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Objectives: We sought to test the hypothesis that late recanalization of infarct-related coronary arteries (IRAs) improves long-term left ventricular (LV) function., Background: Reperfusion within 24 h of an acute myocardial infarction (MI) has been shown to improve myocardial healing and to reduce infarct expansion. Uncontrolled data suggest that there may be a time window of several weeks for such an effect., Methods: Sixteen asymptomatic patients 10 +/- 4 days after a first Q wave anterior wall MI with persistent left anterior descending coronary artery occlusion and infarct-zone akinesia were randomized to immediate (2 weeks) or delayed (3 months) angioplasty. Repeat catheterization and cardiac magnetic resonance imaging (MRI) were performed after 3 and 12 months., Results: Angiography 3 months after MI revealed that LV ejection fraction (LVEF) had increased ([mean +/- SD] 54.4 +/- 4.3% vs. 63.9 +/- 7.4%, p < 0.01) as a result of improved regional function (p < 0.01) and LV end-systolic volume had decreased (p < 0.002), whereas LV end-diastolic volume remained unchanged. With delayed angioplasty, LVEF, infarct zone wall motion and LV volumes did not improve. Cardiac MRI at baseline and at 3 and 12 months confirmed these findings and extended them up to 1 year, indicating that delayed angioplasty could no longer improve LV function because of marked LV dilation (p < 0.01). Immediate angioplasty had a high success rate, but restenosis (50%) was accompanied by new severe angina as a clinical indicator of salvaged myocardium, which did not occur after delayed angioplasty., Conclusions: This pilot study in selected patients supports the hypothesis that myocardial viability persists ("hibernation") for 2 to 3 weeks but not for 3 months after MI, during which time it may be worthwhile to restore blood flow to a large myocardial territory, even in asymptomatic patients, to improve long-term LV function.

In the BASIS study, an improvement in 1 year survival of patients with asymptomatic complex ventricular arrhythmias with low-dose amiodarone was shown in comparison with an untreated control group. To assess whether this beneficial effect would last for a longer follow-up despite discontinuation of amiodarone therapy after one year, we assessed long-term survival and mode of death in the 91 survivors of the first year in the amiodarone treatment group and the 99 survivors in the control group by phone calls to private physicians, patients and hospitals. During a median follow-up of 72 (55-125) months, 184/193 patients (95%) could be reached. Causes of death during the follow-up were sudden (6 vs 14), non-sudden cardiac (8 vs 9), non cardiac (5 vs 9) and unknown (7 vs 6) in patients initially treated with amiodarone versus the control group respectively. The probability of death after 84 months was 30% in the amiodarone group and 45% in the control group, and was significantly lower in amiodarone treated patients with respect to all deaths (p = 0.024) as well as cardiac deaths (p = 0.027). This mortality reduction was only due to amiodarone treatment during the first year after the index infarction, whereas the survival curves did not differ significantly during the late follow-up. Thus, the risk of cardiac death is low after the first year after myocardial infarction and may not justify continued antiarrhythmic therapy in patients with initially complex asymptomatic ventricular arrhythmias.

Background: In the Basel Antiarrhythmic Study of Infarct Survival trial, low-dose amiodarone improved 1-year survival in patients with asymptomatic complex ventricular arrhythmias persisting 2 weeks after myocardial infarction. To assess whether this beneficial effect persisted despite discontinuation of amiodarone after 1 year, the long-term outcomes of all patients of the amiodarone-treated group (initially n = 98) and those of the control group (n = 114) were assessed., Methods and Results: After a mean follow-up of 72 (55-125) months, information on 96% of patients (203 of 212) was obtained regarding survival or cause of death. The probability of death after 84 months according to actuarial life-table analysis (Kaplan-Meier) was 30% for the amiodarone-treated patients and 45% for control patients. For the total follow-up, mortality remained significantly lower in the amiodarone group versus the control group regarding all deaths (p = 0.03) as well as cardiac death (p = 0.047). This mortality reduction was entirely due to the first-year amiodarone effect, since there was no significant mortality difference between groups when considering survival after discontinuation of amiodarone only., Conclusions: These data suggest that the beneficial effect of amiodarone on survival in this high-risk group of patients persists for several years. In addition, the results stress the importance of early treatment after myocardial infarction, whereas the rate of sudden death and all cardiac death is low (1.6% and 4.1% per year, respectively) during late follow-up and therefore may not warrant further therapy.

