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Objective: The purpose of this study is to evaluate the clinical significance of radiographic cardiomegaly in orthotopic heart transplant recipients and to identify causative anatomic and physiologic parameters., Materials and Methods: We retrospectively compared the cardiothoracic ratio (CTR) measured using standard posteroanterior chest radiography with left ventricular end-diastolic diameter and left ventricular ejection fraction measured on two-dimensional echocardiography; right ventricular systolic pressure; and systolic, diastolic, and mean blood pressure measured at biopsy in 46 heart transplant recipients., Results: Twenty-eight (61%) of the 46 patients had radiographic cardiomegaly. When we compared heart transplant recipients who had a CTR greater than 0.5 with recipients who had a CTR less than or equal to 0.5, we found no significant difference between their respective left ventricular end-diastolic diameters, left ventricular ejection fractions, right ventricular systolic pressures, systolic blood pressures, or mean blood pressures. A statistically significant difference existed between the mean values of diastolic blood pressure for transplant recipients with and without radiographic cardiomegaly. We found no significant correlation between CTR and left ventricular end-diastolic diameter, left ventricular ejection fraction, systolic blood pressure, diastolic blood pressure, or mean blood pressure., Conclusion: The statistically significant difference between the mean values of diastolic blood pressure of transplant recipients with and without radiographic cardiomegaly is clinically insignificant and unlikely to account for the finding of radiographic cardiomegaly. We conclude that radiographic cardiomegaly, which occurs frequently in heart transplant recipients, does not correlate with anatomic or physiologic parameters obtained under the same conditions. Radiographic cardiomegaly in heart transplant recipients does not connote allograft dysfunction or heart failure.

The mechanisms responsible for immediate adjustments in cardiac output at onset of exercise, in the absence of neural drive, are not well defined in heart transplant (HT) recipients. Seven male HT recipients (mean +/- SD 57 +/- 6 years) and 7 age-matched sedentary normal control subjects (mean age 57 +/- 5 years) performed constant load cycle exercise at 40% of peak power output (Watts). Cardiac output and plasma norepinephrine were determined at rest and every 30 seconds during the first 5 minutes of exercise and at minutes 6, 8, and 10. All subjects were admitted to the General Clinical Research Center for determination of plasma volume. After 3 days of equilibration to a controlled and standardized diet, plasma volume was measured using a modified Evans Blue Dye (T-1824) dilution technique. Heart rate at rest was higher in the HT group (105 +/- 12 vs 74 +/- 6 beats/min), but during submaximum exercise, heart rates in the control group increased more rapidly (p < or = 0.05) and to a greater magnitude (54 +/- 7% vs 17 +/- 4% above rest). Stroke volume at rest was lower in HT recipients (45 +/- 4 vs 68 +/- 9 ml) but was significantly augmented immediately after onset of exercise (30 seconds) and the relative increase was greater than controls at peak exercise (61% vs 38% greater than baseline). Cardiac output at rest was within the normal range in both groups (4.58 +/- 0.27 vs 4.94 +/- 0.40 L/min). Relative increases in cardiac output were similar (p > or = 0.05) for the HT (106 +/- 12%) and control groups (97 +/- 10%). Plasma norepinephrine did not become significantly greater than resting values until approximately 4 minutes after onset of exercise in both groups. Blood volume, normalized for body weight, was 12% greater in the HT group. Thus, HT recipients with expanded blood volume (12%) augment stroke volume immediately after the onset of exercise. Plasma norepinephrine levels contribute negligibly to the rapid adjustment in cardiac output. Rather, we speculate that abrupt on-transit increases in stroke volume are due to augmented venous return, secondary to expanded blood volume.

Pilots who have received a heart transplant may subsequently want to resume flying. This study was undertaken to determine whether a group of heart transplant recipients who had a particularly low risk of sudden unexpected death could be identified from clinical data. An event, "rapid-onset death," was defined incorporating a number of possible causes of death that could result in a heart transplant recipient-pilot losing control of an airplane. The survival of 3676 patients undergoing a first heart transplantation was 85% and 73% at 1 and 5 years, respectively, the hazard function having a high early phase of risk. When time zero was moved to the beginning of the second year after transplantation, the freedom from "rapid-onset death" at posttransplantation year 2 and posttransplantation year 5 was 96.8% and 88%, respectively. For patients who had both a "normal" coronary angiogram and no episodes of acute heart rejection during the first year transplantation, the probability of "rapid onset death" during the second posttransplantation year was 1.4%, and given the same circumstances, during the third posttransplantation year the risk of "rapid-onset death" was 1.6%. This information is potentially useful to the Federal Aviation Administration for policy decisions regarding this issue.

