Search

It is a pleasure for me to introduce this Heart supplement, commissioned by the British Cardiovascular Intervention Society (BCIS), and generously funded by the BCIS industry partner, the British Cardiovascular Industry Association (BCIA). Under the guidance of BCIS, developments in percutaneous coronary intervention (PCI) in the UK are progressing at an exciting rate. Increasing PCI activity with an annual growth rate of 15–20% has been coupled with the enthusiastic uptake of new technology. As I write, the use of drug eluting stents in the UK is one of the highest in Europe, …

This study was performed to assess whether angiography six months after coronary balloon angioplasty or stent implantation has an influence on clinical management and one-year outcome.The Benestent II study randomized 827 patients to balloon angioplasty or stent implantation. A subrandomization was undertaken allocating patients to six-month clinical follow-up (CF) or clinical and angiographic follow-up (AF).Seven hundred and six patients (349 CF and 357 AF) had no intercurrent angiography, so that restenosis and disease progression elsewhere remained unknown until the time of six-month follow-up. These two groups, which were well matched at enrolment, were compared with respect to symptoms, medication and major cardiac events defined as death, myocardial infarction and need for revascularization at six and 12 months.At six-month follow-up, 53 (15%) of the CF and 76 (21%) of the AF patients had stable angina (p = 0.041), while 5 (1%) and 4 (1%) had symptoms of unstable angina. At 12-month follow-up, 44 (13%) patients in both groups had stable angina, and only 1 patient in the CF group had unstable angina. Seventy-seven patients (27 CF and 50 AF; p0.01) had major cardiac events between 6 and 12 months. Of the 349 patients in the CF group, 21 underwent repeat percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery between 6 and 12 months, compared with 44 of the 357 patients in the AF group (relative risk 2.05 [1.24 to 3.37], p = 0.003).Patients who had AF six months after balloon angioplasty or stent implantation experienced more repeat revascularization procedures than those who had CF. They also had significantly more angina at six-month follow-up but this may be due to bias.

To assess the longer term outlook for patients who have undergone surgery for acquired (postinfarction) ventricular septal defect, we interviewed and studied 60 survivors from a single regional cardiac center between 3 and 144 months after the operation. Including the patients who died within 1 month of the operation, the 5-, 10-, and 14-year survivals (with standard errors) were 69% (65% to 74%), 50% (44% to 57%), and 37% (27% to 46%). Eighty-two percent of patients were in New York Heart Association class I or II. Ten patients (17%) had a persisting but not hemodynamically significant ventricular septal defect. Mean left ventricular ejection fraction was reduced at 0.39 (standard deviation 0.15), but this did not correlate with either New York Heart Association class or exercise tolerance. Twenty-eight patients (47%) had asymptomatic arrhythmias (17 with ventricular premature beats). Angina and other medical problems were not prevalent.

A total of 101 patients (mean age 64.9 years) underwent surgical correction of postinfarction ventricular septal defect at this institution over a 15-year period (1973 to 1988). The overall early mortality rate was 20.8%, although the most recent experience with 36 patients (January 1987 to October 1988) has seen this decline to 11.1%. Factors found to influence early death significantly, when analyzed univariately, were as follows: (1) site of infarction (anterior 12.1%, inferior 32.6%, p = 0.02); (2) time interval between infarction and operation (less than 1 week 34.1%, greater than 1 week 10.5%, p = 0.008); (3) cardiogenic shock (present 38.1%, absent 8.5%, p = 0.001). Nonsignificant variables included preoperative renal function, age, and concomitant coronary artery bypass, although older age (greater than 65 years) became significant when examined in a multivariate fashion. Of the 80 hospital survivors, eight were subsequently found to have a recurrent or residual defect necessitating reoperation, with survival in seven. Late follow-up is 99% complete and reveals an actuarial survival rate for 100 patients of 71.1% at 5 years (95% confidence interval 60.6 to 80.0), and 40.0% at 10 years (95% confidence interval 21.7 to 58.4). A significant recent change in policy of not using coronary angiography in patients with a ventricular septal defect caused by anterior wall infarction has not resulted in any increase in either the early mortality or in the late prevalence of angina. The functional status of 38 surviving patients has been analyzed by a graded treadmill exercise protocol, whereas left ventricular functional assessment was by nuclear scan with additional information on mitral valve function by echocardiogram. Color Doppler flow mapping has been used to determine the presence of a residual defect. Most late survivors have limited exercise tolerance related to both cardiac and noncardiac factors. Left ventricular function is moderately impaired (mean ejection fraction = 0.39). However, many patients are elderly and have adapted to their residual symptoms without significant changes in life-style.

