Physiologic correlates of right ventricular ejection fraction in chronic obstructive pulmonary disease: A combined radionuclide and hemodynamic study

The pathophysiologic correlates of right ventricular ejection fraction, as well as its relation to contractile function as assessed by systolic pressure-volume data, were evaluated in 20 patients with chronic obstructive pulmonary disease. Radionuclide and hemodynamic measurements were obtained simultaneously. Baseline determinations were obtained in all patients. In seven patients, studies were repeated after intravenous administration of sodium nitroprusside. This procedure allowed characterization of right ventricular performance at decreased afterload and provided two points necessary for definition of the right ventricular systolic pressure-volume relation. Seventeen of the 20 patients had a depressed right ventricular ejection fraction (less than 45 percent). There was a strong inverse linear correlation between right ventricular ejection fraction and afterload as assessed by peak or mean pulmonary arterial pressure (r = ?0.81) and pulmonary vascular resistance index (r = ?0.73). Right ventricular ejection fraction also correlated, although less strongly, with preload as assessed by right ventricular end-diastolic volume index (r = ?0.56) and mean right atrial pressure (r = ?0.51). It did not correlate with cardiac index, the ratio of peak pulmonary arterial pressure to right ventricular end-systolic volume index, arterial oxygen tension or left ventricular ejection fraction. After nitroprusside administration, mean arterial pressure, peak pulmonary arterial systolic pressure and pulmonary vascular resistance index decreased significantly. The slope (E) and the volume intercept (V₀) of each pressure-volume line were determined. Administration of dobutamine resulted in a leftward shift from the endsystolic pressure-volume line. There were poor correlations between E and right ventricular ejection fraction, as well as between E and the control ratio between pulmonary arterial systolic pressure and end-systolic volume index.These data demonstrate that, in addition to intrinsic contractile influences, right ventricular ejection fraction is highly dependent on afterload, but less dependent on preload. Right ventricular ejection fraction is a poor indicator of the slope of the systolic pressure-volume relation, raising questions concerning its use as an independent index of chamber contractility.     

Synchronization of the contraction of the right ventricle against an acute afterload increase. Left ventricle-like mechanical function of the right ventricle

AIM: The aim of this study was to demonstrate right ventricular contraction synchronization during acute and moderate afterload increase. MATERIAL AND METHOD: Right and left ventricular pressures, pulmonary and aortic pressures, pulmonary flow, and ventricular volumes by sonomicrometry were measured in seven anesthetized sheep. Pulmonary arterial hypertension was induced by Escherichia coli endotoxemia. RESULTS: Acute increase of the right ventricular afterload, measured as the mean arterial pulmonary pressure (11.9 1.3 to 24 3.6 mmHg) produced the following changes in the right ventricle without preload and contractility changes: a) maximal elastance shifted towards the end of the ejection (127.5 18.5 ms) and the ejection time shortened (57.5 20.3 ms), so that the negative peak of the first ventricular pressure derivative occurred at the end of the ejection; b) the pressure-volume loop became rectangular, i.e.; the systolic and diastolic phases were isovolumic, and c) the ejection showed a single phase. CONCLUSIONS: Asynchronous and sequential right ventricular contraction with normal afterload changed to a synchronic contraction pattern as in the left ventricle during an acute and moderate afterload increase. This left ventricle-like mechanical property establishes a novel mechanical reserve mechanism of the right heart, since it allows the right ventricle to maintain its systolic function during an afterload increase, independently of the preload and contractility.     

Characterisation of the normal right ventricular pressure-volume relation by biplane angiography and simultaneous micromanometer pressure measurements.