In order to assess whether the outcome of MI can be predicted by clinical data alone or whether and how much noninvasive testing is necessary to predict cardiac events or death, 361 patients were prospectively evaluated and followed for up to five years. A recursive partitioning analysis indicated that high-risk patients can be identified clinically after MI with a high degree of accuracy; to separate low-risk patients who need no further investigation or therapy, however, one additional noninvasive test is necessary which allows quantification of myocardial damage as well as exercise-induced ischemia. Additional tests added little to this risk prediction, indicating that multiple noninvasive testing should not be performed.

Carnitine, a quaternary amine (3-hydroxy-4-N-trimethylaminobutyric acid), plays an important physiologic role in fatty acid transport and metabolism as well as in energy production of the myocardial cell. L-carnitine in high doses has been postulated to have an antiarrhythmic effect and this has also been clinically proven. We studied 20 patients with acute myocardial infarction (AMI), 4-12 hours after onset of pain. The patients were randomized and treated double-blind with 5 g L-carnitine (n = 12) or placebo (n = 8) at hours 0, 12, 24, 36, and with 2 x 3 g on days 3 to 7 by intravenous infusion over 2 hours. The two groups were similar for age, sex, infarct site, maximum CPK and conventional antiarrhythmic therapy. 24-hour Holter-ECG was performed on days 1, 2 and 7 and showed no significant difference between the two groups with respect to incidence of ventricular premature beats (VPB) per hour. On the second day following AMI, however, only 4 of 12 carnitine-treated patients showed high-grade VPB (Lown IVa and IVb), in comparison with 7 of 8 patients in the placebo group. The difference is significant: p = 0.028 (Fisher's Exact Test). Carnitine was well tolerated and the efficacy demonstrated on the second day following AMI must be interpreted with caution.

To determine whether the beneficial effect of low-dose amiodarone on survival in patients with complex ventricular arrhythmias after myocardial infarction was dependent on left ventricular (LV) function, results of the Basel Antiarrhythmic Study of Infarct Survival were analyzed. Two hundred twelve patients after acute myocardial infarction with asymptomatic complex arrhythmias were randomly assigned to receive amiodarone 200 mg/day or to a control group and followed up for 1 year. Results of mortality and arrhythmic events were related to baseline radionuclide LV ejection fraction. With preserved (greater than or equal to 40%) LV ejection fraction, there was a significantly lower 1-year cardiac mortality in patients treated with amiodarone (1 of 68 or 1.5%) versus control subjects (5 of 56 or 8.9%; p less than 0.03). This was not the case for patients with LV ejection fraction less than 40%. Similarly, arrhythmic events were significantly reduced only in patients with preserved LV function. These results suggest an interaction between the effects of amiodarone on survival and LV dysfunction in patients after acute myocardial infarction. Because of 2 other small studies with similar results, this finding may be of clinical relevance and should be addressed in ongoing and future research with this drug.

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.

To assess whether myocardial dysfunction after acute reperfusion ('stunning') may show delayed recovery, 33 patients of the European Cooperative Study (rtPA vs placebo) had radionuclide angiocardiography on day 9 and after 3-6 months. Sixteen patients (13 inferior, three anterior infarcts) had a normal left ventricular ejection fraction (LVEF) which remained unchanged (55.4 vs 53.9%). In contrast, LVEF of 17 patients (10 inferior, seven anterior infarcts) with depressed values on day 9 improved during follow-up from 38.8 to 45.2% (P less than 0.01). Improvement was only observed in patients with early reperfusion defined a priori as peak creatine kinase value less than or equal to 15 h of pain onset (from 40.9 to 49.3%; P less than 0.05) in contrast to patients without reperfusion (from 34.0 to 35.2%; ns). Accordingly, LVEF increased in patients with open infarct-related arteries at hospital discharge (n = 8; P = 0.053) but not with persistent occlusion (n = 7; P = 0.11). Thus, a depressed LVEF observed 9 days after reperfusion may show delayed recovery due to prolonged stunning. Therefore, after thrombolysis, left ventricular function may not be evaluated definitively at hospital discharge; results of such studies should be interpreted with caution.

