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  • 1. Aasa, M
    et al.
    Dellborg, M
    Herlitz, Johan
    [external].
    Svensson, L
    Grip, L
    Risk Reduction for Cardiac Events After Primary Coronary Intervention Compared With Thrombolysis for Acute ST-Elevation Myocardial Infarction (Five-Year Results of the Swedish Early Decision Reperfusion Strategy [SWEDES] Trial)2010In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 106, no 12, p. 1685-1691Article in journal (Refereed)
    Abstract [en]

    Primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction compares favorably to thrombolysis. In previous studies the benefit has been restricted to the early postinfarction period with no additional risk decrease beyond this period. Long-term outcome after use of third-generation thrombolytics and modern adjunctive pharmaceutics in the 2 treatment arms has not been investigated. This study was conducted to compare 5-year outcome after updated regimens of PPCI or thrombolysis. Patients with ST-elevation myocardial infarction were randomized to enoxaparin and abciximab followed by PPCI (n = 101) or enoxaparin followed by reteplase (n = 104), with prehospital initiation of therapy in 42% of patients. Data on survival and major cardiac events were obtained from Swedish national registries after 5.3 years. PPCI resulted in a better outcome with respect to the composite of death or recurrent myocardial infarction (hazard ratio 0.54, confidence interval 0.31 to 0.95) compared to thrombolysis. This was attributed to a significant decrease in cardiac deaths (hazard ratio 0.16, confidence interval 0.04 to 0.74). The difference evolved continuously over the 5-year follow-up. After adjustment for covariates, a significant benefit remained with respect to cardiac death or recurrent infarction but not for the composite of total survival or recurrent myocardial infarction (p = 0.07). The observed differences were not seen in patients in whom therapy was initiated in the prehospital phase. In conclusion, PPCI in combination with enoxaparin and abciximab compares favorably to thrombolysis in combination with enoxaparin with a risk decrease that stretches beyond the early postinfarction period. Prehospital thrombolysis may, however, match PPCI in long-term outcome.

  • 2. Albertsson, P
    et al.
    Emanuelsson, H
    Karlsson, T
    Lamm, C
    Sandén, W
    Lagerberg, G
    Herlitz, Johan
    University of Borås, Faculty of Caring Science, Work Life and Social Welfare.
    Morbidity and use of medical resources in patients with chest pain and normal or near normal coronary arteries. Influences of the diagnostic angiogram1997In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 79, no 3, p. 299-304Article in journal (Refereed)
    Abstract [en]

    To evaluate morbidity and use of medical resources in patients with chest pain and normal or near-normal coronary angiograms: 2,639 consecutive patients who underwent coronary angiograms due to chest pain were registered. Two years thereafter all patients who showed normal or near-normal coronary angiograms were approached with a questionnaire regarding hospitalization during the last 4 years (2 years before and 2 years after angiography). All medical files were also examined. Of the patients who underwent angiography, 163 (6%) had no significant stenoses, and of these, 113 showed complete normal angiograms and 50 showed mild (i.e. <50%) stenoses. During the 2 years before diagnostic angiogram, 66% of the patients were hospitalized compared with only 35% during 2 years after angiography (p <0.001). The reduction in hospitalization was due to curtailed utilization of medical resources for cardiac reasons; mean days in hospital was 6.6 days before angiography versus 2.8 days after (p <0.001). There were no significant differences in hospitalization when comparing patients with mild stenoses and completely normal angiograms. There were, furthermore, no differences between patients with positive or negative exercise tests. Thus, the need for hospitalization is significantly reduced after a diagnostic angiogram reveals normal or near-normal coronary arteries.

  • 3. Blohm, M
    et al.
    Herlitz, Johan
    [external].
    Hartford, M
    Karlson, BW
    Risenfors, M
    Luepker, RV
    Sjölin, M
    Holmberg, S
    Consequences of a media campaign focusing on delay in acute myocardial infarction1992In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, ISSN 0002-914, Vol. 69, no 4, p. 411-413Article in journal (Other academic)
  • 4. Engdahl, J
    et al.
    Bång, A
    [external].
    Lindqvist, J
    Herlitz, Johan
    [external].
    Can we define patients with no and those with some chance of survival when found in asystole out of hospital?2000In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 86, no 6, p. 610-614Article in journal (Refereed)
    Abstract [en]