The normal right ventricular pressure-volume relation was studied by recording biplane right ventriculograms with simultaneous high fidelity pressure recordings in 10 adults found to have normal coronary arteries and haemodynamic function at diagnostic cardiac catheterisation. Right ventricular volume was measured frame by frame from digitised ventriculograms by a modification of Simpson's rule. The accuracy of this method was tested in a study of 22 human and animal right ventricular casts. There was excellent agreement between calculated volumes and those measured by fluid displacement. The derived regression equations were used to correct right ventricular volumes calculated from in vivo studies. The mean (SD) end diastolic volume index for the group was 62 (13) ml/m2, the stroke volume index was 43 (8) ml/m2, and the ejection fraction was 62 (6)%. Right ventricular pressure-volume loops were generated by combining simultaneous volume and pressure curves. The normal right ventricular pressure-volume loop was triangular, departing significantly from the square or rectangle of the normal left ventricular pressure-volume loop. Ejection from the right ventricle began early during the pressure rise and continued as right ventricular pressure fell. As a result phases of isovolumic contraction and relaxation were difficult to define. These observations show that normal right ventricular pressure-volume relations differ considerably from those of the normal left ventricle, presumably reflecting the different loading conditions of the two ventricles.     

Study of the relaxation phase of the right ventricle]

The purpose of our study was to investigate the existence or not of an isovolumic relaxation period in the right ventricle in experimental animals with normal pressures in the pulmonary artery. Right and left ventricular pressures, pulmonary and aortic pressures (microtransducers), pulmonary flow, ventricular diameters (sonomicrometer), were recorded at the same time, in 10 sheep anesthetized intravenously with pentobarbital. We obtained "off line" the first ventricular pressures derivative, the ventricular volumes and the pressure-volume loops of both ventricles. The minimum systolic right ventricular volume coincided with 0 pulmonary flow, and both with a diastolic pressure value of 0-5 mmHg in that ventricle. Once the minimum systolic volume was reached, a rapid increase of the right ventricular volume started. The right ventricular pressure-volume loop, unlike the left ventricular one, adopted a non-rectangular shape. The right ventricular ejection period lasted until the beginning of the next filling phase. We concluded that there is no right ventricular isovolumic relaxation period.     

Effect of positive end-expiratory pressure on right ventricular performance. Importance of baseline right ventricular function

Thirty-six patients with diverse baseline right ventricular function were evaluated during incremental positive end-expiratory pressure (PEEP) application. Right heart pressures, cardiac output, right ventricular ejection fractions, and ventricular volumes were obtained at each PEEP level. Right ventricular peak systolic pressure-end-systolic volume relations were analyzed as an index of contractile function. Patients with severely depressed baseline right ventricular ejection fractions (30 percent or less) had an increase in end-diastolic (270 +/- 74 to 391 +/- 76 ml, 0 to 20 cm water (H2O) PEEP, p less than 0.05) and end-systolic volumes (210 +/- 70 to 321 +/- 70 ml, 0 to 20 cm H2O PEEP, p less than 0.05). These patients also had a decline in estimated right ventricular contractile function at 20 cm H2O PEEP as estimated by the slope of systolic pressure-volume relations (0.12 to 0.04 mm Hg/ml, 0 to 15 and 15 to 20 cm H2O PEEP, respectively, p less than 0.05). Patients with normal (40 percent or more) or moderately depressed (31 to 40 percent) baseline right ventricular ejection fractions had no change in right ventricular volumes or estimated contractile function. Therefore, the effect of PEEP on right ventricular function differs depending on the baseline right ventricular ejection fraction.     

Right ventricular dysfunction due to right ventricular outflow tract patch

Doppler tissue imaging analysis was used to examine the relationship between right ventricular function and right ventricular outflow tract damage in 54 patients with repaired tetralogy of Fallot. The patients were divided into three groups: 16 in whom the right ventricular outflow tract was directly sutured (group DS), 23 who had transventricular patch repair (group TVP), and 15 who had transannular patch repair (group TAP). The control group consisted of 16 age-matched patients who underwent patch closure of a ventricular septal defect (group C). The Tei index was obtained from tricuspid and pulmonary Doppler flow velocities. The right ventricular Tei index was significantly greater in groups TVP and TAP than in group DS. Doppler tissue imaging analysis in groups TVP and TAP showed shorter myocardial systolic velocity, diastolic peak velocity, and atrial diastolic peak velocity, lower peak myocardial velocity and acceleration during isovolumic contraction, and prolonged isovolumic relaxation and contraction times compared to groups DS and C. Right ventricular dysfunction is due to the right ventricular outflow tract patch. Thus, the right ventricular outflow tract may be essential for right ventricular ejection and maintenance of right ventricular function.     

