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Background: The benefit of beta-blockers post-myocardial infarction (MI) was established in the late 1970s. Major advances in the treatment of MI have since occurred. However, patients with chronic heart failure (CHF) were excluded from those trials. The purpose of this study was to assess the effect of beta-blockers in post-MI patients with CHF receiving contemporary management., Methods: This was a prespecified subgroup analysis of a double-blind, randomized trial: the Metoprolol CR/XL Randomized Intervention Trial in Heart Failure (MERIT-HF). Patients with CHF in New York Heart Association class II to IV with an ejection fraction (EF) < or =0.40 and a history of being hospitalized for an acute MI (n = 1926) were randomized to metoprolol succinate controlled release/extended release (CR/XL) versus placebo. Mean EF was 0.28, and the mean follow-up was 1 year., Results: Metoprolol CR/XL reduced total mortality by 40% (95% CI 0.20-0.55, P =.0004), and sudden death by 50% (95% CI 0.26-0.66, P =.0004). The combined end point of all-cause mortality/hospitalization for worsening CHF was reduced by 31% (95% CI 0.16-0.44, P <.0001), and cardiac death/nonfatal acute MI by 45% (95% CI 0.26-0.58, P <.0001). A post-hoc analysis showed that the outcome in patients with earlier revascularization (44%) and outcome in those with more severe CHF (20%) was similar to the entire post-MI population., Conclusions: In post-MI patients with symptomatic CHF, beta-blockade continues to exert a profound reduction in mortality and morbidity in the presence of contemporary management that includes early and late revascularization, angiotensin-converting enzyme inhibitors, aspirin, and statins.

In spite of the solid evidence that beta-blockade reduces mortality and morbidity in congestive heart failure (CHF) this therapy continues to be underused in clinical praxis. The reason for this may lie in scarcity of knowledge about the mechanisms of beta-blockade action. The major aim of this study was to investigate in vivo whether selective beta(1)-blockade may improve cardiac energy metabolism in rats with myocardial infarction in early postinfarct remodeling phase. Myocardial infarction (MI) was induced in male Sprague-Dawley rats by ligation of the left coronary artery. Two different groups of rats were studied, rats with MI treated with metoprolol (5 mg/kg/h; n = 9) and rats with MI saline treated (n = 9). The treatment with metoprolol was given by subcutaneously implanted minipumps and was initiated at 3 days postinfarct and during the period of 4 weeks. All rats were investigated with noninvasive methods (31)P magnetic resonance spectroscopy (MRS) and transthoracic echocardiography 3 days after induction of MI and 4 weeks later. Phosphocreatine/ATP ratio was normalized after the treatment with metoprolol while it was 50% lower in the saline group (p < 0.001). In the metoprolol group stroke volume and ejection fraction increased while deceleration time of mitral early filling was longer (all p < 0.05). Left ventricular weight as well as volumes and dimensions were similar between the groups. Plasma levels of noradrenaline (p = 0.058), adrenaline (p < 0.01) and brain natriuretic peptide (p = 0.09) were lower in the metoprolol group. Selective beta(1)-blockade with high dose of metoprolol initiated in the early postinfarct phase improves myocardial energy metabolism and function and prevents overactivation of sympathetic system. The beneficial effect on myocardial bioenergetics may be an important mode of action of beta-blockers which contributes to the clinical benefits of the therapy in CHF., (Copyright 2001 Academic Press.)

The aims of this study were to examine, in vivo, the effects of GH treatment on myocardial energy metabolism, function, morphology, and neurohormonal status in rats during the early postinfarct remodeling phase. Myocardial infarction (MI) was induced in male Sprague Dawley rats. Three different groups were studied: MI rats treated with saline (n = 7), MI rats treated with GH (MI + GH; n = 11; 3 mg/kg x day), and sham-operated rats (sham; n = 8). All rats were investigated with 31P magnetic resonance spectroscopy and echocardiography at 3 days after MI and 3 weeks later. After 3 weeks treatment with GH, the phosphocreatine/ATP ratio increased significantly, compared with the control group (MI = 1.69 +/- 0.09 vs. MI + GH = 2.42 +/- 0.05, P < 0.001; sham = 2.34 +/- 0.08). Treatment with GH significantly attenuated an increase in left ventricular end systolic volume and end diastolic volume. A decrease in ejection fraction was prevented in GH-treated rats (P < 0.05 vs. MI). Myocardial and plasma noradrenaline levels were significantly lower in MI rats treated with GH. These effects were accompanied by normalization of plasma brain natriuretic peptide levels (sham = 124.1 +/- 8.4; MI = 203.9 +/- 34.7; MI + GH = 118.3 +/- 8.4 ng/ml; P < 0.05 vs. MI). In conclusion, GH improves myocardial energy reserve, preserves left ventricular function, and attenuates pathologic postinfarct remodeling in the absence of induction of left ventricular hypertrophy in postinfarct rats. The marked decrease in myocardial content of noradrenaline, after GH treatment, may protect myocardium from adverse effects of catecholamines during postinfarct remodeling.

Aim: To investigate whether uncomplicated chronic coronary artery disease causes changes in heart rate variability and if so, whether the heart rate variability pattern is different from that described in patients with acute myocardial infarction., Methods: Heart rate variability was studied in 65 patients with angina who had no previous myocardial infarcts, no other diseases, and were on no drug that could influence the sinus node. Results were compared with 33 age matched healthy subjects. The diagnosis of coronary artery disease in angina patients was established by coronary angiography in 58, by thallium scintigraphy in six, and by exercise test only in one. Patients and controls were Holter monitored 24 hours outside hospital, and heart rate variability was calculated in the frequency domain as global power (GP: 0.01-1.00 Hz), low frequency peak (LF: 0. 04-0.15 Hz), high frequency peak (HF: 0.15-0.40 Hz), LF/HF in ms(2), and in the time domain as SDNN (SD of normal RR intervals), SDANN (SD of all five minute mean normal RR intervals), SD (mean of all five minute SDs of mean RR intervals), rMSSD (root mean square of differences of successive normal RR intervals) (all in ms), and pNN50 (proportion of adjacent normal RR intervals differing more than 50 ms from the preceding RR interval) as per cent., Results: The mean age in patients and controls was 60.4 (range 32-81) and 59.1 (32-77) years, respectively (NS), the male/female ratio, 57/65 and 24/33 (NS), and the mean time of Holter monitoring, 23.0 (18-24) and 22.8 (18-24) hours (NS). Mortality in angina patients was 0% (0/65) at one year, 0% (0/56) at two years, and 3% (1/33) at three years. Compared with healthy subjects angina patients showed a reduction in GP (p = 0.007), HF (p = 0.02), LF (p = 0.02), SD (p = 0.02), rMSSD (p = 0.01), and pNN50 (p = 0.01). No significant difference was found in RR, LF/HF, SDNN, or SDANN., Conclusions: Uncomplicated coronary artery disease without previous acute myocardial infarction was associated with reduced high and low frequency heart rate variability, including vagal tone. SDANN and SDNN, expressing ultra low and very low frequencies which are known to reflect prognosis after acute myocardial infarction, were less affected. This is in agreement with the good prognosis in uncomplicated angina in this study.