A retrospective review of 15 patients with atrial fibrillation and class III to IV congestive heart failure who underwent atrioventricular nodal ablation demonstrated a marked improvement in their functional abilities. This improvement, however, could not be explained by the improvement in ejection fraction alone.

Thirteen out of 223 consecutive cardiac transplant patients required permanent pacemaker implantation; 11 for sinus node dysfunction and 2 for complete AV block. Patients with sinus node dysfunction were considered for AAIR mode pacemakers if they had intact AV conduction defined as a Wenckebach point of > 120 beats/min. Ten of 11 patients with sinus node dysfunction had a single atrial lead placed. Atrial lead placement was most easily accomplished with a straight, active fixation lead and the use of manually curved stylets to find an optimal position in the donor atrium, although active fixation leads with a preformed atrial J were used as well. Two leads dislodged requiring revision. In contrast, only 1 of 250 atrial leads implanted in nontransplanted hearts dislodged (P < 0.0001). Transvenous endomyocardial biopsies have not caused atrial lead dislodgment. Most transplant recipients requiring permanent pacing have intact AV nodal function and require only atrial pacing. Atrial lead dislodgment requiring lead revision occurs more frequently in heart transplant recipients than in native hearts. Use of a straight active fixation lead with a manually formed curve in the stylet is useful in order to find the optimal position for pacing.

QT dispersion has been cited as a measure of nonuniform myocardial repolarization and a predictor of sudden cardiac death. We describe 38 patients who underwent atrioventricular nodal ablation, 3 of whom had an increase in measured QT dispersion and experienced potentially fatal, pulseless, polymorphic ventricular tachycardia after the procedure.

The purpose of this study was to assess the use of dobutamine stress echocardiography in predicting cardiac events in heart transplant recipients. Dobutamine echocardiography was performed in 63 consecutive heart transplant recipients, 52 males and 11 females ranging in age from 12 to 77 years (mean 54), undergoing routine yearly evaluation. Twenty-one patients had abnormal wall motion at baseline or during dobutamine infusion. Over a mean follow-up of 8 months (range 4 to 14), there were six major cardiac events: five occurred among patients with abnormal echocardiography study results; only one event occurred in a patient with a normal echocardiography result. These data suggest that normal wall motion during dobutamine echocardiography identifies a subset of heart transplant recipients at low risk for development of cardiac events, whereas an abnormal study result serves as an important predictor of subsequent cardiac events.

Background: Orthotopic heart transplantation may interrupt key neural and humoral homeostatic mechanisms that normally adjust Na+ and fluid excretion to changes in intake. Such an interruption could lead to plasma volume expansion., Methods: We measured plasma volume and fluid regulatory hormones under standardized conditions in 11 heart transplant recipients (58 +/- 7 years old; mean +/- standard deviation) 21 +/- 4 months after transplantation, in 6 liver transplant recipients (51 +/- 6 years old) 13 +/- 8 months after transplantation (cyclosporine control group), and in 7 normal healthy control subjects (61 +/- 9 years old). Administration of all diuretics and antihypertensive drugs was discontinued before the study. After 3 days during which subjects ate a constant diet containing 87 mEq of Na+ per 24 hours, plasma volume was measured by a modified Evans blue dye (T-1824) dilution technique. Renal creatinine clearance was measured and blood samples were drawn for determination of plasma levels of vasopressin, angiotensin II, aldosterone, atrial natriuretic peptide, and plasma renin activity., Results: Supine resting plasma renin activity, angiotensin II, and aldosterone (renin-angiotensin-aldosterone axis) and vasopressin levels were not different among the control, heart transplant, and liver transplant groups. However, there was a trend toward elevated angiotensin II (p < or = 0.08) and aldosterone (p < or = 0.08) levels in the heart transplant recipients. Atrial natriuretic peptide levels were significantly elevated two to threefold in the heart transplant recipients when compared with those in the two control groups. Blood volume, normalized for body weight (milliliters per kilogram), was significantly greater (14%) in the heart transplant recipients when compared with that in liver transplant recipients and normal healthy control subjects. Blood volume values did not differ (p > or = 0.05) between the two control groups., Conclusions: Extracellular fluid volume expansion (+14%) occurs in clinically stable heart transplant recipients who become hypertensive. Although hyperactivity of the renin-angiotensin-aldosterone axis is not apparent during supine resting conditions, our data suggest that the renin-angiotensin-aldosterone system is not responsive to a hypervolemic stimulus and this is likely a consequence of chronic cardiac deafferentation. Thus, poor adaptation of the renin-angiotensin-aldosterone system to fluid retention may be partly responsible for the incidence and severity of posttransplantation hypertension in some heart transplant recipients.

