Comparison of ventricular septal surgery and mitral valve replacement for hypertrophic obstructive cardiomyopathy.

We have reviewed the results of two different forms of surgical management of hypertrophic obstructive cardiomyopathy refractory to medical therapy. Twenty-one patients were treated with 22 procedures between 1963 and 1987. Eleven underwent a ventricular septal procedure by myotomy with or without myectomy, and 11 underwent mitral valve replacement (MVR), 1 of whom had previously undergone a ventricular septal procedure. The groups were comparable with respect to severity and duration of symptoms, age range, electrocardiographic features, and hemodynamic changes. Mitral valve replacement produced a greater and more consistent reduction in the left ventricular outflow tract pressure gradient than a ventricular septal procedure (MVR, 68.3 mm Hg preoperatively and 2.5 mm Hg postoperatively; ventricular septal procedure, 60.1 mm Hg preoperatively and 13.4 mm Hg postoperatively). This was associated with better postoperative ventricular configuration in diastole and more apparent loss of midcavity narrowing in systole. Ejection fraction did not fall after a ventricular septal procedure but decreased significantly from a mean of 79% to a mean of 61% after MVR. Similarly, left ventricular end-diastolic pressure remained unchanged after a ventricular septal procedure but fell from a mean of 26.6 mm Hg to 17 mm Hg after MVR. Although both groups experienced a generally satisfactory symptomatic result, this appeared more reliable with MVR. We suggest that MVR offers a more predictable improvement than a ventricular septal procedure and may be the procedure of choice for units with limited experience with ventricular septal procedures.

DNA restriction fragment length polymorphisms as markers of familial coronary heart disease.

246 of 713 men aged 30 to 59 years had first-degree relatives who had had coronary heart disease (CHD) by the age of 60; men with a family history of CHD were twice as likely to have CHD themselves, compared with those without such a family history. At least 75% of the difference was accounted for by CHD in men with minor alleles of 4 restriction fragment length polymorphisms (RFLPs) in the region of the apolipoprotein (apo) AI and apo CIII genes. The RFLPs were identified with the restriction enzymes XmnI, PstI, MspI, and SacI. Each polymorphism has two alleles (major and minor), designated X1 and X2, P1 and P2, M1 and M2, and S1 and S2, respectively. In men with any one of the minor alleles, a family history of CHD was associated with a 234% increase in CHD prevalence. In men with major alleles only, a family history of CHD was not associated with any significant increase in CHD. The effect of the minor alleles was not significantly altered when plasma lipids and other variables except for age were taken into account. The association between the minor RFLP alleles and polymorphic gene variants (probably the apo AI, apo CIII, or both genes) which enhance liability to CHD accounted for almost 20% of total CHD in this population.

Left atrial volume changes in mitral valve disease: a cross-sectional echocardiographic study.

We used cross-sectional echocardiography to study left atrial volume changes in 25 patients with mitral valve disease who underwent cardiac catheterisation. Satisfactory 4 chamber views were obtained in 21. Left atrial systolic overload measured as systolic expansion index did not correlate with the severity of mitral regurgitation as assessed by contrast ventriculography and indicator dilution. The left atrial systolic expansion rate, and the maximum volume increase during the first third of systole, measured as the early systolic expansion index, differentiated well between moderate and severe mitral regurgitation, but not between trivial and moderate regurgitation. Calculation of the early systolic expansion fraction (fraction of total expansion occurring in the first third of systole) gave the best correlation with the degree of mitral regurgitation estimated by other methods.

A prospective evaluation of the Björk-Shiley, Hancock, and Carpentier-Edwards heart valve prostheses.