In an attempt to improve survival of patients with coronary artery disease and high-grade ventricular ectopic activity, several studies using different antiarrhythmic drugs were undertaken. A meta-analysis of all randomized controlled trials using type I antiarrhythmic agents showed that the treatment effect was much more likely to be adverse than beneficial. In contrast to these studies, the pooled results of major secondary prevention trials using beta-blocking agents could demonstrate a significant reduction in the sudden death rate by an average of 24% during observation periods of 9-36 months. In the beta-blocker trials, however, patients with contraindications for this type of drug, such as overt congestive heart failure or chronic obstructive lung disease, were excluded. In these patients a type III antiarrhythmic drug, such as amiodarone, may have a place, and in fact, the Basel Antiarrhythmic Study of Infarct Survival, a prospective, controlled, randomized trial using low-dose amiodarone as an antiarrhythmic agent, could demonstrate a 60% reduction in sudden death rate and a 74% reduction in arrhythmic events incidence during the first year after myocardial infarction. Therefore, in patients with repetitive ventricular ectopic activity after myocardial infarction and adequate left ventricular function, a therapeutic attempt with beta-blockers without intrinsic sympathomimetic activity seems advisable. Beside beta-adrenergic blockade, low-dose amiodarone is an alternative, especially in patients with impaired left ventricular function or other contraindications for beta-blockers.

In view of the high risk of sudden cardiac death and the prognostic importance of complex ventricular ectopic activity, the effects of prophylactic antiarrhythmic treatment were investigated prospectively in patients with persisting asymptomatic complex arrhythmias after myocardial infarction. End points were total mortality and arrhythmic events (sudden death, sustained ventricular tachycardia and ventricular fibrillation). Of 1,220 consecutively screened survivors of myocardial infarction, 312 had Lown class 3 or 4b arrhythmia on 24 h electrocardiographic recordings before hospital discharge and consented to the study. They were randomized to individualized antiarrhythmic treatment (Group 1, n = 100), treatment with low dose amiodarone, 200 mg/day (Group 2, n = 98) or no antiarrhythmic therapy (Group 3 [control group], n = 114). During the 1 year follow-up period, 10 patients in Group 1 died, as did 5 in Group 2 and 15 in Group 3. On the basis of an intention to treat analysis, the probability of survival of patients given amiodarone was significantly greater than that of control patients (p less than 0.05). In addition, arrhythmic events were significantly reduced by amiodarone (p less than 0.01). These effects were less marked and not significant for individually treated patients (Group 1). These findings suggest that low dose amiodarone decreases mortality in the 1st year after myocardial infarction in patients at high risk of sudden death.

In view of today's efforts to preserve myocardial function in acute myocardial infarction, the prevalence and extent of persistent right ventricular dysfunction was analysed in a prospective study of 127 patients admitted with a first myocardial infarction without thrombolysis. Right ventricular ejection fraction measured at hospital discharge by radionuclide angiocardiography was related to the location of infarction as judged electrocardiographically, its size as estimated enzymatically, and by the simultaneously measured left ventricular ejection fraction. Two opposite patterns of right and left ventricular function were observed in relation to the location of infarction: the right ventricular ejection fraction was significantly depressed in inferior, but not in anterior, infarction and the reverse was true for left ventricular ejection fraction (P less than 0.001 between infarct locations for both right ventricular ejection fraction and left ventricular ejection fraction). There were significant correlations between peak levels of creatine kinase and left ventricular ejection fraction for anterior (r = 0.76, P less than 0.001) and inferior (r = 0.57, P less than 0.001) infarction, while peak levels of creatine kinase and right ventricular ejection fraction correlated only in inferior infarction (r = 0.45, P less than 0.01). There was no overall correlation for left ventricular ejection fraction and right ventricular ejection fraction (r = 0.28, P NS), despite the fact that right ventricular ejection fraction was lower in patients with severely reduced left ventricular ejection fraction than in those with normal left ventricular function (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The long-term care of patients following heart transplantation is characterized by the problems associated with long-term immunosuppression. In addition, a specific form of coronary atherosclerosis develops within years in many patients requiring coronary angiography on a yearly basis. The examination of patients after heart transplantation does not reveal characteristic findings, as long as the transplanted heart functions properly and a normally functioning graft allows a functionally almost normal life. The dependence on a specialized center, which may be more or less depending on the clinical course, and the ever present knowledge of the potentially lethal consequences of a graft failure present a severe psychic stress to the patient. This stress is handled more or less well and requires special attention by the treating physicians and, ideally, an intact social environment. The care of patients in a center close to their place of living is less time consuming for the patient and relieves the burden of the transplanting center.

