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To review the development of intracoronary ultrasound, its current utility and the impetus for its continued development as a coronary imaging modality.English-language literature (1966 to 1999) was searched in the MEDLINE database with the key words 'ultra- sound', 'intravascular' and 'intracoronary', and limited to human studies. In addition, an online public access catalogue was searched using the subject headings 'cardiovascular diseases - therapy', 'heart diseases' and 'vascular diseases'.Articles relating to the history of intravascular or intracoronary ultrasound, methods and materials employed, advantages and disadvantages, safety issues and future directions of research in the area of intracoronary ultrasound were selected.Intracoronary ultrasound has been shown to improve upon demonstrated weaknesses of coronary angiography. This imaging technique, while invasive, has not been associated with significant, acute adverse effects and has proved to be useful in guiding interventions, and evaluating the mechanism and extent of their success. Technological limitations with respect to the equipment employed, and the acquisition, processing and display of images are the subject of intense research focus because they hinder more widespread clinical use of intracoronary ultrasound.Intracoronary ultrasound has emerged as a safe and useful tool in the visualization of the coronary vasculature. Technological limitations and questions about long term safety are a concern. Its ability to overcome the inherent limitations of coronary angiography, and to guide and evaluate coronary interventions supports the notion that this technique will continue to assume an ever-expanding role in interventional cardiology.

Nifedipine gastrointestinal therapeutic system (GITS) is a once-daily formulation of nifedipine that provides stable plasma concentrations over the entire 24 h dosing interval. Two-hundred and one patients with Canadian Cardiovascular Society class II to III angina who were on 50 mg of atenolol yet still experiencing angina symptoms were randomized to receive either placebo or nifedipine GITS 30, 60 or 90 mg/day. After four weeks of treatment, the changes in time from baseline to onset of 1 mm ST segment depression in the 183 eligible patients were 26.7+/-10.2 s, 40.9+/-11.3 s, 63.2+/-12.9 s and 70.3+/-12.6 for the placebo, and 30, 60 and 90 mg/day groups, respectively. These differences were significant (P0.05) for the 60 and 90 mg/day groups compared with placebo and for the 60 mg/day group compared with the 30 mg/day group. The times to onset of pain and termination of exercise showed similar prolongation but did not achieve statistical significance. During the one-year open label phase of the study, patients exhibited statistically significant improvements in the time to onset of ST segment depression, time to anginal pain and time to termination of exercise at a mean dose of 52.3 mg/day of nifedipine GITS. Adverse events were primarily vasodilatory in nature. This study supports the use of nifedipine GITS in patients with chronic stable angina inadequately controlled on beta-blocker alone.

This study compared exercise and pharmacologic stress testing using arbutamine delivered by a closed-loop device for the detection of coronary artery disease.Arbutamine, an agent designed to simulate exercise, has been developed in conjunction with a closed-loop delivery device that modulates the rate of administration on the basis of physiologic feedback.Two hundred ten patients (180 men, 30 women) with symptoms and angiographic evidence of coronary artery disease were studied. Ischemia was categorized in three ways: 1) the presence of angina; 2) the occurrence ofor = 0.1-mV horizontal or downsloping ST segment depression or elevation at 60 ms after the J point; or 3) the presence of either condition 1 or 2.In the 210 patients, the mean increase in heart rate and systolic blood pressure evoked by arbutamine and exercise was 51 and 53 beats/min (p = NS) and 36 and 44 mm Hg (p0.0001), respectively. Arbutamine detected ischemia more often than exercise with each of the three ischemic end points. Sensitivity for detecting ischemia by either angina or ST segment change was 84% (95% confidence interval ¿ change was 84% (95% confidence interval [CI] 79% to 89%) for arbutamine and 75% (95% CI 69% to 81%) for exercise testing (p = 0.014). For angina alone, sensitivity was 73% (95% CI 67% to 79%) for arbutamine and 64% (95% CI 57% to 71%) for exercise (p = 0.026). For ST segment change alone, sensitivity was 47% (95% CI 40% to 54%) for arbutamine and 44% (95% CI 37% to 51%) for exercise (p = 0.426). Cardiac events occurred in five patients (1.8%) within 24 h of the arbutamine test.In detecting documented coronary artery disease, the sensitivity of arbutamine testing was equal to that of exercise for the electrocardiographic end point of ST segment change alone. Arbutamine testing was significantly superior to exercise testing for either ST change or angina or for angina alone.

Myocardial rejection is most apt to occur in the first 90 days after heart transplantation. Nevertheless, surveillance endomyocardial biopsies are often performed on a regular basis, indefinitely. The benefit of this approach to patient management is uncertain. Our objective was to determine the frequency of abnormalities and the influence of a routine annual endomyocardial biopsy on patient management.In a consecutive series of 235 transplant recipients who survived 1 year or more, the results of 1123 routine endomyocardial biopsies performed 1 year or more after transplantation were reviewed. The incidence of late rejection, presence of Quilty effect (focal endocardial or myocardial lymphocytic aggregates), and therapeutic reaction to the biopsy result were analyzed.Of 1123 biopsy specimens in 235 patients (1 to 12 years after transplantation), 1115 (99.3%) showed no evidence of significant rejection (grade 0 or 1). Only seven (0.6%) had evidence of rejection grade 2 or worse. Of the seven abnormal biopsy specimens in seven patients, two occurred at 1 year, two at 2 years, and one each at 4, 7, and 8 years. Of these, six were treated for rejection with an increase in the immunosuppressive therapy. One patient was identified as having a symptomatic condition at the time of biopsy. A focal endocardial or myocardial accumulation of lymphocytes (Quilty effect) was present in 311 biopsy specimens (27.6%). Beyond 1 year, 33 patients died, 14 because of graft vascular disease with or without rejection and 19 because of other causes. No deaths were predicted on the basis of a routine surveillance biopsy.Myocardial rejection is rare beyond 1 year after transplantation. The routine endomyocardial biopsy does not significantly impact patient management beyond 1 year. A selective approach to myocardial biopsies, on the basis of a change in clinical status or immunosuppressive medications, is justified.

To evaluate the physiologic basis for the suboptimal peak oxygen uptake observed after heart transplantation, we calculated the functional aerobic impairment ([(peak predicted oxygen uptake-peak observed oxygen uptake)/peak predicted oxygen uptake] x 100) and related it to donor/recipient, operative, and maximal exercise variables. Fifty-seven heart transplant recipients (mean age 50 +/- 10 years, 1 to 9 years after transplantation) underwent maximal upright cycle exercise testing. Concomitant exercise central hemodynamic measurements were obtained in 36 patients (63%).The mean peak oxygen uptake was 21.7 +/- 6.5 ml/kg/min and functional aerobic impairment was 34% +/- 17%. Functional aerobic impairment correlated positively (p0.01) with peak systemic vascular resistance (r = 0.55) and negatively with peak cardiac index (r = -0.62) and peak systemic arteriovenous oxygen difference (r = -0.66). A weak correlation was found between functional aerobic impairment and the duration of cardiac disease (r = 0.35, p0.01) but not the origin of heart failure. No correlation was seen between functional aerobic impairment and donor age, total ischemic time, time since transplantation, recipient age, and resting and exercise right and left ventricular filling pressures.These results suggest that the decreased exercise capacity observed in heart transplant recipients is in part due to increased peripheral vascular resistance and decreased oxygen extraction possibly due to skeletal muscle atrophy. These factors may be the result of irreversible changes from long-standing heart disease, deconditioning, or the effect of cyclosporine and prednisone.

