Mitral valve surgery in the presence of pulmonary hypertension.

Mitral valve surgery was performed in 59 patients with severe pulmonary hypertension (average systolic pulmonary artery pressure 77.1 +/- 18.6 mmHg; range 50-115 mmHg) between 1983 and 1990. Thirty-eight patients had been subjected to mitral valve replacement, 16 patients both mitral and aortic valve replacement, and 5 patients had open mitral commissurotomy, with an operative (30 day) mortality of 5.0%. These 3 deaths happened during the early postoperative period. Survivors were followed up for a period ranging from 6 months to 7 years with a mean of 36 months. Four late deaths (7.1%) occurred in patients with valve replacement. Actuarial survival was 93 +/- 3% at 5 years, and 90.7 +/- 4.4% at 7 years. Right ventricular catheterization was performed on 14 patients a mean of 38 months following operation. Systolic pulmonary artery pressure had decreased from a mean of 77.1 +/- 18.6 to 39.7 +/- 14.0 mmHg (p less than 0.001) and 90% of the survivors were in New York Heart Association Class 1 or II compared to 23.7% preoperatively. The clinical and hemodynamic findings in this series suggest that severe pulmonary hypertension is not a contraindication, and pulmonary hypertension decreases significantly after mitral valve surgery.     

Left ventricular function in pulmonary hypertension

To elucidate left ventricular function in pulmonary hypertension, we measured parameters of left ventricular as well as right ventricular function by echocardiography in 11 patients with pulmonary hypertension (idiopathic pulmonary artery hypertension in 4, chronic thromboembolic pulmonary hypertension in 5, and other pulmonary hypertension in 2). The percent change in these parameters 6 months after treatment with pulmonary artery vasodilators (beraprost in 8 and sildenafil in 3) was assessed. There was a correlation between the relative change in right ventricular systolic pressure (RVSP) and the relative changes in left ventricular outflow tract velocity–time integral (r = ?0.730, P = 0.011) and mitral valve velocity–time integral (r = ?0.621, P = 0.041). However, there was no correlation between the relative change in RVSP and the relative changes in left ventricular ejection fraction, left ventricular diastolic dimension, and systolic blood pressure. The relative change in RVSP was also correlated with the relative change in early diastolic myocardial velocity at the medial mitral annulus (r = ?0.675, P = 0.023). Reduction of RVSP by pulmonary artery vasodilators might increase left ventricular preload, leading to an increase in stroke volume. Right ventricular load reduction might improve left ventricular diastolic function in patients with pulmonary hypertension, possibly through altered interventricular septal performance.     

Simultaneous echocardiographic and catheterisation gradients and mitral valve area during balloon mitral valvuloplasty.

This study was aimed at estimating mean transmitral gradients by simultaneous Doppler echocardiography and cardiac catheterisation and determining mitral valve area by pressure half time, Gorlin's formula and two-dimensional echocardiography so as to assess the relative accuracy of these methods before and after balloon mitral valvuloplasty in patients with rheumatic mitral stenosis. Left atrium-left ventricular, pulmonary artery wedge-left ventricular and echo gradients were simultaneously recorded in 18 patients undergoing balloon mitral valvuloplasty. Mitral valve area was estimated by pressure half time, Gorlin's equation and two-dimensional echocardiography. The correlation between left atrium-left ventricular and echo mean gradient before balloon mitral valvuloplasty was 0.96 (p < 0.03). Between pulmonary artery wedge-left ventricular and echo mean gradient, it was 0.95 (p < 0.04). The correlations between left atrium-left ventricular and pulmonary artery wedge-left ventricular mean gradient were also good. After balloon mitral valvuloplasty, similar good correlations were seen. On subgrouping the patients into those with high and low pulmonary artery pressure, good correlation persisted both before and after balloon mitral valvuloplasty. Mitral valve area by all the methods were similar before balloon mitral valvuloplasty. After balloon mitral valvuloplasty, mitral valve area by pressure half time was the least and by two-dimensional echocardiography, the maximum. All the three methods are equally accurate in estimating transmitral gradients and mitral valve area in mitral stenosis before balloon mitral valvuloplasty. Two-dimensional echocardiography is the best to estimate mitral valve area after balloon mitral valvuloplasty. Echocardiography can replace haemodynamic measurement of gradients and mitral valve area before and after balloon mitral valvuloplasty. But pressure half time is not recommended for measuring mitral valve area immediately after balloon mitral valvuloplasty where two-dimensional echocardiography mitral valve area is to be employed.     