Background: Cytokines produced by host cells infiltrating allogeneic transplants are critical determinants of graft rejection but information on cytokine production during graft rejection remains limited. No reported study on cytokine profiles has compared experimental allograft rejection induced by withdrawal of cyclosporine with clinical transplant rejection that occurs in the presence of therapeutic levels of cyclosporine., Methods: Functional activities of allograft-infiltrating host cells in sequential endomyocardial biopsies obtained before, during, and after acute heart transplant rejection were determined with the use of the reverse transcriptase-polymerase chain reaction to detect cytokine messenger RNA. These results were correlated with histologic findings in both an experimental canine model of heart transplant and rejection and in clinical human heart transplant recipients., Results: When experimental rejection was induced by withdrawal of immunosuppression, rejection was characterized by the presence of mRNA encoding CD4, CD8, interleukin-2 (but not interleukin-4), interleukin-2 receptor, and tumor necrosis factor-beta. These findings are consistent with a classic T-helper, T-cytotoxic cell-mediated response. However, the cytokine profile of human, clinical heart transplant rejection occurring in the presence of therapeutic levels of immunosuppression differed strikingly. In clinical rejection in human beings, histologic evidence of rejection was not associated with detectable interleukin-2 or interleukin-2 receptor mRNA., Conclusions: Human, clinical heart rejection can occur in the absence of locally produced interleukin-2; the degree of immunosuppression achieved with cyclosporine A may explain the different results obtained in the canine withdrawal model versus human clinical allograft rejection.

Infective endocarditis is an infrequent but serious complication in heart transplant recipients. We report successful treatment for this serious complication.

Measures of disease severity used in the evaluation of patients with heart failure include survival data, the New York Heart Association classification, ejection fraction, functional assessments, exercise protocols, rest and exercise hemodynamic data, and biochemical parameters including catecholamine levels and serum sodium. Clinicians must integrate these multiple variables into an overall assessment. An overview of the clinical application of these techniques in the evaluation and treatment of patients with heart failure is presented.

Objectives: The purpose of this study was to determine the effectiveness and safety of diltiazem or lisinopril for treatment of hypertension after heart transplantation., Background: Systemic hypertension is common after heart transplantation, and to date there are no randomized, prospective multicenter treatment trials., Methods: Members of the Cardiac Transplant Research Database Group developed and implemented a prospective, randomized multicenter trial of the effectiveness and safety of diltiazem or lisinopril in the treatment of hypertension in cyclosporine-treated patients after heart transplantation., Results: One hundred sixteen patients with hypertension (blood pressure > or = 140/90 mm Hg) after heart transplantation were randomized for > or = 3 months of treatment. Of 55 diltiazem-treated patients, 21 (38%) were responders (diastolic blood pressure < 90 mm Hg), 23 (42%) were nonresponders (diastolic blood pressure > or = 90 mm Hg), and 11 (20%) were withdrawn from the study. Of 61 lisinopril-treated patients, 28 (46%) were responders, 22 (36%) were nonresponders, and 11 (18%) were withdrawn. There was no difference in baseline characteristics or percent responders between the two groups. Systolic pressure decreased from 157 +/- 2.3 to 130 +/- 2.0 mm Hg (mean +/- 1 SEM) in the diltiazem-treated responders and from 153 +/- 2.1 to 127 +/- 2.7 mm Hg in the lisinopril-treated responders (p < 0.0001). Diastolic pressure decreased from 100 +/- 0.9 to 85 +/- 1.6 mm Hg in the diltiazem-treated responders and from 100 +/- 1.0 to 84 +/- 2.0 mm Hg in the lisinopril-treated responders (p < 0.0001). There were a total of 35 reported adverse events, 22 of which led to withdrawal of the patient from the study. All drug-related side effects were considered minor and resolved with discontinuation of the drug., Conclusions: These results indicate that both diltiazem and lisinopril are safe for treatment of hypertension after heart transplantation, although titrated monotherapy with either drug controlled the condition in < 50% of patients.