Influence of right ventricular hemodynamics on left ventricular diastolic pressure-volume relations in man.

To clarify the mechanism of displacement of the left ventricular diastolic pressure-volume function with alteration of loading conditions, the effects of nitroglycerin on pressure-volume relations in 13 patients were compared with those of amyl nitrite in 13 other patients during cardiac catheterization. After nitroglycerin, average systemic mean arterial pressure declined by 15.1 mm Hg (17%) and left ventricular end-diastolic pressure by 9.4 mm Hg (49%); right ventricular systolic and end-diastolic pressures fell 11.6 mm Hg (36%) and 5 mm Hg (41%), respectively. In all patients diastolic pressure-volume curves were significantly displaced downward and leftward. After amyl nitrite, average systemic mean arterial pressure fell 20.1 mm Hg (22%), but left ventricular end-diastolic pressure and right ventricular systolic and end-diastolic pressures were not significantly reduced. No significant displacement of diastolic pressure-volume curves occurred. Both the rate constant of the exponentially fit diastolic pressure-volume curve, and the rate of diastolic isovolumic relaxation (T) were unchanged after each drug. Thus downward displacement of diastolic pressure-volume functions after nitroglycerin appears to be dependent more upon reduction of right ventricular filling dynamics than coronary perfusion pressures. More favorable effects upon left ventricular function may be associated with reduction of both left ventricular filling pressures and systemic impedance (reflecting both "preload" and "afterload") than of systemic arterial pressures ("afterload") alone.     

Changes in the pressure-volume relation of the right ventricle when its loading conditions are modified

Ventricular pressure-volume diagrams were obtained from the right ventricle in patients before and after relief of right ventricular pressure load, in patients with volume loaded right ventricles, and from the left ventricle in patients after the Mustard procedure for transposition of the great arteries. The patterns of ejection during pressure development and decline were similar in patients after relief of pressure load and in those with isolated volume load. A right ventricular pressure load, however, reduced ejection during the two "isovolumic" periods, and the overall shape of the pressure-volume loop resembled that of the normal left ventricle. Pressure-volume diagrams obtained from the left ventricle after the Mustard procedure were indistinguishable from the normal right ventricle, which accords with the hypothesis that the normal right ventricular contraction pattern is a consequence of loading conditions rather than a reflection of an intrinsic property of the myocardium.     

Changes in the pressure-volume relation of the right ventricle when its loading conditions are modified.

Ventricular pressure-volume diagrams were obtained from the right ventricle in patients before and after relief of right ventricular pressure load, in patients with volume loaded right ventricles, and from the left ventricle in patients after the Mustard procedure for transposition of the great arteries. The patterns of ejection during pressure development and decline were similar in patients after relief of pressure load and in those with isolated volume load. A right ventricular pressure load, however, reduced ejection during the two "isovolumic" periods, and the overall shape of the pressure-volume loop resembled that of the normal left ventricle. Pressure-volume diagrams obtained from the left ventricle after the Mustard procedure were indistinguishable from the normal right ventricle, which accords with the hypothesis that the normal right ventricular contraction pattern is a consequence of loading conditions rather than a reflection of an intrinsic property of the myocardium.     