Several studies have shown that GH can enhance cardiac performance in rats after experimental myocardial infarction and in humans with congestive heart failure. In the present study, the hemodynamic effects of hexarelin (Hex), an analog of GH-releasing peptide-6 and a potent GH secretagogue, were compared with the effects of GH. Four weeks after ligation of the left coronary artery male rats were treated sc twice daily with hexarelin [10 microg/kg x day (Hex10) or 100 microg/kg x day (Hex100)], recombinant human GH (2.5 mg/kg x day), or 0.9% NaCl for 2 weeks. Transthoracic echocardiography was performed before and after the treatment period. GH, but not Hex, increased body weight gain. GH and Hex100 decreased total peripheral resistance (P < 0.05) and increased stroke volume (P < 0.05 and P < 0.01, respectively) and stroke volume index (P = 0.06 and P < 0.01, respectively) vs. NaCl. Cardiac output was increased by GH and Hex100 (P < 0.05), and cardiac index was increased by Hex100 with a borderline significance for GH (P = 0.06). In conclusion, Hex improves cardiac function and decreases peripheral resistance to a similar extent as exogenous GH in rats postmyocardial infarction. The mechanisms of these effects are unclear; they could be mediated by GH or a direct effect of Hex on the cardiovascular system.

Beta blockers have been shown to reduce the risk of sudden cardiac death in more than 50 randomized trials involving more than 55,000 patients. Relative reductions (vs. placebo) in cardiac death in some of these trials ranged from 30 to 50%. These reductions are substantially greater than trials of other drug classes including angiotensin-converting enzyme inhibitors. However, not all beta blockers confer equal benefit to patients at risk of sudden cardiac death. Results from various trials suggest that lipophilic beta blockers--such as timolol, metoprolol, propranolol, bisoprolol, and carvedilol--may be more beneficial than hydrophilic beta blockers. Results of animal studies have indicated that sudden cardiac death is mediated, at least in part, by the central nervous system, which may account for why lipophilic agents have more pronounced clinical effects. Based on the results of numerous clinical and mechanistic studies, it is suggested that beta blockers should be given to all patients at risk for sudden cardiac death, including those patients with previous myocardial infarction, hypertension, or congestive heart failure.

Despite recent advances in the treatment, severe chronic heart failure (CHF) remains a syndrome associated with high mortality. Therefore, the search for new agents to improve both patient symptoms and survival, as well as the pursuit for detailed knowledge about pathophysiology of the failing heart, will continue to depend on relevant animal models. Large acute myocardial infarction (MI) initiates complex changes in the geometrical, structural, and biochemical architecture of both infarcted and non-infarcted regions of ventricular myocardium, which can profoundly affect left ventricular function and prognosis. In this paper we present a new model for non-invasive cardiac (31)P MRS in the rat. Volume-selective (31)P magnetic resonance spectroscopy and echocardiography were used for evaluation of myocardial energy metabolism, cardiac morphology and function in rats 3 days and 3 weeks after induction of large MI. The phosphocreatine:adenosine triphosphate (PCr:ATP) ratio was decreased in rats with MI comparing with controls both at 3 days (1.6+/-0.06 vs 2.7+/-0.04; mean+/-s.e.m. P<0.0001) and 3 weeks (1.6+/-0.07 v 2.7+/-0.02 P<0.0001) postinfarct. The results from the study demonstrate that postinfarct cardiac remodeling is a rapid process of changes not only in cardiac geometry, structure and function but also in myocardial energy metabolism after large transmural MI in the rat., (Copyright 1999 Academic Press.)

The aim of this study is to describe the impact of early treatment with metoprolol on prognosis during 1 year of follow-up in patients with suspected acute myocardial infarction (AMI) and indirect signs of congestive heart failure (CHF). Patients aged 40-74 years who presented within 48 hours of onset of symptoms raising suspicion of AMI were assessed for inclusion. All patients participated in the Göteborg Metoprolol Trial and had indirect indices of CHF according to various clinical criteria. As soon as possible after hospital admission, patients received either placebo or metoprolol (15 mg) divided into 3 intravenous injections, then oral treatment, 200 mg daily for 3 months. Thereafter, most patients in both treatment groups received metoprolol in an open manner. Among the 1,395 randomized patients, 262 (19%) had signs of mild-to-moderate CHF before randomization. Of these, 131 were randomized to metoprolol and 131 to placebo. During the first 3 months, mortality was 10% among patients randomized to metoprolol versus 19% among patients randomized to placebo (p = 0.036). The corresponding figures for the first year were 14% and 27%, respectively (p = 0.0099). Patients randomized to placebo who showed signs of CHF had a 1-year mortality rate of 28% compared with 10% among patients without such signs (p <0.001). The results suggest that early treatment with metoprolol markedly reduces mortality in patients having suspected AMI and signs of CHF.

About half of all deaths after myocardial infarction (MI) are sudden cardiac deaths. Most of these are thought to be due to ventricular fibrillation (VF). A number of interventions and many different antiarrhythmic agents have been investigated, but so far only beta-blocker therapy has been found to produce significant reductions in the risk of sudden cardiac death after MI. Reductions in total mortality and sudden cardiac death were first reported in 1981 in 3 placebo-controlled studies, the Norwegian Timolol Study, the American Beta-Blocker Heart Attack Trial (BHAT), and the Göteborg Metoprolol Trial. A few years later, two very large trials, the Metoprolol in Acute Myocardial Infarction (MIAMI) study and the First International Study of Infarct Survival (ISIS-1), which included 6,000 and 16,000 patients, respectively, showed that beta-blocker therapy could reduce mortality within the first 2 weeks after onset of MI. Data from 24 postinfarction studies with long-term follow-up show an average 20% mortality reduction over 2 years. Pooled results of 28 short-term, randomized, placebo-controlled trials in which beta blockers were given intravenously shortly after onset of MI indicate an average 13% mortality reduction within 2 weeks. In the 16 studies in which the sudden cardiac death rate was reported, the beneficial effect of beta blockade was even more marked: a 34% average reduction of risk. Not all studies with beta blockers, however, have demonstrated a significant reduction in the incidence of sudden cardiac death. Such an effect has been clearly demonstrated only for the more lipophilic beta blockers (timolol, metoprolol, and propranolol). Two of these lipophilic beta blockers, metoprolol and propranolol, have also been shown to prevent VF after MI in clinical studies. Based on observations from animal experiments, it has been proposed that beta blockers with a high degree of lipophilicity penetrate the brain and thereby maintain high vagal tone during stress. A combination of direct anti-ischemic effects due to beta1 blockade and preservation of vagal tone appears to prevent VF in these animal models. Further clinical studies are needed to explore this hypothesis.

