Comparisons between female and male patients with mitral stenosis.

OBJECTIVE--To compare Doppler, echocardiographic, and clinical variables in female and male patients with mitral stenosis. DESIGN--Observational study in consecutive patients with mitral stenosis of cross sectional and Doppler echocardiographic and clinical variables and a retrospective search for a history of systemic embolism. SETTING--A medical centre with 3000 beds, serving both urban and rural populations. PATIENTS--500 consecutive patients with an echocardiographic mitral valve area of 2 cm2 or less. 331 (66.2%) were female and 169 (33.8%) male (mean (SD) ages of 49 (13) and 48 (14) respectively). MAIN OUTCOME MEASURES--Mitral valve areas by echocardiographic planimetry and Doppler pressure half-time method, peak early diastolic mitral velocity and pressure gradient, echocardiographic score of mitral valve, left atrial end systolic diameter, frequency of left atrial thrombus and smoky echoes as well as various valve lesions detected with Doppler and echocardiography, cardiac rhythm, symptomatic functional class of heart failure, and history of systemic embolism. RESULTS--The prevalence of significant tricuspid (22% v 9%, P < 0.001) and pulmonary regurgitation (5% v 1%, P = 0.018) was higher in the female patients than in the male patients. Female patients also had a higher peak regurgitant velocity (3.2 (0.7) v 2.9 (0.7) m/s, P = 0.007) and pressure gradient (41 (21) v 36 (19) mm Hg, P = 0.010) across the tricuspid valve. However, the male patients had a higher echocardiographic score (9.7 (2.4) v 7.0 (2.3), P < 0.001) and a smaller Doppler-derived mitral valve area (0.9 (0.4) v 1.0 (0.4) cm2, P = 0.027). There were no differences between the female and the male patients in mitral valve area measured by planimetry, peak early diastolic mitral velocity and pressure gradient, and left atrial end systolic diameter or in the prevalence of atrial fibrillation, left atrial thrombus, left atrial smoky echoes, significant aortic stenosis, aortic regurgitation, or heart failure of New York Heart Association class III or IV. CONCLUSIONS--Female patients not only had a higher prevalence of mitral stenosis but also had a higher prevalence of associated tricuspid and pulmonary regurgitation along with a higher velocity and gradient of tricuspid regurgitation. The echocardiographic score was higher in male patients, however. These findings suggest that the pathophysiology of mitral stenosis is different in the two sexes and that gender should be taken into account when therapeutic strategies are formulated.     

The clinical spectrum of tricuspid regurgitation detected by pulsed Doppler echocardiography

The clinical diagnosis of tricuspid regurgitation (TR) is often difficult. Two-dimensional pulsed Doppler echocardiography offers a sensitive and specific method for detecting and semi-quantitating tricuspid regurgitation. The clinical, radiographic, radionuclide, echocardiographic, and when available, the right cardiac catheterization findings were evaluated in 36 patients with a diagnosis of tricuspid regurgitation by pulsed Doppler. Ten healthy subjects served as controls. The underlying cardiac cause was rheumatic heart disease in 7 (20%), ischemic heart disease in 12 (33%), dilated cardiomyopathy in 5 (14%), hypertensive heart disease in 2 (5%), aortic valve stenosis and/or regurgitation in 3 (8%), mitral valve prolapse with mitral regurgitation in 1 (3%), and congenital heart disease in 6 (17%). Seven patients (19%) had a temporary or permanent transvenous right ventricular pacing wire. A systolic murmur was heard in 29 patients (81%) with 16 (46%) having an elevated jugular venous pressure. Tricuspid regurgitation was clinically suspected in only 2 patients (6%). Isolated tricuspid regurgitation was uncommon, seen in 6 patients (17%), and usually secondary to congenital heart disease, ischemic heart disease, with the use of a transvenous pacing wire and following mitral valve replacement. Right cardiac catheterization was performed in 10 patients, of which 7 demonstrated elevated right atrial and pulmonary artery pressure. Pulsed Doppler echocardiography offers a practical and accurate method of detecting and evaluating the severity of tricuspid regurgitation. Tricuspid regurgitation is generally a functional disorder, and frequently occurs in association with left sided valvular heart disease, cardiomyopathy or congenital heart disease.     

Simultaneous measurement of left atrial pressure by Doppler echocardiography and catheterization.