Hypercholesterolemia, a common problem after heart transplantation, may be important in the genesis and progression of allograft coronary artery disease. The current study was performed to compare the efficacy of gemfibrozil, simvastatin, and cholestyramine for cholesterol lowering in heart transplant recipients.In this prospective 1-year study, 48 heart transplant recipients with moderate hypercholesterolemia were randomized to therapy with gemfibrozil 600 mg twice daily (n = 17), simvastatin 10 mg daily (n = 13), and cholestyramine 4 gm twice daily (n = 18). Detailed lipoprotein analysis was performed at baseline and after 3, 6, and 12 months of treatment.Total cholesterol and low-density lipoprotein cholesterol were reduced 19% and 29%, respectively, after 3 months of simvastatin therapy (p0.0001) with a sustained reduction in total cholesterol (25%) and low-density lipoprotein cholesterol (39%) at 1 year. Gemfibrozil and cholestyramine treatment did not result in a reduction in cholesterol levels. Apolipoprotein B levels were reduced by 29% at the end of 1 year with simvastatin but not with the other treatments. Serum triglyceride levels were reduced significantly by treatment with gemfibrozil (up to 36%, p0.01) but not by the other treatments. High-density lipoprotein cholesterol initially rose in patients treated with simvastatin and gemfibrozil; however, this effect did not persist to 12 months. However, the ratio of low-density lipoprotein/high-density lipoprotein was favorably affected by simvastatin, with a 38% reduction by 12 months (p0.0001) but not by the other treatments. Over the course of 1 year, 14 patients dropped out of the study: four from the gemfibrozil arm and ten from the cholestyramine arm. Gastrointestinal intolerance was the most common reason for study termination (8 of 14). All patients in the simvastatin treatment arm completed 12 months of therapy. No biochemical abnormalities resulted from any therapy, and no therapy caused significant alteration in cyclosporine blood levels.Of the three therapies studied, simvastatin was found to be the most efficacious and well tolerated for cholesterol lowering in patients after heart transplantation.

A case control study was performed to determine whether previous implantable cardioverter-defibrillator (ICD) insertion adversely affects outcome after heart transplantation. Six male heart transplant recipients who had undergone ICD insertion 12 +/- 5 months before heart transplantation were compared to a cohort of six heart transplant recipients who were matched according to age, preoperative status and hemodynamics, date of transplantation, graft ischemic time, history of a previous cardiac operation, and duration of follow-up. There were no significant differences in operating room time, chest tube drainage, time to extubation, and the duration of intensive care unit or hospital stay between the two groups. Furthermore, there were no significant differences in the number of units of packed cells, fresh frozen plasma, platelets and cryoprecipitate transfused. The number of treated rejection episodes and the number of patients requiring intravenous antibiotics for infection in the first 90 days was identical between groups. It was concluded that heart transplantation after ICD implantation did not appear to carry more risk than heart transplantation after a previous cardiac operation. Our limited experience supports the potential use of the ICD in patients with life-threatening ventricular dysrhythmias who are awaiting transplantation.

In the past decade myocardial biopsy has become a routine diagnostic procedure in cardiology. One of the potential complications is coronary artery--right ventricular fistula. The authors present a case of development and gradual enlargement of a iatrogenous fistula in a heart transplant recipient.

Thirty-nine heart transplant recipients were randomized prospectively to receive OKT3 or antilymphoblast globulin (ALG) for 7 days, having otherwise identical protocols (group 1: OKT3, n = 20 patients; group 2: ALG, n = 19 patients). No preoperative immunosuppression was given. The protocol consisted of methylprednisolone, 500 mg intraoperatively, followed by 1 mg/kg/day, intravenously or orally, tapering to 0.2 mg/kg/day at 1 month; oral cyclosporine starting 3 to 5 days after transplantation; selective use of azathioprine, 1 to 4 mg/kg/day; and either OKT3, 5 mg/day for 7 days, or ALG, 15 mg/kg/day for 7 days. Of the 39 patients in the study, 34 are alive 6 months to 2 years after transplantation. The actuarial survival at 2 years for the OKT3 and ALG groups was 92% (+/- 0.07%) and 83% (+/- 0.09%), respectively (not significant [NS]). The time to first rejection for group 1 was 5.6 weeks and for group 2 was 5.3 weeks (NS). The mean number of rejections for group 1 and group 2 was 2.1 episodes per patient and 1.4 per patient, respectively (NS). Three patients in each group were free of rejection at 6 months. The total number of infections at 6 months was 1.05 per patient in group 1, 0.74 per patient in group 2 (NS), with 35% of patients receiving OKT3 and 52% of patients receiving ALG actuarially free of infection by 6 months after surgery (NS). During the first 24 hours after surgery, no significant differences were noted in mean blood pressure, central venous pressure, or Po2 between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

At the time of hemodynamic assessment three years after cardiac transplantation, a patient developed symptoms and signs of a vasodepressor reaction. In addition to sudden deceleration of heart rate, a 26% fall in mean blood pressure and a 36% fall in cardiac output was observed. Subsequent investigations revealed the presence of respiratory sinus arrhythmia, profound heart rate acceleration on standing and an approximately normal heart rate response during the following exercise. Contrary to current thinking, these observations suggest that certain individuals may develop autonomic re-innervation following orthotopic cardiac transplantation.

Central hemodynamic responses during upright exercise were studied at 1 year in 40 orthotopic cardiac transplant recipients. Hemodynamic responses were characterized by slow rise in heart rate and blunted peak exercise heart rate response, a significant early increase in stroke index followed by a plateau phase, and a steady increase in ventricular filling pressures and pulmonary artery pressure. In spite of exclusive utilization of the Frank-Starling mechanism to augment cardiac output during early exercise, the pressure responses were comparable to those reported in normal subjects. Our observations also indicate that similarly to normal subjects, the heart rate response plays an important role in the cardiac output achieved at maximum exercise. Although patients with younger donor hearts achieved a more favorable maximum heart rate, the other hemodynamic parameters showed no correlation with the donor heart age. Thus, no hemodynamic disadvantage of older donor hearts could be demonstrated. These data provide further enlightenment regarding the mechanisms of the well-preserved functional capacity noted in these patients.