From 1975 to 1979, 540 patients undergoing valve replacement were entered into a randomized trial and received either a Björk-Shiley (273 patients) or a porcine heterograft prosthesis (initially a Hancock valve [107 patients] and later a Carpentier-Edwards prosthesis [160 patients]). Two hundred and sixty-two patients required mitral valve replacement, 210 required aortic valve replacement, 60 required mitral and aortic valve replacement, and eight also required associated tricuspid valve replacement (six mitral valve replacement; two mitral plus aortic valve replacement). Analysis of 34 preoperative and operative variables showed the treatment groups to be well randomized. In-hospital mortality was not significantly different among patients receiving the three prostheses for aortic valve replacement (7.6% overall) and mitral plus aortic valve replacement (10% overall), but there was a higher in-hospital mortality for patients undergoing mitral valve replacement with the Carpentier-Edwards prosthesis (15.5% compared with 8.8% overall; p = .03). This difference could not be explained on the basis of any preoperative or operative variable. Median follow-up was 5.6 (range 2.8 to 8.3) years. Actuarial survival after mitral valve replacement was 56.7 +/- 7.0% at 7 years, that after aortic valve replacement was 69.6 +/- 9.6% at 7 years, and that after mitral plus aortic valve replacement was 62.5 +/- 20.0% at 7 years. There was no significant difference in actuarial survival of patients receiving the three prostheses within the mitral, aortic, and mitral plus aortic valve replacement groups, nor was there a difference when these groups were amalgamated. Thirty-seven patients required reoperation for valve failure (15 with Björk-Shiley, 12 with Hancock, and 10 with Carpentier-Edwards valves; p = NS) and 11 died at reoperation (four with Björk-Shiley, four with Hancock, and three with Carpentier-Edwards valves; overall operative mortality 29.7%). Up to 7 years after surgery, there was no significant difference in the incidence of thromboembolism in patients with different prostheses undergoing mitral or aortic valve replacement. There were too few patients undergoing mitral plus aortic valve replacement for meaningful comparison. There was no significant beneficial effect of anticoagulants in patients undergoing mitral or aortic valve replacement with porcine prostheses, but patients were not randomly allocated to anticoagulant treatment. All patients with Björk-Shiley prostheses received anticoagulants.(ABSTRACT TRUNCATED AT 400 WORDS)

Subclinical chronic Q fever.

Seven patients are described in whom chronic Q fever was detected by serology (Coxiella burneti phase I antibody titre greater than 1:200) during routine screening at admission for cardiac catheterisation. None had clinical evidence of endocarditis, hepatitis or other foci of infection. Three of the patients were kept under observation without antibiotic treatment for periods of six, 18 and 20 months. In two patients of this group, cardiac tissue was obtained at operation and in one patient seroconversion following guinea-pig inoculation indicated the presence of Coxiella burneti infection. Four patients were given antibiotic treatment when Q fever was confirmed by serology. Courses of antibiotic treatment with a combination of two drugs were maintained for four to six years and in three of these patients phase I antibody titres fell to very low levels with no appearance of overt infection. The fourth patient died after resection of an aortic aneurysm, seven months after starting antibiotic treatment. Cases reported in the literature indicate that while endocarditis is the most common manifestation of chronic Q fever, the infection can persist at other sites. Of the seven cases of subclinical chronic Q fever reported here, the infection was localised in only one. Patients with this subclinical form of infection pose the therapeutic dilemma of whether or not they should receive antibiotic treatment.

Persistence of ductus arteriosus with left to right shunt in the older patient.

Eight hundred and four patients with persistence of the ductus arteriosus were seen in Edinburgh between 1940 and 1979. Thirty-seven of them reached the age of 50 years, and in 32 the shunt was exclusively from left to right. Fifteen of the 32 were subsequently treated surgically. None of the 32 was lost to follow-up. Duration of clinical observation averaged 17 years and extended to over 30 years in eight patients. Their features have been correlated with those from reports of 48 comparable patients in an attempt to clarify the management of the persistent ductus in the older patient. Impairment of left ventricular function is shown as the major risk, even when the ductus is small. Bacterial endarteritis is infrequent. Surgical treatment carries greater risk than in childhood and early adult life but usually reduces heart size and restores exercise tolerance. Left ventricular dysfunction, however, occasionally vitiates the benefits; symptoms are then incompletely relieved and death from heart failure may occur months or years after operation. Experience in older patients thus emphasises the value of elective operation in childhood, however well the child, however trivial the shunt. It is concluded that in older patients, the presence or the development of symptoms or cardiac enlargement are almost always indications for surgical treatment. As age increases, especially by the eighth decade, medical treatment may be preferable. Continued follow-up of symptomless patients without cardiomegaly is important because increase in heart size usually precedes further deterioration which can then be prevented by timely surgical treatment.

Pulmonary hypertension and fenfluramine.

Pulmonary hypertension developed in two women who had been taking fenfluramine for over eight months for weight reduction. On withdrawing the drug symptoms and electrocardiographic evidence of pulmonary hypertension disappeared in both cases. In one patient, however, the evidence recurred after rechallenge with fenfluramine.These findings are strong evidence that fenfluramine may cause pulmonary hypertension. Hence any patient taking the drug should report immediately any deterioration in exercise tolerance.

