Extreme pulmonary hypertension caused by mitral valve disease. Natural history and results of surgery.
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Five hundred and eighty six patients with mitral valve disease were studied with cardiac catheterization between 1961 and 1972; 48 (8.2%) had extreme pulmonary hypertension (resting systolic pulmonary artery pressure of 80 mmHg or above and pulmonary vascular resistance of 10 units or greater) and of these patients, 27 underwent cardiac surgery. The operative mortality for mitral valvotomy was 11 per cent and for mitral valve replacement 56 per cent. The overall mortality was 31 per cent. The risks of operation were increased in those with a long history of cardiac symptoms, those over 50 years of age, and in the presence of associated aortic valve disease. The mean survival for those patients not having operation was only 2.4 plus or minus 0.5 years. The mean follow-up period for those surviving operation has been 5.8 plus or minus 0.6 years, and symptomatic improvement has been good. (+info)
Mitral regurgitation in hypertrophic obstructive cardiomyopathy: relationship to obstruction and relief with myectomy.
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OBJECTIVES: This study examined: 1) the impact of myectomy on postoperative mitral regurgitation (MR) and 2) the association between the severity of MR and the left ventricular outflow tract (LVOT) gradient. BACKGROUND: For patients with hypertrophic obstructive cardiomyopathy (HOCM) and MR, controversy exists as to whether myectomy alone is sufficient in eliminating MR. Furthermore, the relationship between the degree of MR and the LVOT peak gradient has not been well defined. METHODS: We performed pre- and postoperative transthoracic as well as intraoperative transesophageal studies in 104 consecutive patients with HOCM undergoing septal myectomy. Left ventricular outflow tract gradient and the nature of MR were assessed. RESULTS: In the 93 patients without independent mitral valve disease, a relationship was observed between MR severity and the LVOT gradient. Left ventricular outflow tract gradient (mean +/- standard deviation) for trivial, mild, moderate and severe MR were: 23.2+/-19.1, 43.8+/-25.4, 70.1+/-21.0 and 104+/-21.0 mm Hg (p < 0.001). Early postoperative, MR was absent or trivial in 80%, mild in 19% and moderate in 1%. None of these patients required additional mitral valve surgery. For patients with independent mitral valve disease (n = 11), five required mitral valve surgery as well as myectomy. The remainder had significant reductions in the degree of MR with myectomy alone. CONCLUSIONS: For patients with HOCM and MR not due to independent mitral valve disease, myectomy significantly reduced the degree of MR, without requirement for additional mitral valve surgery. In these patients the severity of MR was directly related to the magnitude of the LVOT gradient. (+info)
Effect of mitral valve surgery on exercise capacity, ventricular ejection fraction and neurohormonal activation in patients with severe mitral regurgitation.
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OBJECTIVES: The purpose of this study was to prospectively investigate the effects of surgical correction of mitral regurgitation (MR) on exercise performance, cardiac function and neurohormonal activation. BACKGROUND: Little is known about the effect of surgical correction of MR on functional status or on neurohormonal activation. METHODS: Cardiopulmonary exercise test, radionuclide angiography and blood samples for assessment of neurohormonal status were obtained in 40 patients with nonischemic MR before and within one year (216+/-80 days) after surgery. Twenty-four patients underwent mitral valve repair (MVr), and 16 underwent valve replacement (VR) with anterior chordal transection. RESULTS: Despite an improvement in New York Heart Association functional class, exercise performance did not change (peak oxygen consumption: 19.3+/-6.1 to 18.5+/-5.6 ml/kg/min, percentage of maximal predicted oxygen consumption: 79.5+/-18.2% to 76.8+/-16.9%). After surgery, left ventricular (LV) ejection fraction (EF) decreased (64.2+/-10.3% to 59.9+/-11.4%, p = 0.003) while right ventricular (RV) EF increased (41.4+/-9.6% to 44.7+/-9.5%, p = 0.03). Left ventricular EF did not change after MVr (64.3+/-11.5% to 61.5+/-12.2%), but RVEF improved (40.4+/-9.2% to 46.0+/-10.0%, p = 0.02). In contrast, VR was associated with an impairment of LV function in the apicolateral area and a decrease in LVEF (64.1+/-8.5% to 57.4+/-10.0%, p = 0.01), whereas RVEF did not change (42.9+/-10.3% to 42.8+/-8.6%). Moreover, there was only a slight decrease in neurohormonal activation after surgery. CONCLUSIONS: Despite an improvement in symptomatic status, exercise performance was not improved seven months after either MVr or VR for MR, and neurohormonal activation persisted. Compared with MVr, VR resulted in a significant impairment of cardiac function in this study. (+info)
The pathogenesis of acute pulmonary edema associated with hypertension.