The prophylactic effect of beta-blockers in reducing reinfarction and cardiac death after acute myocardial infarction has been proven convincingly in several studies. Whereas anticoagulation is not generally accepted in secondary prophylaxis, it has been shown that in patients where treatment with anticoagulants could be performed without difficulty, withdrawal of the drug is disadvantageous. Large-scale studies have shown the relatively slight effect of drugs which inhibit platelet aggregation. The indication for these drugs, and "prophylactic" surgery to improve prognosis, are discussed with respect to the various risk groups.

We analysed a group of 35 consecutive patients with acute myocardial infarction-23 of the inferior, 12 of the anterior wall-who needed temporary pacing for bradycardiac arrhythmias. We observed in three patients ventricular tachycardias induced by pacemaker stimuli falling onto the vulnerable part of the cardiac cycle due to improper sensing. All three had an inferior myocardial infarction involving the right ventricle. Because the pacemaker electrode in this condition lies in the vicinity of the infarcted myocardium sensing problems occur more frequently and re-entry tachycardias can be triggered more easily. It represents a possible risk of pacemaker treatment in his group of patients who, on the other hand, often need cardiac pacing in the acute phase following the development of transient AV-block.

The longterm effects of early mobilization after myocardial infarction (MI) have been investigated. 122 patients aged under 65 years were reexamined 84.6 +/- 24 weeks after MI. The physical work capacity (PWC) of these men was 22% below the normal value. Patients with angina pectoris after MI had a PWC only 45% of normal. The overwhelming majority (88%) of MI survivors had returned to their jobs by the end of the follow-up period. Of the conventionally treated patients only 70% had returned to work. Age, PWC after MI and psychological status critically influence the rapidity and rate of return to work after MI.

Treatment of patients with acute coronary artery disease in a medium-sized hospital (with multidisciplinary intensive care unit) is compared with treatment in a university hospital. Two groups of 68 patients (under 70 years of age, without preexisting infarction) are comparable in history, physical findings, infarct size and localization, and complications. Quality or care is assessed on the basis of the findings at discharge and the length of hospital stay. We conclude that the quality of care in a medium-sized community hospital (in collaboration with the university hospital) is satisfactory.

Early mobilisation after acute myocardial infarction is said to increase the risk of ventricular aneurysm and -rupture, reinfarction, sudden death, and heart failure. In order to evaluate these possible negative effects, we run a prospective and controlled study: 2 X 100 consecutive patients with acute myocardial infarction were mobilized conventionally (A) and according to an early mobilisation programme (B) respectively-the two groups were comparable according to age, sex, CHD-history, infarction transmural/non transmural and coronary prognostic index (Norris). There was a significant reduction in the average hospital stay from 31.4 days in group A to 25.8 in group B. The patients were followed up for 32 (A) and 46 days (B) respectively. In the early mobilized group we found no increased risk for heart failure, reinfarction, or sudden death. On the other side, early mobilisation has many psychological, oeconomic and social advantages for patients and hospital.

Preliminary experience with thrombolytic therapy in patients with acute myocardial infarction and its practicability in a CCU of a Swiss university hospital are presented. Out of 674 patients with a transmural or non-transmural infarction, 72 (11%) have been treated with thrombolytic agents since March 1986. 53 of these patients were included in the "European Cooperative Study Group" multicenter trial and treated with recombinant tissue plasminogen activator (rt-PA) or placebo; the other 19 patients received streptokinase i.v. with the same inclusion/exclusion criteria. The results corresponded to the well known effects of early thrombolysis with improvement in infarct size reduction, cardiac performance and early mortality.--The importance of the time factor and the implications regarding information of potential patients and practitioners and organization of rapid hospitalization are outlined. Follow-up (after a mean of 14 months) of our 72 thrombolysis patients revealed a high percentage of patients still dependent on medical care, reduced physical capacity in almost half of the patients and (a favourable result) a large number of patients who stopped smoking after the infarction. --In view of the slight additional stress caused by this therapy for patients, physicians and nursing staff, the use of thrombolytic agents in acute myocardial infarction should (with strict inclusion/exclusion criteria) be rapidly generalized in the hospitals of Switzerland.