An analogue computer for pressure-time measurements in valvular heart disease.

Accurate measurement of pressure differences across a diseased heart valve involves either laborious planimetry or elaborate digital computing facilities. An analogue device is described, simple and inexpensive to construct, which derives from the recorder input of two pressure signals the time (seconds/minute) of valve opening and the mean pressure difference during this time. Measurements may be repeated over long periods. The importance of using pressure differences as compared with peak or end diastolic gradients is noted; serious errors in assessment of valvular disease may otherwise occur.

The management of ventricular septal rupture following myocardial infarction.

Twenty-six patients were treated for ventricular septal rupture following myocardial infarction over a five year period. Twenty-three patients underwent full haemodynamic investigation with a view to surgery and nineteen underwent operative closure of the defect. Overall hospital mortality was 47 per cent in the surgical group. Eleven patients had surgery within two weeks of infarction because of marked haemodynamic deterioration soon after septal rupture but only two survived to leave hospital. Eight patients underwent operation two weeks or longer after infaction, all were alive and well at discharge from hospital, six were well at one year and four at three years. Seven patients did not undergo surgery and the maximum survival for these was eight months. No patient in cardiogenic shock before septal rupture benefited from repair. Rapid clinical deterioration following rupture carried a poor prognosis. In all the shunt was large and medical treatment was ineffective. It is concluded that early surgical repair should be considered except when cardiogenic shock antedates the septal rupture.

Regression of multiple pulmonary varices after mitral valve replacement.

A 30-year-old woman with severe mitral insufficiency had large, rounded opacities at the right hilus as seen on her chest x-ray film. These were shown to be varicosities of the right pulmonary veins by pulmonary angiography and by direct injection of contrast medium from a Brockenbrough catheter, which entered the varices from the left atrium. A year after mitral valve replacement there was complete regression of the venous dilatations. When a pulmonary varix is detected there is associated heart disease in 40% of cases. Mitral valve disease (usually mitral insufficiency) is the cardiac abnormality in 27%. This would indicate that pulmonary varix is a complication of mitral insufficiency. Four patients who have undergone valve replacement for mitral reflux have shown regression of the caricosities, suggesting that relief of mitral insufficiency will reduce or eliminate the risk of varix rupture.

Prognosis of patients with acute myocardial infarction admitted to a coronary care unit. I: Survival in hospital.

On a basis of history, clinical examination, and the electrocardiogram it was possible to identify groups of patients with acute myocardial infarction with good and bad prognoses as regards hospital survival. Individual adverse factors were age, prevous history of ischaemic heart disease, anterior infarction, persistent sinus tachycardia, pulmonary crepitations, hypotension, and raised venous pressure. Multivariate analysis showed four factors remaining significant--age, tachycardia, hypotension, and pulmonary crepitations. As a result of treatment of cardiac arrest, hospital mortality, which would otherwise have been 20 percent, was 17 percent. Preceding unstable angina did not worsen the immediate prognosis.

Prognosis of patients with acute myocardial infarction admitted to a coronary care unit. II. Survival after hospital discharge.

The factors adversely affecting long-term prognosis differed from those affecting outcome of acute infarction. Individual factors were previous history of infarction or hypertension, tachycardia, cardiac arrest, ventricular arrhythmia, atrial fibrillation, 3rd heart sound, raised venous pressure, and pulmonary crepitations. Multivariate analysis reduced these to 6--previous infarct or hypertension, sinus tachycardia, cardiac arrest, ventricular arrhythmia, and artial fibrillation. Of those who survived 5 years, approximately half had angina. Two-thirds of the under 60 survivors were at their normal work.

Longitudinal survey of ischaemic heart disease in randomly selected sample of older population.

A group of 215 men and 272 women aged 62 to 90 forming a randomly-selected sample of the older population was studied by cardiovascular survey methods and followed for 5 years. The 5-year mortality of 28 per cent was related to age and was higher in men. Ischaemic heart disease was the certified cause of 28 per cent of the deaths. Mortality was greater in those with systolic hypertension. Among electrocardiographic features ST depression, T inversion, and atrial fibrillation increased overall and ischaemic heart disease mortality independently of their association with age. A positive response to an angina and infarct questionnaire was poorly related to subsequent mortality. Re-examination of 72 per cent of 5-year survivors was possible. Systolic and diastolic blood pressures were significantly lower and the frequency of electrocardiographic abnormalities, particularly left axis deviation, left ventricular hypertrophy, and ST and T wave changes, was increased.