The evolution of resting hemodynamics was studied at 1 week and 1 year in 40 patients following orthotopic cardiac transplantation. Abnormal hemodynamics after transplantation, characterized by elevated ventricular filling pressures (indicating diastolic dysfunction) and also by pulmonary hypertension, showed normalization by 1 year. In the absence of innervation, the resting heart rate of heart transplant recipients should theoretically be close to the intrinsic heart rate predicted by the age of the donor heart. In this study, a high incidence of relative sinus bradycardia (an indicator of sinus node dysfunction) was noted in the first post-operative week, although again there was a tendency to normalization by 1 year. These beneficial changes help to explain the dramatic and sustained improvement in the functional capacity of these patients late after transplantation.

BACKGROUND Although progressive chronic congestive heart failure (CHF) is associated with elevated systemic vascular resistance and increased impedance to ventricular outflow, the contribution of changes in large artery function has not been well documented in humans. METHODS AND RESULTS We studied 45 patients with a broad range of clinical severity of CHF and compared noninvasive measurements of brachial artery diameter, flow, and pulse wave velocity with 22 normal controls of similar age. In CHF, mean arterial pressure was lower than in controls (85 +/- 1 versus 93 +/- 2 mm Hg, p less than 0.001), as were brachial artery diameter (4.07 +/- 0.10 versus 4.53 +/- 0.09 mm, p less than 0.001), flow (40.9 +/- 4.1 versus 70.9 +/- 11.5 ml.min-1, p less than 0.02), compliance (1.29 +/- 0.12 versus 2.00 +/- 0.18 cm4.dyne-1.10(-7), p less than 0.002), and conductance (0.49 +/- 0.05 versus 0.76 +/- 0.13 units, p = 0.06). Limb vascular resistance (40.2 +/- 5.0 versus 20.5 +/- 3.1 units, p less than 0.001) and pulse wave velocity (10.6 +/- 0.5 versus 9.2 +/- 0.4 m.sec-1, p less than 0.03) were higher than in controls. Brachial artery diameter was progressively lower than in controls as severity of CHF increased (New York Heart Association class II, 4.47 +/- 0.23 mm, p = NS; class III, 4.05 +/- 0.10 mm, p less than 0.05; class IV, 3.71 +/- 0.28 mm, p less than 0.05). Similar changes were observed for arterial compliance (class II, 1.76 +/- 0.32 cm4.dyne-1.10(-7), p = NS; class III, 1.21 +/- 0.13 cm4.dyne-1.10(-7), p less than 0.05; class IV, 0.95 +/- 0.10 cm4.dyne-1.10(-7), p less than 0.05). While the lower arterial pressure and flow might be expected to passively reduce arterial diameter, this would be associated with a reduced pulse wave velocity and improved arterial compliance, yet the opposite was observed. Differences in large artery function were not likely caused by underlying atherosclerosis alone, because patients with dilated cardiomyopathy and patients with ischemic heart disease of the same sex, age, left ventricular ejection fraction, and exercise treadmill duration had similar changes in large artery function. CONCLUSIONS We conclude that alterations in brachial artery function are present in patients with moderate and severe CHF. The observed reduction in arterial compliance, if present diffusely throughout the arterial tree, could increase left ventricular end-systolic stress directly and through increased velocity of reflected pressure waves from the periphery.

Despite advances in immunosuppressive therapy and prolonged graft and patient survival, infection after heart transplantation remains problematic. From January 1987 through June 1989, 104 heart transplantations were performed in 100 patients. Immunosuppression induction was by antilymphocyte globulin for 7 days, with oral cyclosporine introduced on stabilization of kidney function (day 3). Steroid therapy was rapidly tapered, and azathioprine was added only in cases of positive donor crossmatch or steroid-resistant rejection. No reverse isolation was used. Twenty-two deaths occurred, one from sepsis. Actuarial survival at 6 months, at 1 year, and at 2 years was 85% +/- 4%, 81% +/- 3%, and 75% +/- 4%, respectively. Fifty-four patients had 81 infections, of which 21 were bacterial; 83% of these episodes were treated. Sixty infections were opportunistic (85% viral), and only 23% necessitated treatment. Actuarial infection-free rates (all types necessitating treatment) at 1 month, at 6 months, and at 2 years were 83% +/- 4%, 75% +/- 5%, and 75% +/- 5%, respectively. Of the 100 transplant recipients, 66% were treated with azathioprine; 47 patients (69%) had an infection, whereas only seven (19%) of the patients not receiving azathioprine became infected (p less than 0.00001). Rejection was noted in 66% of patients, with a median time to the first episode of 4 weeks. A low-intensity immunosuppressive regimen has resulted in fewer serious infections, with acceptable graft loss from rejection. Increased infection surveillance is required for the first 30 days postoperatively and after treatment of rejection episodes.

The number of heart transplantations performed over the past 3 years has plateaued. However, the number of pediatric transplantations continues to slowly increase. Unlike adult heart transplantation, for which cardiomyopathy remains the most frequent indication, structural congenital heart disease is the primary indication in children. This report reviews our experience with orthotopic heart transplantation in the presence of structural congenital heart disease with and without prior palliative repair. The diagnoses included transposition of the great arteries, common atrium, left superior vena cava with and without a bridging innominate vein, dextrocardia, and univentricular configurations. The palliative repairs included Blalock-Taussig shunt, bilateral Glenn shunt, Fontan repair, and Mustard and Rastelli procedure. There were no early deaths. Two rejection-related late deaths have occurred at 8 months and at 3 years postoperatively. Extended use of donor tissue and modifications to surgical technique allowed for successful orthotopic heart transplantation in these patients who had structural congenital heart disease with and without prior surgical palliation.

Of 219 heart transplant patients with follow up for at least 3 months after transplantation, cardiac allograft ischemic time was more than 4 hours in 28% and more than 5 hours in 10%. In 1988 and 1989 grafts with ischemic times longer than 4 hours were used in 44% and 45% of cases, respectively. Overall, donor age has been 35 or more years in 22% and 45 or more in 9%. In 1989 donor age was 35 or more years in 39% of cases and 45 or more in 18%. Fifteen of 20 grafts from donors 45 years or older were used for patients aged 50 or older. There was no relationship between donor age or ischemic time and 90-day graft loss. At 3 and 12 months, cardiac function, assessed by treadmill exercise duration, radionuclide angiography, and rest and peak supine exercise hemodynamics, was also unrelated to donor age or ischemic time. Therefore by careful selection of appropriate donors, extending both graft ischemic time and donor age has increased the potential donor pool and has not to date been associated with increased graft loss or adverse effects on cardiac function 3 months and 1 year after heart transplantation.