Background and Hypothesis: Revascularization has provided an effective treatment of depressed left ventricular function in patients with chronically ischemic or "viable" myocardium. Assessment of viable myocardium can be achieved by several noninvasive techniques including dobutamine stress echo or radionuclides such as flurodeoxyglucose (F18DG). F18DG uptake studies are based on the assumption that enhanced glucose uptake in areas of diminished blood flow provides evidence of viable myocardium. To determine the clinical utility of viability assessment in the management of chronic ischemic left ventricular dysfunction, we reviewed the findings and short-term treatment of a series of patients referred for heart failure evaluation who had subsequent F18DG uptake scans., Methods: We retrospectively reviewed 59 consecutive F18DG viability studies in a series of patients who had documented coronary artery disease and depressed left ventricular function. Single photon emission computerized tomography (SPECT) with F18DG was performed in the patients and these images were compared to SPECT images of resting myocardial perfusion using thallium, sestamibi, or teboroxime. Clinical decisions based on the results of these scans were obtained from chart review. Thirty-day mortality was determined from chart review or contact with the patient's physician. The patients were divided into those without and with F18DG uptake consistent with viable ischemic myocardium. Further analysis included subgroups of patients who were advised to undergo transplantation, revascularization, or to continue medical therapy., Results: Of 34 patients referred for cardiac transplantation, 18 had viable myocardium and 13 underwent revascularization. In the entire study group, 34 of 59 (58%) had evidence of viable myocardium and 29 had subsequent revascularization procedures. Thirty-day survival for all revascularization patients was 86%., Conclusion: Assessment of myocardial viability with F18DG SPECT imaging in patients with ischemic left ventricular dysfunction led to a clinical decision for revascularization in approximately half the patients with severe coronary disease and left ventricular dysfunction who were evaluated for myocardial viability in our institution.

We present the case of a patient with left ventricular pseudoaneurysm following acute myocardial infarction. Survival for 2 years following diagnosis, despite the large size of the aneurysm, and subsequent management with cardiac transplantation represent unusual and interesting aspects of this complication of myocardial infarction.

Objectives: This study was designed to investigate disturbances in arterial blood pressure and body fluid homeostasis in stable heart transplant recipients., Background: Hypertension and fluid retention frequently complicate heart transplantation., Methods: Blood pressure, renal and endocrine responses to acute volume expansion were compared in 10 heart transplant recipients (57 +/- 9 years old [mean +/- SD]) 20 +/- 5 months after transplantation, 6 liver transplant recipients receiving similar doses of cyclosporine (cyclosporine control group) and 7 normal volunteers (normal control subjects). After 3 days of a constant diet containing 87 mEq/24 h of sodium, 0.154 mol/liter saline was infused at 8 ml/kg per h for 4 h. Blood pressure and plasma vasopressin, angiotensin II, aldosterone, atrial natiuretic peptide and renin activity levels were determined before and at 30, 60, 120 and 240 min during the infusion. Urine was collected at 2 and 4 h. Blood pressure, fluid balance hormones and renal function were monitored for 48 h after the infusion., Results: Blood pressure did not change in the two control groups but increased in the heart transplant recipients (+15 +/- 8/8 +/- 5 mm Hg) and remained elevated for 48 h (p < or = 0.05). Urine flow and urinary sodium excretion increased abruptly in the control groups sufficient to account for elimination of 86 +/- 9% of the sodium load by 48 h; the increases were blunted (p < or = 0.05) and delayed in the heart transplant recipients, resulting in elimination of only 51 +/- 13% of the sodium load. Saline infusion suppressed vasopressin, renin activity, angiotensin II and aldosterone in the two control groups (p < or = 0.05) but not in the heart transplant recipients. Heart transplant recipients had elevated atrial natriuretic peptide levels at baseline (p < or = 0.05), but relative increases during the infusion were similar to those in both control groups., Conclusions: Blood pressure in heart transplant recipients is salt sensitive. These patients have a blunted diuretic and natriuretic response to volume expansion that may be mediated by a failure to reflexly suppress fluid regulatory hormones. These defects in blood pressure and fluid homeostasis were not seen in liver transplant recipients receiving cyclosporine and therefore cannot be attributed to cyclosporine alone. Abnormal cardiorenal neuroendocrine reflexes, secondary to cardiac denervation, may contribute to salt-sensitive hypertension and fluid retention in heart transplant recipients.

