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• W2146242058 abstract "The clinical utility of β-adrenergic-receptor blockers in the practice of cardiothoracic and vascular anesthesia is well appreciated by readers of this journal. Few clinicians hesitate to administer them at the first signs of myocardial ischemia, particularly with a hemodynamic profile responsive to their predominant physiologic effects (eg, elevated heart rate with elevated blood pressure or modest hypotension likely to improve with resolution of ischemia). Their well-documented bradycardic and negative inotropic effects significantly lower myocardial oxygen demand and are the major mechanisms by which ischemia is relieved in a variety of clinical settings.1London MJ Drugs affecting adrenoreceptors: Beta-adrenergic antagonists.in: The Pharmacologic Basis of Anesthesiology. Churchill Livingstone, New York, NY1994: 625-668Google Scholar Systolic wall tension usually declines, although varying effects on ventricular size have been reported depending on the clinical setting (eg, acute ischemia in a normal ventricle versus infarction with reperfusion).In contrast to the aforementioned factors modulating demand, effects on myocardial oxygen supply, in particular coronary blood flow, remain controversial after nearly 3 decades of clinical use. In this issue, Coetzee and Coetzee present evidence of a salutary effect of acebutolol, a β1-selective β-adrenergic-receptor blocker with weak intrinsic sympathomimetic activity on myocardial oxygen supply using a pig model of a critical coronary stenosis.2Coetzee A Coetzee G Beta-andrenergic blockade during severe ischemia.J Cardiothorac Vasc Anesth. 2002; 16: 670-678Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar This is a complex topic given the multiplicity of factors involved, including those modulating coronary vascular resistance (eg, neural and humoral factors, extravascular compressive forces, autoregulation, and metabolic control), the duration of diastolic perfusion, and oxygen-carrying capacity (with little evidence to suggest a significant effect of β-blockade on the latter). Some of these are interrelated with the major demand variables (particularly compressive forces and duration of diastole). Recent canine data suggest an independent mechanism by which diastolic time may increase at a constant heart rate during ischemia.3Merkus D Kajiya F Vink H et al.Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced.Circulation. 1999; 100: 75-81Crossref PubMed Scopus (50) Google Scholar β-Adrenergic-receptor blockers may have independent effects on neurohumoral mediators, such as endothelin synthesis (ET-1) and neutrophil chemotaxis and free radical formation.4Garlichs CD Zhang H Mügge A Daniel WG Beta-blockers reduce the release and synthesis of endothelin-1 in human endothelial cells.Eur J Clin Invest. 1999; 29: 12-16Crossref PubMed Scopus (41) Google Scholar, 5Dunzendorfer S Wiedermann CJ Modulation of neutrophil migration and superoxide anion release by metoprolol.J Mol Cell Cardiol. 2000; 32: 915-924Abstract Full Text PDF PubMed Scopus (31) Google Scholar Modulation of endothelial function is now an important focus given evidence of a prognostic role in patients with coronary artery disease and is receiving attention in the perioperative environment.6Gokce N Keaney Jr, JF Hunter LM et al.Risk stratification for postoperative cardiovascular events via noninvasive assessment of endothelial function: A prospective study.Circulation. 2002; 105: 1567-1572Crossref PubMed Scopus (709) Google Scholar Although α-adrenergic–mediated mechanisms seem to be more important in this arena, a new generation β-adrenergic-receptor blocker, nipradilol, has documented vasodilating effects via nitric oxide synthesis.7Hijmering ML Stroes ES Olijhoek J et al.Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation.J Am Coll Cardiol. 2002; 39: 683-688Abstract Full Text Full Text PDF PubMed Scopus (276) Google ScholarThe effects of β-adrenergic-receptor blockers on coronary blood flow vary over the spectrum of settings in which ischemia occurs from subclinical stenoses that may well be the most vulnerable for rupture perioperatively given their thin fibrous caps, to well-developed critical flow-limiting stenoses accompanied by overt regional wall motion abnormalities or subclinical myocardial asynchrony (eg, postsystolic shortening).9Heidland UE Strauer BE Left ventricular muscle mass and elevated heart rate are associated with coronary plaque disruption.Circulation. 