肥厚性心肌病患者右心室结构与功能变化的分析

目的:应用彩色多普勒组织成像(CDTI)技术探讨肥厚性心肌病(HCM)患者右心室结构与功能的变化。方法:HCM患者35例(HCM组),正常对照组30例,应用CDTI测量左、右心室腔大小,室壁厚度,心室流出道等指标,于心尖四腔切面记录舒张期血流频谱,测量右室等容舒张时间(IRT)、等容收缩时间(ICT)、右室射血时间(RVET)及Tei指数。结果:与正常对照组比较,HCM患者右室前壁厚度[(4.56±0.70)mm比(5.43±0.87)mm]、室间隔厚度[(8.66±2.51)mm比(20.53±3.37)mm]、左室后壁厚度[(9.10±2.24)mm比(13.06±1.68)mm]均明显增加(P<0.05或<0.01),右室Tei指数[(0.39±0.61)比(0.80±0.38)]显著升高(P<0.01),右室流出道、右室舒张末期内径两组间无显著差异(P>0.05)。结论:肥厚性心肌病患者中右心室解剖结构与功能均受影响;右室Tei指数可以反映右心收缩及舒张功能变化。     

Noninvasive assessment of pulmonary hypertension from right ventricular isovolumic contraction time

In order to assess a noninvasive method of predicting pulmonary arterial pressure in adults, right ventricular systolic time intervals were determined with echocardiography simultaneously with pulmonary arterial end-diastolic pressure measurements. Right ventricular isovolumic contraction time was measured from echographic recordings of the tricuspid and pulmonary valves. Although this interval was found to increase as pulmonary arterial pressure increased, the method cannot be used to predict quantitatively the level of pulmonary arterial pressure in adults. However, an echocardiographically determined right ventricular contraction time of less than 25 ms suggests a normal pulmonary arterial pressure. In patients with pulmonary parenchymal diseases, echograms of the tricuspid and pulmonary valves are only rarely of such quality as to permit accurate delineation of the valvular events required for these measurements.     

Assessment of right heart function in the athlete's heart

 It is known that the heart of an athlete has been physiologically adapted by prolonged training. There are a large number of echocardiographic studies which have focused on left ventricular wall thickness and dilatation, but there are few studies concerning right heart function in the athlete's heart. The aim of this study was to assess right heart function in elite athletes by conventional and new echocardiographic methods. The study population consisted of 36 elite highly-trained male athletes and 16 age-matched healthy sedentary controls. Right atrial, right ventricular, and inferior vena cava dimensions, and pulsed Doppler measurements of tricuspid inflow and right ventricular outflow were obtained, and systolic (preejection period, ejection time, preejection time/ejection time, QV peak, isovolumic contraction time) and diastolic (E peak, A peak, E/A ratio, decelaration time, isovolumic relexation time) function parameters were measured. The myocardial performance index was calculated as (isovolumetric contraction time + isovolumetric relaxation time)/ejection time. In addition, right ventricular systolic and diastolic functions were determined by Pulsed wave tissue Doppler imaging (S, E, and A velocities) at the lateral corners of the tricuspid annulus. The left ventricular mass index (P < 0.005), and right atrial (P < 0.001), right ventricular (P < 0.001), and inferior vena cava dimensions (P < 0.001) were significantly greater in athletes than in controls. Tricuspid E peak, A peak, E/A ratio, deceleration time, isovolumic relaxation time, preejection period, right ventricular ejection time, preejection time/ejection time, isovolumic contraction time, QV peak, and myocardial performance index were found to be similar in athletes and in controls (P > 0.05). Systolic, early diastolic, and late diastolic tissue Doppler imaging velocities were not significantly different in athletes and controls (P > 0.05). Left ventricular hypertrophy (LV mass index >134 g/m²) was found in 15 of the athletes. Right atrial dimension was greater in the athletes with left ventricular hypertrophy than in those without hypertrophy (P < 0.05). All right ventricular systolic and diastolic echocardiographic parameters were similar in athletes with and without left ventricular hypertrophy (P > 0.05). The results of this study indicate that right ventricular systolic and diastolic functions do not deteriorate in the athlete's heart despite significant chamber dilatation. They suggest that these changes are a normal physiologic adaptation to prolonged training. Received: November 28, 2001 / Accepted: March 8, 2002     

Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index

BACKGROUND: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. OBJECTIVES: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. METHODS: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5-14, n = 11), and group 3: moderate-severe OSA (AHI > or = 15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. RESULTS: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 +/- 0.9, 6.9 +/- 1.0, 7.1 +/- 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 +/- 0.18) than in group 2 patients (0.50 +/- 0.10), and group 1 patients (0.48 +/- 0.08, p < 0.001). CONCLUSIONS: It was suggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.     

Resting right ventricular function in patients with coronary artery disease: pressure volume analysis using conductance catheters

Right ventricular pressure volume cycles from patients with coronary artery disease were created in order to assess their characteristics and the effects of peak ventricular pressure and right and left artery coronary disease. Thirty-three patients undergoing diagnostic catheterisation for ischaemic heart disease underwent right ventricular catheterisation with a micromanometer and a conductance catheter. Simultaneous pressure and volume signals were recorded and analysed as functions of time, and of each other, forming pressure volume cycles. A total of 19/33 (58%) patients had an abnormal pressure volume loop with a clear end systolic shoulder, and an isovolumic relaxation phase. The mean peak ventricular pressure for all patients was raised (35.2 S.D. 11.8 mmHg), but there was no correlation between indices of shape and peak systolic pressure. Values of dP/dt_max were also raised, but there was no significant difference in this or any other index between patients with left or right coronary artery disease. Thus, in patients with coronary artery disease, the right ventricular pressure volume loop is frequently abnormal in a pattern that is recognised as a feature of an increased ventricular afterload.     

Function of the right ventricle in patients with mitral valve diseases

To investigate right ventricular function in mitral valve disease, biplane cineventriculograms of the right and left ventricle were performed in 96 patients-35 with mitral stenosis, 26 with mitral regurgitation, 12 with combined mitral valve disease, 14 with mitral stenosis and tricuspid regurgitation, and nine with mitral regurgitation and tricuspid regurgitation, compared to 18 normals (N). Right ventricular enddiastolic volume index was moderately elevated in patients with mitral stenosis and concomitant tricuspid regurgitation (111.6 +/- 35.3 ml/m2, no significance compared to N: 95.9 +/- 21.8 ml/m2) and with mitral regurgitation and tricuspid regurgitation (107.9 +/- 45.1 ml/m2, no significance compared to N). A reduced right ventricular ejection fraction (RVEF less than or equal to 50%) was found in 40 of the 96 patients. Right ventricular ejection fraction was frequently reduced in patients with mitral regurgitation and tricuspid regurgitation (46.7% +/- 15.1%) and significantly reduced in patients with combined mitral valve disease (45.0 +/- 17.6%, compared to N: 58.0 +/- 7.1%, p less than 0.01). No significant correlations were found between right ventricular ejection fraction and left ventricular enddiastolic volume or left ventricular ejection fraction in patients with mitral valve disease. Moreover, right ventricular ejection fraction did not correlate with systolic pulmonary artery pressure, mean pulmonary artery pressure or mean pulmonary capillary wedge pressure. Local wall motion (mean systolic shortening) was determined for the anterior, anteroapical, and inferior segment in the RAO-projection and for the right ventricular free wall in the LAO-projection. 63% of the patients (n = 25) with reduced right ventricular function (RVEF less than of equal to 50%) showed local wall motion abnormalities, preferably in the anterior segment of the RAO- projection (48%) and the right ventricular free wall (30%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of left and right ventricular end-systolic pressure-volume relations in congestive heart failure