Antithrombotic therapy in native heart valve disease

In establishing the indication for anticoagulation of patients with native heart valve disease, those with thromboembolic events and/or atrial fibrillation (AF) must be distinguished from patients with sinus rhythm. Anticoagulation should be started as a matter of principle in patients with thromboembolic events and/or AF who do not undergo valve replacement. However, a more differentiated procedure is mandatory for patients with sinus rhythm. If the left atrium is enlarged, spontaneous echo contrast is detected, and/or there is no atrial contraction and/or reduced left ventricular pump function (e.g., in patients with mitral valve stenosis), then anticoagulation with a target INR of 2.5 is indicated, even in those with sinus rhythm. Whereas rheumatic mitral valve stenosis predominates in developing countries, aortic stenosis (AS) predominates in developing countries. These AS patients mainly suffer microemboli that often determine the prognosis in patients with calcification of the mitral annulus. Anticoagulation is not recommended in calcific microemboli. If there are simultaneous atherothrombotic plaques of the aortic arch > 5 mm in size owing to an often more complex cardiovascular risk profile, then warfarin treatment is indicated. Mitral valve prolapse (MVP), patient foramen ovale and atrial septal aneurysm are potential sources of embolism that may cause stroke. On their own, these congenital lesions do not entail an indication for anticoagulation. This applies in particular to patients with MVP in whom secondary prevention of stroke can be attained with 100 mg aspirin.     

Massive mitral and pulmonary valve incompetence in a patient with left ventricular, non-compacted myocardium

The case is reported of a patient who underwent cardiac surgery for pulmonary valve stenosis as a child, and presented as an adult with signs and symptoms of severe congestive heart failure. The left ventricle showed an increased trabecular pattern in the region of the apex, the mitral annulus was severely dilated with mitral incompetence, the right ventricular out-flow tract (RVOT) was largely dilated with aneurysm of both pulmonary arteries, and there was evidence of pulmonary valve incompetence. Previously, rare cases have been reported of persistent left ventricular non-compaction in patients with congenital left or RVOT obstruction. Non-compaction of the ventricular myocardium is an inherited autosomal dominant disorder; to date, four genes and one genetic locus have been found to be associated with non-compacted ventricular myocardium. The condition is characterized by arrhythmias, thromboembolic events and heart failure, but affected individuals may not be symptomatic. The present case represented a strange association between non-compacted left ventricle, mitral annular dilation with persistence of a normal leaflet and subvalvular mitral valve apparatus, and RVOT dilation with pulmonary artery aneurysms.     

High Occurrence of Mitral Valve Prolapse in Cardiac Catheterization Patients with Pure Isolated Mitral Regurgitation

ABSTRACT. Danielsen R, Nordrehaug JE, Vik-Mo H (Department of Clinical Physiology, Haukeland Hospital, University of Bergen, Bergen, Norway). High occurrence of mitral valve prolapse in cardiac catheterization patients with pure isolated mitral regurgitation. Acta Med Scand 1987; 221:33–8. The aetiological spectrum of angiographically verified pure isolated mitral regurgitation (MR) was studied in 48 consecutive adult patients (35 males). Severe MR was found in 35 patients (73%) and moderate MR in 13 patients (27%). Mitral valve prolapse (MVP) syndrome was found in 21 patients (44%). These were younger than the rest of the study population (55±13 vs. 62±6 years, p<0.05) and 15 (71%) of them were men. Endocarditis and chordal rupture occurred in 19% and 43% of the MVP patients. Sixteen patients (33%) had MR secondary to myocardial infarction while only three patients (6%) had MR of rheumatic aetiology. Bacterial endocarditis, hypertensive heart disease, hypertrophic obstructive car-diomyopathy and mitral annulus calcification were less frequently found. Mitral valve replacement was done in 20 (57%) of the patients with severe MR and MVP was the underlying disease in 15 (75%) of these patients. In conclusion, MVP is a frequent cause of pure isolated MR and of mitral valve replacement. In contrast to the preponderance of young females amongst MVP patients in population surveys, most of the MVP patients with MR in this study are middle-aged and elderly men.     