Simultaneous, continuous wave Doppler echocardiography, left ventricular systolic and mean pulmonary capillary wedge pressure measurements were performed during cardiac catheterization in 54 patients with mitral regurgitation. Doppler-derived left atrial pressure, which was calculated by subtracting mitral regurgitant gradient from brachial artery systolic pressure, correlated well with mean pulmonary capillary wedge pressure by catheter (r = 0.933, SEE = 2.9 mmHg, P < 0.001); a comparison between non-invasive and invasive systolic gradients across the mitral valve yielded a high correlation (r = 0.91, SEE = 6.0 mmHg, P < 0.001); and there was also a high correlation between brachial artery and left ventricular systolic pressures (r = 0.93, SEE = 4.9 mmHg, P < 0.01). It is concluded that Doppler echocardiography provides a reliable and accurate method for complete non-invasive assessment of left atrial pressure in patients with mitral regurgitation.     

Quantitative assessment of pulmonary hypertension in patients with rheumatic heart disease using continuous wave Doppler ultrasound

The accuracy of Doppler ultrasound in estimating pulmonary arterial systolic pressure non-invasively was evaluated in 50 patients with rheumatic heart disease. In all cases, the maximal velocity of the tricuspid regurgitation jet was measured by continuous wave Doppler ultrasound and the systolic pressure gradient between right ventricle and the right atrium was calculated by the modified Bernoulli equation. There was a close correlation between Doppler estimated and hemodynamically measured transtricuspid systolic gradient (r = 0.86, P less than 0.001). Right ventricular systolic pressure, which equals pulmonary arterial systolic pressure in the absence of right ventricular outflow obstruction, was calculated by adding a constant of 10 to the Doppler gradient and also by using a regression equation. Right ventricular systolic pressure obtained by both of these Doppler methods correlated closely with values at cardiac catheterization (r = 0.82 and 0.83, respectively). Our study suggests that pulmonary arterial systolic pressure can be determined non-invasively with accuracy, by Doppler ultrasound, in patients with rheumatic heart disease.     

Rheumatic tricuspid valve disease: two-dimensional echocardiographic, hemodynamic, and angiographic correlations

From March 1977 through April 1982, 2-dimensional echocardiography detected 372 patients with rheumatic mitral valve disease. Of these patients, 23 (6%) had tricuspid valve involvement. Two-dimensional echocardiographic criteria of rheumatic tricuspid valve disease included thickened leaflets with restriction in motion, diastolic doming, and encroachment of the leaflet tips on the ventricular inlet. These criteria provided a sensitivity of 100%, a specificity of 90%, a predictive accuracy of 21%, and a negative predictive value of 100% in diagnosing hemodynamically significant tricuspid stenosis. Hemodynamic variables in patients with rheumatic tricuspid valve disease (Group I) were compared with those in patients with no rheumatic tricuspid disease (Group II). The only significant difference was mean right atrial pressure (15 +/- 7 mm Hg versus 11 +/- 5 mm Hg, p less than 0.02). Both groups were classified into patients with (A) and without (B) significant tricuspid regurgitation (TR). There was no significant difference in any hemodynamic variable when Group IA was compared with Group IIA. In addition, there was no difference in any hemodynamic variable when patients with functional TR (Group IIA) were compared with those with rheumatic mitral valvular disease without TR (Group IIB). Two-dimensional echocardiography and cardiac catheterization provide complementary diagnostic information in these patients.     

Observations suggesting a high incidence of exercise-induced severe mitral regurgitation in patients with mild rheumatic mitral valve disease at rest