A hemodynamic-radionuclide study was performed to compare the relations between end-systolic pressure and volume in the left and right ventricles in 10 patients with biventricular failure, and to correlate the end-systolic pressure-volume slope with baseline variables of systolic function. During nitroprusside or nitroglycerin infusion, or a combination of both, linear relations were found between end-systolic pressure and volume for both ventricles. In 9 of 10 patients, the end-systolic pressure-volume slope was greater for the left ventricle (mean +/- SD 1.12 +/- 0.36 mm Hg X m2/ml) than for the right ventricle (0.46 +/- 0.27 mm Hg X m2/ml) (p less than 0.001). In all 10 patients, the volume-axis intercept of the pressure-volume relation was greater for the left ventricle (82 +/- 66 ml/m2) than for the right ventricle (2 +/- 30 ml/m2) (p less than 0.005). Right ventricular pressure-volume slope correlated weakly with baseline right ventricular ejection fraction (r = 0.69, p less than 0.05), strongly with the baseline right ventricular end-systolic pressure-volume ratio (r = 0.89) and inversely with baseline right ventricular end-systolic volume (r = -0.86). In conclusion, 1) in patients with severe biventricular failure, changes in systolic pressure influence end-systolic volume more strongly in the right than in the left ventricle. 2) For the right ventricle, the slope of the end-systolic pressure-volume relation is directly related to rest indexes of systolic function. 3) The greater the end-systolic volume at rest, the greater the predicted improvement in right ventricular emptying for any vasodilator-induced reduction in pulmonary artery end-systolic pressure.     

Preload reduction with right ventricular pacing: Effects on left ventricular hemodynamics and contractile pattern

Studies were performed in 32 patients to evaluate left ventricular pressure-volume changes and contractile pattern during right ventricular pacing as compared to normal sinus rhythm. Coronary artery disease was present in 27 patients, while 5 patients (control group) had no evidence of coronary artery or left ventricular disease. Studies were performed during both normal sinus rhythm and right ventricular pacing at comparable heart rates, utilizing angiographic methods to determine heart volumes. Right ventricular pacing in all patients resulted in decreased left ventricular systolic (p< 0.01) and diastolic (p< 0.01) pressures and decreased stroke work (p< 0.001). In the control group, right ventricular pacing caused a decrease in left ventricular end-diastolic volume (p< 0.01) and stroke volume (p< 0.01), with no change in ejection fraction. The patients with coronary artery disease were divided into four groups, dependent on the left ventricular contractile pattern during normal sinus rhythm and the percentage of change in hemiaxis shortening during right ventricular pacing. In group A (six patients with asynergy) and group B (seven patients with asynergy), there was no significant change in the percentage of hemiaxis shortening during right ventricular pacing when compared to normal sinus rhythm. Ventricular volume studies in these patients (groups A and B) were similar to the control groups and no change in contractile pattern was observed during pacing. In group C, twelve patients had asynergy and a 10% increase in percentage of hemiaxis shortening during right ventricular pacing when compared to normal sinus rhythm. Right ventricular pacing resulted in decreased end-diastolic pressure (p< 0.01) and end-diastolic volume (p< 0.001), no change in stroke volume, and an increased ejection fraction (p< 0.01). Contractile patterns improved in all patients in group C during pacing. Group D consisted of two patients with asynergy and a 10% decrease in percentage of hemiaxis shortening during pacing, associated with a decrease in end-diastolic volume and ejection fraction with deterioration of left ventricular contractile pattern. These results indicate that right ventricular pacing in patients with coronary artery disease decreases preload, which may be accompanied by improved left ventricular contractile pattern (11/27) and in some patients (2/27) deterioration of left ventricular function.     

Early detection of right ventricular systolic dysfunction by using myocardial acceleration during isovolumic contraction in patients with mitral stenosis.