Persistent pulmonary hypertension after mitral valve surgery: does surgical procedure affect outcome?

BACKGROUND AND AIM OF THE STUDY: Recently published data suggest that prosthesis-patient mismatch is common after mitral valve replacement (MVR), and manifests as persistent pulmonary hypertension. The study aim was to determine the prevalence and severity of pulmonary hypertension after mitral valve surgery, including mitral valve repair, and to determine whether surgery type affects the prevalence of post-operative pulmonary hypertension. METHODS: Matched preoperative and > or =1 year postoperative Doppler estimates of right ventricular systolic pressure (RVSP) were evaluated in a cohort of 179 patients who underwent MVR or repair (33 after bioprosthetic valve replacement, 20 after mechanical valve replacement, 43 after physiological valve repair (predominantly for myxomatous disease), 78 after undersized annuloplasty for functional regurgitation, and five after repair of rheumatic stenosis). RESULTS: Patients undergoing repair of function mitral regurgitation had a lower left ventricular ejection fraction. The postoperative mean transmitral gradient was slightly higher for patients after bioprosthetic valve replacement (6.9 +/- 2.6 mmHg) compared to mechanical valve replacement (5.2 +/- 2.8 mmHg; p = 0.03), physiological repair (5.2 +/- 2.8 mmHg; p = 0.05), or repair of functional regurgitation (5.5 +/- 2.8 mmHg; p = 0.02). Pulmonary hypertension was common (present in 78% of patients before and 64% after surgery), and there were no significant differences between groups in the prevalence of postoperative pulmonary hypertension. The RVSP tended to decrease in all groups, but reached statistical significance only for patients undergoing bioprosthetic replacement (-9 +/- 24 mmHg; p = 0.04), mechanical replacement (-10 +/- 14 mmHg; p = 0.003) or physiological repair (-6 +/- 16 mmHg; p = 0.01). CONCLUSION: Pulmonary hypertension is common before and after mitral valve surgery. Although there were at least trends toward lower pulmonary artery pressures regardless of surgery type, significant decreases were noted only after MVR and physiological repair. A slightly higher postoperative mean transmitral gradient after bioprosthetic valve replacement may have contributed to postoperative pulmonary hypertension. The physiological repair of organic, non-rheumatic mitral regurgitation appears to offer favorable hemodynamics and a relatively low rate of postoperative pulmonary hypertension.     

Mitralinsuffizienz

Mitral regurgitation is the second most frequent reason for valve surgery. The most important causes of mitral regurgitation are degenerative valve disease (mitral valve prolapse), left ventricular impairment and dilatation (in coronary artery disease or dilated cardiomyopathy), and infective endocarditis. The regurgitation of blood from the left ventricle into the left atrium leads to dilatation of the left atrium, increase in pulmonary capillary pressure and pulmonary congestion. In chronic severe mitral regurgitation, the left ventricle dilates and becomes impaired over time. Key symptoms are fatigue and dyspnea on exertion. The most prominent physical sign is the characteristic systolic murmur. Echocardiography identifies severity, delineates morphology, and estimates the impact of mitral regurgitation on left ventricular function. Importantly, echocardiography identifies candidates for mitral valve repair. Symptomatic patients and asymptomatic patients with impaired left ventricular function should be operated. If possible, valve repair is preferred over valve replacement to better preserve left ventricular function and to avoid the need for postoperative anticoagulation (except if atrial fibrillation persists).     

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.     