Radiologic assessment of the cause of pulmonary parenchymal consolidation in end-stage heart failure may be difficult. From August 1982 to May 1989, 22 patients being considered for orthotopic cardiac allografts had parenchymal consolidation on their chest radiographs, most commonly in the right lower lobe. Our purpose was to determine from standard radiologic studies whether this consolidation represented alveolar pulmonary edema in an atypical basal distribution, pneumonia, or pulmonary infarction. This differentiation is important because pneumonia is an absolute and infarction is a relative contraindication to surgery, whereas successful transplantation can be performed in a setting of pulmonary edema. The chest radiographs were reviewed retrospectively. When available, pulmonary angiograms, nuclear medicine ventilation/perfusion scans, and needle biopsy findings were also evaluated. The radiologic assessment was correlated with the results of surgical, autopsy, or clinical outcome. None of the conventional modalities was very accurate--the plain chest film was correct in only 63%, nuclear medicine studies in 50%. Angiography was the single most useful test, with an accuracy of 75%.

The results of heart-lung transplantation are improving with increasing experience in postoperative management, but obliterative bronchiolitis may still develop late postoperatively. We have performed 19 heart-lung transplants, with 1-month, 1-year, and 2-year actuarial survival rates of 95% +/- 5%, 84% +/- 8%, and 69% +/- 16%, respectively. Three early recipients died of bronchiolitis, and four patients who were operated on more than 2 years ago are currently being followed up with bronchiolitis. Since August 1988, 13 surviving recipients have undergone serial postoperative bronchoscopies and transbronchial biopsies with topical analgesia. Diffuse bronchomalacia, involving the main bronchi down to the fifth-order bronchi bilaterally, has developed in four patients with bronchiolitis 9 +/- 2 months after the diagnosis of bronchiolitis was confirmed. Pulmonary function tests have revealed a lower ratio of forced expiratory volume in 1 second to forced vital capacity, lower specific airway conductance, and higher airway resistance in heart-lung recipients with bronchomalacia than in patients with bronchiolitis alone. We conclude that diffuse bronchomalacia occurs frequently in heart-lung transplant recipients who have obliterative bronchiolitis. Bronchomalacia worsens the functional airflow obstruction caused by bronchiolitis and may play an important role clinically in the declining respiratory status of heart-lung transplant recipients.

Twenty-four patients were randomized to a double-blind, triple placebo controlled, latin square protocol to examine the relative efficacy of propranolol or diltiazem given as monotherapy or in combination with isosorbide dinitrate. Treatment phases were preceded and followed by placebo control periods. At the end of each phase, symptom-limited treadmill exercise stress tests were performed, as well as rest and exercise radionuclide ventriculography. Both forms of monotherapy were effective in reducing episodes of angina and nitroglycerin use, and in improving exercise tolerance. Diltiazem monotherapy was associated with slightly higher treadmill times (509.9 +/- 123 s) compared to propranolol (462.7 +/- 131 s, P less than 0.05). The addition of isosorbide dinitrate to either form of monotherapy allowed no further improvement in any of the measured clinical responses. Radionuclide ventriculography showed no significant difference in resting left ventricular function. The addition of isosorbide dinitrate to propranolol showed a reduction in end diastolic volume in keeping with a reduction in preload. In response to exercise, stress-induced left ventricular dysfunction was equal in all groups except for the diltiazem-nitrate combination, which was associated with a higher ejection fraction (56.2 +/- 8.6%) compared to monotherapy (52.6 +/- 10.9%, P less than 0.01). A higher cardiac output could be achieved in the groups treated with diltiazem; this was related to increased heart rate and maintenance of stroke volume. It was concluded that diltiazem is equally effective as propranolol for the treatment of chronic stable angina and, in terms of exercise capacity and cardiac output, superior to beta-blockade. The addition of isosorbide dinitrate appears to impart no overt benefits, but some evidence suggests a reduction in left ventricular decompensation in the face of stress.

Chronic shortage of donor organs has heightened interest in new strategies for increasing donor availability. Unacceptable hearts for transplant have previously been characterized by donor age greater than 40 years, more than 20% donor/recipient weight mismatch, ischemic time more than 4 hours, and the presence of coronary artery disease. A series of 185 consecutive orthotopic heart transplants were retrospectively examined. A significant number of donor hearts used were unacceptable by one or more of the above criteria. Our current approach is to match donors to recipients using a wide range of criteria. Donors are now accepted from any location in North America. We have accepted donors more than 55 years of age and donors weighing less than 50% of the recipient's body weight. Because of the chronic shortage of donor organs, donor criteria have been effectively liberalized, thereby increasing the donor pool without compromising the overall results of heart transplantation.

Milrinone is a nonglycoside, nonsympathomimetic bipyridine with positive inotropic and systemic vasodilator properties. In order to evaluate the efficacy and safety of a short term infusion of milrinone, 105 patients with stable New York Heart Association (NYHA) class III or IV heart failure received a loading dose (50 micrograms/kg) and a 48 h continuous infusion (0.5 micrograms/kg/min). Administration of the loading dose resulted in a 28% decrease in pulmonary capillary wedge pressure (PCWP) (P less than 0.001), a 38% increase in cardiac index (P less than 0.001), and a 34% increase in stroke volume index (P less than 0.001) within 15 mins. Milrinone infusion maintained an average 27% and 24% reduction in PCWP during the first and second days, respectively (P less than 0.001). Cardiac index was 32% and 34% above baseline during the same intervals (P less than 0.001). There were no clinically significant changes in heart rate or mean arterial blood pressure during the study period. In a subset of 47 patients who underwent Holter monitoring before and during infusion, a significant increase in ventricular arrhythmias (premature ventricular complexes per hour, ventricular couplets per hour and ventricular runs greater than or equal to three) was demonstrated (P less than 0.0001). In general, milrinone was well tolerated. Of the 105 patients entered, one died of an acute myocardial infarction after premature termination of the infusion, and the infusion rate was decreased in two others because of supraventricular arrhythmias. In patients with severe heart failure, intravenous milrinone has significant beneficial hemodynamic effects. ECG monitoring for arrhythmias is recommended during milrinone infusion.

To reduce perioperative hemorrhage following heart-lung transplantation, several technical modifications were introduced in June 1988 to secure better posterior mediastinal hemostasis. The intraoperative and postoperative use of blood and blood products, as well as the chest tube drainage in the first 24 hours postoperatively, were compared in the seven patients operated on since June 1988 with the nine patients operated on before that date. Significant (p less than 0.05) reductions were demonstrated in the intraoperative and postoperative transfusion of packed cells, in the postoperative administration of fresh frozen plasma, and in the chest tube drainage within the first 24 hours postoperatively. The one-month and total hospital mortality rates were 6 percent and 12.5 percent, respectively. It is concluded that newer techniques to obtain optimal posterior mediastinal hemostasis have significantly reduced blood loss following heart-lung transplantation in our experience and have contributed to our excellent early postoperative results.