    We describe the epidemiology, prognosis, and circumstances at resuscitation among a consecutive population of patients with out-of-hospital cardiac arrest (OHCA) with asystole as the arrhythmia first recorded by the Emergency Medical Service (EMS), and identify factors associated with survival. We included all patients in the municipality of Göteborg, regardless of age and etiology, who experienced an OHCA between 1981 and 1997. There were a total of 4,662 cardiac arrests attended by the EMS during the study period. Of these, 1,635 (35%) were judged as having asystole as the first-recorded arrhythmia: 156 of these patients (10%) were admitted alive to hospital, and 32 (2%) were discharged alive. Survivors were younger (median age 58 vs 68 years) and had a witnessed cardiac arrest more often than nonsurvivors (78% vs 50%). Survivors also had shorter intervals from collapse to arrival of ambulance (3.5 vs 6 minutes) and the mobile coronary care unit (MCCU) (5 vs 10 min), and they received atropine less often on scene. There were also a greater proportion of survivors with noncardiac etiologies of cardiac arrest (48% vs 27%). Survivors to discharge also displayed higher degrees of consciousness on arrival to the emergency department in comparison to nonsurvivors. Multivariate analysis among all patients with asystole indicated age (p = 0.01) and witnessed arrest (p = 0.03) as independent predictors of an increased chance of survival. Multivariate analysis among witnessed arrests indicated short time to arrival of the MCCU (p < 0.001) and no treatment with atropine (p = 0.05) as independent predictors of survival. Fifty-five percent of patients discharged alive had none or small neurologic deficits (cerebral performance categories 1 or 2). No patients > 70 years old with unwitnessed arrests (n = 211) survived to discharge.

  • 5.
    Herlitz, Johan
    [external].
    Comparison of lisinopril versus digoxin for congestive heart failure during maintenance diuretic therapy1992In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 70, no 10, p. 84-90Article in journal (Refereed)
    Abstract [en]

    Lisinopril 5–20 mg once daily was compared with digoxin 0.125–0.375 mg once daily in a double-blind, randomized, parallel-group study involving 217 patients with mild-to-moderate heart failure (New York Heart Association [NYHA] grades II–III) who were maintained on optimized diuretic therapy. After 6 weeks of treatment, digoxin and lisinopril had increased exercise duration by 18 seconds (p = 0.015) and 32 seconds (p = 0.0007), respectively, versus the baseline run-in period. The difference between treatments was not statistically significant (p = 0.1343). After 12 weeks, digoxin and lisinopril had increased exercise duration by 29 seconds and 51 seconds, respectively. The effect of digoxin compared with the baseline value was not significant but that for lisinopril was (p = 0.0027). The difference between treatments approached statistical significance (p = 0.0813). There was no difference between lisinopril and digoxin with regard to their effects on the frequency of ventricular ectopic counts, couplets, or nonsustained ventricular tachycardia. Blood pressures were not significantly different between treatments, although both systolic and diastolic blood pressure were consistently lower in the lisinopril group throughout randomized treatment. The proportions of patients demonstrating an improvement in NYHA grading were similar for both lisinopril and digoxin. Both treatments had similar effects on the symptoms of heart failure. Both drugs appeared to be equally well tolerated with a similar frequency of adverse events reported for both drugs (30% for lisinopril vs 29% for digoxin). Withdrawals from treatment were of a similar frequency for both treatments. It is concluded that lisinopril may be a useful alternative to digitalis in patients with heart failure who remain symptomatic on diuretic therapy.

  • 6.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Arrhythmias. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 35-38Article in journal (Refereed)
    Abstract [en]

    Forty-five patients in the placebo (1.5%) and 29 in the metoprolol (1%) groups, respectively, were receiving antiarrhythmic drugs on a long-term basis before entry into the trial. Before randomization, 2.2% (n = 64) of the placebo and 1.7% (n = 50) of the metoprolol patients developed ventricular fibrillation (VF) in the hospital. The corresponding figures for atrial fibrillation or flutter were 3% (n = 87) and 3.3% (n = 94). After randomization, there was no significant difference in the number of patients who developed VF in the placebo (n = 52) and the metoprolol (n = 48) groups. The total number of episodes of VF tended to be fewer in the metoprolol group (n = 67) compared with the placebo group (n = 96). The tendency was, however, not apparent until after 5 days. When the occurrence of VF was related to high- and low-mortality risk groups, any beneficial effect of metoprolol was confined mainly to the high-risk group. A similar proportion of patients underwent electric conversion for ventricular tachyarrhythmia in the 2 groups. Although antiarrhythmic drugs were intended to be given only for major ventricular tachyarrhythmias a large proportion of patients received such treatment. Significantly more patients were treated with antiarrhythmics in the placebo (21.5%) than in the metoprolol group (19.2%, p = 0.03) during the study period, but predominantly during the first 5 days. Atrial fibrillation or flutter and other supraventricular tachyarrhythmias were significantly less frequent in the metoprolol than in the placebo group, as was the use of cardiac glycosides.

