Protective Effect of Propranolol in Threatened Myocardial Infarction

Norris, R. M.; Sammel, Neville; Clarke, E.D.; Smith, Warren; Williams, Barbara F.

doi:10.1016/s0140-6736(78)91628-8

Cited by 159 publications

(26 citation statements)

References 14 publications

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“…By the compartment model, the ascending and descending parts of the curve are determined separately, as opposed to the log normal model. The distribution space for CK molecules equals the plasma volume (PV)9' 29: PV = (100 -hematocrit) X blood volume80 (6) Blood volume was estimated according to Feldschuh and Enson.30 Serum activities of CK-MB were corrected to constant levels of either serum a2-macroglobulin or serum protein to eliminate changes in plasma volume during the blood sampling period. The corrections for changes in plasma volume were done by multiplying the enzyme activities by the correction factor AO/At.…”

Section: Methodsmentioning

confidence: 99%

Estimation of acute myocardial infarct size in man by serum CK-MB measurements.

Grande¹,

Hansen²,

Christiansen³

et al. 1982

Circulation

136

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SUMMARY This study was performed to determine the relationship between myocardial infarct size estimated by serum CK-MB methods and the extent of irreversible injury in acute myocardial infarction. In 321 consecutive patients, infarct size was estimated by different mathematical models, and in 22 patients who died in hospital, the extent of myocardial necrosis was determined by autopsy. We also investigated the depletion of CK-MB in infarcted tissue, the recovery of CK-MB in the plasma volume, and the elimination of CK-MB from plasma.Myocardial CK-MB depletion was relatively greater in the larger infarcts, whereas the recovery of enzyme in plasma was independent of the infarct size. Correction of serum CK-MB for changes in plasma volume improved the estimate significantly (p < 0.05). The correlation between the measured infarct size (g) and the estimated infarct size (units per liter and gram-equivalents) was highly significant (r = 0.85-0.89, SEE = 23-27%, p < 0.001). Thus, a semiquantitative expression of the extent of myocardial necrosis can be determined in vivo. AMI. Of these, 72 were excluded: 48 because the symptoms of AMI had lasted more than 15 hours before admission or because the second blood sample did not show higher CK-MB activity than the first and 24 because not enough blood samples had been obtained because patients died or were transferred to another department. The remaining 321 patients form the study group. Forty-three of these patients died within 18 days and were divided into group A, which included 22 patients in whom a detailed heart autopsy was performed, and group B, which included 21 patients in whom no detailed heart autopsy was performed. All patients autopsied had survived for at least 48 hours from the appearance of CK-MB activity in serum and there were no signs of reinfarction before death. Furthermore, all plasma curves showed a pure elimination phase (first-order kinetics).The 22 patients in group A included 12 women and 10 men who died at a mean age of 69.7 years (range 49-88 years). The median time from onset of symptoms until death was 6.4 days (range 2-14 days). Cardiogenic shock was the main cause of death in 12 patients and recurrent ventricular fibrillation in six patients. Two died from asystole and two from noncardiac causes.Heart biopsies were taken postmortem every 6 hours for 30 hours in eight patients from group B. The total enzyme depletion in whole heart homogenates was measured in 10 other patients.In 10 patients who died without signs of heart disease, myocardial biopsies were made to estimate CK and CK-MB activity. Tissue extracts were made from about 0.3 g tissue (wet weight) in a mixture of 10 ml 0.25 mol/ 1 sucrose, 3 ml 0.01 mol/l TRIS buffer (pH 7.4), 3 ml 1 mmol/l EGTA (pH 7.4) and 3 ml 1 mmol/ I mercaptoethanol, and homogenized on ice in an Ultra Turax blender for 1 minute. The homogenate was centrifuged (3500 g) and the supernatant was used to determine isoenzyme activity. The samples were diluted with heat-inactivated serum or TRIS buffer to the line...

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Section: Methodsmentioning

confidence: 99%

Estimation of acute myocardial infarct size in man by serum CK-MB measurements.

Grande¹,

Hansen²,

Christiansen³

et al. 1982

Circulation

136

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“…The 18 articles that met all criteria make up the basis for this evidence-based medicine review. 4,[7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] There were several large and often-quoted studies using beta-blockers in acute myocardial infarction that did not meet our strictly time-limited inclusion criteria. The Beta-Blocker Heart Attack trial 24 was a randomized double-blinded multicenter study of propanolol given to patients (n = 3,837) at least 5 days post-MI and followed for 2 to 4 years.…”

Section: Search Resultsmentioning

confidence: 99%

“…The smallest of the studies included only 43 patients. 11 The largest (COMMIT) enrolled 45,852 patients. 23 Only six studies enrolled more than 500 patients (Norris et al, 15 the MIAMI group, 16 Salathia et al, 18 ISIS-1,…”

Section: Study Characteristicsmentioning

confidence: 99%

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Does the Early Administration of Beta‐blockers Improve the In‐hospital Mortality Rate of Patients Admitted with Acute Coronary Syndrome?