Congenital heart disease as an indication for heart transplantation accounts for a small number of the total heart transplant experience--less than 3% in most centers. We have performed heart transplantation in eight such patients, accounting for 4% of our total experience. All these patients had specific anatomic anomalies relevant to transplantation. None had morbidity directly related to their anatomic defect and subsequent transplant. Six of the eight had undergone no prior palliative or corrective repairs. One child had a left Blalock-Taussig shunt, and one had bilateral Glenn shunts and a Fontan repair. Technical considerations for orthotopic heart transplantation are described for transposition of the great arteries, left superior vena cava with and without bridging innominate vein, common atrium, presence of Blalock-Taussig shunt, bilateral Glenn shunts, and Fontan repair. Anatomic congenital heart disease is becoming a more frequent indication in heart transplantation. Heart transplantation in the presence of structural congenital heart disease may be technically challenging. Nevertheless, transplantation offers an effective therapeutic alternative for patients with end-stage congestive heart failure and congenital heart disease.

In recent years, new approaches for the medical treatment for heart failure have evolved. While the use of vasodilators and specifically angiotensin converting enzyme inhibitors has improved both functional status and survival, long term prognosis unfortunately remains poor [1–4]. Since the initial human heart transplant over 20 years ago, there has been a progressive improvement in long-term survival [5]. Moreover, cardiac transplantation results in marked alleviation of symptoms and improved quality of life in patients with end stage heart failure. Indeed, patients undergoing successful cardiac transplant are capable of resuming normal physical activity which is in sharp contrast with their severe physical limitations prior to surgery. With the availability of cyclosporine [6], the cardiac transplantation program at University Hospital, London, Canada commenced in April 1981. Between then and December 1988, 186 transplants were performed in 179 patients with end-stage heart disease. Heart failure was the result of ischemic heart disease (IHD) in 86 patients and cardiomyopathy (CM) in 80 patients. In the remainder, transplantation was for end-stage valvular heart disease in eight, congenital heart disease in five, and seven patients required retransplantation. In this discussion only the patients with IHD and CM will be evaluated. Of the 80 patients with CM, one patient had amyloidosis, two hypertrophic CM, one postpartum CM, one adriamycin-induced CM, and one patient had acute myocarditis. In the remainder no identifiable cause of dilated CM was identified.

Cibenzoline is a new antiarrhythmic agent with predominant Vaughan-Williams type 1 properties. The safety, tolerance, and adverse effects of incremental single intravenous doses of this agent were investigated. A total of 28 patients received incremental doses of 0.25 mg/kg (four patients), 0.5 mg/kg (five patients), 0.75 mg/kg (seven patients), 1.0 mg/kg (six patients), or 1.2 mg/kg (six patients) cibenzoline. Another six patients received 2.0 mg/kg disopyramide. Left ventricular function by radionuclide ventriculography and plasma cibenzoline levels were measured at frequent intervals. In the patients who received 1.0 mg/kg and 1.2 mg/kg cibenzoline or patients who received 2.0 mg/kg disopyramide, right and left ventricular filling pressures and cardiac output were measured with a Swan-Ganz catheter. At low-dose cibenzoline (0.25 to 0.75 mg/kg) there was a modest drop in ejection fraction (60% ± 7% to 53% ± 7%). With the higher doses of cibenzoline (1.0 or 1.2 mg/kg) there was a more profound fall in ejection fraction (69% ± 8% to 49% ± 8%) that persisted for approximately 2 hours. This was associated with a rise in end diastolic volume index (74 ± 24 to 85 ± 27 ml/m2) and end systolic volume index (29 ± 15 to 43 ± 18 ml/m2) and a fall in cardiac index (2.65 ± 0.62 to 2.14 ± 0.24 L/min/m2). These hemodynamic changes were similar to those of disopyramide infused at a dose of 2.0 mg/kg: a fall in ejection fraction (57 ± 9 to 48 ± 8), rise in end-end diastolic index (81 ± 44 to 95 ± 55 ml/m2) and end systolic volume index (37 ± 22 to 49 ± 26 ml/m2), and a fall in cardiac index (2.51 ± 0.15 to 2.13 ± 0.16 L/min/m2) and stroke volume (39 ± 8 or 30 ±4 ml/m2). After intravenous infusion, cibenzoline results in significant dose-related negative inotropic effects. An infusion of 1.0 to 1.2 mg/kg results in a similar decline in left ventricular function as does disopyramide infused at a dose of 2.0 mg/kg. Clinical Pharmacology and Therapeutics (1987) 41, 537–545; doi:10.1038/clpt.1987.69

The possible value of myocardial imaging with 201thallium as a screening procedure for the detection of latent disease has not been previously shown. Fifty-eight asymptomatic men underwent exercise 201thallium imaging together with a risk score profile based on the Framingham criteria for predicting future coronary events. Six subjects (10%) developed perfusion defects compatible with myocardial ischemia. The risk score for the population with an abnormal test was 7.7 +/- 2.9%, compared to 2.0 +/- 2.2% (p less than 0.001) for those men with normal tests. Three of the subjects with abnormal scans underwent selective coronary arteriograms; all three had normal coronary arteries. During a 30-month follow-up, all individuals remained physically active and free of cardiac symptoms. Exercise myocardial imaging is not a cost-effective means of detecting coronary artery disease in an asymptomatic population and should not be used as a screening procedure.

Spontaneous regression of a left anterior descending coronary artery lesion was diagnosed by noninvasive testing (stress electrocardiography and thallium-201 myocardial imaging) and confirmed on selective coronary angiography in a 46-year-old man. The patient's clinical improvement, normalization of stress ECG and thallium-201 imaging, together with the loss of collateral filling, confirm that the regression is genuine. This case provides evidence that regression of coronary atherosclerosis can occur in man.

The contribution of a liaison psychiatrist to a cardiac transplant programme is described. Ninety one patients were referred to the transplant unit for assessment over four years, and of these, 86 were assessed by the psychiatrist. A high prevalence of preoperative anxiety and depression was found. Thirty four transplants were performed on 33 patients during the study and 22 patients survived. Six patients developed transient delirious episodes during the first 10 postoperative days, three showed symptoms of considerable anxiety, and three developed social and behavioural problems during the convalescent period. Subjects with higher scores on the somatic scale of the general health questionnaire showed increased postoperative mortality. In conclusion, the liaison psychiatrist is useful in evaluating and managing heart transplant patients before and after operation.