  • 7.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Development of myocardial infarction. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 23-26Article in journal (Refereed)
    Abstract [en]

    The effect of metoprolol on the development of an acute myocardial infarction (AMI) during days 0 to 3 and on late first and recurrent infarctions during days 4 to 15 has been investigated. Signs on electrocardiogram (ECG) were well balanced between the treatment groups at entry; 70% of patients had signs of suspected AMI and 19% of patients had normal ECGs. The remaining patients had abnormal ECGs but actual infarction could not be localized. The localization of suspected AMI was equivalently distributed in the 2 groups before randomization. Metoprolol altered the distribution of patients diagnosed during days 0 to 3 as having definite, possible or no AMI (p less than 0.02). In the placebo group, there were more patients with definite AMI (72.5% vs 70.5%) and less with possible AMI (5.6% vs 7.4) than in the metoprolol group. A larger proportion of patients developed a Q-wave infarction during days 0 to 3 in the placebo group (53.9%) compared with the metoprolol group (50.9%, p = 0.024). No difference in the effect of metoprolol regarding localization of the early AMI was observed. Late first myocardial infarction development (days 4 to 15) was observed in 20 patients (0.7%) in each group. Recurrent myocardial infarction tended to develop more frequently during days 4 to 15 in the placebo group compared with the metoprolol group (3.9% vs 3.0%, p = 0.08).

  • 8.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Enzymatic estimation of infarct size. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 27-29Article in journal (Refereed)
    Abstract [en]

    The maximum serum activity for aspartate aminotransferase (s-ASAT) during the first 3 days was recorded in 5,507 patients with suspected or definite acute myocardial infarction. The s-ASAT activity was corrected for the normal range from each center. The median s-ASAT activity was 4.9 arbitrary units in the placebo group versus 4.6 arbitrary units in the metoprolol group (p = 0.072). Univariate analyses indicated that the delay time between onset of symptoms and randomization and sympathetic activity at entry significantly influenced the effect of metoprolol. A similar decrease in serum enzyme activity after metoprolol treatment was observed independent of signs of infarct localization on the entry electrocardiogram.

  • 9.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Mortality. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 15-22Article in journal (Refereed)
    Abstract [en]

    After 15 days there were 142 deaths in the placebo group (4.9%) and 123 deaths in the metoprolol group (4.3%), a difference of 13% (p = 0.29). The 95% confidence limits for the relative effect of metoprolol ranged from an 8% excess (-8%) to a 33% reduction (+33%) in mortality. There was generally a lower mortality rate for metoprolol-treated patients in most subgroups and a consistent tendency for a more pronounced difference between the treatment groups in those subgroups with a placebo mortality rate higher than the average for all placebo patients. Most deaths were cardiac and occurred among patients who developed a definite myocardial infarction (97%) and most of these had a Q-wave infarction (83%). Using a simple model, the placebo mortality was found to increase with increasing number of 8 risk predictors defined from prestudy experience, from 0% in patients with no risk predictors to 11.6% in patients with any 5 or more of these risk factors. Similarly, there was an increase in the difference between the treatment groups in favor of metoprolol with increasing number of placebo risk factors. Metoprolol had no apparent effect in a low-mortality risk group (less than or equal to 2 risk factors), but there was a difference in mortality of 29% in favor of metoprolol in a high-risk group (greater than or equal to 3 risk factors) comprising one-third of the trial population.

  • 10.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Narcotic analgesics and other antianginal drugs. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 30-34Article in journal (Refereed)
    Abstract [en]

    The effect of metoprolol on chest pain has been assessed in terms of the duration and the use of narcotic analgesics, nitrates and calcium-channel blockers. Fewer metoprolol-treated patients in the MIAMI trial were given narcotic analgesics (49% of the placebo patients vs 44% of the metoprolol patients, p less than 0.001), nitrates (55% vs 53%, p = 0.10) and calcium-channel blockers (12% vs 9%, p less than 0.001). A total number of 6,697 dose equivalents of narcotic analgesics were given to the placebo group compared with 5,493 dose equivalents to the metoprolol group, a difference of 18% (p less than 0.001). Mean dose equivalents were 2.3 and 1.9, respectively. The analysis of the total use of the 3 types of treatment for ischemic chest pain showed a significantly less frequent use of treatment for chest pain in the metoprolol group than in the placebo group (p less than 0.004). The relative difference in the incidence of drug treatment tended to be more striking for patients with maximal therapy, i.e., receiving high doses of narcotic analgesics, nitrates and calcium-channel blockers. There were 22% fewer patients receiving 4 or more doses of narcotic analgesics in the metoprolol group than in the placebo group. A multivariate analysis disclosed that site of suspected infarction, delay time, entry systolic blood pressure and metoprolol treatment all had a significant effect on the use of narcotic analgesics. There was a nonsignificant tendency for heart rate to be of importance. In the placebo group the use of narcotic analgesics increased with decreasing delay time and increasing systolic blood pressure.