Objectives. The aim of this study was to determine the hemodynamic effects of upright bicycle ergometry in symptomatic patients with mild, mixed mitral stenosis and regurgitation.Background. Patients with seemingly mild rheumatic mitral valve disease often complain of exertional dyspnea or fatigue. These symptoms are usually ascribed to flow-dependent increases in the gradient across the stenotic mitral valve. Although catheterization studies in these patients may demonstrate an increase in mitral valve gradient proportional to an increase in cardiac output, this approach does not specifically address the underlying mechanism of any observed increases in mitral gradient or left atrial (i.e., pulmonary capillary wedge) pressure. Exercise echocardiography is uniquely suited to the dynamic assessment of exercise-induced hemodynamic changes.Methods. Fourteen symptomatic patients with exertional dyspnea and mild mitral stenosis and regurgitation at rest performed symptom-limited upright bicycle ergometry with quantitative two-dimensional, Doppler and color Doppler echocardiographic analysis.Results. Average pulmonary artery systolic pressure in the 13 patients with adequate spectral signals of tricuspid regurgitation increased from 36 ± 5 mm Hg (mean ± SD) at rest to 63 ± 14 mm Hg at peak exercise (p < 0.001). The mean transmitral pressure gradient in all patients increased from 4.5 ± 1.4 mm Hg at rest to 12.7 ± 2.7 mm Hg at peak exercise (p < 0.001). Five patients developed severe mitral regurgitation during exercise.Conclusions. Patients with exertional dyspnea and mild mitral stenosis and regurgitation at rest demonstrate a marked increase in pulmonary artery systolic pressure and mean transmitral pressure gradient during dynamic exercise. In a subset of these patients, marked worsening of mitral regurgitation appears to be the underlying mechanism of this hemodynamic deterioration. Because of the small sample size, this novel observation must be considered preliminary with respect to the true prevalence of exercise-related development of severe mitral regurgitation. If additional studies confirm the importance of this phenomenon, it has important implications for the management of patients with rheumatic mitral valve disease.     

Reappraisal by transesophageal echocardiography of the significance of left atrial thrombi in the prediction of systemic arterial embolization in rheumatic mitral valve disease.

Systemic arterial embolization imparts a significant risk of serious complications throughout the lives of patients with rheumatic heart disease. Left atrial (LA) thrombi have been thought to be the major source of emboli. A transesophageal echocardiography (TEE) study of 260 consecutive patients with rheumatic mitral valve disease was performed during a period of 24 months, with particular reference to understanding the association between LA thrombi and embolic complications. Of these patients, 155 had predominant mitral stenosis, 24 had significant mitral regurgitation, and the remaining 81 with xenograft mitral valve replacement developed valvular dysfunction (25 resulted in predominant mitral stenosis and 56 in significant mitral regurgitation). LA thrombi were detected in 38 patients (group A) and absent in 222 (group B). Group A patients had a higher frequency of recent (less than or equal to 1 week before TEE study) and remote (greater than 1 week before) embolization than did group B patients (recent: 26.3 vs 5.4% [p less than 0.001]; remote: 18.4 vs 5.0% [p less than 0.01]). The frequency of atrial fibrillation was also greater in group A patients (100 vs 74.3%; p less than 0.001). The exclusion of patients with significant mitral regurgitation and sinus rhythm had no effect on the association between LA thrombi and evidence of previous embolization. It is concluded that TEE is a convenient diagnostic modality that can be used to identify a subset of patients with rheumatic mitral valve disease at high risk for systemic embolization. Consequently, preventive anticoagulation for possible embolic complications should be more vigorously adhered to in patients with rheumatic mitral valve disease and LA thrombi.     

Surgical experience with diseases of the tricuspid valve. Cross-sectional and Doppler echocardiographic evaluation following DeVega's repair

Seventy-eight patients undergoing mitral valve surgery with or without replacement of the aortic valve also underwent procedures on the tricuspid valve over a period of 10 years. All patients were in functional class III or IV preoperatively. The procedures were performed in all patients with organic disease of the tricuspid valve (N = 44) and in those with moderate or severe functional tricuspid valvar regurgitation (N = 34). Seventy-one patients underwent DeVega's annuloplasty with or without commissurotomy. The overall mortality was 11.5%. 65 long-term survivors were followed up for a period of 6 months to 10 years (mean 5.3 years). Sixty-three patients were in functional class I or II at the last follow-up. Six patients had clinical evidence of mild to moderate tricuspid regurgitation. Regression of cardiomegaly (as judged by the chest radiograph and right ventricular hypertrophy seen in the electrocardiogram) was evident in most cases. Fifty-one of 54 patients evaluated by cross-sectional echocardiography were reported to have a functionally normal tricuspid valve. Doppler echocardiography in 28 patients showed no significant tricuspid regurgitation or stenosis in 26 patients. Eleven consecutive patients undergoing DeVega's annuloplasty were studied prospectively with pre- and postoperative Doppler echocardiography. Good correlation existed between right ventricular systolic pressures predicted by Doppler with those obtained preoperatively at cardiac catheterization. Postoperative Doppler echocardiography in these 11 patients showed complete restoration of competence of the tricuspid valve as well as normalisation of the right ventricular systolic pressure in 10 patients.     

Functional tricuspid regurgitation following replacement of the mitral valve.

