxation process prior to the onset of right ventricular systole and the configuration of the tricuspid diastolic pressure gradient. The tricuspid opening snap was recorded in the right ventricular inflow tract and occurred at the time of a notch at the termination of the Y descent of the right atrial pressure pulse V wave, while right atrial pressure exceeded right ventricular pressure. The sound-pressure events were consistent with angiographic and echocardiographic studies, which showed doming or ballooning of the mobile, fused, stenotic tricuspid valve into the right ventricle during the Y descent of the right atrial pressure pulse. The tricuspid opening snap occurred at the time of the termination of the diastolic movement of the fused tricuspid unit into the right ventricle. These observations are presented within the framework of previous studies in order to trace the development of medical ideas about the pathophysiologic basis for the sound and pressure events of tricuspid stenosis.     

Early diastolic clicks after the Fontan procedure for double inlet left ventricle: anatomical and physiological correlates

M mode echocardiograms and simultaneous phonocardiograms were recorded in four patients with early diastolic clicks on auscultation. All had double inlet left ventricle and had undergone the Fontan procedure with closure of the right atrioventricular valve orifice by an artificial patch. The phonocardiogram confirmed a high frequency sound occurring 60-90 ms after aortic valve closure and coinciding with the time of maximal excursion of the atrioventricular valve patch towards the ventricular mass. One patient had coexisting congenital complete heart block. The M mode echocardiogram showed "reversed" motion of the patch towards the right atrium during atrial contraction. Doppler flow studies showed that coincident with this motion there was forward flow in the pulmonary artery with augmentation when atrial contraction coincided with ventricular systole. The early diastolic click in these patients was explained by abrupt cessation of the motion of the atrioventricular valve patch towards the ventricular mass in early diastole. In one patient atrial contraction led to a reversal of this motion and was associated with forward flow in the pulmonary artery.     

Early diastolic clicks after the Fontan procedure for double inlet left ventricle: anatomical and physiological correlates.

M mode echocardiograms and simultaneous phonocardiograms were recorded in four patients with early diastolic clicks on auscultation. All had double inlet left ventricle and had undergone the Fontan procedure with closure of the right atrioventricular valve orifice by an artificial patch. The phonocardiogram confirmed a high frequency sound occurring 60-90 ms after aortic valve closure and coinciding with the time of maximal excursion of the atrioventricular valve patch towards the ventricular mass. One patient had coexisting congenital complete heart block. The M mode echocardiogram showed "reversed" motion of the patch towards the right atrium during atrial contraction. Doppler flow studies showed that coincident with this motion there was forward flow in the pulmonary artery with augmentation when atrial contraction coincided with ventricular systole. The early diastolic click in these patients was explained by abrupt cessation of the motion of the atrioventricular valve patch towards the ventricular mass in early diastole. In one patient atrial contraction led to a reversal of this motion and was associated with forward flow in the pulmonary artery.     

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.     

Diastolic function of the right ventricle in patients with lung diseases as evidenced by Doppler echocardiography]

The study was undertaken to examine the most informative Doppler echocardiographic parameters to determine right ventricular diastolic function in 46 pulmonological patients with pulmonary hypertension and right ventricular failure and 11 healthy individuals. The patients exhibited the highest blood velocity in the rapid filling phase, as compared to the healthy persons. They also demonstrated increased maximum blood velocities in the rapid filling phase on atrial systole and prolonged late blood flow in the rapid filling phase. Thus, Doppler echocardiography may be useful in the non-invasive diagnosis of right ventricular diastolic dysfunctions.     

Pulmonary artery and left heart end-diastolic pressure relations.

The exponential fall of the pulmonary pressure curve from its systolic peak to left atrial pressure previously described in the presence of normal intraventricular conduction has been investigated in patients with right bundle-branch block. We have been able to show once more that the pulmonary artery diastolic pressure seeks the left atrial level: when right ventricular systole is delayed the pulmonary artery pressure continues to fall with the left atrial 'x' descent.     