This study provides descriptive data on the prevalence of symptoms and quality of life of cardiac transplantation recipients and tests the predictive validity of a pre-cardiac transplantation psychological assessment battery on posttransplantation quality of life. Following the formation of four cluster groups of pretransplantation MMPI profiles based on previous research, frequency analysis found that the cluster groups were not equally represented among cardiac recipients, such that the "Distressed/Confused" cluster had only one recipient member. Tests of significance among the three remaining cluster groups on the posttransplantation quality of life variables found no significant differences. Regression analyses to test the predictive validity of other pretransplantation medical and psychological variables indicated that trait anxiety was a significant predictor of increased symptom frequency and symptom problems and decreased mental health among recipients. Collectively, modest support was found for the use of pretransplantation psychological variables as predictors of posttransplantation quality of life. Interpretation of psychological test data in the context of other psychosocial variables is discussed.

Background: Previous studies of allograft rejection have focused on early episodes and risk factors from pretransplant variables., Methods: This multiinstitutional study compared early (< 1 year) and late (> 1 year) rejection episodes and risk factors for recurrent rejection from variables both before and after transplantation among 1251 patients who underwent primary heart transplantation and available follow-up of greater than 1 year., Results: There were a total of 1882 rejection episodes over a mean follow-up of 26 +/- 0.3 months. The hazard function (instantaneous risk per patient per month) peaked at 1 month followed by a low constant risk of rejection after 12 months. By multivariable analysis, the most dominant risk factors for recurrent rejection during the first posttransplantation year were a shorter time interval since transplantation and a shorter time since a previous rejection episode. Other factors included young age, female gender, female donor, positive cytomegalovirus serology, prior infections, and OKT3 induction. In contrast, after the first year, the dominant risk factors for rejection were a greater number of rejections during the first year and the presence of prior cytomegalovirus infections., Conclusions: These data show a striking time dependency for rejection episodes among heart transplant recipients. Factors that increase risk for rejection in the first year differ from risk factors for rejection in subsequent years. These data suggest that it may be possible to tailor rejection surveillance protocols and immunosuppression intensity, according to specific patient and time-related risk factors.

Preview Inactivity adds to the decline of patients with congestive heart failure (CHF). However, in prescribing exercise in these patients, three principles must be understood: ejection fraction does not predict functional capacity, exercise can bring marked peripheral improvement without changing ejection fraction or hemodynamics, and benefits accrue slowly. The authors review the mechanisms of exercise intolerance in CHF and the factors to keep in mind when designing an exercise program.

The clinical success of cardiac transplantation requires clinical cardiologists to become familiar with care of the post-transplant patient. This review emphasizes five major post-transplant problems: (1) infection/immunosuppression, (2) metabolic problems, (3) post-transplant hypertension, (4) exercise intolerance, and (5) graft coronary disease. The evolution of these problems after transplantation is emphasized, so that clinical cardiologists and internists sharing the management of these patients can develop a context in which to work.

Objectives: The purpose of this study was to determine whether heart transplantation has an adverse effect on pulmonary diffusion and to investigate the potentially deleterious effects of impaired pulmonary diffusion on arterial blood gas dynamics during exercise in heart transplant recipients., Background: Abnormal pulmonary diffusing capacity is reported in patients after orthotopic heart transplantation. Abnormal diffusion may be caused by cyclosporine or by the persistence of preexisting conditions known to adversely affect diffusion, such as congestive heart failure and chronic obstructive pulmonary disease., Methods: Eleven patients (mean age 50 +/- 14 years) performed pulmonary function tests 3 +/- 1 months before and 18 +/- 12 (mean +/- SD) months after heart transplantation. Transplant patients were assigned to groups with diffusion > 70% (n = 5) or diffusion < 70% of predicted values (n = 5). The control group and both subsets of patients performed 10 min of cycle exercise at 40% and 70% of peak power output. Arterial blood gases were drawn every 30 s during the 1st 5 min and at 6, 8 and 10 min., Results: Significant improvements in forced vital capacity (17.4%), forced expiratory volume in 1 s (11.7%) and diffusion capacity (6.6%) occurred in the patients; however, posttransplantation vital capacity, forced expiratory volume and diffusion were lower (p < or = 0.05) compared with values in 11 matched control subjects. Changes in blood gases were similar among groups at 40% of peak power output. At 70% of peak power output, arterial blood gases and pH were significantly (p < or = 0.05) lower in transplant patients with low diffusion (arterial oxygen pressure 15 to 38 mm Hg below baseline) than in patients with normal diffusion and control subjects. Cardiac index did not differ (p > or = 0.05) between transplant patients with normal and low diffusion at rest or during exercise. Posttransplantation mean pulmonary artery pressure was significantly related to exercise-induced hypoxemia (r = 0.71; p = 0.03)., Conclusions: Abnormal pulmonary diffusion observed in patients before heart transplantation persists after transplantation with or without restrictive or obstructive ventilatory defects. Heart transplant recipients experience exercise-induced hypoxemia when diffusion at rest is < 70% of predicted. Our data also suggest that abnormal pulmonary gas exchange possibly contributes to diminished peak oxygen consumption in some heart transplant recipients; however, direct testing of this hypothesis was beyond the scope of the present study. This possibility needs to be investigated further.