In this series, the effect of replacement of the mitral valve was examined in 86/900 (9.6%) patients who had developed moderate functional tricuspid regurgitation, secondary to rheumatic mitral valvar disease. These patients were subdivided according to the severity of pulmonary hypertension and impairment of right ventricular function. Forty-six patients presented with severe pulmonary hypertension and 40 patients had moderate pulmonary hypertension (mean main pulmonary arterial pressure: 78 +/- 14 mmHg vs 41 +/- 6 mmHg; P less than 0.05). The latter had more advanced disease, greater impairment of right ventricular function and dilatation of the right heart chambers. Functional tricuspid regurgitation regressed in 38/42 survivors with severe pulmonary hypertension and persisted or progressed significantly in 22/34 survivors with impaired right ventricular function despite successful replacement of the mitral valve. The latter underwent replacement of the tricuspid valve (n = 16) or tricuspid annuloplasty (n = 6), at a mean interval of 44 +/- 4.4 months after replacement of the mitral valve, which resulted in 8/22 (23.5%) early deaths. Functional tricuspid regurgitation is more likely to persist in patients with advanced right ventricular failure. Tricuspid valvar competence should be restored in these patients at initial replacement of the mitral valve.     

Echocardiographic predictors of pulmonary hypertension in patients with severe aortic stenosis.

BACKGROUND: Pulmonary hypertension complicating severe aortic stenosis increases morbidity and mortality. Causes and mechanisms of this are unclear. METHODS: This is a retrospective observational study of 626 patients with severe aortic stenosis who had measurable pulmonary arterial pressure by Doppler echocardiography. Clinical, echocardiographic and pharmacological data were related to the presence of pulmonary hypertension. RESULTS: Of the 626 patients, 119 (19%) had severe pulmonary hypertension defined as pulmonary artery systolic pressure > or =60 mmHg. Patients with severe pulmonary hypertension had a smaller aortic valve area (P < 0.0001), a lower left ventricular ejection fraction (P < 0.0001), a higher mitral E/A velocity ratio (P < 0.0001) indicating a higher filling pressure and a higher prevalence of 3 or 4+ mitral regurgitation (P < 0.001). They were less likely to be on a beta blocker (P = 0.05) or a statin (P = 0.02). Smaller aortic valve area, left ventricular dysfunction, mitral regurgitation and lack of statin use were independent predictors of severe pulmonary hypertension. CONCLUSIONS: Severity of aortic stenosis, left ventricular dysfunction, and mitral regurgitation are risk factors for the genesis of pulmonary hypertension and statins may potentially be protective in patients with severe aortic stenosis.     

Comparison of Doppler echocardiography and cardiac catheterization in patients requiring valve surgery: search for a 'gold standard'.

OBJECTIVE: To compare the sensitivities of Doppler echocardiography and cardiac catheterization in the diagnosis of severe valvular heart disease in patients requiring valve surgery. DESIGN: Retrospective analysis of Doppler echocardiograms and cardiac catheterizations. SETTING: Tertiary referral cardiovascular centre in a university setting. PATIENTS: Sixty-nine patients undergoing valve surgery between July 1988 and July 1990. RESULTS: The sensitivities of echocardiography and cardiac catheterization were 84 and 87%, respectively (P = 1.0) in 32 patients who underwent aortic valve surgery primarily for severe aortic stenosis; 83 and 67%, respectively (P = 1.0) in six patients with severe aortic regurgitation, and 100 and 85%, respectively (P = 1.0) in seven patients with combined severe aortic stenosis and regurgitation. The sensitivities of echocardiography and cardiac catheterization in 11 patients who underwent mitral valve surgery for severe mitral stenosis were 73 and 91%, respectively (P = 0.6) and 69 and 92%, respectively (P = 0.3) in 13 patients with severe mitral regurgitation. Sensitivities of echocardiography and cardiac catheterization in the diagnosis of severe tricuspid regurgitation in five patients who had tricuspid valve repair were 100 and 80%, respectively (P = 1.0). Two patients with severe aortic stenosis by echocardiography, but not by catheterization, did not undergo aortic valve replacement during valvular surgery; both required aortic valve replacement within two years of initial surgery because of heart failure. Four patients with severe tricuspid regurgitation identified by echocardiography did not have tricuspid repair; three had pulmonary hypertension and these patients had resolution of tricuspid regurgitation on follow-up. One patient with severe tricuspid regurgitation and absence of pulmonary hypertension required reoperation for tricuspid valve repair 10 months after initial operation. CONCLUSIONS: The sensitivity of echocardiography and cardiac catheterization in the detection of severe valvular lesions requiring surgery is similar. Discordant results should be reviewed carefully with knowledge of the inherent pitfalls of both techniques in order to ensure optimal patient outcome.     