Detection and assessment of severity of tricuspid regurgitation using first-pass radionuclide angiography and comparison with pulsed Doppler echocardiography

Noninvasive detection and semiquantitative assessment of tricuspid regurgitation (TR) were performed using first-pass radionuclide angiography (RNA), by sampling a region of interest over the right atrium for any tracer entering the right atrium during right ventricular systole. The relative amount of tracer entering the right atrium was quantitated and the results were compared with semiquantitative Doppler echocardiographic grading of TR severity. Using the right ventricular time-activity curve to define end-diastolic and end-systolic frames, the right atrial counts for the 2 or 3 cardiac cycles after the peak right ventricular counts were summed. The right atrial "injection fraction" was calculated using the following formula: [(end-systolic counts - end-diastolic counts)/(end-diastolic counts)] X 100%. The right atrial injection fraction was examined in 51 patients who had good quality RNA and Doppler studies. Of 27 patients with no evidence of TR by Doppler, 26 had a negative right atrial injection fraction. All 24 patients with a positive Doppler for TR had a positive right atrial injection fraction. Comparison of right atrial injection fraction grade ranges with semiquantitative grades of TR severity on Doppler revealed identical grades in 21 of the 24, with a single grade difference in the remaining 3 patients. Thus, right atrial time-activity curve quantitation during routine first-pass RNA allows detection and grading of the severity of TR, with results very similar to pulsed Doppler echocardiography. This simple procedure is easily appended to the evaluation of ventricular performance with first-pass RNA.     

Echocardiographic assessment of tricuspid regurgitation during ventricular demand pacing

Twenty patients from our pacemaker clinic population were assessed clinically and by saline contrast echocardiography (subxiphoid view) to determine the prevalence of tricuspid regurgitation (TR) and, if TR was present, its mechanism. The patients had no known TR before lead placement, a single transvenous right ventricular pacing lead present more than 6 months (mean 52, range 7 to 138), ventricular demand pacing alternating with sinus rhythm and rate programmability. Each patient was studied in sinus rhythm and during ventricular pacing. Using the criterion of inferior vena cava (IVC) contrast reflux during ventricular systole to diagnose TR, no patient had evidence of TR in sinus rhythm, consistent with clinical examination. During ventricular demand pacing, jugular venous pulse cannon A waves developed in 10 patients, and 18 patients (including these 10) had IVC contrast reflux during ventricular systole. Analysis of the timing of IVC reflux revealed its close temporal relation to the timing of atrial systole rather than a fixed timing during ventricular systole. This reflux occurred with loss of normal atrioventricular (AV) synchrony and the underlying mechanism in all cases was shown to be right atrial contraction against a closed tricuspid valve. Two patients who did not have such a pattern with pacing maintained normal AV synchrony. These observations indicate that: TR is an uncommon accompaniment of ventricular demand pacing; the jugular venous pulse and IVC echocardiographic contrast patterns during ventricular demand pacing simulate TR when AV asynchrony [corrected] occurs; and the IVC contrast pattern of pacing induced AV asynchrony [corrected] is best termed the cannon A wave synchronous pattern.     

Hemodynamic importance of systolic ventricular interaction, augmented right atrial contractility and atrioventricular synchrony in acute right ventricular dysfunction

To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 +/- 5 to 18 +/- 4 mm Hg) and decreased left ventricular systolic pressure (100 +/- 18 to 80 +/- 18 mm Hg) and stroke volume (14 +/- 4 to 10.3 +/- 3.5 ml) (all p less than 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular end-diastolic size (155 +/- 13% of control), but decreased left ventricular size (69 +/- 11% of control) (both p less than 0.05). Right atrial pressure increased (5.8 +/- 2.5 to 7.6 +/- 2.8 mm Hg, p less than 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and bulged paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of ventricular septal motion. Influence of relative right and left ventricular size.