Background: Allograft vasculopathy after heart transplantation is thought to represent a response to endothelial injury in the graft vessels. To assess endothelial function before the onset of anatomic disease, coronary vasomotor responses to adenosine, acetylcholine, and nitroglycerin were evaluated in transplant recipients by intravascular ultrasound imaging and Doppler flow studies., Methods and Results: Nine patients were studied 1 year after heart transplantation. Acetylcholine provoked significant vasoconstriction to 82% of maximal coronary diameter but was associated with an increase in mean coronary blood flow from 63.1 to 204 ml/min. Coronary blood flow increased fivefold in response to adenosine, a normal response., Conclusions: The vasomotor response to acetylcholine at 1 year after heart transplantation is consistent with endothelial dysfunction in the epicardial conduit vessels. Microvascular function as judged by coronary flow reserve appears to be normal.

The spectacular clinical success of heart transplantation (HTTX) in the cyclosporine era has engendered challenging new clinical problems that include long-term management of patients with severely compromised systolic function, preparation of potential HTTX recipients for major surgery followed by immunosuppression, and ethical and rational distribution of limited numbers of donated organs. The magnitude of these challenges may seem overwhelming. Fortunately, clinicians have the luxury of dealing with the issues involved one patient, and one step, at a time. The continued efforts of clinical investigators have clarified important management principles. There is a growing appreciation of the pivotal importance of mitral valve function in determining the response to medical therapy and long-term prognosis in this patient population. Enthusiasm for pharmacologic control of asymptomatic ventricular ectopy has waned; instead, the restoration and maintenance of normal atrial function has clearly taken precedence. In preparation for surgery, new endoscopic techniques offer great advantages. The use of high-technology support devices as "bridges to transplantation" has been re-examined in view of the relatively poorer short- and long-term prognosis of patients managed with these devices. Increasingly, the optimal scenario for HTTX entails transplantation of a severely compromised but medically stable patient. As specific therapy, HTTX today has relatively limited application to the vast majority of patients with heart failure (HF). Seventeen hundred heart transplants will do little to directly affect the 400,000 patients in the United States who each year develop symptomatic HF.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative serial coronary angiograms performed annually over a 3-year period after transplantation in 26 orthotopic heart transplant recipients showed persistently normal nitroglycerin-induced vasodilation. The vasodilator response to nitroglycerin did not predict development of graft arteriopathy; the presence of graft arteriopathy did not prevent a substantial vasodilator response to nitroglycerin.

Quantitative angiographic studies with use of cine-videodensitometry after maximal coronary vasodilation with nitroglycerin in 18 "angiographically normal" heart transplant recipients demonstrated significant loss of lumen diameter between years 1 and 3. When sensitive angiographic techniques are used, graft arteriopathy appears to be ubiquitous in heart transplant recipients.