Mitral regurgitation

Mitral regurgitation is the second most frequent reason for valve surgery. The most important causes of mitral regurgitation are degenerative valve disease (mitral valve prolapse), left ventricular impairment and dilatation (in coronary artery disease or dilated cardiomyopathy), and infective endocarditis. The regurgitation of blood from the left ventricle into the left atrium leads to dilatation of the left atrium, increase in pulmonary capillary pressure and pulmonary congestion. In chronic severe mitral regurgitation, the left ventricle dilates and becomes impaired over time. Key symptoms are fatigue and dyspnea on exertion. The most prominent physical sign is the characteristic systolic murmur. Echocardiography identifies severity, delineates morphology, and estimates the impact of mitral regurgitation on left ventricular function. Importantly, echocardiography identifies candidates for mitral valve repair. Symptomatic patients and asymptomatic patients with impaired left ventricular function should be operated. If possible, valve repair is preferred over valve replacement to better preserve left ventricular function and to avoid the need for postoperative anticoagulation (except if atrial fibrillation persists).     

Continuity from normal to prolapsed mitral valves: two-dimensional and color Doppler echocardiographic investigations]

To investigate the continuity between the normal and prolapsed mitral valves (MVP), two-dimensional echocardiography (2DE) and color Doppler echocardiography (CDE) were performed in 508 healthy boys aged 12 to 13 years old. The distance from the plane of the mitral annulus to the coaptation of the mitral valve "c", the maximum distance between the anterior leaflet and a straight line connecting the anterior mitral annulus and the coaptation of the mitral valve "d", and the maximum distance between the posterior mitral leaflet and the straight line connecting the posterior mitral annulus and the coaptation of the mitral valve "e" were measured in the parasternal long-axis view. The locations of the anterior and posterior mitral annuli were determined to be the hing point of the anterior leaflet on the left ventricular side and the junction of the posterior leaflet on the ventricular side, respectively. Mitral regurgitation (MR) was evaluated by CDE in the parasternal long-axis view. The ratio of the duration of regurgitation to ejection time (DT/ET) was measured by M-mode CDE in the subjects with and without MVP. The values of "c" ranged from +10 mm to -3 mm, and those of "d" from +5 mm to -4 mm (minus denotes prolapse into the left atrium). Approximately normal distributions were demonstrated with the parameters "c" and "d". The value of "e" could not be measured because of a poor image of the posterior leaflet. The incidence of MVP varied from 2.5 to 13.5% depending on the criterion for applied MVP. Fifty-nine of the 487 healthy subjects turned out to have MR (12%). Coaptation of the mitral valve deviated from the posterior commissure significantly to the left atrium more in the subjects with MR than in those without MR (2.46 +/- 1.93 vs 3.41 +/- 1.84, p < 0.01). The DT/ET ratio of the MR subjects with MVP tended to be higher than that of the boys without MVP. The presence of continuity between the normal and prolapsed mitral valves suggests that MVP may be a multifactorial disorder of the valve. Associated asymptomatic MR may be related not only to the severity of MVP but also to other factors, especially in MR of normal healthy subjects.     

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.     

Factors determining early improvement in mitral regurgitation after aortic valve replacement for aortic valve stenosis: a transthoracic and transesophageal prospective study

BACKGROUND: Mitral regurgitation (MR) is frequently associated with aortic stenosis. Previous reports have shown that coexisting mitral insufficiency can potentially regress after aortic valve replacement. HYPOTHESIS: This study sought to assess the frequency and severity of MR before and after aortic valve replacement for aortic stenosis and to define the determinants of its postoperative evolution. METHODS: For this purpose, 30 adult patients referred for aortic valve surgery underwent pre- and postoperative transthoracic and transesophageal echocardiography and color Doppler examination. RESULTS: Mean preoperative left ventricular ejection fraction was 57 +/- 16% and remained unchanged postoperatively. Preoperative MR was usually mild to moderate and correlated with aortic stenosis severity and left ventricular systolic dysfunction. The color Doppler mitral regurgitant jet area significantly decreased during the postoperative period (p = 0.016) as left ventricular loading conditions returned to normal, suggesting an early decrease of the functional part of MR. On the other hand, the mitral regurgitant jet width at the origin remained unchanged. Statistical analysis found pulmonary artery pressure (p = 0.02) an d indexed left ventricular mass (p = 0.009) to be preoperative predictive factors of postoperative MR improvement. Predictive factors of postoperative MR severity were left atrial diameter (p = 0.02), pulmonary artery pressure (p = 0.003), and the presence of mitral calcifications (p = 0.004). CONCLUSION: In our cohort of patients with normal left venticular ejection fraction, the majority of moderate MR, associated with severe aortic stenosis, regresses early after aortic valve replacement. Mitral calcifications and/or left atrial dilation seem to be predictive factors of fixed MR.     