In 1986/87, emergency-PTCA in acute myocardial infarction was performed in 13 patients in whom thrombolysis was contraindicated. All infarct-related arteries could be opened with PTCA. Patency rate after one week was 94%. Reopening of the vessel resulted in immediate cessation of ischemic chest pain and in stable cardiac rhythm and hemodynamics. Prior cardiopulmonary resuscitation and/or cardiogenic shock did not influence short- or longterm outcome. In nine of eleven patients an improvement of left ventricular function was found after four to six months as compared to one to four weeks after PTCA. The functional result proved to be better if PTCA was performed early; PTCA within 90 minutes was associated with normal left ventricular function. Thus, PTCA is feasible as an emergency procedure in patients with acute myocardial infarction and contraindications to thrombolysis. It can salvage myocardium and improve or prevent severe infarct complications when performed early after onset of pain. Rapid hospital admission through the primary care physician importantly influences the outcome for these patients.

To assess the prognostic significance of right ventricular dysfunction after a first myocardial infarction for complex ventricular arrhythmias and or sudden cardiac death in relation to infarct location, size and left ventricular function, a series of 127 consecutive patients was prospectively studied and followed up for one year. Prior to hospital discharge, a 24-hour electrocardiographic recording and radionuclide angiocardiography were performed. Right ventricular ejection fraction was related to inferior infarct location and size (r = 0.45, P less than 0.01): similarly left ventricular ejection fraction was related to anterior infarct location and size (r = 0.76, P less than 0.001). The incidence of severe ventricular arrhythmias was significantly higher in patients with isolated right or left ventricular dysfunction compared to patients with normal function; it was highest in patients with severe depression of both ventricles. Patients with complex ventricular arrhythmia and/or sudden cardiac death had significantly reduced left and right ventricular ejection fractions. Detailed analysis in patients with left ventricular ejection fraction greater than 0.40 vs. less than or equal to 0.40 showed that presence of complex ventricular ectopic activity and/or sudden cardiac death after myocardial infarction was related not only to left, but also independently to right ventricular dysfunction. These results imply a significant prognostic contribution of right ventricular dysfunction to the occurrence of severe ventricular arrhythmias and/or sudden cardiac death after myocardial infarction independent of and additive to left ventricular dysfunction.

The short- and long-term results of provisional pacemaker therapy in fresh myocardial infarction have been investigated. In this cardiac unit in the period 1975--1977 provisional pacemakers were implanted in 48 patients due to severe conduction disturbance or sinus node syndrome with non-tolerated heart failure. 16 patients had bifascicular block (11 anterior, 3 diaphragmatic, and 2 non-localizable infarctions): in 9 (56%) of them, progression to complete AV block occurred. 27 patients exhibited AV block of 2nd to 3rd degree without evidence of fascicular blockades (21 diaphragmatic, 3 anterior, and 3 non-localizable infarctions). In 5 patients, sinus node dysfunction was the reason for pacemaker implantation. Hospital mortality in the group was 31.2% and thus was twice as high as the hospital mortality in all patients hospitalized in this unit with myocardial infarction during the same period (16.5%). The hospital mortality in patients with anterior infarction was 57.2% compared with a mortality of 16.7% in patients with diaphragmatic infarction. Late mortality (18 months after myocardial infarction) in the group was 46.8%. None of the patients with diaphragmatic infarction died during this observation period. In the patient group with anterior infarction, the mortality rose to 85.8%. Of the 14 patients who died in hospital, death in 12 was due to severe heart failure: neither bradycardic nor tachycardic arrhythmias were immediate factors in death. At autopsy, all patients exhibited severe coronary sclerosis with extensive myocardial infarction. Only 2 patients died from arrhythmia (atrial fibrillation/asystole). In 6 of the 34 survivors, a definitive pacemaker was implanted. 3 of these patients died in the first year after the myocardial infarction. Death was sudden in all three.