In order to determine the significance of abnormalities of diastolic function in patients with left ventricular hypertrophy, exercise echocardiography to heart rates of 140 to 150 beats/min was performed in 18 normal subjects and 14 patients after aortic valve replacement. Simultaneous echo-, phono-, and electrocardiograms were recorded. Left ventricular cavity size was determined at end-diastole and end-systole. The timing of mitral valve opening and closure was measured, and hence left ventricular filling time derived, expressed either as ms/beat, or s/min when multiplied by heart rate. Isovolumic relaxation was taken as the interval between A2 and mitral valve opening. Systolic function, assessed from cavity dimensions, peak VCF, and QA2 interval was normal in all but two patients at rest and on exercise. Isovolumic relaxation was prolonged at rest in the patients to 85 +/- 8 ms (normal 69 +/- 9 ms), but left ventricular filling times were normal. With exercise, in normal subjects, isovolumic relaxation remained constant, but filling times dropped strikingly from 380 +/- 66 ms/beat, or 27 +/- 2 s/min at rest to 115 +/- 10 ms/beat or 16 +/- 2 s/min. In patients with left ventricular hypertrophy, isovolumic relaxation dropped on exercise to 41 +/- 15 ms. Filling periods were normal at rest, 367 +/- 67 ms/beat or 27 +/- 3 s/min, but failed to show the normal drop with exercise, being 240 +/- 44 ms/beat or 28 +/- 4 s/min. At heart rates above 120/min, separation between the two groups was complete. Thus, striking abnormalities of left ventricular filling can be demonstrated on exercise in patients with left ventricular hypertrophy. They appear to represent loss of mechanisms whereby rapid diastolic filling is achieved in the normal subject.

Digitised M mode echocardiograms were analysed in 22 patients with possible Björk-Shiley mitral prosthetic dysfunction. Patients with paraprosthetic mitral regurgitation had a significantly greater shortening fraction, an increased peak rate of dimension change during systole, and an increased peak velocity of circumferential fibre shortening than those with poor left ventricular function. Patients with a clotted prosthesis had lower values for shortening fraction and peak rate of dimension change during systole than patients with paraprosthetic regurgitation. In this latter group, the peak rate of dimension change during diastole and peak lengthening rate were greater than in either those patients with poor left ventricular function or those with a clotted prosthesis. In addition, the peak lengthening rate was greater in those with a clotted prosthesis than in those with poor left ventricular function. Thus M mode echocardiography is a useful method of assessing mitral prosthetic dysfunction and allows patients with paraprosthetic regurgitation to be distinguished from those with either poor left ventricular function or a clotted prosthesis.

Between 1970 and 1981, 12% of patients undergoing mitral valve surgery were found to have chordal rupture. Spontaneous or primary rupture accounted for 74.6% of patients (primary group); in the remainder (secondary group) chordal rupture complicated chronic rheumatic valvular disease (8.9%), bacterial endocarditis on both normal (8.5%) and rheumatic valves (4.7%), ischaemic heart disease (2.3%), acute rheumatic fever (0.5%), and osteogenesis imperfecta (0.5%). Isolated posterior rupture was seen most frequently (54%), with anterior rupture in 36% and rupture of both mitral cusps in 10% of patients. A short symptomatic history of acute mitral regurgitation was rare, occurring in only 4% of patients in either the primary or secondary groups, suggesting that mitral regurgitation due to ruptured chordae is a progressive disease. In contrast to previous reports the clinical presentation did not help to differentiate the aetiology of the chordal rupture.