Angiocardiographic evaluation of the left ventricular function in adult and pediatric subjects with interatrial defect of the ostium secundum type]

In order to assess left ventricular function in adults and children with ostium secundum atrial septal defect (ASD), 42 patients were examined by hemodynamic and angiocardiographic techniques. Patients were divided into three groups: Group I, 18 patients (mean age 42 years) with ASD; Group II, 14 patients (mean age 9 years) with ASD; Group III, 10 patients without cardiopathies who represented the control group. The following parameters of ventricular function were assessed: left ventricular end diastolic volume, global and regional left ventricular ejection fraction, left ventricular telediastolic pressure, mean pulmonary artery pressure, the ratio between pulmonary flow and systemic flow (QP/QS). Group I patients showed higher values of left ventricular end diastolic pressure and mean pulmonary artery pressure (16 +/- 0.6 mmHg; 33 +/- 1.5 mmHg) in relation to those of Group II (5.1 +/- 0.4 mmHg; 14 +/- 1.4 mmHg) and Group III (8.1 +/- 0.5 mmHg; 18 +/- 1.6 mmHg). In both cases the difference was statistically significant (p less than 0.001). A significant difference (p less than 0.05) was also noted in the incidence of mitral valve prolapse between patients in Group I and II. There was no significant difference (p = NS) however, between overall ejection fraction values in the three groups of patients; a lower regional ejection fraction (postero-basal segment) was recorded in Group I patients with mitral valve prolapse in comparison to patients in the other two groups (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Assessment of Mitral Annulus Velocity by Doppler Tissue Imaging in the Evaluation of Left Ventricular Diastolic Function

Objectives. This study assessed the clinical utility of mitral annulus velocity in the evaluation of left ventricular diastolic function.Background. Mitral inflow velocity recorded by Doppler echocardiography has been widely used to evaluate left ventricular diastolic function but is affected by other factors. The mitral annulus velocity profile during diastole may provide additional information about left ventricular diastolic function.Methods. Mitral annulus velocity during diastole was measured by Doppler tissue imaging (DTI) 1) in 59 normal volunteers (group 1); 2) in 20 patients with a relaxation abnormality as assessed by Doppler mitral inflow variables (group 2) at baseline and after saline loading; 3) in 11 patients (group 3) with normal diastolic function before and after intravenous nitroglycerin infusion; and 4) in 38 consecutive patients (group 4) undergoing cardiac catheterization in whom mitral inflow velocity and tau as well as mitral annulus velocity were measured simultaneously.Results. In group 1, mean ± SD peak early and late diastolic mitral annulus velocity was 10.0 ± 1.3 and 9.5 ± 1.5 cm/s, respectively. In group 2, mitral inflow velocity profile changed toward the pseudonormalization pattern with saline loading (deceleration time 311 ± 84 ms before to 216 ± 40 ms after intervention, p < 0.001), whereas peak early diastolic mitral annulus velocity did not change significantly (5.3 ± 1.2 cm/s to 5.7 ± 1.4 cm/s, p = NS). In group 3, despite a significant change in mitral inflow velocity profile after nitroglycerin, peak early diastolic mitral annulus velocity did not change significantly (9.5 ± 2.2 cm/s to 9.2 ± 1.7 cm/s, p = NS). In group 4, peak early diastolic mitral annulus velocity (r = −0.56, p < 0.01) and the early/late ratio (r = −0.46, p < 0.01) correlated with tau. When the combination of normal mitral inflow variables with prolonged tau (≥50 ms) was classified as pseudonormalization, peak early diastolic mitral annulus velocity <8.5 cm/s and the early/late ratio <1 could identify the pseudonormalization with a sensitivity of 88% and specificity of 67%.Conclusions. Mitral annulus velocity determined by DTI is a relatively preload-independent variable in evaluating diastolic function.     