To assess the hemodynamic influence of posture during radionuclide cardiac studies, rest and exercise electrocardiographically gated blood pool cardiac scintigraphy was performed in the supine and sitting positions in 22 normal subjects and in 20 patients with coronary artery disease (CAD). In normal subjects, left ventricular ejection fraction was higher in the sitting position both at rest (67 +/- 6% versus 64 +/- 5%, p less than 0.01) and during exercise (79 +/- 9% versus 76 +/- 6%, p less than 0.05). Left ventricular end-diastolic volume in the sitting position was smaller at rest (by 19 +/- 26%, p less than 0.001), but this variable was similar in both positions during exercise (p greater than 0.05). Left ventricular end-systolic volume was smaller in the sitting position both at rest, by 26 +/- 31 percent, and during exercise, by 14 +/- 20% (p less than 0.001). Left ventricular end-diastolic volume increased from rest to exercise, in the sitting position by 31 +/- 23% (p less than 0.001) and in the supine position by 6 +/- 22% (p greater than 0.05). In patients with CAD, similar left ventricular ejection fractions in both postures were found at rest and during exercise. Left ventricular end-diastolic volume in the sitting posture was smaller at rest by 16 +/- 22% (p less than 0.01) and during exercise by 8 +/- 18% (p less than 0.05). Sitting left ventricular end-systolic volume was smaller by 18 +/- 20% (p less than 0.001) at rest and by 14 +/- 21% (p less than 0.01) during exercise. Left ventricular end-diastolic volume increased from rest to exercise, in the sitting position by 45 +/- 36% (p less than 0.001) and in the supine position by 32 +/- 51% (p less than 0.01). Despite significant hemodynamic differences, the value of rest-exercise radionuclide cardiac studies to detect CAD was similar in the 2 positions.

To investigate the role of intrinsic sympathomimetic activity on left ventricular (LV) function during antianginal therapy with beta-adrenoreceptor antagonists, 23 patients with chronic, exercise-induced angina pectoris and normal or near normal LV function underwent radionuclide ventriculography at rest and during exercise, during 3 randomly allocated periods: (a) treatment with oral propranolol, a drug without intrinsic sympathomimetic activity, 40 to 80 mg 4 times a day; (2) treatment with pindolol, a drug with marked intrinsic sympathomimetic activity, 5 to 10 mg 2 times a day; and (3) a control period. During the control period, the LV ejection fraction decreased from rest (58.9 +/- 8.2%) to exercise (54.3 +/- 10.7%), and the wall motion score decreased from 0.57 +/- 1.08 at rest to 2.39 +/- 2.10 during exercise, p less than 0.001. After propranolol, the ejection fraction did not change significantly at rest (57.2 +/- 8.1%) but improved during exercise (56.8 +/- 11.8%), compared with control values. After pindolol, the ejection fraction did not change at rest (57.9 +/- 8.6%) but improved during exercise (56.9 +/- 8.1%), compared with control values. Similarly, the wall motion score after administration of both agents did not change significantly at rest, but improved during exercise (p less than 0.001). The number of anginal episodes, nitroglycerin tablets consumed, and magnitude of S-T segment depression decreased significantly with both pindolol and propranolol. With both drugs, a similar improvement in exercise tolerance and a similar decrease in exercise heart rate and blood pressure were obtained. It is concluded that pindolol and propranolol, beta-adrenoreceptor antagonists with and without intrinsic sympathomimetic activity, respectively, have similar effects on global and regional LV function in patients with angina pectoris, at doses producing equal suppression of exercise heart rate and similar antianginal effect.

High temporal resolution radionuclide angiography was performed in 24 normal volunteers and 31 healthy cardiac transplant recipients two to 43 months (mean 13 +/- 14 months) postoperatively in order to obtain cardiac volumes and parameters of left ventricular ejection and filling at rest and during supine exercise. The peak left ventricular ejection rate was significantly higher in transplant patients at rest (2.73 +/- 0.62 versus 1.98 +/- 0.29, P less than 0.0001). During submaximal exercise, however, in contrast to normal subjects, peak ejection rate increased in transplant recipients only during later exercise, corresponding to an increase in heart rate. Peak left ventricular filling rate was also significantly higher among transplant recipients at rest (3.52 +/- 0.96 versus 2.36 +/- 0.45, P less than 0.0001) and during submaximal exercise. Peak filling rate increased in transplant patients on initiation of exercise, associated with an increase in the end diastolic volume in the absence of an increase in heart rate. In 13 patients studied more than one year post cardiac transplantation, the peak ejection rate and peak filling rates did not differ from those studied less than one year post transplant. Therefore, in transplant patients, no defect of myocardial filling was apparent either at rest or during exercise. Systolic performance improved in later exercise, presumably as levels of circulating catecholamines and heart rate increased.

The left ventricular (LV) volume response to supine exercise (EX) was studied in 15 normal volunteers (mean age 44, asymptomatic, with normal resting ECG and treadmill stress test) and 28 coronary artery disease patients (CAD, documented by cardiac catheterization) with no previous myocardial infarction. Each individual underwent stress gated equilibrium radionuclide angiography (RNA) and was on no medication. A nongeometric count based LV volume programme developed in our laboratory (correlation to biplane cineangiography R = .98), was used to calculate end diastolic volume index (EDI), end systolic volume index (ESI), stroke volume index (SVI), cardiac index (CI), and ejection fraction (EF). In normal individuals, end diastolic volume did not change from rest to exercise, while end systolic volume decreased by an average of 16%. In the patients with coronary artery disease, however, both end diastolic volume and end systolic volume increased (14% and 15% respectively). Furthermore, our preliminary data suggest that the extent of the changes may be dependent upon the extent of the underlying CAD. While all the CAD patients had an increase in their end diastolic volumes, there was no change in the end systolic volume in those with single vessel disease, an 11% increase in patients with double vessel disease and a 19% in patients with triple vessel disease.

Myocardial injury was assessed with the use of enzyme indexes in 40 patients randomly assigned to one of two groups undergoing coronary artery bypass surgery. Twenty patients received cold cardioplegia delivered by retrograde coronary sinus perfusion and 20 received cardioplegic solution by anterograde aortic root perfusion. Creatine kinase isoenzyme MB and lactate dehydrogenese isoenzyme 1 and isoenzyme 2 assays were carried out on blood samples obtained from the coronary sinus before aortic cross-clamping and 0, 5, and 30 min after aortic unclamping. Levels of these enzymes were also obtained from venous blood samples before aortic cross-clamping and 3, 8, 14, and 20 hr after aortic unclamping and 2, 3, 4, and 5 days after surgery. Preoperative and postoperative hemodynamic measurements (Swan-Ganz catheter) and radionuclide wall motion studies were also obtained for comparison. There was no overall significant difference between the two groups postoperatively in terms of enzyme indexes, hemodynamic measurements, or results of wall motion studies. We conclude that retrograde coronary sinus perfusion is an alternative to aortic root perfusion in delivering cold cardioplegia. More studies are required to determine which subgroup of patients with coronary artery disease may benefit from retrograde coronary perfusion.