Unlabelled: Heart rate variability (HRV) reflects autonomous activity that influences the heart. It has been shown that HRV is depressed during acute myocardial infarction (AMI) and that it recovers with time. Beta-blockers reduce mortality after AMI and changes in sympathico-vagal activity have been suggested to be of importance. Under certain animal experimental conditions, metoprolol has been reported to increase vagal tone more than atenolol, which could have clinical implications. The purpose of the present study was to compare the effects of atenolol and metoprolol treatments on HRV during 6 weeks after AMI and to follow the post MI changes in HRV in patients on betablockers., Methods: In an open, randomised cross-over study, 28 patients were randomised to 3+3 weeks' treatment with atenolol or metoprolol starting 2-5 days after AMI. Twenty-four hour Holter recordings were made before randomisation and after 3 and 6 weeks. HRV was analysed as HR, SDRR, SDANN, SD, rMSSD and pNN50 in the time domain and as coefficient of component variance (CCV) of HF and LF, and as LF/HF ratio in the frequency domain., Results: The average daily dose in our study population was 106 mg of metoprolol and 54 mg of atenolol. There were trends toward lower heart rates daytime, lower LF/HF ratio daytime and higher rMSSD on atenolol compared to metoprolol. In the total group of 28 patients we found during the first 3 weeks, a significant increase of SDNN, SDANN (p<0.0001) and LF/HF ratio daytime and CCV-HF night-time (p<0.01). All differences and trends were unchanged between 3 and 6 weeks., Conclusions: There was no evidence of more increased vagal tone with metoprolol compared to atenolol as has been suggested from animal models. In patients also on chronic treatment with beta blockers, an increase of HRV was seen during the first weeks post MI.

Accumulating evidence suggests from experimental and clinical studies beneficial effects of growth hormone (GH) on contractility, although concomitant cardiac hypertrophy, generally considered to be a cardiovascular risk factor, has also been reported. In the present study, we combine a rat model with impaired cardiac performance after myocardial infarction (MI) with echocardiographic evaluation of GH effects on cardiac structure and function. We have used a rat model with ligation of the left coronary artery in normal, growing male rats resulting in subsequent impaired cardiac performance. After 6 weeks' recovery, blind transthoracic echocardiography was performed to determine infarction size, cardiac geometry and performance. Rats with no signs of myocardial infarction were excluded from the study. After randomization, the rats were treated with daily s.c. injections of saline (n = 8) or recombinant human growth hormone (rhGH) (n = 6) at a dose of approximately 1 mg kg-1 body weight for 1 week. A new blind echocardiography examination was performed after treatment demonstrating a 13% increase in ejection fraction (EF) and a 50% increase in cardiac index in GH-treated rats compared with control rats (P < 0.01). Moreover, GH caused a significant decrease in end-systolic volume. There were no significant changes in left ventricular (LV) or interventricular wall thickness, LV dimensions, heart rate or diastolic function. No effects were seen on LV weight, cardiac insulin-like growth factor (IGF) I, IGF-I receptor and GH receptor mRNA content. GH in a physiological dose improves systolic function in an experimental model of heart failure without signs of hypertrophy, suggesting a potential role as a therapeutic agent in the treatment of heart failure and merits further investigation.

A study was undertaken to evaluate the 1-year risk of cardiac death for patients with chest pain/suspected acute myocardial infarction in the emergency department (ED) and express the prognosis in a statistical model. Clinical variables and electrocardiogram were correlated to cardiac death during 1 year. Cox regression model was used to estimate the risk of death as a continuous function of a risk score and the time interval. From these, the prognosis for each patient can be calculated. There were 6,794 visits by 5,303 patients followed for 1 year, during which 604 patients died. The absolute risk of cardiac death can be calculated from the independent predictors for cardiac death: age; sex; histories of diabetes mellitus, hypertension, and congestive heart failure; and symptoms, electrocardiographic pattern, and degree of suspicion of acute myocardial infarction on admission. This model allows estimation of the prognosis for every patient with chest pain/suspected acute myocardial infarction from data easily available in the ED.

Objective: To evaluate whether prophylactic treatment with metoprolol for two years after coronary artery bypass grafting improves working capacity and reduces the occurrence of myocardial ischaemia in patients with coronary artery disease., Methods: After coronary artery bypass grafting, patients were randomised to treatment with metoprolol or placebo for two years. Two years after randomisation, a computerised 12-lead electrocardiogram was obtained during a standardised bicycle exercise test in 618 patients (64% of all those randomised)., Results: The median exercise capacity was 140 W in the metoprolol group (n = 307) and 130 W in the placebo group (n = 311) (P > 0.20). An ST depression of > or = 1 mm at maximum exercise was present in 34% of the patients in the metoprolol group and 38% in the placebo group (P > 0.20) and an ST depression of > or = 2 mm at maximum exercise was present in 11% in the metoprolol group and 16% in the placebo group (P = 0.09). The median values for maximum systolic blood pressure were 200 mm Hg in the metoprolol group and 210 mm Hg in the placebo group (P < 0.0001), while the median values for maximum heart rate were 126 beats/min in the metoprolol group and 143 beats/min in the placebo group (P < 0.0001). The occurrence of cardiac and neurological clinical events two years postoperatively among exercised patients was comparable in the treatment groups., Conclusions: Treatment with metoprolol for two years after coronary artery bypass grafting did not significantly change exercise capacity or electrocardiographic signs of myocardial ischaemia.

Most studies have suggested that patients with anterior myocardial infarction have an adverse prognosis compared with patients with inferior infarction. The objective of this study was to compare the mortality and morbidity in anterior versus inferior acute myocardial infarction (AMI) during 1 year in a consecutive series of patients hospitalized with AMI. All patients fulfilling the criteria for AMI who were admitted to a single hospital during 21 months (n = 921) participated in the study. Patients with anterior infarction (n = 312) had a 1-year mortality rate of 26% versus a rate of 24% for patients with inferior infarction (n = 269) (p > 0.2). The corresponding figures for patients with no previous infarction who developed Q waves were 27 and 21%, respectively (p > 0.2). Reinfarction, thromboembolic events, and other aspects of morbidity during long-term follow-up appeared with similar frequency in the two groups. Thus, in a nonselected group of patients admitted to a single hospital because of AMI, the prognosis was found to be similar among patients with inferior and those with anterior infarction. In the subset of patients with a first myocardial infarction who developed Q waves, there was a trend indicating higher mortality in anterior infarction.

A large number of studies have shown the prognosis after acute myocardial infarction (AMI) to be favorably affected by treatment with beta blockers. Whether such treatment also will have a favorable effect on the prognosis in patients in whom AMI was not confirmed has not been shown. A study was undertaken at Sahlgren's Hospital, Göteborg, to determine risk indicators for death and prognosis among 1,443 patients in whom AMI was not confirmed and who survived hospitalization in relation to whether or not beta blockers were prescribed at discharge. One-year mortality was determined and p values were corrected for differences at baseline. Of the 1,443 patients who participated in the analyses, 44% were prescribed beta blockers. They differed from the remaining patients by younger age, predominance of men, a more frequent history of AMI, angina pectoris, and hypertension, and a less frequent history of congestive heart failure. Patients in whom beta blockers were prescribed had a 1-year mortality of 6% compared with 16% in those not on beta blockers (p < 0.001). The difference was similar in various subgroups according to clinical history.