  • 11.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Other clinical findings and tolerability. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 39-46Article in journal (Refereed)
    Abstract [en]

    Fifteen minutes after injection there was a fall in mean heart rate (18%, p less than 0.001), systolic blood pressure (10%, p less than 0.001) and rate-pressure product (27%, p less than 0.0001) in the metoprolol group of patients in the MIAMI trial. Hypotension and bradycardia not necessarily associated with withdrawal of drug were more common in the metoprolol group (p less than 0.001). Atrioventricular block I was more common in the metoprolol group (p less than 0.03), whereas no such difference was observed for atrioventricular block II and III, asystole or pacemaker implantations. Left ventricular failure was observed no more often in the metoprolol group. The occurrence of cardiogenic shock also did not differ between the groups. Cardiac glycosides were used more in the placebo group, but diuretic and furosemide usage did not differ. For all patients mean furosemide doses and number of diuretic injections were similar in both treatment groups. Atropine (4.1 vs 6.4%) and sympathomimetic (3.2 vs 4.6%) agents were used more often in the metoprolol group during days 0 to 5 (p less than 0.05). The trial medication was withdrawn temporarily more often in the metoprolol than in the placebo group (p less than 0.001). However, permanent withdrawal of trial medication occurred with a similar frequency overall in both groups. More patients were withdrawn from the study because of cardiovascular reasons in the metoprolol group (9%) than in the placebo group (5%, p less than 0.001).

  • 12.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Patient population. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 10-14Article in journal (Refereed)
    Abstract [en]

    During the recruitment phase of the MIAMI trial (December 1982 to March 1984), data on 26,439 patients eligible for inclusion were entered. Of these, 5,778 patients were included. Current treatment with either beta blockers or calcium-channel blockers (51%) was the most predominant reason for exclusion. The randomized and excluded patients differed. The randomized patients were younger and more often men. The mean age of the patients was 59 years in both the placebo and the metoprolol groups. The 2 groups were evenly balanced with regard to basic demographic variables. The median delay between onset of symptoms and randomization was 7 hours, and 25% of the patients were included within 4 hours. Previous clinical history and pharmacologic treatment given before admission were well balanced in the groups. Mean heart rate for the 2 groups before randomization was 83 beats/min and systolic blood pressure was 141 mm Hg. Approximately 15% of randomized patients presented with pulmonary rales. Before randomization 20% of the patients had normal electrocardiograms; 70% could be classified as having electrocardiographic signs of acute myocardial infarction; and 10% presented with other electrocardiographic abnormalities. Electrocardiographic signs at entry suggested a predominance of anterior wall infarctions. The randomized patients were not representative of eligible patients and the treatment groups were well balanced at entry.

  • 13.
    Herlitz, Johan
    [external].
    Metoprolol in acute myocardial infarction. Patients and methods. The MIAMI Trial Research Group1985In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 56, no 14, p. 3-9Article in journal (Refereed)
    Abstract [en]

    The effects of early intervention with metoprolol in patients with suspected or definite acute myocardial infarction (AMI) have been assessed in a randomized, double-blind, placebo-controlled international study. Patients aged 75 years or younger were eligible for entry if they presented to a coronary care unit within 24 hours of the onset of symptoms of an AMI. Exclusion criteria included current treatment with a beta blocker or calcium-channel blocker, heart rate less than or equal to 65 beats/min, systolic blood pressure less than or equal to 105 mm Hg, contraindications and other administrative reasons. Treatment began with an intravenous loading dose (3 X 5 mg injections of metoprolol or placebo at 2-minute intervals) followed by an oral regime of 200-mg metoprolol daily or placebo. The study period was 15 days in addition to the day of randomization. The patients' clinical history and status at entry were documented. The following outcome variables were recorded: mortality, development of AMI, serum enzyme activity, electrocardiographic signs of AMI, late or recurrent AMI, arrhythmias, treatment of chest pain, concomitant treatment, adverse events and details of treatment with trial medication.

  • 14.
    Herlitz, Johan
    [external].
    Rationale, design, and organisation of the metoprolol CR/XL randomized trial in heart failure (MERIT-HF)1997In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 80, no 9B, p. 54-58Article in journal (Other academic)
    Abstract [en]

    Metoprolol is a cardioselective beta blocker that has been shown to improve left ventricular function and symptoms of congestive heart failure (CHF) and also to decrease the number of hospitalizations due to CHF. However, the effects of metoprolol on mortality in patients with CHF have yet to be determined. Accordingly, the Metoprolol CR/XL Randomized Intervention Trial in Heart Failure (MERIT-HF) has been designed to investigate the effect of once-daily dosing of metoprolol succinate controlled release/extended release (CR/XL) when added to standard therapy in patients with CHF. A total of 3,200 patients will be recruited for this international, double-blind, randomized, placebo-controlled survival study. The 2 primary objectives of MERIT-HF are to determine the effect of metoprolol CR/XL on (1) total mortality and (2) the combined endpoint of all-cause mortality and all-cause hospitalizations (time to first event). Eligible patients are 40-80 years old, with a reduced left ventricular ejection fraction (< or =0.40) and symptoms of CHF (New York Heart Association functional classes II-IV). After a 2-week placebo run-in period, an optimal allocation procedure will be used to randomize patients in a 1:1 ratio to metoprolol CR/XL or matching placebo. After an initial titration phase starting with 12.5 mg or 25 mg once daily (depending on functional class), the target dose will be 200 mg in all patients who tolerate this dose. The mean follow-up is estimated to be 2.4 years. The study data will be analyzed on an intention-to-treat basis. An Independent Safety Committee will monitor the safety aspects of the trial, and an Independent Endpoint Committee will classify all endpoints.