Full assessment of coronary atherosclerotic disease necessitates not only the determination of symptoms, but also the coronary anatomy, collateral circulation patterns and left ventricular function. The coronary arteriogram does not measure regional myocardial perfusion at the capillary level, while the left ventricular angiogram cannot distinguish between reversible and irreversible myocardial dysfunction. Such evaluation is becoming more important as the number of patients being considered for aorto-coronary by-pass surgery increases. The delivery of additional blood to heavily scarred myocardium is a needless procedure. Myocardial perfusion as measured by the labelled albumin particle method (1, 2) is a promising technique which appears to be capable of distinguishing between scarred myocardium and ischemic, yet viable, myocardial tissue. We have assessed this technique in patients undergoing diagnostic coronary angiography and would like to present the results in our first 400 patients.

Evaluation of patients for aotocoronary bypass (ACB) surgery is dependent on the findings at cardiac catheterization. Left ventricular angiography cannot distinguish between reversible and irreversible myocardial dysfunction. In 82 patients macroaggregates of human serum albumin, labelled with iodine-131, were injected before operation into the right coronary artery and technetium-99m labelled microspheres were injected into the left coronary artery. Two weeks after operation similar technetium-99m and iodine-131 injections were made into the native vessels and grafted vessels, respectively. Myocardial distribution of the 20 mu particles was visualized with a rectillinear scanner. Sixty-seven patients had normal myocardial perfusion scans preoperatively even though wall motion was abnormal in 34. There was substantial improvement in the left ventricular function of these 34 patients; the mean ejection fraction increased from 56 to 65%. Fifteen patients had abnormal myocardial perfusion scans; improvement in left ventricular function in this group occurred only if the bypass graft was made to an area with normal regional perfusion preoperatively. It is certain that an adequate capillary bed is present if the myocardial scan is normal, regardless of the degree of critical stenosis in either coronary artery. The patient with a completely occluded coronary artery and normal myocardial scan is a good candidate for ACB and will show improved left ventricular contraction if the ACB is patent

The effects of mitral valve replacement or commissurotomy on cardiac function were studied using radionuclide ventriculography in 13 patients with chronic mitral stenosis and in 8 with chronic mitral regurgitation, before and after mitral valve surgery. The stenosis resulted from rheumatic heart disease in all instances while regurgitation was due to mitral valve prolapse in three patients and rheumatic heart disease in five. Fourteen patients had a Carpentier-Edwards valve inserted and 4 a Lillehei-Kaster disc valve. Three patients with mitral stenosis had an open commissurotomy. All patients underwent supine-rest and symptom-limited exercise radionuclide ventriculography shortly before and 6 to 12 months after operation. The data obtained showed that left ventricular function remained unchanged postoperatively in patients with mitral stenosis but deteriorated in those with mitral regurgitation. Right ventricular function improved postoperatively in those with mitral stenosis but remained unchanged in patients who had regurgitation.

Current immunosuppression protocols in heart transplantation commonly employ an inductive phase preoperatively, which often is followed by triple therapy (azathioprine, cyclosporine, and prednisone). From 1981 to June 1987, 119 heart transplants were performed in 114 patients. Group I (n = 19) received cyclosporine preoperatively and postoperatively, as well as steroid intraoperatively and postoperatively. Group II (n = 100) received antilymphocyte globulin postoperatively and interval cyclosporine orally 5 to 7 days postoperatively when the antilymphoblast globulin was discontinued. Methylprednisolone was given intraoperatively, and 1 mg/kg was given postoperatively. Steroid was tapered to 20 mg/day within 4 weeks. Cyclosporine was removed from the early postoperative regimen to reduce the deleterious renal effects. Steroid was used in low doses and tapered quickly to lessen steroid-related complications. There was one cyclosporine-related kidney failure in group I and none in group II. In no patient was cyclosporine discontinued because of adverse effects. The rate of rejection remains acceptable. There have been eight deaths as a result of rejection (three in group I and five in group II). Three patients have died of infection (one in group I and two in group II). Since January 1987 no postoperative protective isolation has been used. Overall survival is 77%, and no patient has exhibited late coronary atherosclerosis on follow-up coronary angiography. The regimen of immunosuppression that has evolved is safe and effective and has long-term benefits.

Six left atrial myxomas were detected at one hospital in a 15-month period. These tumours are not as rare as was once thought and they frequently cause systemic problems. The diagnosis may easily be missed, but echocardiography is a simple way of establishing the diagnosis. Excision of the tumour usually results in marked symptomatic improvement.

The authors have reviewed the literature in search of the coexistence of single coronary artery with significant coronary artery disease. Two cases of single right coronary artery are described. In both, the anomalies were unsuspected and diagnosed roentgenographically in life. Both patients had angina pectoris, positive graded-exercise stress tests, and hemodynamically significant obstruction or occlusion to the coronary arteries. In neither case was the stenosis proximal or amenable to bypass surgery. ImagesFIG. 1FIG. 2

In a 14-month period mitral leaflet prolapse was diagnosed in 85 patients by echocardiography or cineangiography. Chest pain alone was the presenting complaint in 30 patients and linked with palpitation, dyspnoea, or syncope in 9. Eleven presented with major neurological disturbances (9 had transient ischaemic attacks), 10 with palpitation, 4 with undue and persistent fatigue, 2 with dyspnoea, and 2 with dizziness. Seventeen were referred not because of symptoms but because of clicks and murmurs. Overall, chest pain affected 61 patients and unless associated with coronary artery disease was not anginal. Palpitation was admitted by 42 patients; dizziness, lightheadedness, or paraesthesiae by 15, and syncope by 12. Systolic auscultatory abnormalities were noted in 69: 25 had single clicks, 3 had multiple clicks, 19 had both click(s) and murmur, and 22 had a murmur alone. Electrocardiography revealed ST segments flat for greater than 0-10 s in 21, prolonged QTc in 18, and T wave flattening or inversion in inferior limb and lateral chest leads in 14. The exercise stress test was abnormal in 13 of 27 patients. Mitral valve echograms showed definite mitral leaflet prolapse in 61, 'possible' prolapse in 14, and were normal in 8 patients with angiographic proof of mitral leaflet prolapse. Cardiac catheterization with left ventriculography showed prolapse of posterior mitral leaflet in 36, of both leaflets in 2, and left ventricular wall motion abnormalities in 16 cases. Selective coronary arteriography in 31 cases showed major vessel narrowing of larger than or equal to 80 per cent lumen diameter in 4, all with angina. This consecutive series indicates that the physical event of mitral leaflet prolapse is more common than hitherto appreciated, is priminently associated with non-anginal chest pain, palpitation, and neurological disturbances, and in 90 per cent of cases could be shown echocardiographically.