Background: We evaluated the impact of diabetes mellitus on the prognosis in hypertensive patients admitted to hospital as a result of acute chest pain., Patients: All patients in this study had a history of hypertension and were admitted to the Emergency Department at Sahlgrenska Hospital, Göteborg, Sweden, complaining of chest pain, or other symptoms suggestive of acute myocardial infarction, between 15 February 1986 and 9 November 1987., Methods: All patients were prospectively registered on admission to the Emergency Department and followed for 1 year in terms of mortality and morbidity., Results: Of the 1274 patients who fulfilled the inclusion criteria, 187 (15%) had a history of diabetes mellitus. The 1-year mortality rate for all hypertensive patients was 18%, whereas it was 24% for those who also had diabetes mellitus, and 16% for hypertensive patients without diabetes mellitus (P < 0.05). However, in a multivariate analysis considering age, sex, and history of cardiovascular diseases, the following appeared as independent predictors of death in the hypertensive patients: age (P < 0.001), a history of congestive heart failure (P < 0.001), and male sex (P < 0.01)., Conclusion: Hypertensive patients who were admitted to the Emergency Department of Sahlgrenska Hospital with acute chest pain had a poor prognosis, which was even worse if they also had a history of diabetes mellitus. The relationship between diabetes mellitus and hypertension could not, however, be clearly defined.

In all patients hospitalized in one single hospital due to acute myocardial infarction (AMI) during a period of 21 months, we describe the prognosis in relation to smoking habits and other risk indicators with death. Of 862 AMI patients, 37% reported smoking at the onset of AMI. Of the patients who smoked at the onset of AMI and who survived the first year, 53% reported having quit smoking. Patients who had quit smoking reported fewer symptoms of chest pain (p < 0.01), headache (p < 0.01) and dizziness (p < 0.001) as compared with patients who continued to smoke after one year. Of the patients who had quit smoking, the mortality during the subsequent 4 years was 17% as compared with 31% for patients who continued to smoke (p < 0.05). However, patients who quit smoking less frequently had a previous history of myocardial infarction and congestive heart failure. When correcting for such dissimilarities, quitting smoking did not remain significantly associated with prognosis.

This study aims at describing the in-hospital prognosis of patients admitted with suspected acute myocardial infarction, focusing on the possibility of emergency room prediction of the risk for death and severe complications. From 7157 consecutive patients with chest pain or other symptoms suggestive of acute myocardial infarction in the emergency room, 4690 were hospitalized. Of these, 246 (5%) died in hospital, with a mortality rate among the 921 patients who developed myocardial infarction of 14%, and among those without infarction of 3%. From the clinical history, examination and electrocardiogram in the emergency room, independent predictors of death and death or any severe complication were determined by logistic regression analysis. These included age, initial degree of suspicion of infarction, electrocardiographic pattern, history of diabetes mellitus, history of congestive heart failure and on admission arrhythmias, loss of consciousness, acute congestive heart failure, or unspecific symptoms. From these analyses the probability of death or death or any severe complication can be calculated. Thus, 18% of patients hospitalized due to suspected acute myocardial infarction suffered a severe complication or died in hospital. From a statistical model it is possible to predict the in-hospital prognosis of every such patient.

The purpose of this study was to relate the 1-year risk of death and development of acute myocardial infarction among diabetics with acute chest pain to whether they had a history of hypertension or not. All patients with a history of diabetes mellitus who, during 21 months, were admitted to the Emergency Room in Sahlgrenska Hospital, Göteborg, due to chest pain or other symptoms suggestive of acute myocardial infarction, were included. Among the 427 patients with a history of diabetes mellitus 44% also had a history of hypertension. These hypertensives had a 1-year mortality rate of 22% as compared with 26% in diabetics without such a history (p > 0.2). The corresponding values for development of myocardial infarction during 1 year were 33 and 30%, respectively (p > 0.2). We did not find a history of hypertension to adversely affect the prognosis among diabetics with acute chest pain.

Based on selected patient populations, several randomized trials have shown beta blockers to decrease mortality after acute myocardial infarction (AMI). The purpose of this study was to describe the use of beta blockers in various subsets of patients admitted to Sahlgren's Hospital between February 15, 1986, and November 9, 1987, with AMI, and the relation of AMI to other risk indicators for death and to a 1-year mortality rate. Beta blockers, mainly metoprolol, were prescribed for 66% of all survivors at discharge. They were more frequently prescribed for younger patients and for those with a previous history of AMI and hypertension, but less frequently for those with a history of congestive heart failure and diabetes mellitus. Patients for whom beta blockers were not prescribed haa a 1-year mortality of 27% versus 11% for the rest (p < 0.001). Independent predictors of 1-year mortality after discharge were age (p < 0.001), history of hypertension (p < 0.001), prescription of beta blockers at discharge (p < 0.001), congestive heart failure during hospitalization (p < 0.001), and a history of AMI (p < 0.01). P values were corrected for baseline differences. Beta blockers were not prescribed at discharge for one-third of survivors after AMI. This group had a very high mortality during the first year. When simultaneously considering various risk indicators for death, prescription of beta blockers at discharge was associated with an increased rate of survival.

Background: The majority of patients hospitalized due to suspected acute myocardial infarction (AMI) will eventually not develop infarction. Information about the long-term prognosis in this patient population is limited., Aim: To describe the mortality during 10 years of follow-up in patients hospitalized due to an initially strong suspicion of AMI, but in whom the diagnosis of AMI could not be confirmed., Patients: All patients participating in an early intervention trial with metoprolol in suspected AMI, but in whom the diagnosis was not confirmed. Patients were included during 1976-1981., Results: In all 1395 patients were included in the study, of whom 586 did not fulfil the criteria for confirmed AMI. The overall mortality during 10 years of follow-up in this population was 26%. In a multivariate analysis considering age, sex, history of cardiovascular diseases, initial heart rate and various complications during the hospital stay, including congestive heart failure, severe ventricular arrhythmias, tachycardia, hypotension, high degree AV-block and severe chest pain, the following appeared as independent predictors of death: previous infarction (P < 0.001), age (P < 0.001), history of diabetes mellitus (P < 0.001) history of smoking (P < 0.05), history of hypertension (P < 0.05), male sex (P < 0.05), and the initial heart rate (P < 0.05)., Conclusion: Among patients in whom AMI was not confirmed the major risk indicators for death during 10 years of follow-up were: a history of cardiovascular diseases and smoking, age, male sex and high heart rate on admission to hospital.

Objective: To describe the relation between the extent of a myocardial infarct, measured according to maximum serum enzyme activity of lactate dehydrogenase, and mortality at 10 years., Patients: In 759 patients with acute myocardial infarction in whom serum activity of heat stable lactate dehydrogenase had been determined every 12 hours for 108 hours after randomisation in an early intervention trial with metoprolol., Main Outcome Measure: Mortality at 10 years in relation to quartile of maximum serum lactate dehydrogenase activity and history of cardiovascular disease., Results: Among all patients mortality at 10 years was 39% in the lowest quartile, 51% in the second quartile, 50% in the third, and 59% in the fourth (p < 0.001 for relation between infarct size and 10 year mortality). Among patients without a history of myocardial infarction, angina pectoris, diabetes mellitus, or hypertension the mortality in each quartile was 29%, 32%, 41%, and 56%, respectively (p < 0.001 for relation between infarct size and 10 year mortality). Among patients with any of these risk indicators the association between the estimated infarct size and mortality at 10 years was weak (p < 0.05)., Conclusion: Estimated size of a myocardial infarct and mortality over 10 years seem to be related but mainly in patients without a history of cardiovascular disease.

