Effect of Propranolol in Myocardial Infarction

Snow, P.J.D.

doi:10.1016/s0140-6736(65)90863-9

Cited by 239 publications

(53 citation statements)

References 11 publications

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“…13 Several subsequent studies, including the β-Blocker Heart Attack (BHAT) trial (propranolol reduced all-cause mortality by 26%) 14 and the Norwegian Multicenter Study Group trial (timolol reduced all-cause mortality by 39%), 15 have confirmed this observation. Therefore, BB are widely used in the treatment of hypertension and post-MI patients, and national and international guidelines recommended BB as first-line agents.…”

Section: Discussionmentioning

confidence: 93%

Secondary Preventive Effects of a Calcium Antagonist for Ischemic Heart Attack - Randomized Parallel Comparison With .BETA.-Blockers -

Nakagomi

Kodani

Takano

et al. 2011

Circ J

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Section: Discussionmentioning

confidence: 93%

Secondary Preventive Effects of a Calcium Antagonist for Ischemic Heart Attack - Randomized Parallel Comparison With .BETA.-Blockers -

Nakagomi

Kodani

Takano

et al. 2011

Circ J

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“…However if propranolol were to be given to patients with overt cardiac failure, it is possible that this would be exacerbated, and it is likely that temporary support for the myocardium by such methods as intra-aortic balloon counterpulsation might be necessary. Again This study has shown lower CPK levels in patients treated with propranolol less than 4 hours following the onset of symptoms of subsequently proven acute myocardial infarction. In view of continuing controversy about the measurement of myocardial infarct size, similar trials need to be conducted using different methods of infarct size measurement.…”

Section: Discussionmentioning

confidence: 53%

“…One difficulty in interpretation of these results arises from the fact that three of the treated patients in the under 4 figure 1) in treated and control patients entering the trial, less than 4 hr or more than 4 hr after the onset of infarction. Filled circles indicate patients with anterior infarction, unfilled circles those with inferior infarction and S patients who had ST-segment elevation in the ECG at the time of entry to the trial but who subsequently developed T wave inversion without Q waves, indicating subendocardial infarction.…”

Section: Methodsmentioning

confidence: 99%

“…Although these patients had been randomized to groups, and met the criteria required for entry to the trial, we believed that cases should be strictly comparable if conclusions were to be drawn concerning the effects of therapy. Accordingly, the data were further analyzed by omitting these cases and comparing 19 control with 15 treated patients who entered the trial within 4 hours of onset of chest pain and who subsequently went on to develop pathological Q waves. When the data were analyzed in this way, the differences between control and treated cases were still apparent.…”

Section: Methodsmentioning

confidence: 99%

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Reduction of enzyme levels by propranolol after acute myocardial infarction.