Mitral valve surgery utilizing homografts: early results

BACKGROUND AND AIM OF THE STUDY: Mitral valve repair is superior to prosthetic valve replacement due to preservation of the subvalvular apparatus. We used cryopreserved homografts for mitral valve replacement in selected cases, in whom valve repair would not have been successful. METHODS: Cryopreserved homografts were used in 10 patients (four males, six females; mean age 47 +/- 8 years; range: 27-65 years), for either complete (n = 7) or partial (n = 3) mitral valve replacement. Surgery was indicated due to acute endocarditis (n = 3), stenosis (n = 4) or combined mitral valve disease (n = 3). Transesophageal echocardiography (TEE) was performed to determine correct homograft size; these values were compared with intraoperative measurements of valvular dimensions. The function of the implanted grafts was examined intraoperatively by TEE. Follow up included clinical examination, electrocardiography and echocardiography. RESULTS: All patients survived surgery. Intraoperative TEE revealed mild insufficiency (grade I) in six cases and no insufficiency in four. The papillary muscle-mitral annulus distance was the most reliable preoperative echocardiographic parameter to determine the required homograft. Mean pressure gradients were 3.2 +/- 0.7 mmHg for complete and 2.4 +/- 0.5 mmHg for partial homograft replacement. Sinus rhythm was present in all cases at discharge. Mean follow up was 24 months (range: 6-36 months). At six-month and one-year follow up, the pressure gradients had risen slightly to 3.4 +/- 0.6 mmHg (complete) and 2.8 +/- 0.6 mmHg (partial). To date, four patients had competent grafts, and six presented with an insufficiency (grade I). All patients had normal left ventricular function (EF 65 +/- 6%) at their last follow up; there were no signs of endocarditis during the follow up period. CONCLUSION: Mitral homografts for valve replacement or repair are recommended in selected cases in whom conservative reconstruction techniques are not possible. The avoidance of long-term anticoagulation therapy and preservation of left ventricular geometry are clear advantages to other mitral valve prostheses.     

The Impact of Pulmonary Venous Hypertension on the Pulmonary Circulation in the Young

Objective and Design. Pulmonary venous hypertension is a well‐characterized cause of pulmonary hypertension in adults, but little is known regarding the relationship between left atrial pressure and pulmonary arteriolar resistance in the young. Also, in adults relief of pulmonary venous hypertension results in a marked fall in pulmonary arteriolar resistance, but this could be different in children because vascular changes are more severe in young patients than adults with mitral stenosis. We inspected records of children at Children's Hospital Boston having mitral balloon valvuloplasty, and patients ≤5 years old having mitral valve replacement, to determine (1) the relationship between left atrial pressure and pulmonary arterial pressure and resistance (n = 94 children, median age 17.8 months) and (2) how pulmonary arteriolar resistance changes after mitral valve replacement. Results. The average indexed pulmonary arteriolar resistance was 7.8 ± 5.9 units and was unrelated to age but was positively related to left atrial pressure. There was great variability in pulmonary arteriolar resistance for any given left atrial pressure. Pulmonary arterial pressure (n = 16) and pulmonary arterial resistance (n = 9) were measured before and after mitral valve replacement (median = 29.4 months old). Despite preoperative indexed pulmonary arterial resistance of ≥5 units in 11 of 15 patients, postoperative pulmonary arterial pressure was substantially lower in all save three, and two patients with high pulmonary arterial pressure still had high left atrial pressure postoperatively (25 mmHg). Conclusions. We conclude that in young children, as in adults, pulmonary arterial resistance generally falls greatly with reduction in left atrial pressure.     