Previous descriptions of the prognosis after acute myocardial infarction (AMI) have mainly included patients admitted to coronary care units, often with an upper age limit. This study describes the prognosis, with emphasis on morbidity, during 1 year in 921 patients admitted to one single hospital with AMI regardless of age and regardless of whether or not they were admitted to the coronary care unit. During the first year, 29% of the patients died and 16% developed a reinfarction. Fifty-four percent required rehospitalization for various reasons, mainly for AMI, chest pain of other origins, and congestive heart failure. After 1 year, 52% of the surviving patients had symptoms of angina pectoris. Among patients younger than 65 years, only 37% were back to work full time after 1 year. Of patients alive after 1 year, 25% fulfilled the following criteria: no reinfarction, no rehospitalization, and no angina pectoris. Of patients aged less than 65 years at follow-up, 12% fulfilled the same criteria and were back to work full time after 1 year. In this unselected, consecutive series of patients with AMI, mortality and morbidity were high during the first year. Only a small percentage of patients were free of events or symptoms of angina pectoris.

Background: About 20% of patients admitted to a medical emergency room have chest pain or other symptoms raising suspicion of acute myocardial infarction., Aim: To describe the place and mode of death in such patients during 1 year of follow-up., Patients: All patients (n = 5362) admitted to a single hospital during 21 months because of such symptoms., Results: In all, 565 patients (11%) died. Death rate was directly related to the initial degree of suspicion of acute myocardial infarction. Of these patients, 196 (35%) died during initial hospitalization and only 89 (16%) died outside the hospital. The overall autopsy rate was 53%. Of the deaths that occurred during initial hospitalization, the majority were judged as cardiac, most being due to acute myocardial infarction, particularly if the patients died in the coronary care unit. Among patients who died after discharge from hospital, non-cardiac factors contributed more substantially to death, particularly in patients who died during rehospitalization. The cause of death was not established in a high proportion of patients who died outside hospital., Conclusion: The results suggest that, among patients admitted to the emergency room because of suspected acute myocardial infarction, causes of death other than a documented cardiac event become increasingly important when the interval between admittance to the emergency room and death increases.

Previous studies have compared the outcome between patients with and without a confirmed acute myocardial infarction (AMI) mainly during the first few years after its onset. Our aim was to compare the prognosis between patients with and without a confirmed AMI during 10 years of follow-up. Patients participating in an early intervention trial with metoprolol in suspected AMI between 1976 and 1981 took part in this evaluation. The total 10-year mortality rate including hospital mortality was 51% for patients with confirmed AMI as compared with 32% for patients with a possible AMI and 23% for patients in whom AMI was definitely ruled out (p < 0.001). The 10-year mortality after discharge from hospital was in AMI 46%, possible AMI 32% and in definitely ruled out AMI 23% (p < 0.001). When simultaneously considering age, sex, previous history of cardiovascular disease and smoking, the development of AMI appeared as an independent predictor of death (p < 0.001). Thus, among patients hospitalized due to suspected AMI, 10-year mortality after discharge from hospital was directly related to the diagnosis during the first 3 days in hospital.

Background: Previous studies on the prognosis after acute myocardial infarction (AMI) have mainly focused on the first few years. In this study, we aimed to describe the mortality rate during 10 years of follow-up after development of AMI in relation to clinical history and observations during the hospital stay., Methods: We prospectively followed for 10 years all patients with suspected AMI, enrolled between 1976 and 1981, participating in an early intervention trial with metoprolol who fulfilled given criteria for AMI., Results: A total of 809 patients developed AMI during the first 3 days in hospital, of whom 399 were randomly assigned to receive metoprolol and 410 to receive placebo. The overall 10-year mortality rate, including initial in-hospital mortality, was 51%. In a multivariate analysis considering age, sex, history of cardiovascular diseases, estimated infarct size, and the occurrence of various complications during initial hospitalization (i.e. congestive heart failure, severe ventricular arrhythmias, tachycardia, hypotension, high-degree atrioventricular block and severity of pain) the following appeared as independent predictors of death: a history of diabetes mellitus (P < 0.001), congestive heart failure during hospitalization (P < 0.001), age (P < 0.001), and a history of previous myocardial infarction (P < 0.001)., Conclusion: Independent predictors of death during the first 10 years after AMI were a history of diabetes mellitus, congestive heart failure during hospitalization, age, and previous myocardial infarction.

Background: Previous studies suggest a gender-related difference in prognosis among patients with ischaemic heart disease. In the present study, we aimed to describe the characteristics and prognosis among patients with suspected ischaemic heart disease in relation to gender., Methods: During the 21 months of the study, all patients who came to the medical emergency room of one single hospital as a result of chest pain or other symptoms suggestive of acute myocardial infarction were prospectively followed for 1 year., Results: A total of 5362 patients were admitted on 7157 occasions; men accounted for 55% of the admissions. The 1-year mortality rate was 11% for men compared with 10% for women. The women were older and had a higher prevalence of known congestive heart failure and hypertension, whereas the prevalence of previous myocardial infarction was higher in men. When correcting for the dissimilarities in age and history of cardiovascular diseases, male gender appeared as an independent predictor of death. Development of myocardial infarction occurred in 25% of the men and 16% of the women (P < 0.001) during 1 year. The symptoms that brought patients to the emergency room were interpreted as being caused by myocardial infarction or myocardial ischemia in 29% of men compared with 21% of women (P < 0.001)., Conclusions: In a consecutive series of patients with chest pain or other symptoms suggesting acute myocardial infarction in the emergency room, male gender was an independent risk indicator for death during 1 year. This might be explained by a higher occurrence of coronary artery disease in men than in women in this patient population.

We evaluated the prognosis of 858 patients with acute myocardial infarction (MI), of whom 97 (11%) had a history of diabetes mellitus. Among patients with diabetes the 1-year mortality rate was 41% versus 26% for non-diabetic patients (p < 0.01), and the 1-year reinfarction rates were 23% and 14%, respectively (p = 0.05). Diabetic patients with a history of hypertension had a similar mortality rate as compared with diabetic patients without hypertension. In a multivariate analysis including age and history of cardiovascular disease, diabetes did not significantly contribute to death or reinfarction. Among diabetic patients the only independent risk factor for death was age. The place and mode of death appeared similar in the two groups. Patients with and without a history of diabetes had a similar infarct size. We conclude that diabetic patients with acute myocardial infarction have a very poor prognosis. Within 1 year nearly half of them are dead and one-quarter develop reinfarction. The mode of death appeared to be similar in diabetic patients as compared with non-diabetic patients.