  • 15.
    Herlitz, Johan
    [external].
    Very early trombolytic therapy in suspected acute myocardial infarction1990In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 65, no 7, p. 401-407Article in journal (Refereed)
    Abstract [en]

    Three hundred fifty-two patients with suspected acute myocardial infarction (AMI) were randomized to placebo (175) or tissue-type plasminogen activator (rt-PA) (177). Patients were eligible if evaluated within 165 minutes from onset of chest pain and if age was <75 years. Electrocardiographic criteria were not required. A mobile coronary care unit with a cardiologist present was used to initiate treatment at home in 29% of the patients. Primary endpoints were infarct size (serum lactate dehydrogenase isoenzyme1 activity), left ventricular function (radioangiography) and exercise capacity at 30 days. AMI was diagnosed in 59% of all randomized patients. The incidence was similar in the 2 groups (placebo, 108, rt-PA, 101). Among all randomized patients, rt-PA was associated with significantly decreased infarct size and an increased ejection fraction. Among rt-PA-treated patients there were significantly fewer Q-wave infarctions. No difference in exercise capacity could be detected. No benefit was found in subgroups of patients without ST-segment elevation on the initial electrocardiogram. There were 18 (10.3%) and 11 (6.2%) deaths (p = 0.23) within 30 days in the placebo and rt-PA groups, respectively. Adverse reactions were similar in both groups with no excess of complications in the home-treated group. Very early treatment with rt-PA in patients with a strong suspicion of AMI and ST-segment elevation limits infarct size and improves left ventricular function. The infarct pattern is shifted from Q-wave to non-Q-wave infarcts by rt-PA. The study suggests that thrombolysis can be given before hospital admission without additional risk. Furthermore, etectrocardiographic records are useful for selection of patients.

  • 16.
    Herlitz, Johan
    et al.
    [external].
    Edwardsson, N
    Holmberg, S
    Rydén, L
    Waagstein, F
    Waldenström, A
    Swedberg, K
    Hjalmarson, Å
    Göteborg Metoprolol Trial: effects on arrhythmias1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 27-31Article in journal (Refereed)
    Abstract [en]

    During the initial hospitalization, ventricular fibrillation (VF) developed in 6 metoprolol-treated patients (0.9%) vs 17 placebo-treated patients (2.4%) after inclusion in the study (p = 0.035). There were 6 episodes of VF in the metoprolol group compared with 41 episodes in the placebo group (p less than 0.001). During the same period, 14 metoprolol-treated patients had treated ventricular tachycardia vs 26 placebo-treated patients (p = 0.076). Similar favorable results were found when the incidence of severe ventricular arrhythmias during the first rehospitalization within the 3-month double-blind treatment period was analyzed.

  • 17.
    Herlitz, Johan
    et al.
    [external].
    Ejdebäck, J
    Swedberg, K
    Waagstein, F
    Hjalmarson, Å
    Göteborg Metoprolol Trial: electrocardiographically estimated infarct size1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 22-26Article in journal (Refereed)
    Abstract [en]

    In 236 patients with anterior myocardial infarction (MI), infarct size was estimated by analyzing the R- and Q-wave amplitude in 24 precordial leads 4 days after randomization. In 254 patients with inferior MI, the final R- and Q-wave amplitude was evaluated in leads II, III and aVF. Electrocardiographic signs of a smaller MI were observed in anterior MI in the metoprolol group compared with the placebo group when treatment was started 12 hours or less after the onset of pain, but no difference was found when treatment was started later. There was no sign of an effect of metoprolol in inferior MI. An immediate reduction in ST-segment elevation was observed after metoprolol treatment regardless of infarct localization or delay between the onset of pain and treatment.

  • 18.
    Herlitz, Johan
    et al.
    [external].
    Elmfeldt, D
    Hjalmarson, Å
    Holmberg, S
    Málek, I
    Nyberg, G
    Rydén, L
    Swedberg, K
    Vedin, A
    Waagstein, F
    Waldenström, A
    Waldenström, J
    Wedel, H
    Wilhelmsen, L
    Wilhelmsson, C
    Effect of metoprolol on indirect signs of the size and severity of acute myocardial infarction1983In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 51, no 8, p. 1282-1288Article in journal (Refereed)
    Abstract [en]