Coronary artery dissection is an infrequent but serious complication of coronary angioplasty that can lead to periprocedural vessel occlusion, emergency bypass surgery, myocardial infarction or death. Recently, a perfusion balloon catheter was developed that permits passive perfusion of blood through the central lumen of the catheter. It enables prolonged balloon inflations to be performed and has been used to provide distal blood flow after coronary occlusion. To evaluate the effectiveness of the perfusion balloon catheter in patients with major coronary dissections, 36 consecutive patients treated with the perfusion balloon catheter were compared with 46 consecutive patients treated before its availability. The 2 groups were similar in terms of clinical, angiographic and initial procedural characteristics. Use of the perfusion balloon catheter permitted a significantly longer inflation than standard balloon inflation (average 18 +/- 5 min). Angiographic success was significantly greater with the perfusion balloon catheter (84 vs 62% for conventional therapy), whereas complications were markedly reduced (48 vs 78%). With the perfusion balloon catheter there were fewer deaths (2 vs 6%), myocardial infarctions (14 vs 40%) and emergency bypass operations (11 vs 25%). The findings of this retrospective comparison demonstrate that the perfusion balloon catheter is effective for the management of major dissections after coronary angioplasty. The use of the perfusion balloon catheter should be considered when a major coronary dissection occurs and when emergency bypass surgery is contemplated.

Long-term follow-up of patients undergoing coronary artery bypass graft surgery indicates that as many as 50% eventually experience recurrent angina pectoris. Rational management of these individuals requires an understanding of the natural history of coronary bypass grafts, the risks and benefits of both reoperation and angioplasty, as well as a structure within which to integrate these data. This report reviews the literature and employs formal decision analysis to develop a strategy for management of recurrent angina. Our analysis supports the strategy that patients experiencing recurrent angina within 3 years after surgery should undergo prompt angiographic re-evaluation and angioplasty if anatomically suitable. Symptoms beginning more than 6 years after surgery should be managed medically, reserving surgery for refractory symptoms.

The patient had collateral flow from the right coronary to left circumflex coronary artery in the absence of proximal obstructive disease. This supports the hypothesis that the intercoronary collaterals seen in coronary atherosclerotic disease are present in the normal heart.

Two female patients with carcinoid heart disease, ages 56 and 32 years, underwent pulmonic valve resection surgery and tricuspid valve replacement with a porcine bioprosthesis. Preoperatively, both patients were in function class 4 with severe right-side congestive failure and signs of tricuspid regurgitation and pulmonic stenosis. Both underwent surgery for porcine tricuspid valve replacement (33 and 31 mm valves) and pulmonic valve resection. Postoperatively, both patients had only minimal symptoms, including trace ankle edema and soft pulmonic murmurs, despite persistence of the systemic symptoms of carcinoid syndrome. Pre- and postoperative catheterization data documented hemodynamic improvements. One patient eventually died of hepatic failure due to metastatic disease. At autopsy, her bioprosthesis was free of carcinoid valvular changes.

Clinical, electrocardiographic and cineventriculographic data in two patient groups were analyzed to define the natural history of S-T segment elevation after myocardial infarction. In sixteen of 22 patients (73 percent) with acute inferior myocardial infarction, S-T segment elevation was present on hospital admission, persisting in 1 (5 percent) by the 2nd week. S-T segment elevation was present on admission in 18 of 23 patients (78 per cent) with acute anterior myocardial infarction and persisted in 13 after 1 week and in 9 of 14 (64 percent) during a follow-up period of 1 to 6 months. S-T segment elevation lasting more than 2 weeks after myocardial infarction did not resolve. Compared with patients with inferior myocardial infarction or anterior infarction without persistent S-T segment elevation, patients with anterior infarction and persistent S-T segment elevation had a higher level of mean maximal serum creatine phosphokinase (CPK), more severe left ventricular decompensation and a greater frequency of death in the early follow-up period. In a separate series of 95 patients with cineangiographically documented coronary artery disease, 40 of 65 patients (62 percent) with advanced anterior and apical asynergy had persistent S-T segment elevation. By contrast, only 1 of 30 (3 percent) with coronary disease and normal ventriculograms had persistent S-T segment elevation. We concluded that (1) the natural history of S-T segment elevation after myocardial infarction is resolution within 2 weeks in 95 percent of inferior but in only 40 percent of anterior infarctions; (2) S-T segment elevation persisting more than 2 weeks after myocardial infarction does not resolve; (3) persistent S-T segment elevation is associated with clinically more severe myocardial infarction; and (4) in patients with coronary artery disease, persistent S-T segment elevation after myocardial infarction is a specific but insensitive index of advanced asynergy.

In 2 patients cardiac rhythm disturbances clearly caused falls and hip fractures. This prompted us to study patients with hip fractures to determine if any combination of clinical and laboratory findings identified those with fractures due to arrhythmia.