Hemodynamic measurements before and during graded leg-up tilt were performed in 20 patients on the 1st and 3rd day following myocardial infarction. In those with an elevated pulmonary capillary pressure (greater than 11 mm Hg), independent of the cardiac index, the tilt-test (i.e. an additional increase in preload) unmasked heart failure. When applied to test drug responses, furosemide (n = 7) reduced the tilt-stimulated cardiac index with an attendant fall in pulmonary capillary pressure; nitroglycerine (n = 7) did not change cardiac index but reduced the pulmonary capillary pressure.

In order to assess the effect of prophylactic antiarrhythmic therapy in asymptomatic patients with persistent complex ventricular ectopic activity after myocardial infarction, a prospective controlled trial was started in 1981 and is still ongoing. Until August 1986, 965 consecutive patients less than or equal to 70 hospitalized for acute myocardial infarction were screened without antiarrhythmic drugs by 24-h ECG before discharge from the hospital. In this group, 238 patients (28%) had ventricular arrhythmias Lown class III-IVb during at least 2 of 24 hours; they were randomly assigned to three treatment groups: (1) individualized antiarrhythmic therapy based on efficacy in multiple 24-h ECGs and drug level determinations (starting with mexiletine or quinidine; n = 79), (2) treatment with low-dose amiodarone (200-400 mg/day after a loading phase; n = 73), and (3) no antiarrhythmic therapy (n = 86). The three groups were comparable regarding age, gender, previous infarction, Q-wave infarction, ejection fraction, as well as incidence and severity of ventricular ectopic activity. Follow-up, including 24-h ECGs, was performed after 3, 6, and 12 months. Based on the results of this study which will be completed by the end of June 1988, it should be possible to estimate the benefit--or harm--of antiarrhythmic drug therapy as well as its cost in postmyocardial infarction patients with asymptomatic ventricular ectopic activity and to decide whether such treatment may improve survival.

Incidence and course of complex ventricular ectopic activity (VEA) after myocardial infarction was prospectively evaluated in 217 patients in relation to infarct size, location, ventricular function and signs of persistent ischemia. Complex VEA (Lown greater than III) was found acutely in 138 patients (63.6%) and at hospital discharge in 42 (19.3%). Of 79 patients with VEA Lown less than or equal to III in the first 24 hours, 93.7% remained VEA-free at follow-up. Patients with persistent complex VEA differed from those who became VEA-free only in left and right ventricular ejection fraction, whereas all the other infarct related factors had no influence on the course of VEA.

The relationship between clinical findings and invasively measured hemodynamic data was investigated in a prospective trial of 70 patients with acute myocardial infarction. In 26 out of 27 consecutive patients without clinical signs of disturbed myocardial function, normal hemodynamic values were also found invasively. In 43 patients, depressed myocardial function was diagnosed on the basis of the clinical findings. These findings were verified in 38 patients (88%) by means of cardiac catheterization; 5 patients (12%) had normal hemodynamic values. In 26 patients with clinical signs of congestive heart failure, an attempt was made to identify non-invasively those with a low output (cardiac index less than 2/min/m2). Only 3 of the 6 patients with a low output could be identified by clinical examination alone. In one patient a low output was clinically diagnosed despite normal cardiac function measured invasively. In 16 patients, 48 subsequent clinical examinations were performed during treatment of congestive heart failure to identify either persistent elevated left ventricular filling pressure or low output; 15 (31%) were found to be incorrect when compared with the cardiac catheterization data. Patients with acute myocardial infarction and normal ventricular function can be identified with high accuracy by means of clinical examination alone. The clinical diagnosis of congestive heart failure was incorrect in 12% of the patients. A low output state in acute myocardial infarction is often overlooked in clinical examination alone. Of the clinical examinations on patients during therapy, 30% were incorrect. Invasive hemodynamic monitoring in acute myocardial infarction therefore appears to be unnecessary in patients with normal clinical findings, but in those with clinically diagnosed congestive heart failure it is mandatory for precise indication and evaluation of therapy.