To test the hypothesis that the ventricular septum moves during systole toward the center of the ventricular mass (so that the end-diastolic position of the septum within the heart should determine both the direction and the magnitude of septal motion during systole), echocardiograms from patients with several different hemodynamic burdens were analyzed. A linear relation was noted between the end-diastolic intracardiac position of the ventricular septum and the direction and magnitude of systolic septal motion in 1) forty three patients with an atrial septal defect )regression coefficient r = 0.80), 2) fourteen patients with other causes of right ventricular volume overload (r = 0.82), 3) nineteen patients with left ventricular volume overload (r = 0.74), 4) ten patients with right ventricular pressure overload (r = 0.93), 5) ten patients with left ventricular pressure overload (r = 0.80), 6) twenty-eight normal subjects (r = 0.82). We conclude that, in the presence of normal ventricular activation and contraction, the direction and magnitude of sepatal motion during systole is determined by the intracardiac position of the septum at enddiastole.     

Reduced atrial contribution to left ventricular filling in patients with severe tricuspid regurgitation after tricuspid valvulectomy: a Doppler echocardiographic study

Patients undergoing valvulectomy for isolated tricuspid valve endocarditis offer the unique opportunity to study the effects of acquired right ventricular volume overload on left ventricular filling in persons free of pulmonary hypertension and preexisting left heart disease. Eleven patients who had undergone total or partial removal of the tricuspid valve were compared with 11 age-matched control subjects; Doppler echocardiographic techniques were used to quantify changes in left ventricular filling and to relate them to changes in left ventricular and left atrial geometry caused by right ventricular and right atrial distension. The late diastolic fractional transmitral flow velocity integral, a measure of the left atrial contribution to left ventricular filling, was significantly decreased in patients undergoing tricuspid valvulectomy compared with control subjects (0.22 +/- 0.11 versus 0.32 +/- 0.09; p less than 0.04). Severe tricuspid regurgitation in these patients resulted in marked right atrial distension, reversal of the normal interatrial septal curvature and compression of the left atrium such that left atrial area was significantly smaller than in control subjects (5.9 +/- 2.2 versus 8.6 +/- 1.2 cm2/m2; p less than 0.005). Acting as a receiving chamber, the left ventricle was maximally compressed by the volume-overloaded right ventricle in late diastole, coincident with the timing of atrial systole, resulting in a significant increase in the left ventricular eccentricity index compared with that in control subjects (1.35 +/- 0.14 versus 1.03 +/- 0.1; p less than 0.001). Thus, right ventricular volume overload due to severe tricuspid regurgitation results in left heart geometric alterations that decrease left atrial preload, impair left ventricular receiving chamber characteristics and reduce the atrial contribution to total left ventricular filling.     

Influence of left ventricular dysfunction on the role of atrial contraction: an echocardiographic-hemodynamic study in dogs

OBJECTIVES: The purpose of this study was to understand the significance of an effective atrial systole and the interactions between atrial and ventricular function. BACKGROUND: The significance of atrial function is controversial, particularly in the setting of left ventricular (LV) dysfunction. METHODS: Serial, rapid pacing in five dogs that had undergone radiofrequency ablation and implantation of right atrial and ventricular pacemakers produced reversible atrial and ventricular dysfunction (alone and in combination). Atrial function (echocardiograph-determined transmitral diastolic flow, left atrial appendage emptying, and pulmonary venous flow), cardiac output, and right heart pressures were measured at matched paced heart rates of 80 beats/min. RESULTS: Isolated rapid atrial pacing (LV ejection fraction approximately 60%) decreased atrial booster pump in the body and appendage of the left atrium, but increased the conduit function of the left atrium. Isolated LV dysfunction (LV ejection fraction approximately 34%) increased atrial booster pump function. The decreased atrial booster pump function in animals with combined atrial and ventricular dysfunction was incompletely compensated by the redistribution of the reservoir and conduit functions of the left atrium. As a result, cardiac output decreased and right heart pressures increased only after superimposed pacing. CONCLUSIONS: In the presence of a normal left ventricle (LV), atrial failure has little effect on cardiac output and right heart pressures because of compensatory conduit function, but when early LV dysfunction coexists, changes in reservoir and conduit functions are insufficient to compensate for an impairment of atrial contraction.     

Reduction of cardiac ejection fraction as a problem of pacemaker treatment

Ventricular pacing often is associated with a decrease of left ventricular output leading to symptoms of diminished cerebral perfusion. This is caused by a loss of properly timed atrial systole. The contribution of the atrial contribution of the atrial contraction to left ventricular output can reach 40% especially in patients with myocardial failure. A particular diminution of cardiac performance can be observed when ventriculoatrial conduction follows ventricular pacing. AV-sequential pacing, however, with a coordinated atrial systole leads to an obvious increase of cardiac output.     

