Early Intravenous Atenolol Treatment in Suspected Acute Myocardial Infarction

Yusuf, Salim; Ramsdale, David R.; Pető, Richárd; Furse, L.; Bennett, David; Bray, Colin; Sleight, Peter

doi:10.1016/s0140-6736(80)90231-7

Cited by 208 publications

(30 citation statements)

References 15 publications

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“…These observations suggested that the protective effect of intravenous propranolol was dependent on residual flow to the ischemic region rather than on the systemic effect of the drug. Several clinical investigations have found a reduction in infarct size after ,(3-adrenergic blockade on the basis of enzymatic'l'3 and electrocardiographic11 11 analyses. In contrast, some studies failed to demonstrate a reduction in the extent of myocardial necrosis.…”

Section: Resultsmentioning

confidence: 99%

Myocardial protection during transient coronary artery occlusion in man: beneficial effects of regional beta-adrenergic blockade.

Zalewski¹,

Goldberg²,

Dervan³

et al. 1986

Circulation

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The goal of this study was to verify whether myocardial protection could be achieved via the intracoronary administration of propranolol in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Accordingly, 21 patients undergoing PTCA were randomly assigned to receive either intracoronary placebo (group A, n = 10) or intracoronary propranolol (group B, n = 11). Three balloon inflations (i.e., coronary artery occlusions) were performed in each patient. Inflations I and II (maximum duration 60 sec) served as control occlusions. Inflation III (maximum duration 120 sec) was performed either after intracoronary administration of saline (2 ml) or propranolol (1.1 + 0.2 mg). The following electrocardiographic index of myocardial ischemic injury were measured: (1) time to the development of ST segment elevation equal to 0.1 mV and (2) magnitude of ST segment elevation after 60 sec of coronary artery occlusion. Both indexes did not differ significantly between the groups during inflations I and LI. In group A the time to development of ST segment elevation of 0.1 mV remained unchanged between the second and third occlusions (25 + 5 and 26 ± 4 sec during inflations II and III, respectively). In group B subselective injection of propranolol into the affected coronary artery significantly prolonged the time to ST segment elevation of 0. 1 mV from 19 + 4 sec (inflation II) to 53 ± 9 sec (inflation III; p < .001). Administration of placebo did not change the magnitude of ST segment elevation 60 sec after coronary artery occlusion between the second and third occlusion in group A (0. 16 + 0.02 and 0. 18 ± 0.03 mV, respectively). In group B, after intracoronary administration of propranolol, ST segment elevation 60 sec after occlusion decreased significantly from 0.23 0.06 mV (inflation II) to 0.12 ± 0.04 mV (inflation III; p < .005). There were no significant differences in heart rate and mean aortic pressure between groups A and B during inflations I, II, and III. In conclusion, our results suggest that (1) repetitive episodes of transient coronary artery occlusion are associated with similar degrees of myocardial ischemic injury, (2) intracoronary propranolol significantly reduces the electrocardiographic indexes of myocardial ischemic injury, and (3) the myocardial protection afforded by intracoronary propranolol is most likely mediated by a regional effect of the drug.

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Section: Resultsmentioning

confidence: 99%

Myocardial protection during transient coronary artery occlusion in man: beneficial effects of regional beta-adrenergic blockade.

Zalewski¹,

Goldberg²,

Dervan³

et al. 1986

Circulation

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“…Studies in man after acute myocardial infarction suggest that ,Badrenoceptor blocking drugs reduce the extent of the infarct, provided they are administered sufficiently promptly. This has been shown with post-infarct ST segment mapping (Pelides et al, 1972), monitoring cardiac enzyme changes (Peter et al, 1978;Yusuf et al, 1980;Jurgensen et al, 1981), R wave changes (Yusuf et al, 1980) and chest pain (Andersen et al, 1979); all parameters showing improvement after P-adrenoceptor blockade. Overall trials of ,3-adrenoceptor blocking drugs post-infarction indicate the drugs produce benefit (Baber & Lewis, 1982;Hampton, 1982;Lancet, 1982;Rose, 1982;Turi & Braunwald, 1983), although like all drugs, there is a benefit risk ratio (Breckenridge, 1982).…”

Section: /3-adrenoceptor Blocking Drugsmentioning

confidence: 82%

The management of hypertension.

Prichard¹,

Owens²

1986

Brit J Clinical Pharma

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“…Complications that developed after taking APSAC included bruising (eight patients), nausea and flushing (seven), and minor bleeding (three)-mostly streaks of blood from the mouth or the upper respiratory tract or in vomit. One patient had an unusual shower of emboli to the lower trunk and legs 18 hours after infarction, resulting in numerous patches of skin and muscle necrosis and, ultimately, in gangrene of the toes. His illness had been complicated from the start by refractory pulmonary oedema, and the prognosis was therefore poor; his death three months after the attack might, nevertheless, have been hastened by the emboli.…”

Section: Methodsmentioning

confidence: 99%

Treatment of acute myocardial infarction with anisoylated plasminogen streptokinase activator complex.

Ikram¹,

Lewis²,

Bucknall³

et al. 1986

BMJ

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A controlled trial in 149 patients admitted to a district hospital with probable myocardial infarction tested the effect of 30 units of anisoylated plasminogen streptokinase activator complex (APSAC) on indices of infarct size. Patients were grouped prospectively according to whether they entered the trial within two and a half hours (early entry) or between two and a half and four hours (late entry) after onset ofthe symptoms. Sixty seven of 73 patients in the control group showed increased plasma activity of myocardial creatine kinase isoenzyme that was diagnostic of infarction compared with only 60 of 76 who received APSAC. The difference was significant overall but occurred predominantly in the early entry group. The patients who received APSAC had more early ventricular arrhythmias, compatible with reperfusion, and showed greater preservation of R waves during admission to hospital. Unwanted effects were generally minor and more common in the actively managed group than the control group (26% v 3%). After nine to 12 months offollow up 12 patients in the control group had died compared with seven in the actively managed group.The ease of administration and the apparent efficacy of APSAC suggest that it is suitable for use in a district hospital for patients with suspected acute myocardial infarction. IntroductionThrombus obstructing an atherosclerotic artery is the commonest precipitating cause of acute transmural myocardial infarction.' 2 When intravenous streptokinase was introduced nearly 30 years ago it seemed a logical treatment to use early in an attack; the first paper on this was published in 1959.3 Although early results were promising,45 subsequent studies, including Australian and British multicentre trials,"7 did not show any evidence of benefit from this treatment, and it was not used much outside mainland Europe.The intracoronary administration of streptokinase was associated with cineangiographic evidence of reperfusion, and this led to a resurgence of interest.-" Relatively few patients, however, can be admitted to hospitals that have facilities for immediate coronary angiography. Moreover, a recent review of published data on the influence of thrombolytic treatment on mortality does not support the belief that intracoronary administration is superior to intravenous administration.'2 Efficacy and safety may be enhanced by fibrin specific agents that become concentrated at the site of a recent thrombus, thus improving the ratio of local effect to systemic effect. These agents include tissue plasminogen activator," 14 prourokinase," and anisoylated plasminogen streptokinase activator complex (APSAC or BRL 26921).'

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Early Intravenous Atenolol Treatment in Suspected Acute Myocardial Infarction

Cited by 208 publications

References 15 publications

Myocardial protection during transient coronary artery occlusion in man: beneficial effects of regional beta-adrenergic blockade.

Myocardial protection during transient coronary artery occlusion in man: beneficial effects of regional beta-adrenergic blockade.

The management of hypertension.

Treatment of acute myocardial infarction with anisoylated plasminogen streptokinase activator complex.

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