Plasma adrenaline (A) and noradrenaline concentrations (NA) were determined in 41 patients admitted to the coronary care unit (CCU). Eleven with suspected acute myocardial infarction (AMI), subsequently excluded as a diagnosis, had significantly elevated A and NA compared with 20 normal resting subjects. Patients with proven infarcts but no ventricular fibrillation had even higher levels of A and NA. Nine patients with ventricular fibrillation as a complication of AMI showed the highest plasma catecholamine values on admission. Patients with AMI and congestive heart failure exhibited substantially increased A, while NA was only slightly elevated compared with that of AMI patients without congestive heart failure. High plasma catecholamines and the relationship between adrenaline and the severity of ventricular arrhythmias suggest that the sympathetic nervous system plays an important role in sustaining a vicious circle of increased myocardial damage and increased irritability during the acute phase of AMI.

With the Swan-Ganz catheter it has become possible to measure the hemodynamics repeatedly in patients with acute myocardial infarction. It was shown that the majority of these patients have an elevated filling pressure but cardiac output and stroke volume remain normal. The clinical signs of a third sound, rales and elevated venous pressure are therefore due to the initial backward failure but are not signs of depressed cardiac output. However, in a small group of patients with clinical signs of flow output, treatment with diurectis and vasodilators is necessary. The mean filling pressure of the left ventricle in this subgroup was 26.2 +/- 2 mm Hg at entrance and could be effectively lowered with both treatments. On the other hand, the cardiac index at entrance (2.3 +/- 0.21/min/m2) did not change significantly under vasodilation but in some cases fell dangerously under furosemide. It is therefore considered that in patients with a low output syndrome hemodynamic monitoring is necessary not only when they are treated with vasodilators but also under furosemide.

Between 1980 and 1985 nine patients under the age of 30 were admitted to our hospital with acute myocardial infarction. They represented 4% of all patients with acute myocardial infarction. Coronary angiography was performed in 8 patients and in a high proportion (5 patients) no stenotic lesion was found. In these patients, vasospasm seems to be the most likely pathogenesis. In one patient no angiography was performed; he had stopped anticoagulation therapy after aortic valve replacement and therefore coronary embolism was the obvious reason for the infarct. After a median of 5 years (2-7) no patient had died or had suffered a new coronary event. The 5 patients with angiographically normal coronary arteries had ceased taking medication and were all back to work full time. Psychological evaluation showed impaired ability to express aggression in all 9 patients.

Ten patients with severe congestive heart failure after acute myocardial infarction were treated with 40 mg isosorbiddinitrate-retard every 4 hours and additional sublingual nitroglycerine. There was a prompt improvement of hemodynamic parameters which was maintained for 24 hours: pulmonary capillary wedge pressure (PCW) decreased within 10 min from 26 +/- 5 (X +/- SEM) to 17 +/- 2 mm Hg (p less than 0.01) and mean arterial pressure from 109 +/- 7 to 98 +/- 6 mm Hg. The heart rate remained constant, and the cardiac index improved from 2.3 +/- 0.2 to 2.5 +/- 0.21/min/m2. The fall in blood pressure was dependent on the pretreatment pressure: it was significantly greater in patients with elevated blood pressure and only slight in those with a low pretreatment blood pressure. In the presented series of patients neither adverse effects or symptoms nor a critical reduction of blood pressure were observed. Combined oral treatment with isosorbiddinitrate and nitroglycerine can therefore be carried out without invasive blood pressure monitoring.

A series of 63 patients were studied by gated radionuclide angiocardiography 51/2 weeks after their first acute myocardial infarction. Left (LVEF) and right (RVEF) ventricular ejection fraction were assessed in three groups of patients: 12 patients with transmural anterior infarctions, 35 patients with transmural inferior infarctions and 16 patients with non-transmural infarctions. LVEF was depressed only in the group of patients with anterior infarctions (34.4 +/- 16.3%) but remained within normal limits in the other two groups. RVEF was reduced in 64% of patients with inferior infarctions; the mean value in this group was 36.3 +/- 10.2% (normal range 48 +/- 8%, p less than 0.02). In the other two groups RVEF was only rarely reduced and the mean values were within normal limits. Regional wall motion abnormalities ( WMA ) were found in 47% of all patients, those localised in the left ventricle matching ECG localisation of necrosis in 86% of cases. Only patients with infarctions of the inferior left ventricular wall were found to have WMA in the right ventricle. Functional signs of ischemia (decrease of RVEF or LVEF during physical exercise) were found in 34% of patients with transmural infarctions and 57% of patients with non-transmural infarctions. Radionuclide angiocardiography showed itself a valuable method for assessing persistent dysfunction after acute myocardial infarction not only of the left but also of the right ventricle, a phenomenon not easily detected clinically.