The prognosis during 1 year of follow-up in 715 patients admitted to one single hospital due to suspected acute myocardial infarction (AMI) with a history of unstable angina pectoris immediately preceding hospitalization is described. AMI developed in 192 patients (27%) during the first three days and in 255 patients (38%) during the first year. The mortality during hospitalization was 7% (50 patients) and during 1 year 19% (130 patients). Of the nonsurvivors, 54% died of AMI, 28% of congestive heart failure, and 20% of cardiogenic shock. Based on simple clinical parameters on admission to the emergency room, risk indicators for death during the following year could be identified as follows, in the order of significance: high age (p < 0.001), ST-segment depression on admission (p < 0.001), and a history of diabetes mellitus (p < 0.05). At admission to the emergency room, risk indicators for development of AMI during the following year were as follows: initial degree of suspicion of AMI (p < 0.001), electrocardiographic signs of acute ischemia on admission (p < 0.001), ST-segment elevation on admission (p < 0.01), age (p < 0.05), and lack of a previous history of chronic stable angina pectoris (p < 0.05). We conclude that, among patients admitted to hospital due to suspected AMI with a history of unstable angina pectoris immediately preceding hospitalization, 38% developed a confirmed infarction and 19% died during the following year.

In 917 patients with acute myocardial infarction (AMI) we evaluated the impact of previous angina pectoris on the prognosis. Thirty-four percent of the patients had chronic angina prior to AMI, and 22% had angina pectoris of short duration. Patients with chronic angina pectoris differed from the remaining patients having a more frequent previous history of AMI, diabetes mellitus, hypertension, and congestive heart failure. They less frequently developed a Q-wave AMI, and had smaller infarcts according to maximum serum-enzyme activity as compared with the remaining patients. They had a higher one-year mortality rate (36%) as compared with those having angina pectoris of short duration (22%), and those with no angina pectoris (26%). Their reinfarction rate was also higher (26%) as compared with that in the other two groups (15% and 9% respectively). In a multivariate analysis considering age, sex, clinical history, initial symptoms, initial electrocardiogram and estimated infarct size, previous chronic angina pectoris was not an independent risk factor for death, but was independently associated with the risk of reinfarction (P < 0.001). Among patients with a history of angina pectoris the outcome was related to medication prior to onset of AMI and at discharge from hospital. Patients in whom beta-blockers were prescribed at discharge had a one-year mortality of 13% as compared with 30% in the remaining patients (P < 0.001).

In 292 patients with suspected acute myocardial infarction given thrombolytic agents, we describe the delay time between the onset of pain and the start of thrombolysis and relate the observations to the prognosis. In 3%, treatment was started 1 h or less and in 22% 2 h or less after onset of symptoms. The median delay time between onset of symptoms and arrival in hospital was 1 h 38 min, and the median delay time between the arrival in hospital and start of thrombolysis was 1 h 25 min. A very strong association between delay time to thrombolysis and mortality during 2 weeks and 1 year of follow-up was observed.

Objectives: A previous history of hypertension is overrepresented among patients with ischaemic heart disease. The present study aims at describing the influence of a previous history of hypertension upon the prognosis among patients hospitalized due to acute myocardial infarction., Design: Patients were followed for 1 year. Mortality and morbidity are described during hospitalization and after discharge from hospital., Setting: Sahlgrenska Hospital, serving half of the area of Gothenburg in Sweden., Patients: All patients admitted to Sahlgrenska Hospital during 21 months due to acute myocardial infarction regardless of age and whether they were admitted to the coronary care unit., Results: Among all patients with confirmed acute myocardial infarction (n = 917) a previous history of hypertension was reported in 324 patients. Hypertensives more frequently had a previous history of acute myocardial infarction, angina pectoris, congestive heart failure and diabetes mellitus. Their mortality during hospitalization was similar to that in normotensives. However, the total mortality during 1 year of follow-up was 35% in hypertensives and 25% for normotensives (P < 0.01), and a previous history of hypertension was an independent risk indicator for death after discharge from hospital. Place and mode of death appeared similar in normotensives and hypertensives. Reinfarction was twice as common in hypertensives as in normotensives, and a previous history of hypertension was an independent risk indicator for reinfarction., Conclusions: Among patients with acute myocardial infarction a previous history of hypertension indicates a poor prognosis, one-third of patients dying and one-quarter developing reinfarction during the first year after onset of acute myocardial infarction.

In all 4,232 patients admitted to a single hospital during a 21-month period due to initially suspected acute myocardial infarction (AMI), the prognosis and risk factor pattern were related to whether patients had chest pain or not. Symptoms other than chest pain that raised a suspicion of AMI were mainly acute heart failure, arrhythmia, and loss of consciousness. In 377 patients (9%) symptoms other than chest pain raised an initial suspicion of AMI. These patients developed a confirmed infarction during the first three days in hospital with a similar frequency (22%) as compared with patients having chest pain (22%). However, patients with "other symptoms" had a one-year mortality of 28% versus 15% for chest pain patients (p less than 0.001). Patients with "other symptoms" more often died in association with ventricular fibrillation and less often in association with cardiogenic shock as compared with chest pain patients. Among the 921 patients who developed early AMI, 64 (7%) had symptoms other than chest pain. They had a one-year mortality of 48% versus 27% for chest pain patients (p less than 0.001). We conclude that in a nonselected group of patients hospitalized due to suspected AMI, those with symptoms other than chest pain have a one-year mortality, which is nearly twice that of patients with chest pain.

In 857 consecutive patients with acute myocardial infarction (AMI), the occurrence of chest pain more than 24 h after hospital admission is described and related to death or reinfarction during one year of follow-up. Prolonged chest pain was observed in 333 patients (39%). In this group 15% died and 7% developed reinfarction during the first month as compared with 10% (p < 0.05) and 2% (p < 0.01) respectively in patients without prolonged pain. However, during one year of follow-up mortality did not differ significantly between patients with (27%) and without (24%) prolonged pain. The 1-year reinfarction rate was similar in the two groups (18% and 14%, respectively; NS). We conclude that AMI patients with prolonged chest pain have a particularly high mortality during the first month. However, during a longer follow-up the prognosis is similar in patients with and without prolonged chest pain.

Several postinfarction trials have evaluated the effect of secondary prophylaxis with different beta-blockers. Although so called meta-analysis of the results from all the trials have shown a beneficial effect of postinfarction beta-blockade, many of the individual studies have shown inconclusive results, mainly due to low statistical power. In order to obtain an evaluation of the merits of postinfarction therapy with metoprolol, data from the five available studies with metoprolol have been pooled into one database. In the total material 5474 patients (4353 men, 1121 women) have been studied during double-blind therapy with metoprolol 100 mg twice daily or matching placebo. The follow-up ranges from 3 months to 3 years. In total 4732 patient years of observation have been obtained. In total there were 223 deaths in the placebo-treated patients as compared to 188 deaths in the metoprolol-treated patients (P = 0.036), which corresponds to mortality rates of 97.0 and 78.3 per 1000 patient years, respectively. The mortality reduction was found both in men and women. As has been reported from individual postinfarction beta-blocker trials, the pooled results showed a marked reduction in sudden deaths (104 in the placebo group, 62 in the metoprolol group, P = 0.002). In a Cox regression model the influence of sex, age and smoking habits on the effect of metoprolol was evaluated. None of these factors influenced the metoprolol effect significantly. It is concluded that metoprolol therapy after acute myocardial infarction reduces the total number of deaths, and especially sudden cardiac deaths. The mortality reduction was independent of gender, age and smoking habits. Available data support a continuous beneficial effect.