AIM: The aim of the study was to determine if the tissue Doppler imaging (TDI)-derived myocardial acceleration during isovolumic contraction (IVA) of tricuspid lateral annulus could be used in early detection of RV systolic dysfunction in patients with mitral stenosis (MS), before the clinical signs of systemic venous congestion occur. METHODS: One hundred and twelve patients with rheumatic MS without relevant regurgitation and 60 control subjects were enrolled in the study. Conventional echocardiographic parameters (mitral valve area, transmitral diastolic gradients, pulmonary artery pressure, RV fractional shortening, pulmonary flow acceleration time, tricuspid annular plane systolic excursion) and TDI-derived systolic velocities of tricuspid annulus (isovolumic myocardial acceleration: IVA, peak myocardial velocity during isovolumic contraction: IVV, peak systolic velocity during ejection period: Sa and RV Tei index) were recorded from all patients. RESULTS: TDI-derived IVA, IVV, Sa and Tei index were found to be significantly decreased in patients with MS. IVA was the only parameter which had a significant negative correlation with the traditional echocardiographic parameters and RV Tei index in patients with MS. Additionally, in subgroup analyses, IVA was significantly lower in patients with severe degree of MS. CONCLUSION: TDI-derived right ventricular IVA may be used as an adjunctive, reliable, noninvasive parameter for the early detection of right ventricular systolic dysfunction in patients with MS but without signs of systemic venous congestion.     

Immediate and delayed effects of successful percutaneous transvenous mitral commissurotomy on global right ventricular function in patients with isolated mitral stenosis

Global right ventricular function of the pressure-overloaded right ventricle in patients with mitral stenosis and pulmonary hypertension after successful percutaneous transvenous mitral commissurotomy (PTMC) has not been well-defined. With the use of a recently developed Doppler method for estimating right ventricular function in human beings, we studied 25 consecutive patients with isolated rheumatic mitral stenosis before, immediately after (mean, 40+/-12 h) and at a mean follow-up of 11.5 months after PTMC. Immediately after percutaneous mitral commissurotomy, there was a significant increase in mitral valve area (P = 0.000017) along with a decrease in mean pulmonary pressure (P = 0.001). The index was not affected immediately after successful PTMC (0.70+/-0.25 vs., 0.58+/-0.18; P = 0.06); however, at follow-up of about one year, the index showed a significant decrease (0.697+/-0.28 vs. 0.380+/-0.13; P = 0.0008, n = 24). The change in the index was characterised by a significant prolongation of the right ventricular ejection time, with a decrease in the isovolumic intervals. The Doppler index of combined right ventricular function was significantly correlated to the mean pulmonary artery pressure (r = 0.695, P<0.001) and systolic pulmonary artery pressure (r = 0.60, P = 0.007) before PTMC and also immediately after the procedure; however, at follow-up, the index had no correlation with the Doppler estimated pulmonary artery systolic pressure (r = 0.07). Despite a larger mitral valve area following PTMC, right ventricular isovolumic indices remain abnormal on mid-term follow-up, although global function tends to normalise in two-thirds of the patients.     

Right ventricular myocardial function after atrial switch operation for transposition of the great arteries

Postoperative right ventricular (RV) myocardial function was evaluated in 6 patients who underwent atrial switching for simple transposition of the great arteries (TGA). The average age at study was 5.5 years. RV function was evaluated at rest and during administration of methoxamine by cardiac catheterization and RV angiography. The data were compared with left ventricular function in a control group, which consisted of 6 patients, 3 with functional murmur and 3 with pulmonary valvar stenosis. During stress, the TGA group showed a significant increase in end-diastolic pressure, minute work index and end-diastolic and end-systolic volume indexes, along with a significant decrease in ejection fraction. The control group also showed an increase in these variables except for ejection fraction during stress, which did not change. The slope of the work-function curve for the TGA group was lower than that for the control group (p = 0.02). The TGA group had a lower slope of the peak systolic pressure-volume relation than the control group (p = 0.005). There was no significant correlation between the slope of the peak systolic pressure-volume relation and age at repair or study. This study shows that RV pump dysfunction observed in postoperative TGA patients may be caused by depressed myocardial function.