2001; 104: 1477-1482Crossref PubMed Scopus (324) Google Scholar The latter is a relatively mature laboratory measurement that is just now being evaluated clinically using high temporal resolution tissue Doppler ultrasound.10Foex P Leone BJ Pressure-volume loops: A dynamic approach to the assessment of ventricular function.J Cardiothorac Vasc Anesth. 1994; 8: 84-96Abstract Full Text PDF PubMed Scopus (20) Google Scholar Overt myocardial infarction, with or without reperfusion, and the complex effects of ventricular remodeling (which is most susceptible to angiotensin-converting enzyme inhibition) lie at the end of this spectrum.11Trambaiolo P Tonti G Salustri A et al.New insights into regional systolic and diastolic left ventricular function with tissue Doppler echocardiography: From qualitative analysis to a quantitative approach.J Am Soc Echocardiogr. 2001; 14: 85-96Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar The associated physiologic milieu, most notably hemodynamics (eg, resting physiology or induced exercise) and the level of sympathetic tone (assessed by circulating catecholamine levels), are important cofactors. The latter is of particular interest given the secondary preventive effects of β-adrenergic-receptor blockers for sudden death in chronic congestive heart failure and as more recent evidence suggests, a beneficial effect on ventricular function with even short-term clinical use during a single episode of cardiopulmonary bypass.12Kramer CM Nicol PD Rogers WJ et al.Beta-blockade improves adjacent regional sympathetic innervation during postinfarction remodeling.Am J Physiol. 1999; 277: H1429-H1434PubMed Google Scholar, 13Foody JM Farrell MH Krumholz HM Beta-blocker therapy in heart failure: Scientific review.JAMA. 2002; 287: 883-889Crossref PubMed Scopus (278) Google Scholar, 14Zaugg M Schaub MC Pasch T Spahn DR Modulation of beta-adrenergic receptor subtype activities in perioperative medicine: Mechanisms and sites of action.Br J Anaesth. 2002; 88: 101-123Crossref PubMed Scopus (93) Google Scholar, 15Booth JV Spahn DR McRae RL et al.Esmolol improves left ventricular function via enhanced beta-adrenergic receptor signaling in a canine model of coronary revascularization.Anesthesiology. 2002; 97: 162-169Crossref PubMed Scopus (22) Google Scholar This is likely due to prevention of translocation of agonist-induced β-adrenergic-receptor kinase, which binds the inhibitor protein, β-arrestin, responsible for acute left ventricular dysfunction via dampened myocardial β-adrenergic-receptor signaling.15Booth JV Spahn DR McRae RL et al.Esmolol improves left ventricular function via enhanced beta-adrenergic receptor signaling in a canine model of coronary revascularization.Anesthesiology. 2002; 97: 162-169Crossref PubMed Scopus (22) Google Scholar The underlying molecular pharmacology of the adrenergic receptor has been reviewed in this journal and is rapidly coming to the forefront of clinical practice.16Smiley RM Kwatra MM Schwinn DA New developments in cardiovascular adrenergic receptor pharmacology: Molecular mechanisms and clinical relevance.J Cardiothorac Vasc Anesth. 1998; 12: 80-95Abstract Full Text PDF PubMed Scopus (32) Google Scholar Genetic polymorphisms in the β2-receptor are recognized to modulate vascular reactivity and hemodynamic responses to noxious clinical stimuli (eg, intubation) and may in the not-too-distant future influence the clinician's choice of a particular β-adrenergic-receptor blocker on a patient level.17Kim NS Lee IO Lee MK et al.The effects of beta2-adrenoceptor gene polymorphisms on pressor response during laryngoscopy and tracheal intubation.Anaesthesia. 2002; 57: 227-232Crossref PubMed Scopus (26) Google Scholar, 18Cockcroft JR Gazis AG Cross DJ et al.Beta2-adrenoceptor polymorphism determines vascular reactivity in humans.Hypertension. 2000; 36: 371-375Crossref PubMed Scopus (142) Google Scholar, 19Schwinn DA Booth JV Genetics infuses new life into human physiology: Implications of the human genome project for anesthesiology and perioperative medicine.Anesthesiology. 