The relationship of pulmonary artery wedge pressure to the posterior aortic wall echocardiogram in patients free of obstructive mitral valve disease

Aortic wall echocardiograms were obtained simultaneously with pulmonary artery wedge pressures (PAWP) in 21 patients free of obstructive mitral valve disease. There was a significant (p < 0.001) negative correlation between the fraction of passive posterior aortic wall motion occurring in the first third of diastole (the atrial emptying index-AEI) and the pulmonary artery wedge pressure (r = ?0.91). The AEI for patients with normal PAWP (≤ 12mm. Hg) was 0.94 ± 0.06 (mean ± S.D.) compared with 0.61 ± 0.20 for those with abnormal PAWP (> 12 mm. Hg). No patient with a normal PAWP had an AEI < 0.80, and no patient with a PAWP > 18 mm. Hg had an AEI > 0.66. These data suggest that analogous to the reported use of the AEI to estimate severity of mitral obstruction, the index provides a noninvasive measure of left ventricular filling pressure when the mitral valve is normal.     

Isolated chronic mitral regurgitation with preserved systolic left ventricular function and severe pulmonary hypertension

Pulmonary hypertension in chronic mitral valve disease has been related most commonly to left ventricular dysfunction or mitral stenosis; its association with chronic, isolated mitral regurgitation and preserved left ventricular systolic function is unclear. In 41 catheterized patients with chronic mitral regurgitation (known history of mitral regurgitation for greater than 18 months) and preserved left ventricular systolic function (ejection fraction greater than 0.55), historic, electrocardiographic, echocardiographic and hemodynamic variables were analyzed. Ten patients (Group I) had normal pulmonary artery systolic pressure (less than 30 mm Hg), whereas 31 patients had pulmonary hypertension. Pulmonary artery systolic pressure was mildly increased (30 to 49 mm Hg) in 13 patients (Group II) and was greater than or equal to 50 mm Hg in 18 patients (Group III). Univariate analysis showed the more frequent occurrence of male gender and ruptured chordae tendineae in the groups with pulmonary hypertension. Mean pulmonary capillary wedge pressure, size of the V wave in pulmonary capillary wedge pressure and pulmonary arteriole resistance were higher, whereas cardiac index was lower in the hypertension groups. Multivariate stepwise analysis revealed higher mean pulmonary capillary wedge pressure and pulmonary arteriole resistance as the only variables independently differing among groups. In conclusion, pulmonary hypertension occurs frequently (76% of cases) in patients with chronic, isolated mitral regurgitation with preserved left ventricular systolic function. In these patients, a severe increase in pulmonary capillary wedge pressure is associated with elevation in pulmonary artery resistance, a finding similar to that in mitral stenosis.     

Echocardiographic characteristics and causal mechanism of physiologic mitral regurgitation in young normal subjects

Background: It has become evident that mitral regurgitation (MR) is not uncommon in healthy subjects, and Doppler color flow mapping is a technique that imparts important information relevant to its detection. Hypothesis: Using transthoracic echocardiography, this study evaluated the mechanism of physiologic MR in young normal subjects using transthoracic echocardiography. Methods: The study population consisted of 48 young normal subjects (mean 21 ± 5 years) with MR (physiologic MR group), 40 age-matched young normal subjects (mean 20 ± 5 years) without MR (control group), 45 patients (mean 41 ± 15 years) with mitral valve prolapse with MR (MVP group), and 27 patients (mean 59 ± 13 years) with ruptured chordae tendineae (rupture group). Results: Men were predominant in the rupture group, whereas there were no significant gender differences in the other three groups. Left ventricular end-diastolic dimension and left atrial systolic dimension were slightly smaller in the physiologic MR group than in the control group, but were significantly smaller than those in the MVP and rupture groups. The ratio of the maximum anteroposterior diameter to the maximum transverse diameter on chest radiography and the ratio of the short- to long-axis diameter of the left ventricular cavity at end diastole, determined from two-dimensional short-axis echocardiogram, were significantly lower in the physiologic MR group than in the other three groups. Mitral regurgitation occurred more frequently at the posteromedial commissural site in the physiologic MR and MVP groups, whereas there was no preference for location in the rupture group. Early systolic MR was often observed in the physiologic MR group, whereas pansystolic MR was common in the MVP and rupture groups. Conclusion: As a causal mechanism for physiologic MR detected in young normal subjects, “flattening” of the thorax during growth may cause morphologic abnormalities of the left atrial and ventricular cavities, resulting in spatial imbalance of the mitral complex and resulting in malcoaptation of the valve.