    In a double-blind randomized trial, 1,395 patients with suspected acute myocardial infarction (MI) were investigated to evaluate the possibility of limiting indirect signs of the size and severity of acute MI with the beta1-selective adrenoceptor antagonist metoprolol. Metoprolol (15 mg) was given intravenously and followed by oral administration for 3 months (200 mg daily). Placebo was given in the same way. The size of the MI was estimated by heat-stable lactate dehydrogenase (LD[EC 1.1.1.27]) analyses and precordial electrocardiographic mapping. Lower maximal enzyme activities compared with placebo were seen in the metoprolol group (11.1 ± 0.5 μkat · liter−1)when the patient was treated within 12 hours of the onset of pain (13.3 ± 0.6 μkat · liter−1; n = 936; p = 0.009). When treatment was started later than 12 hours, no difference was found between the 2 groups. Enzyme analyses were performed in all but 20 patients (n = 1,375). Precordial mapping with 24 chest electrodes was performed in patients with anterior wall MI. The final total R-wave amplitude was higher and the final total Q-wave amplitude lower in the metoprolol group than in the placebo group. Patients treated with metoprolol ≤12 hours also showed a decreased need for furosemide, a shortened hospital stay, and a significantly reduced 1-year mortality compared with the placebo group, whereas no difference was observed among patients treated later on. After 3 months, however, there was a similar reduction in mortality among patients in whom therapy was started 12 hours and >12 hours after the onset of pain. The results support the hypothesis that intravenous metoprolol followed by oral treatment early in the course of suspected myocardial infarction can limit infarct size and improve longterm prognosis.

  • 19.
    Herlitz, Johan
    et al.
    [external].
    Elmfeldt, D
    Holmberg, S
    Málek, I
    Nyberg, G
    Pennert, K
    Rydén, L
    Swedberg, K
    Vedin, A
    Waagstein, F
    Waldenström, A
    Waldenström, J
    Wedel, H
    Wilhelmsen, L
    Wilhelmsson, C
    Hjalmarson, Å
    Göteborg Metoprolol Trial: mortality and causes of death1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 9-14Article in journal (Refereed)
    Abstract [en]

    During the 3-month blind treatment period there were 40 deaths in the metoprolol group compared with 62 deaths in the placebo group (p = 0.024). During the first year (after 3 months the 2 groups were treated similarly) there were 64 deaths in the metoprolol group vs 93 in the placebo group (p = 0.017) and during 2 years 92 patients died in the metoprolol group vs 120 in the placebo group (p = 0.043). The relative incidence of different causes of death did not differ significantly between the 2 treatment groups, indicating that metoprolol reduced all causes of death to the same extent as its effect on overall mortality.

  • 20.
    Herlitz, Johan
    et al.
    [external].
    Emanuelsson, H
    Swedberg, K
    Vedin, A
    Waldenström, A
    Waldenström, J
    Hjalmarson, Å
    Göteborg Metoprolol Trial: enzyme-estimated infarct size1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 15-21Article in journal (Refereed)
    Abstract [en]

    In 1,375 patients serum activity of heat-stable lactate dehydrogenase (LD; E.C.1.1.1.27.) was analyzed every twelfth hour for 48 to 108 hours. The mean maximum LD activity was 11.1 +/- 0.4 mu kat X 1(-1) in the metoprolol group vs 12.4 +/- 0.5 mu kat X 1(-1) in the placebo group (p = 0.054). In patients in whom treatment was started 12 hours or less after the onset of pain, a 17% reduction in LD activity was observed (p = 0.009) and similar results were found in patients randomized 8 hours or less. Groups in which the effect after metoprolol treatment was more pronounced were those with an initially higher heart rate and also those with anterior myocardial infarction.

  • 21.
    Herlitz, Johan
    et al.
    [external].
    Hartford, M
    Aune, S
    Karlsson, T
    Occurence of hypotension during streptokinase infusion in suspected acute myocardial infarction, and its relation to prognosis and to metoprolol therapy1993In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 71, no 12, p. 1021-1024Article in journal (Refereed)
    Abstract [en]

    In all patients who received streptokinase infusion for strongly suspected acute myocardial infarction in 1 hospital during 1989 to 1990, the occurrence of hypotension during infusion is described and related to prognosis. In 54% of patients, the β blocker metoprolol was simultaneously administered intravenously. The median systolic blood pressure (BP) before infusion was 135 mm Hg, and the median value for the lowest systolic BP recorded during infusion was 100 mm Hg (p < 0.001). A positive correlation between systolic BP before streptokinase and the lowest systolic BP during infusion was found (r = 0.53; p < 0.001). Among patients administered streptokinase and metoprolol, 23% had systolic BP < 90 mm Hg, and 12% had <80 mm Hg at any time during infusion; corresponding values for patients administered streptokinase only were 47 and 30%, respectively. Patients with the lowest systolic BP < 80 mm Hg during infusion had a mortality during the first 2 weeks of 22 vs 11% for those with between 80 and 100 mm Hg, and 8% for those with >100 mm Hg (p < 0.001). However, in a multivariate analysis the systolic BP before infusion rather than the lowest systolic BP during infusion was independently associated with death. It is concluded that although patients with low systolic BP during streptokinase infusion have a high mortality, the level of systolic BP before infusion is more strongly associated with the outcome. Simultaneous use of intravenous β blockade does not increase the occurrence of hypotension during streptokinase infusion.