2002; 96: 261-263Crossref PubMed Scopus (17) Google ScholarA critical variable to be considered on the supply side is the status of the collateral circulation. As evidenced by the isoflurane controversy and by the daily decisions of the cardiac surgeon to attempt revascularization of a particular coronary lesion, the degree of collateral flow can significantly attenuate the amount of ischemia and the size of an infarct and mitigate adverse effects on ventricular function during ischemia. Striking species-specific differences in the ability to form collateral vessels (dogs>humans>pigs) must be considered, especially in studies of acute ischemia. Adrenergic receptor types and subtypes vary by location in the coronary circulation with β1 predominant in epicardial vessels, β2 in arterioles, and a mixed population in collateral vessels. β-Adrenergic-receptor blockers may antagonize β-mediated vasodilation in these vessels, causing vasoconstriction and reduction in flow to ischemic zones. Although α-receptors are not present in collaterals, they are present in the precollateral circulation and as such likewise can reduce flow. Clinical and laboratory studies are inconclusive in this regard, although the weight of evidence suggests a reduction in collateral flow, offset by a reduction in myocardial oxygen demand.20Kyriakides ZS Kolettis T Antoniadis A et al.Beta-adrenergic blockade decreases coronary collateral blood flow in patients with coronary artery disease.Cardiovasc Drugs Ther. 1998; 12: 551-559Crossref PubMed Scopus (10) Google ScholarEarlier animal and human studies for the most part reported a reduction in coronary blood flow associated with decreased myocardial oxygen consumption causing an increase in coronary vascular resistance. Their effects on coronary flow reserve (flow during maximal vasodilation from ischemia or a potent vasodilator such as adenosine divided by resting flow) are less well studied. In this regard, in vivo studies using newer methods for assessing flow reserve, such as intracoronary Doppler flow velocity and positron emission tomography, show greater flow reserve with β-adrenergic-receptor blockers as a result of enhanced flow with maximal vasodilatory stimuli.21Bottcher M Czernin J Sun K et al.Effect of beta1-adrenergic receptor blockade on myocardial blood flow and vasodilatory capacity.J Nucl Med. 1997; 38: 442-446PubMed Google Scholar, 22Billinger M Seiler C Fleisch M et al.Do beta-adrenergic blocking agents increase coronary flow reserve?.J Am Coll Cardiol. 2001; 38: 1866-1871Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar Even if resting flow is reduced, a greater increase in flow with maximal vasodilation (eg, in response to ischemia) will increase coronary flow reserve and lessen the potential for development of ischemia or infarction during stress.The effects of β-adrenergic-receptor blockers on the function of nonischemic adjacent segments have received some attention given the well-recognized clinical finding of compensatory hyperkinesis. Limited clinical data suggest a small but measurable effect of acute β-adrenergic-receptor blocker administration to decrease the latter and improve function in the infarct zone (most notable with dyskinetic segments).23Grines CL Booth DC Nissen SE et al.Acute effects of parenteral beta-blockade on regional ventricular function of infarct and noninfarct zones after reperfusion therapy in humans.J Am Coll Cardiol. 1991; 17: 1382-1387Abstract Full Text PDF PubMed Scopus (21) Google Scholar Although compensatory hyperkinesis is thought to be a helpful reflex, this acute effect may be protective against the relatively rare event of cardiac rupture (which is supported by larger scale epidemiologic studies).24Freemantle N Cleland J Young P et al.Beta-blockade after myocardial infarction: Systematic review and meta regression analysis.BMJ (Clin Res Ed). 1999; 318: 1730-1737Crossref PubMed Google ScholarThe controversy over perioperative β-blockade for the prophylaxis of short-term and long-term cardiac morbidity and mortality in patients with coronary artery disease or known risk factors undergoing noncardiac surgery has been well reviewed.25Auerbach AD Goldman L Beta-blockers and reduction of cardiac events in noncardiac surgery: scientific review.JAMA. 2002; 287: 1435-1444Crossref PubMed Google Scholar, 26Auerbach AD Goldman L Beta-blockers and reduction of cardiac events in noncardiac surgery: clinical applications.JAMA. 2002; 287: 1445-1447Crossref PubMed Google Scholar The revised guidelines of the American College of Cardiology/American Heart Association Committee on Perioperative Cardiovascular Evaluation address this topic using the limited number of randomized, controlled trials available, granting class I and IIa recommendations for their use in high-risk and moderate-risk patients undergoing vascular and other noncardiac procedures, although the optimal timing, dose, duration, and class of β-blocker are not well delineated.27Eagle KA Berger PB Calkins H et al.ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery—executive summary a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery).Circulation. 