The role of propranolol in the treatment of acute myocardial infarction

Mueller, Hiltrud S.; Ayres, Stephen M.

doi:10.1016/0033-0620(77)90018-4

Cited by 66 publications

(9 citation statements)

References 63 publications

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“…24,25,32 A parallel reduction in LV function and oxygen consumption would also be expected early in therapy. 29 In the current study LV function was maintained with metoprolol at a lower rate of oxidative metabolism, supporting the idea that some recovery occurred and that there is an energy-sparing effect of ␤-blocker therapy. Longer follow-up (beyond 3 months) may have shown an improved ejection fraction as well.…”

Section: Beanlands Et Alsupporting

confidence: 66%

“…By reducing heart rate and inotropy, ␤-blockers should reduce myocardial energy demands and oxygen consumption. 29 Reduction in demand from ␤-blockade would permit the repletion of energy stores. 6 This may allow energy to be directed to repairing cell injury and restoring contractile elements.…”

Section: Potential Role Of An Energy-sparing Effect Of ␤-Blockadementioning

confidence: 99%

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The Effects of β ₁ -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

et al. 2000

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Background-The mechanism for the beneficial effect of ␤-blocker therapy in patients with left ventricular (LV) dysfunction is unclear, but it may relate to an energy-sparing effect that results in improved cardiac efficiency. C-11 acetate kinetics, measured using positron-emission tomography (PET), are a proven noninvasive marker of oxidative metabolism and myocardial oxygen consumption (MV O 2 ). This approach can be used to measure the work-metabolic index, which is a noninvasive estimate of cardiac efficiency. Methods and Results-The aim of this study was to determine the effect of metoprolol on oxidative metabolism and the work-metabolic index in patients with LV dysfunction. Forty patients (29 with ischemic and 11 with nonischemic heart disease; LV ejection fraction Ͻ40%) were randomized to receive metoprolol or placebo in a treatment protocol of titration plus 3 months of stable therapy. Seven patients were not included in analysis because of withdrawal from the study, incomplete follow-up, or nonanalyzable PET data. The rate of oxidative metabolism (k) was measured using C-11-acetate PET, and stoke volume index (SVI) was measured using echocardiography. The work-metabolic index was calculated as follows: (systolic blood pressureϫSVIϫheart rate)/k. No significant change in oxidative metabolism occurred with placebo (kϭ0.061Ϯ0.022 to 0.054Ϯ0.012 per minute). Metoprolol reduced oxidative metabolism (kϭ0.062Ϯ0.024 to 0.045Ϯ0.015 per minute; Pϭ0.002). The work-metabolic index did not change with placebo (from 5.29Ϯ2.46ϫ10 6 to 5.14Ϯ2.06ϫ10 6 mm Hg ⅐ mL/m 2 ), but it increased with metoprolol (from 5.31Ϯ2.15ϫ10 6 to 7.08Ϯ2.36ϫ10 6 mm Hg ⅐ mL/m 2 ; PϽ0.001). Conclusions-Selective ␤-blocker therapy with metoprolol leads to a reduction in oxidative metabolism and an improvement in cardiac efficiency in patients with LV dysfunction. It is likely that this energy-sparing effect contributes to the clinical benefits observed with ␤-blocker therapy in this patient population.

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Section: Beanlands Et Alsupporting

confidence: 66%

Section: Potential Role Of An Energy-sparing Effect Of ␤-Blockadementioning

confidence: 99%

The Effects of β ₁ -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

et al. 2000

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“…By enhancing the disparity between myocardial oxygen supply and demand, catecholamines have been shown to augment the severity of myocardial ischemia [1 , 29]. Beta-blockers are thought to decrease myocardial oxygen consumption and to favorably shift myocardial metabolism from lactate production to lactate extraction [30,31]. Although the ability of beta-blockers to reduce the severity of myocardial ischemia is well established, their effects upon infarct size appear to be somewhat variable.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effects of acute and chronic beta-blockade on infarct size in the dog after circumflex occlusion