  • 22.
    Herlitz, Johan
    et al.
    [external].
    Hartford, M
    Blohm, M
    Karlsson, BW
    Ekström, L
    Risenfors, M
    Wennerblom, B
    Luepker, R
    Holmberg, S
    Effect of media campaign on delay times and ambulance use in suspected acut myocardial infarction1989In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 64, no 1, p. 90-93Article in journal (Refereed)
    Abstract [en]

    The early phase in suspected acute myocardial infarction (AMI) is particularly critical. More than 50% of deaths from coronary artery disease occur outside the hospital mainly due to ventricular fibrillation.1 Recent experiences strongly indicate that early intervention with thrombolysis2–4 and β blockers5,6 can limit myocardial damage and thereby improve prognosis. Delay times in suspected AMI have remained stable over the years. Therefore, a media campaign was started in the urban area of Göteborg, Sweden, with the intention to shorten delay times and to increase ambulance use in patients with suspected AMI.

  • 23.
    Herlitz, Johan
    et al.
    [external].
    Hartford, M
    Pennert, K
    Swedberg, K
    Waagstein, F
    Waldenström, A
    Wedel, H
    Wilhelmsson, C
    Hjalmarson, Å
    Goteborg Metoprolol Trial: clinical observations1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 37-45Article in journal (Refereed)
    Abstract [en]

    Heart rate, systolic blood pressure and rate-pressure product were analyzed during the first 18 hours and 4 days after intravenous metoprolol or placebo. On injection of metoprolol there was an immediate decrease in mean heart rate from 72.9 0.6 to 62.7 0.4 beats/min, but no change was found in the placebo group. The difference in heart rate remained during the first 4 days. Systolic blood pressure was reduced from 144.1 0.9 to 134.6 0.9 mm Hg after intravenous metoprolol and was lower than that in the placebo group during 4 days of follow-up. Indirect signs of congestive heart failure tended to be less severe in patients given metoprolol within 12 hours of the onset of symptoms than in those given placebo. The duration of hospitalization also tended to be shorter in patients given early metoprolol treatment than in those given placebo early.

  • 24.
    Herlitz, Johan
    et al.
    [external].
    Holmberg, S
    Pennert, K
    Swedberg, K
    Vedin, A
    Waagstein, F
    Waldenström, A
    Waldenström, J
    Wedel, H
    Wilhelmsen, L
    Wilhelmsson, C
    Hjalmarsson, Å
    Göteborg Metoprolol Trial: design, patient characteristics and conduct1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 3D-8DArticle in journal (Refereed)
    Abstract [en]

    The Göteborg Metoprolol Trial was a double-blind, placebo-controlled, stratified trial aimed at evaluating the effect of the beta 1-selective blocker, metoprolol, in suspected acute myocardial infarction and during 2 years of follow-up. The primary end-point was 3-month mortality (blind treatment period). Secondary end-points were 2-year mortality, indirect signs of infarct size, chest pain, arrhythmias and tolerability. The entry criteria were fulfilled in 2,802 patients, 1,395 of whom were included in the trial. Treatment started as soon as possible after arrival in hospital with intravenous administration followed by oral treatment for 3 months. All patients were randomized 48 hours or less after estimated onset of infarction and 69% were randomized at 12 hours or less. The blind treatment had to be withdrawn in 19% of all randomized patients before the end of the 3-month follow-up.

  • 25.
    Herlitz, Johan
    et al.
    [external].
    Pennert, K
    Wedel, H
    Vedin, A
    Wilhelmsson, C
    Wilhelmsen, L
    Hjalmarson, Å
    Göteborg Metoprolol Trial: tolerance1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 46D-50DArticle in journal (Refereed)
    Abstract [en]

    During a 3-month follow-up, 131 patients (19.1%) withdrew from blind treatment in both metoprolol- and placebo-treated groups. More metoprolol-treated than placebo-treated patients withdrew because of cardiovascular adverse experience mainly during the very early phase. In all, 45 (6.5%) metoprolol-treated vs 14 (2.0%) placebo-treated patients were not given either a full intravenous dose or a full oral dose 15 minutes later. Bradycardia and hypotension were more common in the metoprolol group, whereas severe atrioventricular block did occur in a similar number of patients in both groups and severe congestive heart failure was more common in the placebo group. Results indicate that tolerance is generally good after intravenous and oral treatment with metoprolol in patients with suspected acute myocardial infarction.

  • 26.
    Herlitz, Johan
    et al.
    [external].
    Waagstein, F
    Lindqvist, J
    Swedberg, K
    Hjalmarson, Å
    Effect of metoprolol on the prognosis among patients with suspected acute myocardial infarction and indirect signs of congestive heart failure. (A subgroup analysis of the Göteborg Metoprolol Trial)1997In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 80, no 9B, p. 40J-44JArticle in journal (Refereed)
    Abstract [en]

    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.