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BACKGROUND: Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (> or =0.50). However, the pulmonary edema may not have resulted from isolated diastolic dysfunction but, instead, may be due to transient systolic dysfunction, acute mitral regurgitation, or both. METHODS: We studied 38 patients (14 men and 24 women; mean [+/-SD] age, 67+/-13 years) with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg. We evaluated the ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and one to three days after treatment. RESULTS: The mean systolic blood pressure was 200+/-26 mm Hg during the initial echocardiographic examination and was reduced to 139+/-17 mm Hg (P< 0.01) at the time of the follow-up examination. Despite the marked difference in blood pressure, the ejection fraction was similar during the acute episode (0.50+/-0.15) and after treatment (0.50+/-0.13). The left ventricular regional wall-motion index (the mean value for 16 segments) was also the same during the acute episode (1.6+/-0.6) and after treatment (1.6+/-0.6). No patient had severe mitral regurgitation during the acute episode. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment. In 16 of these 18 patients, the ejection fraction was at least 0.50 during the acute episode. CONCLUSIONS: In patients with hypertensive pulmonary edema, a normal ejection fraction after treatment suggests that the edema was due to the exacerbation of diastolic dysfunction by hypertension--not to transient systolic dysfunction or mitral regurgitation. (+info)
Left ventricular mechanics during and after acute rheumatic fever: contractile dysfunction is closely related to valve regurgitation.
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OBJECTIVES: The purpose of this study was to characterize left ventricular (LV) mechanics during acute rheumatic fever (ARF) and to define factors influencing remodeling after the acute event. BACKGROUND: Acute rheumatic fever is associated with varying degrees of valvulitis and myocarditis, but the impact of these factors on LV mechanics is poorly defined. METHODS: Echocardiograms and clinical data were reviewed in 55 patients aged 11.2 +/- 2.6 years during ARF. Valve regurgitation was absent or mild in 33 (group I) and moderate or severe in 22 (group II). Forty-two children (75%) underwent a further examination after ARF. RESULTS: Group I patients demonstrated a mildly elevated LV size during ARF and had normal indexes at follow-up. Group II patients demonstrated a markedly elevated LV size (end-diastolic dimension z-score 3.6 +/- 1.8, p < 0.01 compared with the normal population) and decreased shortening fraction (z-score -0.8 +/- 1.4, p < 0.05). The stress-velocity index, a z-score describing the velocity of shortening-afterload relationship, was normal in group II patients with mitral regurgitation (-0.2 +/- 1.2, p = NS) but was depressed in those with aortic regurgitation or both (- 1.4 +/- 1.4, p < 0.01). At follow-up the stress-velocity index remained depressed (-1.2 +/- 1.0, p < 0.01) and had deteriorated in those treated nonsurgically compared with those treated surgically (interval change nonsurgical -0.7 +/- 1.2 vs. surgical 1.3 +/- 1.3, p = 0.005). CONCLUSIONS: The evolution of contractile dysfunction during and after ARF is dependent on the degree and type of valve regurgitation and may be influenced by surgical intervention. These findings suggest that mechanical factors are the most important contributors to myocardial damage during and after ARF. (+info)
Optimization of atrioventricular delay and follow-up in a patient with congestive heart failure with an implanted DDD pacemaker: case report.