Furosemide was administered intravenously to 11 patients with cardiac failure after acute myocardial infarction. After an initial loading dose furosemide was given four-hourly if the pulmonary capillary wedge pressure (PCW) was not normalized, i.e. less than or equal to 15 mm Hg. The comparison of the hemodynamic results with the results of a previous study with nitrates was as follows: like the nitrates furosemide lowered the PCW early, i.e. within 15 minutes from 22 +/- 3 to 18 +/- 5 mm Hg, but the therapeutic objective (PCW less than or equal to 15 mm Hg) was reached later than with nitrates. During the 24-hour observation period PCW and total peripheral resistance decreased steadily. The decrease of cardiac index to critical low values in some patients after a mean of 7.5 hours of therapy, and of the mean arterial pressure from 100 +/- 13 to 91 +/- 14 mm Hg, may limit the use of furosemide alone in these patients. During nitrate therapy PCW started to rise again after 12 hours in some patients, necessitating higher doses of nitrates with a corresponding decrease of diuresis. A combination of both forms of therapy may be of value and needs further investigation.

To assess the incidence of silent ischemia after myocardial infarction, a prospective series of 100 consecutive patients was studied 5 weeks after the acute event. Objective evaluation of myocardial ischemia included a 9-lead ECG, thallium-201 scintigraphy and radionuclide ventriculography, each at rest and during symptom-limited bicycle ergometry. Diagnostic criteria were ECG: greater than or equal to 1 mm horizontal or downsloping ST depression or greater than or equal to 1 mm ST elevation; thallium scintigraphy: a clearly reversible perfusion defect at rest, detectable only after exercise; radionuclide ventriculography: an exercise-induced decrease in global LVEF greater than or equal to 5% and/or in anyone regional EF greater than or equal to 14%. Presence of ischemia was assumed if at least 2 of 3 objective ischemic signs were found. This was the case in 28 of 100 patients. During exercise, 15 of 100 patients complained of chest pain, but only 8 (54%) had objective evidence of ischemia. Thus, silent ischemia was demonstrated in 20 of 100 patients. The sensitivity of both nuclear cardiology procedures was markedly superior to that of the ECG in diagnosing post-myocardial ischemia.

In a prospective series of 190 patients under the age of 70 with a first myocardial infarction, the risk profile for ischemia, heart function and arrhythmias was investigated at the time of hospital discharge. Fifteen of these 190 patients had had ventricular fibrillation within 24 hours after admission which could be converted into sinus rhythm. In comparison, patients with ventricular fibrillation had a significantly larger infarct as estimated with the thallium-defect score (11.0 +/- 5.8 vs. 7.3 +/- 5.4; p less than 0.02)). In addition, left ventricular ejection fraction at rest was lower, at 42.7 +/- 17.4% compared to 50.0 +/- 14.0, but the p-value reached only 0.07. Persistent arrhythmias and ischemia were not significantly different in the two groups. In the first year after infarction none of these 15 patients died, compared to 8/175 patients.

In a consecutive group of 125 patients three weeks after myocardial infarction an ergometer bicycle test was performed in order to obtain an objective assesment of the physical fitness. The patients were exercised on 3 different workloads during a total time of six minutes. It was attempted to reach the training heart rate which was calculated from the resting heart rate plus 60% of the maximum increase, the maximal heart rate being "215-age in years". The Physical Work Capacity (PWC) was compared with the fitness of on age correlated control group. We could show that the PWC at hospital discharge, i.e. 3 weeks after myocardial infarction, was 79.6 +/- 23% of the normal value. Three weeks later it had improved by another 9%. A positive correlation with the CPJ of Norris and with the degree of physical activity prior to the acute illness could be demonstrated.