2002; 105: 1257-1267Crossref PubMed Scopus (77) Google Scholar It seems that many clinicians are awaiting larger scale epidemiologic studies to better evaluate clinical effectiveness, some of which have started or are in planning stages (in Canada and the Department of Veterans Affairs). Substantial logistical issues are required for the institution and monitoring of perioperative β-blockade, factors not previously well considered.28Schmidt M Lindenauer PK Fitzgerald JL Benjamin EM Forecasting the impact of a clinical practice guideline for perioperative beta-blockers to reduce cardiovascular morbidity and mortality.Arch Intern Med. 2002; 162: 63-69Crossref PubMed Scopus (47) Google Scholar Data suggest a more aggressive role for β-blockers in coronary artery bypass graft surgery, although similar to the noncardiac surgery studies, methodologic limitations limit immediate generalization of results. In particular, the large Society of Thoracic Surgeons database analysis showed extremely small differences in outcomes and suggested an adverse effect in patients with a preoperative ejection fraction of <0.35.29Ferguson Jr, TB Coombs LP Peterson ED Preoperative beta-blocker use and mortality and morbidity following CABG surgery in North America.JAMA. 2002; 287: 2221-2227Crossref PubMed Scopus (216) Google Scholar The growth of off-pump coronary artery bypass graft surgery, with reduction in use of cardiopulmonary bypass and growing appreciation of pharmacologic preconditioning effects of volatile anesthetics via modulation of the mitochondrial ATP-sensitive potassium (KATP) channel are factors that may temper β-adrenergic-receptor blocker use.30DeHert SG tenBroecke PW Mertens E et al.Sevoflurane but not propofol preserves myocardial function in coronary surgery patients.Anesthesiology. 2002; 97: 42-49Crossref PubMed Scopus (295) Google ScholarThe news for clinicians interested in expanding their own (and perhaps more importantly their surgeons' and internists') use of β-adrenergic-receptor blockers perioperatively—the porcine data of Coetzee and Coetzee, new-generation cardiac catheterization studies using Doppler velocity and intravascular ultrasound to assess coronary vascular resistance more accurately, molecular pharmacology studies documenting salutary effects on the toxic effects of catecholamines on signal transduction pathways, and the emerging role of pharmacogenomics in clinical practice—is good. β-Adrenergic-receptor blockers have multiple salutary effects, and new information such as presented in this issue of the Journal of Cardiothoracic and Vascular Anesthesia continues to expand the knowledge base. The biggest task for the clinician is how to evaluate clinical efficacy among other therapies appreciated to be of value (eg, angiotensin-converting enzyme inhibition, statin use) or those on the horizon (eg, modulation of endothelial function and the inflammatory response, sodium/hydrogen ion inhibitor therapy). Despite this contention, it is likely that β-adrenergic-receptor blockers will remain one of the primary weapons in the armamentarium for treating ischemia for many years to come.31Freemantle N Urdahl H Eastaugh J Hobbs FD What is the place of beta-blockade in patients who have experienced a myocardial infarction with preserved left ventricular function? Evidence and (mis)interpretation.Prog Cardiovasc Dis. 2002; 44: 243-250Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar The clinical utility of β-adrenergic-receptor blockers in the practice of cardiothoracic and vascular anesthesia is well appreciated by readers of this journal. Few clinicians hesitate to administer them at the first signs of myocardial ischemia, particularly with a hemodynamic profile responsive to their predominant physiologic effects (eg, elevated heart rate with elevated blood pressure or modest hypotension likely to improve with resolution of ischemia). Their well-documented bradycardic and negative inotropic effects significantly lower myocardial oxygen demand and are the major mechanisms by which ischemia is relieved in a variety of clinical settings.1London MJ Drugs affecting adrenoreceptors: Beta-adrenergic antagonists.in: The Pharmacologic Basis of Anesthesiology. Churchill Livingstone, New York, NY1994: 625-668Google Scholar Systolic wall tension usually declines, although varying effects on ventricular size have been reported depending on the clinical setting (eg, acute ischemia in a normal ventricle versus infarction with reperfusion). In contrast to the aforementioned factors modulating demand, effects on myocardial oxygen supply, in particular coronary blood flow, remain controversial after nearly 3 decades of clinical use. In this issue, Coetzee and Coetzee present evidence of a salutary effect of acebutolol, a β1-selective β-adrenergic-receptor blocker with weak intrinsic sympathomimetic activity on myocardial oxygen supply using a pig model of a critical coronary stenosis.2Coetzee A Coetzee G Beta-andrenergic blockade during severe ischemia.J Cardiothorac Vasc Anesth. 