Twelve patients fulfilling strict criteria for chronic obstructive bronchitis recorded serial peak expiratory flow rates (PEFR) five times daily for a two-week period. Despite a 9.2% improvement in forced expiratory volume in one second (FEV1) with ipratropium bromide, and an 11.3% improvement with ipratropium bromide plus salbutamol, the inherent diurnal variation in PEFR while on no medication was greater than the improvement caused by either bronchodilator. In the group as a whole, the difference between the highest and the lowest daily PEFR over the two weeks was 24% of the mean daily value. Using cosinor analysis, 10 of the 12 patients showed a significant rhythm in PEFR with a computed mean amplitude between highest and lowest readings of 8.6% of the mean daily value. This is no greater than that found in normal subjects, but is considerably less than the variation in PEFR in patients with bronchial asthma.

During the period 1970-81, 183 patients underwent mitral valve surgery for chordal rupture. Of these, 82 (45%) patients were treated by mitral valve repair and 101 (55%) by mitral valve replacement. Mean age at surgery was 57 years. The early mortality was nine of 183 (4.9%) patients, of whom five had undergone replacement and four repair. During the follow up period (mean 3.6 years, range 0.8-12.2 years) a further 27 patients died; 23 of these had undergone mitral valve replacement and four mitral valve repair. Cerebrovascular events accounted for 35% of the deaths after mitral valve replacement and none of those after mitral valve repair. In 11 patients repair was technically unsatisfactory, and mitral valve replacement was undertaken at the same operation; a further five patients required late replacement (mean 1.4 years) for pronounced mitral regurgitation. Actuarial curves predict a six year survival of 68 +/- 5.7% (mean +/- SD) for all patients after mitral valve replacement compared with 88 +/- 6.9% (mean +/- SD) after repair (p less than 0.01). Actuarial survival curves favour mitral valve repair as the procedure choice for chordal rupture, and in isolated posterior cusp repair breakdown of the repair is a rare occurrence.

A young man who presented with a short history of angina was found to have syphilitic coronary ostial stenosis six years after the primary infection. He was successfully treated with bilateral internal mammary grafts.

Between May, 1981, and December, 1984, thirteen combined heart-lung transplants were performed in 12 patients for the treatment of Eisenmenger's syndrome. The age range of the recipients was 22 to 42 years. Two patients had undergone previous open cardiac operations; in addition, one had had closure of a persistent ductus arteriosus, one an open lung biopsy, one a pulmonary artery banding, and one patient received a second heart-lung transplant after 3 years. Four recipients died before hospital discharge, one at operation and three at 4, 10, and 33 days after operation. Early symptomatic results and cardiopulmonary function were excellent in all of the survivors. Two patients died 14 and 15 months after transplantation of accelerated graft arteriosclerosis and respiratory failure, respectively, and six remain alive 7 to 44 months after transplantation. Four of these surviving patients and the two patients who died late subsequently had major pulmonary complications. Symptoms included progressive breathlessness, cough (often productive), and fever with physical signs of diffuse crepitations and expiratory rhonchi. Serial pulmonary function tests showed progressive obstructive physiology in all six patients with superimposed restrictive defects in four. Histologic examination of tissue from open lung biopsy or autopsy displayed bronchiolitis obliterans in five of these patients, one of whom required retransplantation. It is possible that these late changes are the result of rejection, since similar changes in one other patient have now been reversed with augmented immunosuppression. Further understanding of the causes and manifestations of late pulmonary deterioration should improve the late functional results of this operation for Eisenmenger's syndrome.

Pulmonary function measurements were performed before and after heart-lung transplantation in nine patients who had undergone surgery for end-stage pulmonary hypertension. In seven of them, sequential follow-up studies were performed at variable times postoperatively with the longest period 27 months. Pre-transplant studies showed a mild restrictive defect in 33 percent and obstructive disease in 50 percent of the patients, respectively. Arterial hypoxemia was present in all patients. The degree of mechanical changes found did not appear severe enough to account for the marked dyspnea and disability characterizing this group of patients with pulmonary hypertension. Following transplantation, all patients showed striking improvement of symptoms and general physical status. In the early post-transplant period, there was a marked decrease in most lung volumes resulting in a moderately severe restrictive ventilatory defect. Flow parameters that were reduced could be related to decreased volumes and not to intrinsic airway obstruction. Arterial O2 tensions improved dramatically and gas exchange was maintained at essentially normal levels. Lung function tended to improve progressively following transplantation with the passage of time. Heart-lung transplant is consistent with an adequate long-term pulmonary functional state which has the capacity to sustain the normal activities of daily living. From the standpoint of lung function, heart-lung transplantation appears to be acceptable as a form of therapy in selected patients.