中老年心房间隔缺损患者经导管封堵术后心功能变化

目的　探讨 40岁以上心房间隔缺损患者用导管封堵术治疗后的心功能变化。方法　采用封堵术治疗 2 1例40岁以上心房间隔缺损患者 ,并于术后 6个月进行随访 ,观察心脏彩超和心电图所得结果与术前比较。结果　心房间隔缺损封堵术后 6个月 ,心脏彩色多谱勒超声提示心脏收缩末期右房最大容积和右室舒张末期容积显著降低 ;左室舒张末期容积、射血分数和左室短轴缩短率显著提高 ;心电图提示PR间期和QRS宽度明显缩短。结论　40岁以上心房间隔缺损患者行心房间隔封堵术能够降低右心室的容量负荷 ,提高左心室的收缩功能 ,改善心房和心室的电传导     

Relation of third and fourth heart sounds to blood velocity during left ventricular filling.

To investigate the relation between changes in left ventricular inflow velocity and the timing of third and fourth heart sounds, simultaneous phonocardiograms and continuous wave Doppler traces were recorded in 48 patients (aged 17-78) with heart disease and in 21 normal children. The onset of the first vibration of the third heart sound coincided with peak left ventricular inflow blood velocity to within 5 ms in all but two of the patients. The mean (SD) difference between the two events was 5 (5) ms, which did not differ significantly from zero. The relation was similar in patients with primary myocardial disease (11), and in those with valve disease (26), hypertension (five), and coronary artery disease (four). In the normal children, the mean interval was 2.5 (5) ms--not significantly different from zero. By contrast, the first deflection of the fourth heart sound consistently preceded the timing of peak atrial inflow velocity by 55 (10) ms. Agreement was much closer between the onset of atrial flow and the onset of the atrial sound (mean difference 1 (5) ms, not significantly different from zero). Gallop sounds seem to be closely related to changes in ventricular inflow velocity, and thus to the effects of forces acting on blood flow. The forces underlying the third sound seem to arise within the ventricle and are responsible for sudden deceleration of flow during rapid ventricular filling. The fourth sound, occurring at the onset of the "a" wave, is more likely to arise from dissipation of forces causing acceleration of blood flow--that is, atrial systole itself.     

Relation of third and fourth heart sounds to blood velocity during left ventricular filling

To investigate the relation between changes in left ventricular inflow velocity and the timing of third and fourth heart sounds, simultaneous phonocardiograms and continuous wave Doppler traces were recorded in 48 patients (aged 17-78) with heart disease and in 21 normal children. The onset of the first vibration of the third heart sound coincided with peak left ventricular inflow blood velocity to within 5 ms in all but two of the patients. The mean (SD) difference between the two events was 5 (5) ms, which did not differ significantly from zero. The relation was similar in patients with primary myocardial disease (11), and in those with valve disease (26), hypertension (five), and coronary artery disease (four). In the normal children, the mean interval was 2.5 (5) ms--not significantly different from zero. By contrast, the first deflection of the fourth heart sound consistently preceded the timing of peak atrial inflow velocity by 55 (10) ms. Agreement was much closer between the onset of atrial flow and the onset of the atrial sound (mean difference 1 (5) ms, not significantly different from zero). Gallop sounds seem to be closely related to changes in ventricular inflow velocity, and thus to the effects of forces acting on blood flow. The forces underlying the third sound seem to arise within the ventricle and are responsible for sudden deceleration of flow during rapid ventricular filling. The fourth sound, occurring at the onset of the "a" wave, is more likely to arise from dissipation of forces causing acceleration of blood flow--that is, atrial systole itself.     