The characteristics and the prognosis in 921 consecutive patients with acute myocardial infarction (AMI) admitted to one single hospital are described and related to whether they were treated in the coronary care unit or not. Patients treated in the coronary care unit (n = 779) had a 1-year mortality rate of 26% as compared with 41% for patients treated in general wards (n = 115; p < 0.001) and 74% for patients treated in the intensive care unit (n = 27; p < 0.001). Patients treated outside the coronary care unit had a different risk factor pattern including a higher age and a higher prevalence of a previous cardiovascular disease. Independent clinical risk indicators for death among patients in the coronary care unit were in order of significance, high age (p < 0.001), arrhythmia on admission (p < 0.01), acute congestive heart failure on admission (p < 0.01) and a history of diabetes mellitus (p < 0.05). In patients treated in general wards, the only risk indicator for death was a history of congestive heart failure.

We evaluated the prognosis of 599 diabetics who came to the emergency department with chest pain or other symptoms suggestive of acute myocardial infarction (AMI). They made up 8% of the patients with such symptoms (n = 7,157). Diabetics had a 1-year mortality rate of 25% as compared with 10% for nondiabetics (p less than 0.001). The difference remained significant regardless of whether there was a strong or a vague initial suspicion of AMI. On admission, independent risk factors for death were age, acute congestive heart failure and initial degree of suspicion of AMI. We conclude that among diabetics who appear in the emergency department with chest pain or other symptoms suggestive of AMI, 25% are dead within 1 year. The prognosis is directly related to the initial suspicion of AMI.

By the mid 1960s a beneficial effect of post-myocardial infarction treatment with beta-blockade had been proposed. However, it was not until 1981 that large clinical trials clearly demonstrated a beneficial effect both in terms of reduction in mortality and morbidity. Today treatment with beta-blockers both in the acute phase of acute myocardial infarction as well as in the stable post-myocardial infarction patient is well established. In this review article, different aspects of early and late treatment with beta-adrenoceptor blockers are discussed. The cardioprotective effects of beta-blockers on mortality and morbidity should not be considered class effects valid for all beta-blockers. Pooled data have clearly demonstrated that beta-blockers with intrinsic sympathomimetic activity have less marked effects. Impressive effects on mortality and morbidity have been obtained with propranolol, timolol, and metoprolol, which are noncardioselective as well as more beta 1-selective (metoprolol), but they are all lacking intrinsic sympathomimetic activity and, furthermore, have a relatively high degree of lipophilicity. It is clear that acute beta-adrenoceptor blockade in suspected acute myocardial infarction reduces mortality and morbidity as well as complications such as chest pain and ventricular arrhythmias during the acute phase. In post-myocardial infarction treatment, it is clear that both mortality and morbidity are reduced. Reports from extended follow-ups after termination of initial double-blind beta-blocker studies in postinfarction patients indicate that withdrawal of the active treatment may increase mortality after cessation of treatment. This is observed despite measures having been taken to avoid so-called acute withdrawal phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)

In a totally nonselected group of patients with acute myocardial infarction (AMI) (n = 921) admitted from the emergency department to the coronary care unit or other hospital ward, the occurrence of non-Q-wave AMI and the prognosis in these patients was determined and compared with those in whom Q waves were developed. Fifty-two percent had AMI without new Q waves. Patients with a non-Q-wave AMI differed from patients with Q-wave AMI, more frequently having a previous history of AMI (p less than 0.001), angina pectoris (p less than 0.01), diabetes mellitus (p less than 0.05), congestive heart failure (p less than 0.001), and a higher mean age (p less than 0.001), whereas smoking was more common in Q-wave AMI. Patients with non-Q-wave AMI had a 1-year mortality of 31% compared with 26% in Q-wave AMI (p greater than 0.2) and a reinfarction rate of 20% compared with 12% for Q-wave AMI (p less than 0.01). Among patients aged less than 75 years without a previous history of AMI, congestive heart failure, and diabetes mellitus, the 1-year mortality rate was 16% for patients with Q waves versus 15% for those without Q waves (NS). Appearance of Q waves was not independently associated with death. We conclude that in a nonselected group of patients with AMI the occurrence of a non-Q-wave AMI is much higher than previously reported. The prognosis in AMI during one year of follow-up is not associated with development of Q waves.

Consecutive patients admitted to our hospital with suspected acute myocardial infarction during 21 months were prospectively evaluated. One-year mortality after discharge from hospital was related to whether or not an infarction developed (infarct versus non-infarct patients). Of patients discharged alive after developing an infarct, there was a mortality of 17% (n = 777) versus 12% (n = 1830) (P less than 0.001) for all patients not developing infarction. In a high risk group (any of the following: age greater than or equal to 75 years, previous history of myocardial infarction, diabetes mellitus or congestive heart failure) patients developing infarction had a mortality of 24% (n = 457) versus 17% (n = 1221) for those who did not (P less than 0.001). In a low risk group (none of the high risk criteria), the corresponding mortality was 8% (n = 316) for patients suffering infarction and 3% (n = 603) for those not having infarction (P less than 0.001). The difference in mortality between patients with and without infarction was most marked in women (21% vs 11%; P less than 0.01) and in hypertensives (25% vs 12%; P less than 0.001), but less marked in men (16% vs 13%; NS) and in patients without hypertension (13% vs 12%; NS). Among patients not suffering infarction, mortality was particularly high in those with previous congestive heart failure (23%) and diabetes mellitus (21%).

All 7157 patients (55% men) admitted to the emergency room with chest pain or other symptoms indicative of acute myocardial infarction during a period of 21 months were registered consecutively. Chest pain was reported by 93% of the patients. On the basis of history, clinical examination, and electrocardiogram in the emergency room, all patients were prospectively classified in one of four categories: (i) obvious infarction (4% of all patients); (ii) strongly suspected infarction (20%); (iii) vague suspicion of infarction (35%); and (iv) no suspected infarction (41%). In patients with no suspected infarction (n = 2910), musculoskeletal (26%), obscure (21%) and psychogenic origins (16%) of the symptoms occurred most frequently. We conclude that few of the patients had an obvious infarction on admission, and that a musculoskeletal origin of the symptoms occurred most frequently in patients with no suspected infarction.

The possibility of early prediction of acute myocardial infarction (AMI) was assessed in 7,157 consecutive patients coming to our emergency room during a 21-month period with chest pain or other symptoms suggestive of AMI. Of these patients 921 developed an AMI during the first 3 days in the hospital. Of the 4,690 patients admitted to hospital, 1,576 (34%) had a normal admission electrocardiogram, and 90 of these (6%) developed AMI. Of 1,964 patients with an abnormal electrocardiogram without signs of acute ischemia (42% of those admitted), 268 (14%) developed AMI, and 563 (51%) of 1,109 patients with acute ischemia on the electrocardiogram (24%) developed AMI. All patients were prospectively classified in the emergency room on the basis of history, clinical examination and electrocardiogram into 1 of 4 categories, according to the initial degree of suspicion of AMI. Of 279 admitted patients judged to have an obvious AMI (6% of the 4,690), 245 (88%) actually developed AMI; of 1,426 with a strong suspicion of AMI (30%), 478 (34%) developed one; of 2,519 with a vague suspicion of AMI (54%), 192 (8%) developed one; and of 466 with no suspicion of AMI (10%), 6 (1%) developed one. Thus, only a low percentage of the patients with a normal initial electrocardiogram or a vague initial suspicion of AMI developed a confirmed AMI.