Euler

Hughes

Scanlon

1988

Cardiovasc Drug Ther

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In order to compare the effects of acute and chronic beta-blockade on infact size, the left circumflex coronary artery was occluded for 6 hours in 33 anesthetized dogs. The dogs (18 to 22 kg) were divided into three groups; group 1 (N = 10) served as controls, group 2 received intravenous nadolol (average dose 1.25 mg/kg) just prior to coronary occlusion, and group 3 received oral nadolol (80 mg) twice daily for 16 days prior to coronary occlusion. To ensure equivalent degrees of beta-blockade at the time of occlusion, group 2 and 3 dogs were given incremental doses of intravenous nadolol to abolish the chronotropic response to isoproterenol (2 mu/kg IV). Left ventricular pressure, its first derivative (dP/dt), and heart rate were monitored. The anatomic risk region was determined antemortem by Evan's blue staining while the infarct zone was delineated postmortem by tetrazolium staining. Compared to Group 1, heart rate was 22% lower in group 2 and 15% lower in group 3 dogs 6 hours after occlusion (p less than 0.05). There were no differences among groups in peak left ventricular systolic pressure or mean arterial pressure. Infarct size as a function of the area at risk was 68 +/- 3% in group 1, 52 +/- 7% in group 2, and 44 +/- 8% in group 3. A significant difference was found only between groups 3 and 1. The data suggest that chronic beta-blockade provides greater protection against ischemic-induced necrosis than does acute beta-blockade. The greater protective effect of chronic beta-blockade may be due to chronic adaptive changes in either blood flow or metabolism.

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“…Catecholamines also increase fatty acid extraction and oxidation [194,195], which are an inefficient source of myocardial high energy phosphates [187]. Indeed, adrenergic agents decrease myocardial efficiency [184,[188][189][190], whereas β-blockers reduce myocardial energy demands, oxygen consumption and enhance efficiency [196]. In type 1 diabetes, no regional differences in LV C-11 acetate clearance have been identified after metabolic standardization [197].…”

Section: Regional Cardiac Adrenergic Activation or Denervation May Immentioning

confidence: 99%

Oxidative-Nitrosative Stress as a Contributing Factor to Cardiovascular Disease in Subjects with Diabetes

Stevens¹

2005

CVP

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In diabetes, clear evidence has emerged for the presence of oxidative-nitrosative stress, which may be a consequence of a glucose-mediated imbalance of systemic antioxidant buffering capacity, coupled with increased production of free radical species. Although multiple metabolic pathways have been identified, which may contribute to oxidative stress in diabetes, the principal pathogenetic pathways and their key down-stream targets remain to be established. Evidence links oxidative stress in particular, to elevations of postprandial glucose and lipids, which also have recently emerged as major risk factors for cardiovascular events. Indeed, considerable evidence suggests that increased oxidative stress in diabetes may play an important role in the development or progression of cardiovascular disease by a number of different mechanisms, including alterations of cardiovascular sympathetic nervous system tone and integrity, elevation of acute phase reactants, disruption of endothelial function and facilitation of myocardial injury. Despite the disappointments of recent large scale clinical trials evaluating the efficacy of antioxidants in cardiovascular disease, many therapeutic agents which have been used successfully in diabetic subjects at high risk for cardiovascular disease have a mechanism of action which includes an antioxidant capacity. Therefore, incorporating an antioxidant action in future therapeutic approaches to combat cardiovascular disease complicating diabetes, appears to remain justified and warrants further evaluation.

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The role of propranolol in the treatment of acute myocardial infarction

Cited by 66 publications

References 63 publications

The Effects of β ₁ -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

The Effects of β ₁ -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

Comparison of the effects of acute and chronic beta-blockade on infarct size in the dog after circumflex occlusion

Oxidative-Nitrosative Stress as a Contributing Factor to Cardiovascular Disease in Subjects with Diabetes

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The role of propranolol in the treatment of acute myocardial infarction

Cited by 66 publications

References 63 publications

The Effects of β 1 -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

The Effects of β 1 -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

Comparison of the effects of acute and chronic beta-blockade on infarct size in the dog after circumflex occlusion

Oxidative-Nitrosative Stress as a Contributing Factor to Cardiovascular Disease in Subjects with Diabetes

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The Effects of β ₁ -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction

The Effects of β ₁ -Blockade on Oxidative Metabolism and the Metabolic Cost of Ventricular Work in Patients With Left Ventricular Dysfunction