Incidence and concomitant factors of tricuspid valve insufficiency in patients with aortic and mitral valve diseases

Invasive data about the frequency and associated factors of tricuspid regurgitation in normals and in patients with aortic and mitral valve disease are still rare. Thus, right ventricular biplane angiograms (RAO/LAO projection), the mean pulmonary artery pressure and the presence of atrial fibrillation were analyzed with regard to tricuspid regurgitation in 30 normals and 165 patients with pure mitral regurgitation, mitral stenosis, aortic regurgitation, aortic stenosis, combined mitral valve disease or combined aortic valve disease. Patients with tricuspid stenosis or coronary artery disease were excluded. In 52 of the 195 patients tricuspid regurgitation was present. Tricuspid regurgitation occurred statistically more often in patients with mitral stenosis (33%), mitral regurgitation (48%) or combined mitral valve disease (68%) than in patients with aortic regurgitation (4%) or combined aortic valve disease (3%). In patients with aortic stenosis and in normals tricuspid regurgitation was not present. In patients with combined mitral valve disease, tricuspid regurgitation was more often present than in patients with pure mitral stenosis (p less than 0.002), despite comparable values of the mean pulmonary artery pressure, the right ventricular enddiastolic and endsystolic volume indexes, the right ventricular ejection fraction and the frequency of atrial fibrillation. Only in patients with pure mitral regurgitation tricuspid regurgitation was associated with an elevated mean pulmonary artery pressure (p less than 0.02). Differences in the right ventricular size and function did not occur between normals and patients with mitral or aortic valve disease. Therefore, the mean pulmonary artery pressure, atrial fibrillation and the size and function of the right ventricle are not major determinants for the occurrence of tricuspid regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulsed Doppler echocardiographic evaluation of valvular regurgitation in patients with mitral valve prolapse: comparison with normal subjects

Pulsed Doppler echocardiography was used to determine prospectively the prevalence of mitral, aortic, tricuspid and pulmonary regurgitation in 80 consecutive patients with mitral valve prolapse and 85 normal subjects with similar age and sex distribution. Mitral valve prolapse was defined by posterior systolic displacement of the mitral valve on M-mode echocardiography of 3 mm or more (40 patients), the presence of one or more mid- or late systolic clicks (61 patients), or both. Mitral regurgitation, detected by pulsed Doppler techniques in 53 patients with prolapse, was holosystolic in 24, early to mid-systolic in 6, late systolic in 15 and both holosystolic and late systolic behind different portions of the valve in 8. Definitive M-mode findings were present in only 27 of the 53 patients, and only 21 had mitral regurgitation audible on physical examination. Tricuspid regurgitation was evident by pulsed Doppler echocardiography in 15 patients (holosystolic in 9, early to mid-systolic in 1, late systolic in 4 and both holosystolic and late systolic in 1); 12 of these 15 patients, including all with an isolated late systolic pattern, had an echocardiographic pattern of tricuspid prolapse, but none had audible tricuspid regurgitation. A Doppler pattern compatible with aortic regurgitation was recorded in seven patients, all without echocardiographic aortic valve prolapse and only two with audible aortic insufficiency. A Doppler shift in the right ventricular outflow tract in diastole, suggestive of pulmonary regurgitation, was recorded in 16 of the 78 patients with an adequate Doppler examination: only 1 of the 16 had audible pulmonary insufficiency. Of the 85 normal subjects without audible regurgitation, pulsed Doppler examination detected mitral regurgitation in 3 subjects (holosystolic in 1 and early to mid-systolic in 2), aortic regurgitation in none, tricuspid regurgitation in 9 (holosystolic alone in 8 and both holosystolic and late systolic in 1) and right ventricular outflow tract turbulence compatible with pulmonary insufficiency in 15. The prevalence of valvular regurgitation, detected by pulsed Doppler echocardiography, is high in patients with mitral valve prolapse. Regurgitation may involve any of the four cardiac valves and is clinically silent in the majority of patients. The prevalence rates of mitral and aortic regurgitation are significantly higher in patients with mitral prolapse than in normal subjects, suggesting that alterations in underlying valve structure in the prolapse syndrome may indeed be responsible for this regurgitation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Tricuspid valve disease