Brandler

Paladino

Sinert

2010

Academic Emergency Medicine

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Objectives: Beta-blockade is currently recommended in the early management of patients with acute coronary syndromes (ACS). This was a systematic review of the medical literature to determine if early beta-blockade improves the outcome of patients with ACS. Methods:The authors searched the PubMed and EMBASE databases for randomized controlled trials from 1965 through May 2009 using a search strategy derived from the following PICO formulation of our clinical question: Patients included adults (18+ years) with an acute or suspected myocardial infarction (MI) within 24 hours of onset of chest pain. Intervention included intravenous or oral beta-blockers administered within 8 hours of presentation. The comparator included standard medical therapy with or without placebo versus early beta-blocker administration. The outcome was the risk of in-hospital death in the intervention groups versus the comparator groups. The methodologic quality of the studies was assessed. Qualitative methods were used to summarize the study results. In-hospital mortality rates were compared using a forest plot of relative risk (RR; 95% confidence interval [CI]) between beta-blockers and controls. Statistical analysis was done with Review Manager V5.0.Results: Eighteen articles (total N = 72,249) met the inclusion ⁄ exclusion criteria. For in-hospital mortality, RR = 0.95 (95% CI, 0.90-1.01). In the largest of these studies (n = 45,852), a significantly higher rate (p < 0.0001) of cardiogenic shock was observed in the beta-blocker (5.0%) versus control group (3.9%).Conclusions: This systematic review failed to demonstrate a convincing in-hospital mortality benefit for using beta-blockers early in the course of patients with an acute or suspected MI. ACADEMIC EMERGENCY MEDICINE 2010; 17:1-10 ª 2010 by the Society for Academic Emergency MedicineKeywords: adrenergic beta-antagonists, coronary artery disease, chest pain, myocardial infarction, angina CLINICAL SCENARIOA 48-year-old man presents to the emergency department (ED) with new onset chest pain of 45 minutes' duration that occurred for the first time today. The pain was centrally located in the chest when it began and did not radiate. It dissipated after 10 minutes of rest and is no longer present at the time of evaluation. The pain was associated with some shortness of breath, but no nausea, vomiting, diaphoresis, or palpitations. The patient has hypertension and non-insulin-dependent diabetes and has smoked 1 to 1.5 packs of cigarettes per day for 20 years. His father died of a heart attack at age 45. The physical exam and vital signs are all within normal limits. The heart rate is 95 beats ⁄ min, blood pressure is 170 ⁄ 94 mm Hg, and finger stick blood sugar is 230 mg ⁄ dL. An electrocardiogram demonstrated deep and symmetrical T-wave inversions in the precordial leads V4-V6. The initial troponin is normal. The patient receives aspirin, and you decide to admit him to the telemetry unit for possible acute coronary syndrome (ACS). The patient's family physician requests that yo...

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“…However, the risks of sudden withdrawal of these drugs in patients with coronary heart disease is now clearly established (Diaz, Somberg & Freeman, 1973;Alderman et al, 1974;Miller et al, 1975;Shiroff et al, 1978); in clinical emergencies continuation of medication may only be possible by their intravenous administration. Medical interest in the use of intravenous /8-adrenoceptor blocking drugs in patients with coronary heart disease has also been stimulated by their potential to reduce infarct size (Norris et al, 1978;Yusef et al, 1980) and abort dysrhythmias (Singh & Jewitt, 1974;Taylor & Burley, 1977) following myocardial infarction. In all of these situations it is important to know the speed of onset of the cardioprotective activity of these drugs.…”

Section: Introductionmentioning

confidence: 99%

Speed of onset of pharmacodynamic activity of propranolol, practolol, oxprenolol and metoprolol after intravenous infection in man.

Lochan¹,

Silke²,

Taylor³

1981

Brit J Clinical Pharma

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1 The speed of onset of the pharmacodynamic activity of intravenous propranolol, practolol, oxprenolol and metoprolol was determined, using attenuation of isoprenaline‐induced tachycardia as the end‐point, in 16 patients with clinically coronary heart disease. 2 Antagonism was evident within 15 s of injection into the central circulation of all four drugs. The time to maximum attenuation of isoprenaline tachycardia was significantly more rapid with propranolol and oxprenolol than with practolol and metoprolol.

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Protective Effect of Propranolol in Threatened Myocardial Infarction

Cited by 159 publications

References 14 publications

Estimation of acute myocardial infarct size in man by serum CK-MB measurements.

Estimation of acute myocardial infarct size in man by serum CK-MB measurements.

Does the Early Administration of Beta‐blockers Improve the In‐hospital Mortality Rate of Patients Admitted with Acute Coronary Syndrome?

Speed of onset of pharmacodynamic activity of propranolol, practolol, oxprenolol and metoprolol after intravenous infection in man.

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