This study describes the outcome in terms of health-related quality of life (QL) five years after onset of symptoms in 397 patients with an initial suspicion of acute myocardial infarction (MI) but in whom the diagnosis was not confirmed. The patients were approached by means of a postal inquiry that comprised two questionnaires. The most pronounced impairment in health-related QL was expressed as decreased energy, whereas social life was the least affected area. The overall QL was very similar to that in patients who had a confirmed MI. Subsets of patients with impaired QL were those given the diagnosis of angina pectoris or possible infarction.

We evaluated the prognosis for 419 patients admitted to hospital due to suspected acute myocardial infarction (AMI) who developed ST-T changes, but no rise in serum enzyme activity, and compared it to that of 508 patients developing non-Q-wave AMIs. We conclude that these patients have a high 1-year mortality (13%), although significantly lower than in patients with non-Q-wave AMIs (31%). The mortality is higher in patients with only ST depression (n = 86; 22%) than in patients with only T-wave inversion (n = 264; 8%).

During a 21-month period, the prognosis in all patients admitted to a hospital ward from the emergency room with suspected acute myocardial infarction (AMI) was prospectively recorded and related to the time between onset of symptoms and arrival in hospital. They were classified as early arrivers (less than or equal to 2 h), intermediate arrivers (2-8 h) and late arrivers (greater than 8 h). Among patients developing a confirmed AMI (n = 909) the 1-year mortality rate was 26.0% in early arrivers, 28.1% in intermediate arrivers and 32.6% in late arrivers. The corresponding figures for patients in whom AMI was ruled out (n = 2,035) were 15.2, 15.1 and 17.6%, respectively. In AMI patients, various morbidity aspects during hospitalization and 1 year of follow-up appeared mainly independent of delay time, whereas among those in whom AMI was ruled out congestive heart failure during hospitalization was most common in early arrivers. We conclude that patients with suspected AMI who do not arrive early in hospital have a high 1-year mortality rate regardless of whether they develop AMI or not. Whether their prognosis can be improved by shortening of delay time remains to be clarified.

Circadian variation of onset of acute myocardial infarction has been noted in many studies and may carry important implications. However, only a few previous studies have attempted subgroup analysis. In 4,796 patients with documented acute myocardial infarction, the time of symptom onset was recorded. As in other studies, a peak occurred in the morning hours from 6 A.M. to noon with 28% of the population (1.16 times the average percent for the other time periods) experiencing symptom onset in that period (p less than 0.001). There was a second lower peak (25%) in the evening hours between 6:01 P.M. and midnight, also observed in some previous studies. Whether the presence of subgroups with specific clinical characteristics would exhibit different patterns and thereby contribute to these peaks in the overall population was then determined. In patients with a history of congestive heart failure (n = 606) or with non-Q-wave infarction (n = 832), a pronounced peak (29%) occurred only in the evening hours. In patients greater than 70 years of age (n = 1,422), smokers (n = 2,057), diabetics (n = 767), women (n = 1,213) and patients taking beta blocking drugs (n = 847), 2 nearly equal peaks were observed. Finally, in patients with previous myocardial infarction (n = 1,104), no peaks were observed. In a subgroup of patients (n = 1,084) free from the most important modifying factors, there was a single very pronounced late morning peak (32%), 1.39 times the average percent for the other time periods (p less than 0.001), without evidence of a second evening peak.(ABSTRACT TRUNCATED AT 250 WORDS)

Based on the registration of all the 7,157 patients admitted during a 21-month period to the emergency ward of a single hospital in an urban area with chest pain or other symptoms suggestive of acute myocardial infarction, we studied eligibility for intravenous thrombolysis in suspected acute myocardial infarction. We have limited the present analysis to those 1,715 patients with a strong suspicion of myocardial infarction, and for these patients, we have calculated the percentages eligible for thrombolysis when various electrocardiographic and delay time criteria are applied, but we have not considered contraindications to thrombolysis. We have also calculated the proportions of all infarctions in this group that would thereby receive the treatment, and the proportions of patients treated that would develop a confirmed infarction. Using the criteria ST elevation on the initial electrocardiogram and arrival in hospital within 6 hours from onset of symptoms, 18% of patients would have been given early intravenous thrombolysis, 37% of confirmed infarctions would have been treated, and 91% of all treated patients would have developed a confirmed infarction; with a delay time criterion of 12 hours, these percentages would have been 20%, 41%, and 91%, respectively; with a criterion of 24 hours, they would have been 22%, 45%, and 90%, respectively. By not considering the initial electrocardiogram and applying only the criterion of delay time, these percentages would have been 70%, 72%, and 45%, respectively, for a delay time of 6 hours; 83%, 84%, and 45%, respectively, for a delay time of 12 hours; and 91%, 92%, and 44%, respectively, for a delay time of 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

From a large randomized multicentre trial of metoprolol in suspected acute myocardial infarction (n = 5778) we report on the outcome during 1 year of follow-up, in relation to early diagnosis. Patients who developed a confirmed infarction had a 1-year mortality rate of 12.8%. This was significantly higher than the mortality rate of 6.3% (P less than 0.001) in patients with possible infarction and it was also higher than that in patients with no infarction, which was 5.0% (P less than 0.001). A multivariate analysis showed that independent risk predictors in the clinical history of patients without confirmed infarction were a history of angina pectoris, chronic use of digitalis and advanced age. After 1 year, angina pectoris was most common in patients with an initial possible infarction. These patients were also in most urgent need of bypass surgery. We thus conclude that the mortality during 1 year of follow-up among patients with an initially strongly suspected acute myocardial infarction was clearly related to whether or not the patient developed a myocardial infarction.

From a randomized multicenter trial with metoprolol in suspected acute myocardial infarction (n = 5778) we report on the outcome during a one-year follow-up in patients with confirmed infarction (n = 4106) in relation to whether or not they developed Q waves. Patients with Q waves had another pattern of risk factors, including lower age and a lower occurrence of previous infarction, angina pectoris, and congestive heart failure. After one year follow-up, 14.3% of the patients with Q waves had died versus 9.0% of those without Q waves (p less than 0.001). Reinfarction during the first year occurred in 8.2% of patients with Q waves and 12.5% of patients without Q waves (p less than 0.001). After one year, other morbidity aspects appeared relatively independent of the original presence of Q waves. In conclusion, during the first year after development of acute myocardial infarction the appearance of Q waves during the first three days is associated with a higher mortality and a lower reinfarction rate, whereas other morbidity aspects appear to be relatively independent of its presence.