The influence of atrial systole on ventricular capture by failing artificial pacemakers. II. Experimental observations

The mechanism by which atrial systole influences the efficacy of ventricular capture by a failing pacemaker was investigated in 12 dogs with atrioventricular heart block. Atrial systole caused facilitation of ventricular capture in eight dogs, and inhibition of capture in 10 dogs. Interpolating atrial extrasystoles caused an enhancement or depression of the hemodynamic performance of the atrial systole that affected the efficacy of the pacemaker stimulus. These interpolation experiments showed that atrial systole influenced the efficacy of capture by a mechanical mechanism and not by an electrotonic mechanism. Atrial systole probably caused motion of the endocardial pacing catheter and/or ventricular myocardium. This motion increased or decreased the contact between the pacing electrode and the endocardium with subsequent changes in the efficacy of capture. In three dogs with pacing through epicardial electrodes, atrial systole had no effect on the efficacy of capture.     

Importance of sequential atrioventricular pacing in obstructive myocardiopathy with atrioventricular block]

A case of atrioventricular block (AVB) complicating hypertrophic obstructive cardiomyopathy is reported and analysed with respect to the results of cardiac catheterisation. The installation of 2nd degree AVB was associated with an increase of the intraventricular pressure gradient from 36 to 128 mmHg. This aggravation was related to the lenghtening of diastole which lowered the aortic diastolic pressure and allowed a more forceful ventricular contraction with a reduction in the calibre of the intraventricular stenosis. The sudden lenghtening of diastole also led to an increased contractility of the following systole. In complete AVB the increased gradient was related to a reduction in ventricular volume secondary to the loss of atrial systole. The 33 mmHg pressure gradient disappeared when spontaneous atrial systole or an atrial systole provoked by sequential atrioventricular pacing preceded ventricular contraction. Sequential atrioventricular pacing would seem to be the most appropriate pacing technique in hypertrophic obstructive cardiomyopathy complicated by complete AVB.     

An echocardiographic assessment of atrial mechanical behaviour

Relations between movement of the atrioventricular ring and changes in left atrial and ventricular dimensions were studied by echocardiography and compared with apexcardiography and Doppler mitral flow velocity traces in 20 healthy controls and in patients with left ventricular hypertrophy (n = 28) or dilatation (n = 16). During left ventricular systole the atrioventricular ring, a structure common to ventricle and atrium, moved towards the ventricular apex, thus increasing left atrial volume. This action matched pulmonary venous return because it was in phase with the transverse left atrial dimension measured from aortic root to posterior left atrial wall. During early diastole, the mitral ring moved rapidly towards the atrium as transmitral flow accelerated. This requires a force directed from ventricle to atrium, likely to be the result of elastic recoil arising from compression of the ventricular myocardium or stretching of the atrial myocardium during ventricular systole. Two additional mechanisms of ventricular filling with atrial systole were recognised: (a) an increase in ventricular volume as the atrioventricular ring moved upwards and (b) transverse left ventricular expansion by pressure driven transmitral flow. The former is undetectable by Doppler from the apex; it accounted for 10% of ventricular filling in the healthy controls, but for significantly less in those with ventricular dilatation. In left ventricular hypertrophy, left ventricular filling was maintained by both mechanisms compensating for the reduced increase in volume early in diastole. Interactions between the atrium and ventricle are functionally important during ventricular systole, early diastole, and in atrial systole. They are not included in the traditional separation of atrial function into reservoir, conduit, and pump functions.     

Non-invasive observations on initial low frequency vibrations of the first heart sound--correlation with the 'presystolic' murmur in mitral stenosis.

The initial low frequency component of the first heart sound, 'M', has been studied in normal subjects, and in patients with vario-s prosthetic mitral valves and with mitral stenosis, using simultaneous low frequency phonocardiography, echocardiography, and apex cardiography. The techniques showed 'M' to have a constant morphology in preisovolumic systole. In mitral stenosis, 'M' and the preisovolumic 'presystolic' murmur appear to be the same phonocardiographic phenomenon. While 'M' was present in sinus rhythm, augmentation of this normal vibration occurred particularly during the short cycles of atrial fibrillation. Leaflet coaption and movement of the ventricular wall as detected echocardiographically do not appear to play a role in its pathogenesis but the sound could emanate from the ventricular wall as it tautens and decreases its compliance at the onset of systole.