A 35 year old female patient was referred for investigation and treatment of recurrent ventricular tachycardia. Cardiac examination and the echocardiogram were normal. Equilibrium radionuclide ventriculography demonstrated a reduction in right ventricular ejection fraction (rest and exercise) while left ventricular ejection fraction was normal. It is proposed that radionuclide ventriculography may be the noninvasive study of choice to screen patients for arrhythmogenic right ventricular dysplasia. The right ventricular response to exercise may provide additional evidence for right ventricular dysfunction based on relative changes compared to the left ventricle. The diagnosis of arrhythmogenic right ventricular dysplasia may be subsequently confirmed by right ventricular angiography or endomyocardial biopsy, both of which are techniques which may not be performed during routine cardiac catheterization in the absence of the radionuclide ventriculography findings to suggest right ventricular dysfunction.

Left ventricular function and volume changes during supine isotonic exercise were assessed in 32 patients with coronary artery disease (CAD) and 12 normal subjects by electrocardiographically gated blood pool cardiac scintigraphy. Ejection fraction (EF) in normal subjects was 49 +/- 10% at rest, 54 +/- 10% during intermediate exercise (P less than 0.05 vs. rest), and 62 +/- 14% during maximal exercise (P less than 0.01 vs. rest). In patients with CAD the resting EF was 42 +/- 14%, 43 +/- 23% at intermediate exercise (P = nonsignificant vs. rest) and 36 +/- 11% at maximal exercise (P less than 0.01 vs. rest). Changes of average and maximal ejection rates from rest to exercise were similar to those of EF but had a lesser degree of statistical significance. End-diastolic volume index (EDVI) in patients with CAD, at intermediate exercise was equal to that at rest, but it increased during maximal exercise (P less than 0.01). In normal subjects EDVI did not change with exercise. Thus, during supine exercise the Frank-Starling mechanism is apparent in patients with CAD but not in normal subjects. Analysis of EF response to exercise is a highly sensitive technique to detect CAD provided that adequate exercise is achieved.

Few studies have assessed the effect of severity of mitral stenosis (MS) on ventricular function. Using equilibrium radionuclide ventriculography to measure ejection fraction and volume changes, 63 patients were studied during supine, symptom-limited exercise. To more carefully assess the 12 patients with MS and impaired left ventricular function, 2 groups of patients were formed. Group I (n = 51) had a normal (less than 50%) resting left ventricular (LV) ejection fraction (EF) and group II (n = 12) had an abnormally low (less than 50%) resting LVEF. Both groups were divided into mild (greater than 1.4 cm2), moderate (1.1-1.4 cm2) and severe (less than 1.0 cm2) MS. There were no differences in mean rest or exercise LVEF for group I. Exercise LVEF increased significantly (p less than 0.05) from rest with mild MS, but not with moderate or severe MS. The decrease in exercise LVEF was due to a decrease in exercise end-diastolic volume of 9 +/- 23% and 15 +/- 18% for moderate and severe MS, respectively. Exercise end-systolic volume decreased normally for all degrees of MS severity. Exercise right ventricular (RV)EF did not increase for any degree of MS severity due to an increase in end-systolic volume. All patients in group II had an RVEF of less than 40%. For this group, severity of MS had no effect on resting LVEF and the response to exercise was similar to group I. We conclude that in patients with MS, resting LVEF is unaffected by MS severity whereas exercise LVEF decreases with increased severity of MS due to impaired diastolic filling.(ABSTRACT TRUNCATED AT 250 WORDS)

Serial electrocardiography, technetium-99m pyrophosphate scintigraphy and measurement of myocardial creatine kinase (CK2) and lactic dehydrogenase isoenzyme activity (specifically the LD1 to LD2 ratio) were evaluated prospectively in 26 patients who underwent aortocoronary bypass grafting and 11 patients who underwent valvular or other thoracic surgery, as methods of diagnosing perioperative myocardial infarction. Of the 26 patients who had aorto coronary bypass grafting, 7 (group 1) had myocardial infarction perioperatively; of these, only 2 had positive results from all four diagnostic tests. The other 19 patients (group 2) had no perioperative myocardial infarction and the only diagnostic method yielding positive results was the LD1 to LD2 ratio, in 7 of the 19. In the 11 patients who did not undergo aortocoronary bypass grafting (group 3), only 1 patient had myocardial infarction perioperatively; results from the measurement of CK2 isoenzyme activity and LD1 to LD2 ratio were positive while electrocardiography and 99mTc pyrophosphate scintigraphy yielded negative results. The respective sensitivity (%) and specificity (%) of the four diagnostic methods were as follows: electrocardiography: 38, 100; 99mTc pyrophosphate scintigraphy: 88, 100; LD1 to LD2 ratio: 100, 68; CK2: 38, 100. When the CK2 criterion was redefined, using patients in group 2 as controls, the sensitivity and specificity of this method became 100 and 90 respectively. The authors conclude that 99MTc pyrophosphate scintigraphy and measurement of myocardial creatine kinase isoenzyme are of comparable value and are the most reliable indicators of perioperative myocardial infarction.

The efficacy of gated synchronous acquisition (GSA) after cardiac blood pool labelling in assessing left ventricular function (ejection fraction and regional wall motion) was evaluated in 31 patients within 24 hours of contrast left ventricular angiography. With the R-wave of the electrocardiogram as a physiologic marker, radionuclide data recorded into an on-line computer allowed construction of cardiac blood pool images during sequential periods of the cardiac cycle. The images, of high count density, have good spatial resolution and can be viewed repetitively in real time in a cine mode. The ejection fractions calculated from the left ventricular time-activity curves corrected for background activity correlated well with the ejection fractions determined from dimension analysis of the contrast left ventricular angiograms (r = 0.87). The results were highly reproducible (r = 0.97). Results of analysis of left ventricular wall motion were similar with the two types of angiograms in 26 of the 31 subjects. GSA is a simple, safe means of evaluating left ventricular ejection fraction and regional wall motion noninvasively.

The efficacy of two beta-receptor antagonists, propranolol and pindolol, was compared with that of a calcium antagonist, verapamil, in the treatment of exertional angina pectoris in 22 men (mean age 51 years). The clinical response and left ventricular function were evaluated with treadmill exercise and with radionuclide ventriculography performed while the patient was at rest or exercising supine with a bicycle ergometer. All the treatments significantly prolonged exercise duration (p less than 0.001) and reduced the number of patients terminating treadmill exercise because of angina (p less than 0.05). The resting heart rate was decreased markedly (p less than 0.001) by propranolol but only slightly (p less than 0.05) by pindolol and verapamil. The left ventricular ejection fraction during rest was unchanged by any treatment, but that during exercise was improved (p less than 0.05) by all the treatments. Patients who failed to gain relief from angina with one of the drugs often responded to another, and adverse reactions occurring with one drug did not necessarily occur with another. In summary, pindolol and verapamil were safe and effective alternatives to propranolol in the treatment of the exertional angina pectoris of these patients.