Arteriovenous differences (A-V) of all naturally occurring amino acids, lactate, and oxygen were measured simultaneously with coronary sinus blood flow (CSBF) in 8 normal subjects and 11 patients with coronary artery disease at rest and during pacing stress. Mean values for CSBF and myocardial oxygen consumptions (MVO2) for the two groups were similar at rest and during pacing, although mean CSBF and MVO2 increased significantly in both groups in the paced as compared to the rest state. Alanine (ala) was the only amino acid released by the myocardium, while only glutamic acid(glu) demonstrated uptake. Mean A-V ala was negative at rest in the control and coronary disease groups (-4.8+/-3.8 vs. -22.0+/-3.0 nmol/ml, respectively), but was significantly more negative in the coronary group (P less than 0.001) and not statistically different than zero in the normals. A-V ala became significantly negative with pacing in the normals (-10.0+/-4.3 nmol/ml), remained unchanged in the coronary group (-23.0+/-2.9 nmol/ml), and was significantly more negative in the coronary group (P less than 0.05). Calculation of data on the basis of net ala flux ([A-V] X [CSBF X hematocrit]) yielded similar results as that obtained with A-V differences. A-V glu was significantly positive in normals (27.7 +/- 8.9 nmol/ml, P less than 0.01) and coronary patients (59.9 +/- 8.9 nmol/ml, P less than 0.01) at rest but significantly greater in the latter group (P less than 0.001). With pacing, A-V glu remained significantly greater than zero in coronary patients (35.3 +/- 6.3 nmol/ml) and decreased to zero in the normals (4.3 +/- 11.8 nmol/ml). Calculation of net glu flux (nmol/min) at rest yielded data similar to that based on A-V difference. With pacing, net glu flux in the coronary patients did not decrease due to the augmentation of CSBF. No relation between A-V glu or ala and CSBF, MVO2 or A-V lactate was noted. The data demonstrate that specific alterations of myocardial amino acid metabolism characterize patients with chronic ischemic heart disease.

Data from exercise tolerance testing should be incorporated into clinical decision making. A strategy for stratification of individual patients into high, indeterminate, and low-risk categories using Bruce protocol exercise testing is outlined. This approach will help to ensure further evaluation of high-risk individuals without excessive testing of patients having excellent long-term prognoses.

We describe a patient with an unusual coronary anatomic variant in which the first septal perforator gives rise to the posterior descending artery. The angiographic features and clinical recognition of this anomaly are reviewed.

To assess possible coronary vasoconstriction in patients with ischemic heart disease, we measured coronary vascular resistance in 12 patients with normal hearts and 12 with coronary disease before and during the initial 50 seconds of cold pressor test, a stimulus known to produce systemic vasoconstriction. Control coronary vascular resistance was similar in the two groups, and although it did not change in patients with normal vessels, it rose by 27 per cent (P less than 0.005) in the group with coronary disease during the cold pressor test. In three of 12 patients with coronary disease coronary flow actually declined despite an increase in arterial pressure; in four, angina was precipitated. Phentolamine abolished increases in arterial pressure and coronary vascular resistance during the test in three patients with coronary disease. Adrenergically mediated coronary vascular tone may be an important determinant of coronary blood flow and may contribute to ischemia in patients with coronary disease.

The risk of embolic stroke during sick sinus syndrome before cardiac pacemaker insertion is substantial, but stroke after pacemaker insertion has not been well studied. We observed 10 sick sinus syndrome patients who developed an ischemic stroke 4 days to 112 months after pacemaker insertion. Nine patients represented 6% of the 156 ischemic stroke patients observed during a 30-month period. Eight had a ventricular-demand pacemaker, one had a dual-chamber pacemaker, and one had an atrial-inhibited pacemaker. Six patients were in atrial fibrillation at stroke onset, but none had atrial fibrillation when the pacemaker was inserted. Six patients were taking aspirin, and one was anticoagulated when stroke occurred. Stroke in sick sinus syndrome after pacemaker insertion is not rare, and pacing does not appear to be protective. Sick sinus syndrome patients who convert to atrial fibrillation or who have a ventricular-demand pacemaker might represent high-risk groups for stroke.

A "new" shallow left anterior oblique view of the right coronary artery allows better visualization of the distal vessel in selected patients. This paper describes the angiographic technique; retrospective data suggest that the view is useful in approximately 20% of patients. An illustrative case is presented.