  • 27. Holmberg, S
    et al.
    Holmberg, M
    Herlitz, Johan
    [external].
    The problem of out-of-hospital cardiac arrest prevalence of sudden death in Europe today1999In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 83, no 5B, p. 88D-90DArticle in journal (Refereed)
    Abstract [en]

    In Europe, 40% of all deaths of individuals who are 25-74 years of age are caused by cardiovascular disease. Cardiac disease is the underlying cause in two-thirds of out-of-hospital sudden deaths. The 28-day case fatality rate for the combined population of out-of-hospital coronary artery disease deaths and hospitalized acute myocardial infarction patients is approximately 50% in 29 of the regions included in the World Health Organization (WHO) Monitoring Trends and Determinants in Cardiovascular Disease registry. Of 14,065 patients included in the Swedish Cardiac Arrest Registry, resuscitation procedures were started in 10,966 patients. The remaining 3,099 were considered definitely dead; 70% were witnessed, cardiac arrests and 32.3% had been given bystander cardiopulmonary resuscitation (CPR). The incidence of ventricular tachycardia (VT)/ventricular fibrillation (VF) in all patients was 43%, in witnessed cases 54%, and in nonwitnessed cases, 31%. The initial incidence of VT/VF was calculated to be approximately 60% in the whole population and 80-85% in those with probable cardiac disease. Survival to 1 month was 5.0% in the total population, 9.5% for those with VT/VF on the first electrocardiogram compared with 1.6% for those not in VT/VF. Survival rate was also calculated in relation to delay time to first defibrillation. Survival was 50% when defibrillation was performed immediately and decreased gradually to 0% for those with a delay time of 20 minutes. The survival rate after bystander CPR was 2.6-fold higher than the rate for those where no treatment was given until the ambulance arrived.

  • 28. Karlsson, BW
    et al.
    Herlitz, Johan
    [external].
    Wiklund, O
    Richter, A
    Hjalmarson, Å
    Early prediction of acute myocardial infarction from clinical history, examination and electrocardiogram in the emergency room1991In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 68, no 2, p. 171-175Article in journal (Refereed)
    Abstract [en]

    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.

  • 29. McGovern, PG
    et al.
    Herlitz, Johan
    [external].
    Pankow, JS
    Karlsson, T
    Dellborg, M
    Shahar, E
    Luepker, RV
    Comparison of medical care and one and 12-month mortality of hospitalized patients with acute myocardial infarction in Minneapolis-St Paul, Minnesota, United States of America and Göteborg, Sweden1997In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 80, no 1, p. 557-562Article in journal (Refereed)
    Abstract [en]

    We compared medical care and mortality through 1-year of hospitalized acute myocardial infarction (AMI) patients in 2 large metropolitan areas in the United States and Sweden. All hospitalized AMI discharges (International Classification of Diseases, 9th revision [ICD9] codes 410) occurring among 30 to 74-year-old residents of the Minneapolis-St. Paul metropolitan area in 1990 and Göteborg, Sweden, in 1990 to 1991 were identified and their medical records examined. There were dramatic differences in medical care during the index hospitalization of AMI patients between Minneapolis-St. Paul and Göteborg. Use of thrombolytic therapy, coronary angioplasty, bypass surgery, calcium antagonists and lidocaine was more common in Minneapolis-St. Paul; beta blockers were more frequently used in Göteborg, and aspirin use was similar. Despite these large differences, neither 28-day nor 1-year mortality of hospitalized AMI patients differed significantly. The marked differences found in the early treatment of AMI between Minneapolis-St. Paul and Göteborg, combined with the negligible differences observed in short- and long-term mortality, raise questions about the most effective and efficient allocation of medical resources.

  • 30. Richterova, A
    et al.
    Herlitz, Johan
    [external].
    Holmberg, S
    Swedberg, K
    Waagstein, F
    Waldenström, A
    Vedin, A
    Wennerblom, B
    Wilhelmsson, C
    Hjalmarson, Å
    Goteborg Metoprolol Trial: effects on chest pain1984In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 53, no 13, p. 32-36Article in journal (Refereed)
    Abstract [en]

    The effect of metoprolol on chest pain was compared with that of placebo in all randomized patients. The pain score before and 15 minutes after the injection of trial medication was registered and a reduction in chest pain was observed in the metoprolol group. Increasing chest pain after blind injection was observed in only 16 and 9 patients from the placebo and metoprolol groups, respectively. Comparison with the placebo as well as detailed analysis of clinical data revealed that in these patients the increasing pain could not be explained by coronary spasm evoked by beta-blockade. Similarly, metoprolol did not exhibit any unfavorable effect on the 14 patients who were withdrawn (together with the 28 patients given placebo) from blind treatment due to angina pectoris. Either metoprolol does not induce coronary vasospasm or spasm does not play a role in these patients with definite and suspected acute myocardial infarction as well as unstable angina pectoris. Metoprolol reduced the need for analgesics during the first 4 days and shortened the duration of pain. The effects were similar in patients with early and late treatment, but may depend on initial heart rate, blood pressure and site of infarction.

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