At Stanford University Medical Center from January 1968 until January 1984, 288 patients received 313 heart transplants. The immunosuppressive regimen before December 1980 consisted of azathioprine and prednisone, with or without rabbit antithymocyte globulin. After that time cyclosporine replaced azathioprine. In 92 recipients of 95 heart allografts, the 1- and 3-year survival rates were 82% and 65% to 70% respectively. In the 3 years from March 1981 to March 1984, successful heart-lung transplantation was accomplished in 13 of 19 recipients, using cyclosporine-based immunosuppression. Survival ranged from 1 to 38 months. While it is true that cyclosporine has improved survival in heart transplant recipients, has allowed successful heart-lung transplantation to be performed, has shortened intensive care unit and total hospital stays and therefore hospital costs, and has allowed easier management of rejection and infection, several disconcerting problems have not yet been resolved. These include hypertension that is difficult to control and renal dysfunction in all patients, and the fact that cellular and humoral rejection still occurs, as manifested by graft atherosclerosis, bronchiolitis obliterans and classic acute rejection. Better understanding and application of cyclosporine immunosuppression will undoubtedly minimize both cyclosporine- and non-cyclosporine-related postoperative complications and will improve survival even further.

To assess the long-term hemodynamic consequences of combined heart and lung transplantation, we investigated six rhesus monkeys 2.6 to 4.6 years (mean 4.0) after operation. Total follow-up was 24.0 primate-years. Autotransplantation had been carried out in four animals and allotransplantation in two, and the hemodynamic results were compared with those in three normal monkeys of similar size. Each animal underwent simultaneous right and left heart catheterization and pulmonary arteriography. Hemodynamic measurements were made at three levels of inspired oxygen. Arterial oxygen tension was within normal limits in all animals, and pulmonary artery pressure and pulmonary vascular resistance index did not change significantly with changes in the levels of inspired oxygen. Indices of left ventricular systolic function were normal in all animals. Values for pulmonary artery pressure and pulmonary vascular resistance index were similar in the autograft and normal groups: in the allograft group, the average pressure was 30/17 mm Hg (mean 24) and the index was 5.6 units . m2--both levels significantly higher than normal (pressure was 16/10 mm Hg, mean 13, [p less than 0.001] and index was 2.5 units . m2 [p less than 0.02]). Pulmonary arteriography in the allograft group with the highest pulmonary vascular resistance index (6.1 units . m2) was compatible with pulmonary vascular disease. Pulmonary arteriograms in the remaining eight monkeys were normal. Prolonged survival following combined heart and lung transplantation is possible in primates. Autotransplantation (and probable persisting denervation of the cardiopulmonary axis) does not necessarily result in abnormal long-term hemodynamics. The elevation in pulmonary artery pressure and pulmonary vascular resistance index in the allograft group may be related to previous episodes of pulmonary rejection, infection, or drug reaction.

A patient-activated ambulatory electrocardiogram device with a solid-state memory loop was used to investigate 100 unselected patients experiencing palpitation, dizziness, or syncope. Clinically useful information was obtained in 68% of patients. Frequently, sinus rhythm had been restored by the time the patient activated the device, but the arrhythmia had been stored in the pre-event segment of the memory--a distinct advantage over many other patient-activated devices. This recorder is complementary to conventional 24 hour electrocardiographic monitoring in the investigation of possible arrhythmias and is particularly suitable for patients with infrequent symptoms. Because the stored data can be rapidly analysed by any commercially available electrocardiograph the device is suitable for use in district general hospitals.