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It has been reported that cardiac function can be improved by implanting a DDD pacemaker (PM) and setting a short atrioventricular (AV) delay in patients with impaired cardiac function. A previous report found that the critical AV delay that induces diastolic mitral regurgitation (MR) may represent the upper limit of the optimal AV delay. The optimal AV delay can be predicted by a simple method: slightly prolonged AV delay minus the interval between the end of the atrial kick and complete closure of the mitral valve (duration of diastolic MR) at the AV delay setting. The patient was a 84-year-old man with an old myocardial infarction. He had repeated admissions to hospital for congestive heart failure. ECG showed prolongation of the PQ interval (0.28 s) and complete left bundle branch block. Cardiac function was improved by AV sequential pacing when the AV delay was set at 120ms. After DDD-PM implantation, the cardiothoracic ratio decreased from 57 to 45% and cardiac function was improved from New York Heart Association class III to I. The AV delay was optimized during follow-up. Four years after PM implantation, the patient was in good condition without further hospital admission. (+info)
Natural history of cardiovascular manifestations in Marfan syndrome.
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AIMS: To investigate the natural history of mitral valve and aortic abnormalities in patients with Marfan syndrome during childhood and adolescence. METHODS: Fifty two patients with Marfan syndrome were followed for a mean of 7.9 years. Occurrence of adverse cardiovascular outcomes was measured clinically and by ultrasound examination. RESULTS: Mitral valve prolapse (MVP) was diagnosed in 46 patients at a mean age of 9.7 years, more than 80% of whom presented as "silent MVP". Mitral regurgitation (MR) occurred in 25 patients, aortic dilatation in 43, and aortic regurgitation (AR) in 13. Both MVP and aortic dilatation developed at a constant rate during the age period 5-20 years. In 23 patients MVP was diagnosed before aortic dilatation, in 18 the reverse occurred, and in 11 patients the two abnormalities were diagnosed simultaneously. During follow up, 21 patients showed progression of mitral valve dysfunction; progression of aortic abnormalities occurred in 13. Aortic surgery was performed in 10; two died of subsequent complications. Mitral valve surgery was performed in six. In sporadic female Marfan patients the age at initial diagnosis of MVP, MR, aortic dilatation, and AR was lowest, the grade of MR and AR most severe, the time lapse between the occurrence of MVP and subsequent MR as well as between dilatation and subsequent AR shortest, and the risk for cardiovascular associated morbidity and mortality highest. CONCLUSIONS: During childhood and adolescence in Marfan syndrome, mitral valve dysfunction as well as aortic abnormalities develop and progress gradually, often without symptoms, but may cause considerable morbidity and mortality by the end of the second decade, especially in female sporadic patients. (+info)
Echocardiographic evaluation of the fetus with congenital cystic adenomatoid malformation.
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OBJECTIVES: The development of nonimmune hydrops is a known complication of congenital cystic adenomatoid malformation (CCAM) in the fetus. The aim of this study was to investigate the impact of CCAM on hemodynamics in the fetus and to determine whether cardiac dysfunction contributes to the development of hydrops in this patient population. METHODS: The echocardiographic data from 41 consecutive fetuses diagnosed prenatally with CCAM were reviewed. The presence or absence of hydrops was noted in each patient. Two-dimensional ultrasonographic and Doppler data were compared between the two groups (with or without hydrops). RESULTS: The mean gestational age for the study group at the time of imaging was 23.2 +/- 3.0 weeks. Hydrops was noted in 15 of 41 fetuses (36.5%). The fetuses that developed hydrops had a lower cardiac/thoracic ratio than those which did not develop hydrops (0.18 vs. 0.23, P = 0.001). The fetuses with hydrops also demonstrated an increase in early ventricular filling. The ratio of early ventricular filling to atrial contraction (E/A ratio) at both the tricuspid and mitral valves was significantly higher in the fetuses with hydrops (P = 0.005 and P = 0.03, respectively). Doppler interrogation of the inferior vena cava demonstrated a greater degree of reversal with atrial contraction in the hydrops group (29.7% vs. 15.1%, P = 0.003). The development of significant atrioventricular valve insufficiency was rare in the fetuses with hydrops (one of 15 cases). CONCLUSIONS: Cystic adenomatoid malformation can result in significant cardiac compression in the fetus. This alters hemodynamics and may result in hydrops on the basis of elevated central venous pressure. (+info)