The normal tricuspid valve anatomy and function have several dissimilarities to the corresponding mitral valve in the left heart, in part, based on lower pressures in the right heart chambers. The functional abnormalities resulting from tricuspid valve disease are classified as primary and secondary. Primary valve disease is any associated intrinsic valve pathology. The list of responsible conditions includes congenital, rheumatic, infective endocarditis, carcinoid heart disease, toxic effects of chemicals, tumors, blunt trauma, and myxomatous degeneration. The secondary tricuspid valve disease does not involve intrinsic anatomic abnormalities of the valve apparatus, aside from tricuspid annular dilation secondary to right ventricular dilation and dysfunction. The most common cause of tricuspid valve disease is secondary to left heart disease, either myocardial, valvular, or mixed. Although bedside diagnosis of advanced tricuspid valve disease is feasible, echocardiography provides valuable clues to the presence and severity of tricuspid valve stenosis and/or regurgitation with considerable accuracy. The tricuspid regurgitation signal using Doppler techniques is utilized for estimation of right ventricular systolic pressure, which, in the absence of right ventricular outflow obstruction, corresponds to pulmonary arterial systolic pressure. This is clinically useful since nearly 80 to 90% of patients exhibit some degree of tricuspid regurgitation. The treatment of tricuspid valve disease is guided by underlying etiology and pathology. Tricuspid valve repair is increasingly advocated for patients with advanced tricuspid regurgitation, especially when combined with surgery on the left heart pathology. Primary tricuspid valve disease is often treated by surgical approach specific to the underlying pathology.     

Doppler echocardiography diagnosis and classification of the degree of aortic valve insufficiency in patients with aortic stenoses and mitral valve diseases

To test the capacity of pulsed Doppler echocardiography in the detection and quantification of aortic regurgitation, 64 consecutive patients with aortic and mitral valve disease were examined clinically and by echocardiography before cardiac catheterization. The severity of aortic regurgitation was determined angiographically (I-IV) and compared with the extent of the regurgitant jet in the left ventricle measured by pulsed Doppler echocardiography. In 15 of 64 patients neither angiography nor pulsed Doppler echocardiography showed aortic regurgitation (specificity 100%). Apart from 3 patients with poor echo quality pulsed Doppler echocardiography correctly detected aortic regurgitation in 46 of 49 patients (sensitivity 94%). Clinical examination (63%) and M-mode echocardiography (63%) were significantly less sensitive than Doppler echocardiography (p less than 0.001). The pulsed Doppler echocardiographic degree of aortic regurgitation correlated strongly with angiography (corrected contingency coefficient 0.91). In patients with severe aortic stenosis (systolic gradient greater than 50 mm Hg) aortic regurgitation I was slightly overestimated by pulsed Doppler echocardiography (p less than 0.003). Differentiation of aortic regurgitation III and IV was not possible. Mitral valve disease did not affect quantification of aortic regurgitation (n = 23).     

Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease.

OBJECTIVE--To determine how severe tricuspid regurgitation influences exercise capacity and functional state in patients who have undergone successful mitral valve replacement for rheumatic mitral valve disease. DESIGN--9 patients in whom clinically significant tricuspid regurgitation developed late after mitral valve replacement were compared with 9 patients with no clinical evidence of tricuspid regurgitation. The two groups were matched for preoperative clinical and haemodynamic variables. Patients were assessed by conventional echocardiography, Doppler echocardiography, and a maximal treadmill exercise test in which expired gas was monitored by mass spectrometry. SETTING--University Hospital of Wales, Cardiff. SUBJECTS--18 patients who had been reviewed regularly since mitral valve replacement. MAIN OUTCOME MEASURE--Objective indices of exercise performance including exercise duration, maximal oxygen consumption, anaerobic threshold, and ventilatory response to exercise. RESULTS--Mitral valve prosthetic function was normal in all patients and estimated pulmonary artery systolic pressure and left ventricular function were similar in the two groups. Right ventricular diameter (median (range) 5.0 (4.3-5.6) v 3.7 (3.0-5.4) cm, p less than 0.01) and the incidence of paradoxical septal motion (9/9 v 3/9, p less than 0.01) were greater in the group with severe tricuspid regurgitation. Exercise performance--assessed by exercise duration (6.3 (5.0-10.7) v 12.7 (7.2-16.0) min, p less than 0.01), maximum oxygen consumption (11.2 (7.3-17.8) v 17.7 (11.8-21.4) ml min-1 kg-1, p less than 0.01), and anaerobic threshold (8.3 (4.6-11.4) v 0.7 (7.3-15.5) ml min-1 kg-1, p less than 0.05)--was significantly reduced in the group with severe tricuspid regurgitation. The ventilatory response to exercise was greater in patients with tricuspid regurgitation (minute ventilation at the same minute carbon dioxide production (41.0 (29.9-59.5) v 33.6 (26.8-39.3) l/min, p less than 0.01). CONCLUSIONS--Clinically significant tricuspid regurgitation may develop late after successful mitral valve replacement and in the absence of residual pulmonary hypertension, prosthetic dysfunction, or significant left ventricular impairment. Patients in whom severe tricuspid regurgitation developed had a considerable reduction in exercise capacity caused by an impaired cardiac output response to exercise and therefore experienced a poor functional outcome. The extent to which this was attributable to the tricuspid regurgitation itself or alternatively to the consequences of right ventricular dysfunction was not clear and requires further investigation.     

Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease.

OBJECTIVE--To determine how severe tricuspid regurgitation influences exercise capacity and functional state in patients who have undergone successful mitral valve replacement for rheumatic mitral valve disease. DESIGN--9 patients in whom clinically significant tricuspid regurgitation developed late after mitral valve replacement were compared with 9 patients with no clinical evidence of tricuspid regurgitation. The two groups were matched for preoperative clinical and haemodynamic variables. Patients were assessed by conventional echocardiography, Doppler echocardiography, and a maximal treadmill exercise test in which expired gas was monitored by mass spectrometry. SETTING--University Hospital of Wales, Cardiff. SUBJECTS--18 patients who had been reviewed regularly since mitral valve replacement. MAIN OUTCOME MEASURE--Objective indices of exercise performance including exercise duration, maximal oxygen consumption, anaerobic threshold, and ventilatory response to exercise. RESULTS--Mitral valve prosthetic function was normal in all patients and estimated pulmonary artery systolic pressure and left ventricular function were similar in the two groups. Right ventricular diameter (median (range) 5.0 (4.3-5.6) v 3.7 (3.0-5.4) cm, p less than 0.01) and the incidence of paradoxical septal motion (9/9 v 3/9, p less than 0.01) were greater in the group with severe tricuspid regurgitation. Exercise performance--assessed by exercise duration (6.3 (5.0-10.7) v 12.7 (7.2-16.0) min, p less than 0.01), maximum oxygen consumption (11.2 (7.3-17.8) v 17.7 (11.8-21.4) ml min-1 kg-1, p less than 0.01), and anaerobic threshold (8.3 (4.6-11.4) v 0.7 (7.3-15.5) ml min-1 kg-1, p less than 0.05)--was significantly reduced in the group with severe tricuspid regurgitation. The ventilatory response to exercise was greater in patients with tricuspid regurgitation (minute ventilation at the same minute carbon dioxide production (41.0 (29.9-59.5) v 33.6 (26.8-39.3) l/min, p less than 0.01). CONCLUSIONS--Clinically significant tricuspid regurgitation may develop late after successful mitral valve replacement and in the absence of residual pulmonary hypertension, prosthetic dysfunction, or significant left ventricular impairment. Patients in whom severe tricuspid regurgitation developed had a considerable reduction in exercise capacity caused by an impaired cardiac output response to exercise and therefore experienced a poor functional outcome. The extent to which this was attributable to the tricuspid regurgitation itself or alternatively to the consequences of right ventricular dysfunction was not clear and requires further investigation.     

Impact of atrial fibrillation on clinical status, atrial size and hemodynamics in patients after mitral valve replacement.