Peter¹,

Norris²,

Clarke³

et al. 1978

Circulation

200

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SUMMARY The effect of propranolol (0.1 mg/kg intravenously followed by 320 mg given over 27 hour orally) on serum levels of creatine kinase enzyme was studied in a randomized trial involving 95 patients seen within 12 hours of onset of symptoms of uncomplicated myocardial infarction. In 15 patients who were treated with propranolol within 4 hours of onset, and who eventually developed pathological Q waves, peak measured enzyme levels were 27% (P < 0.0125) lower than in 19 control patients who were also seen THE WELL-KNOWN EFFICACY of beta-adrenergic blocking drugs for the treatment of angina pectoris53 suggests that these drugs should also be effective for the acute imbalance between oxygen supply and demand which occurs during the early stages of myocardial infarction. Apart from an encouraging report by Snow in 1965,4 however, a number of carefully randomized early clinical trials of beta blockers5-9 showed no effect on hospital mortality from infarction nor on the incidence of arrhythmias in treated patients compared with controls.A number of recent developments suggest, however, that the use of beta-adrenergic blocking drugs in the acute stage of myocardial infarction should be re-investigated. First, there is the evidence that long-term beta blockade prolongs life after myocardial infarction'0 11 and that this may be due in part to the prevention of new ischemic events.'2 Second, there is evidence that propranolol given prophylactically to experimental animals reduces myocardial infarct size;3-5 this suggests that measurements of infarct size should be used as an end-point for therapeutic trials in man. Third, doses of propranolol used in previous trials (40-80 mg per day) were comparatively low and were administered orally and comparatively late after the onset. Patients given this low dose do not develop blood levels within the therapeutic range for 24-48 hours after first administration of the drug. 16The present trial proposed to investigate the effect of highloading doses of propranolol given within 12 hours of onset of symptoms of infarction on serum creatine phosphokinase (CPK) levels.'7', Results show that CPK levels were reduced by propranolol if the drug was given within four hours of onset of the most severe chest pain.Patients and MethodsWe included in this study those infarctions which were of moderate severity since we postulated they would ultimately within 4 hours of the onset but had no specific treatment. Total calculated enzyme appearance was also lower in the treated patients (reduced 25%, P < 0.05) as was the calculated rate of appearance (33%, P < 0.005). No significant difference was found for treated compared with control patients entering the trial more than 4 hours after the onset of chest pain. This evidence suggests that propranolol may reduce the size of uncomplicated infarctiops if it is given intravenously within 4 hours of the onset.cause a moderately high enzyme release for which a reduction would be both easily measurable and clinically meaningful. At the same time it was r...

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“…In 1965 Snow reported that propranolol reduced mortality in patients with acute myocardial infarction (Snow, 1965). The number of patients was, however, small (n=97) and the trial was neither randomized nor doubleblind.…”

Section: Beta Adrenergic Blockadementioning

confidence: 99%

Secondary prevention after myocardial infarction: Subgroup analysis of patients at risk in the norwegian timolol multicenter study

Gundersen¹

1985

Clinical Cardiology

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Timolol treatment after myocardial infarction is generally related to a significant reduction in both morality and reinfarction compared with placebo. Retrospective analyses of the timolol study are performed on subgroups of patients with a high placebo mortality. The present study shows that these patients are target groups for secondary prevention, as they benefit most from timolol treatment after myocardial infarction. In patients 65‐75 years of age, the number of cardiac deaths and reinfarctions prevented by timolol treatment is twice as high as that of patients below 65 years of age. Timolol treatment is well tolerated in the older age group and the contraindications for timolol treatment are independent of age up to 75 years. The reduction in mortality and reinfarction is independent of heart size at baseline. However, in patients with cardiomegaly and compensated heart failure on treatment with digitalis and diuretics, timolol treatment may be of special importance because of the very high incidence of cardiac death in this group of patients. In patients with compensated heart failure on treatment with digitalis and diuretics, timolol treatment does not precipitate heart failure. Patients with stable diabetes mellitus basically behave like nondiabetic patients regarding inclusion rate, side effects, and timolol‐related reduction in mortality and reinfarction. Decisions concerning secondary prevention with timolol should be independent of preinfarction and postinfarction angina. In conclusion, 70‐80% of all the patients below 75 years of age surviving myocardial infarction, without contraindication to betablocker treatment, can be treated with timolol 10 mg twice daily to reduce mortality and reinfarction. In contrast to previous routines, secondary prevention with beta blockers should be especially directed to high‐risk patients.

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Effect of Propranolol in Myocardial Infarction

Cited by 239 publications

References 11 publications

Secondary Preventive Effects of a Calcium Antagonist for Ischemic Heart Attack - Randomized Parallel Comparison With .BETA.-Blockers -

Secondary Preventive Effects of a Calcium Antagonist for Ischemic Heart Attack - Randomized Parallel Comparison With .BETA.-Blockers -

Reduction of enzyme levels by propranolol after acute myocardial infarction.

Secondary prevention after myocardial infarction: Subgroup analysis of patients at risk in the norwegian timolol multicenter study

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