BACKGROUND AND AIM OF THE STUDY: The association between mitral valve disease and atrial fibrillation (AF) is well known, but few data exist regarding the impact of AF after mitral valve replacement (MVR) on NYHA functional class, atrial size and hemodynamic parameters. The present study was conducted to evaluate these issues. METHODS: Eighty-six patients (26 men, 60 women) who underwent MVR were evaluated by transthoracic echocardiography. Fifty-nine patients had chronic AF (AF group), and 27 were in sinus rhythm (sinus group). Variables analyzed included end-systolic left atrial and right atrial areas, tricuspid regurgitation, and presence and duration of AF. Peak and mean transprosthetic mitral valve gradients and pulmonary pressure were estimated by Doppler echocardiography. RESULTS: Groups were matched for age, sex and time from MVR (mean 6.6 years). Sixty-four patients (77%) had rheumatic heart disease, 18 (21%) had mitral valve disease, and two (2%) had mitral valve prolapse. Mean duration of AF was 11+/-12 years (range: 8-50 years). Preoperatively, AF patients had a worse NYHA class than sinus patients (2.8+/-0.8 versus 1.1+/-0.7, p = 0.001), but both had similar fractional shortening of the left ventricle and preserved prosthetic mitral valve function. Multivariate analysis identified AF as a single predictor of NYHA class after MVR. Although left and right atrial areas were larger in AF patients (47+/-25 versus 27+/-7 cm2, p = 0.0001 and 30+/-12 versus 17+/-5 cm2, p = 0.0001, respectively), the left:right atrial size ratio was not significantly different between groups. Multivariate analysis identified mean transmitral gradient and duration of AF as independent predictors of left atrial size after MVR (p = 0.01 and p = 0.0001, respectively). Tricuspid regurgitation and duration of AF were independent predictors of right atrial size (p = 0.003 and p = 0.0001, respectively). CONCLUSION: The presence of AF after MVR is associated with a worse NYHA functional class, increased transmitral gradients, and larger areas of both atria, when compared with sinus rhythm. Hence, a special effort should be made to correct arrhythmia during surgery, and in case of paroxysmal arrhythmia, earlier surgery should be considered before the condition becomes chronic.     

Serial assessment of mitral regurgitation by pulsed Doppler echocardiography in patients undergoing balloon aortic valvuloplasty

Mitral regurgitation was serially assessed by pulsed Doppler echocardiography in 144 patients undergoing balloon aortic valvuloplasty for symptomatic aortic stenosis. Regurgitant scores of 0, 1, 2 and 3 were assigned to pulsed Doppler patterns corresponding to no, mild, moderate and severe mitral regurgitation, respectively. Before balloon aortic valvuloplasty, mitral regurgitant score correlated significantly (p less than 0.005) but weakly with aortic valve area (r = -0.24), left ventricular ejection fraction (r = -0.34) and left ventricular systolic pressure (r = 0.23). There was no significant correlation between mitral regurgitation and either mean catheterization or mean Doppler aortic valve gradient. Balloon aortic valvuloplasty produced significant decreases in both catheterization and Doppler mean transvalvular aortic valve gradients (56 +/- 19 to 31 +/- 12 and 60 +/- 19 to 48 +/- 16 mm Hg, respectively; both p less than 0.0001) and a significant increase (p less than 0.0001) in aortic valve area assessed by catheterization (0.6 +/- 0.2 to 0.9 +/- 0.3 cm2). Left ventricular ejection fraction did not change, but cardiac output increased (p less than 0.001) and pulmonary capillary wedge pressure decreased (p less than 0.0001). Pulsed Doppler findings of mitral regurgitation were present in 102 of the 144 patients. Eighty-eight patients had a score compatible with mild or more severe degrees of mitral regurgitation, and 49 had a score indicative of moderate or severe valvular insufficiency. In the entire group of 144 patients, mitral regurgitant score decreased significantly from 1.1 +/- 1.0 to 1.0 +/- 1.0 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mitral valve prolapse in patients with prior rheumatic fever

It is known that rheumatic heart disease frequently results in isolated mitral regurgitation without concomitant mitral stenosis, especially in countries with a high prevalence of rheumatic fever. However, more recent surgical pathologic data also have demonstrated a high incidence of mitral valve prolapse in cases of rheumatic heart disease, which suggests that rheumatic fever may be a cause of mitral valve prolapse. To determine whether this association of mitral valve prolapse and rheumatic heart disease is present in a stable clinic population, we studied 30 patients who had an apical systolic murmur and a well-documented history of rheumatic fever with dynamic auscultation, two-dimensional echocardiography, and pulsed Doppler examinations. Twenty of the 30 patients (67%) had findings on physical examination consistent with isolated mitral regurgitation and 25 patients (84%) had mitral regurgitation by Doppler examination. Echocardiography demonstrated mitral valve prolapse in 24 patients (80%), whereas only one of the total study group had echocardiographic findings consistent with mitral stenosis. We conclude that (1) the presence of an isolated systolic murmur in patients with a history of rheumatic fever frequently represents pure mitral regurgitation secondary to mitral valve prolapse and (2) postinflammatory changes in valvular tissue resulting from rheumatic fever may be the etiology of mitral valve prolapse in these patients.