2002; 16: 670-678Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar This is a complex topic given the multiplicity of factors involved, including those modulating coronary vascular resistance (eg, neural and humoral factors, extravascular compressive forces, autoregulation, and metabolic control), the duration of diastolic perfusion, and oxygen-carrying capacity (with little evidence to suggest a significant effect of β-blockade on the latter). Some of these are interrelated with the major demand variables (particularly compressive forces and duration of diastole). Recent canine data suggest an independent mechanism by which diastolic time may increase at a constant heart rate during ischemia.3Merkus D Kajiya F Vink H et al.Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced.Circulation. 1999; 100: 75-81Crossref PubMed Scopus (50) Google Scholar β-Adrenergic-receptor blockers may have independent effects on neurohumoral mediators, such as endothelin synthesis (ET-1) and neutrophil chemotaxis and free radical formation.4Garlichs CD Zhang H Mügge A Daniel WG Beta-blockers reduce the release and synthesis of endothelin-1 in human endothelial cells.Eur J Clin Invest. 1999; 29: 12-16Crossref PubMed Scopus (41) Google Scholar, 5Dunzendorfer S Wiedermann CJ Modulation of neutrophil migration and superoxide anion release by metoprolol.J Mol Cell Cardiol. 2000; 32: 915-924Abstract Full Text PDF PubMed Scopus (31) Google Scholar Modulation of endothelial function is now an important focus given evidence of a prognostic role in patients with coronary artery disease and is receiving attention in the perioperative environment.6Gokce N Keaney Jr, JF Hunter LM et al.Risk stratification for postoperative cardiovascular events via noninvasive assessment of endothelial function: A prospective study.Circulation. 2002; 105: 1567-1572Crossref PubMed Scopus (709) Google Scholar Although α-adrenergic–mediated mechanisms seem to be more important in this arena, a new generation β-adrenergic-receptor blocker, nipradilol, has documented vasodilating effects via nitric oxide synthesis.7Hijmering ML Stroes ES Olijhoek J et al.Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation.J Am Coll Cardiol. 2002; 39: 683-688Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar The effects of β-adrenergic-receptor blockers on coronary blood flow vary over the spectrum of settings in which ischemia occurs from subclinical stenoses that may well be the most vulnerable for rupture perioperatively given their thin fibrous caps, to well-developed critical flow-limiting stenoses accompanied by overt regional wall motion abnormalities or subclinical myocardial asynchrony (eg, postsystolic shortening).9Heidland UE Strauer BE Left ventricular muscle mass and elevated heart rate are associated with coronary plaque disruption.Circulation. 2001; 104: 1477-1482Crossref PubMed Scopus (324) Google Scholar The latter is a relatively mature laboratory measurement that is just now being evaluated clinically using high temporal resolution tissue Doppler ultrasound.10Foex P Leone BJ Pressure-volume loops: A dynamic approach to the assessment of ventricular function.J Cardiothorac Vasc Anesth. 1994; 8: 84-96Abstract Full Text PDF PubMed Scopus (20) Google Scholar Overt myocardial infarction, with or without reperfusion, and the complex effects of ventricular remodeling (which is most susceptible to angiotensin-converting enzyme inhibition) lie at the end of this spectrum.11Trambaiolo P Tonti G Salustri A et al.New insights into regional systolic and diastolic left ventricular function with tissue Doppler echocardiography: From qualitative analysis to a quantitative approach.J Am Soc Echocardiogr. 2001; 14: 85-96Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar The associated physiologic milieu, most notably hemodynamics (eg, resting physiology or induced exercise) and the level of sympathetic tone (assessed by circulating catecholamine levels), are important cofactors. The latter is of particular interest given the secondary preventive effects of β-adrenergic-receptor blockers for sudden death in chronic congestive heart failure and as more recent evidence suggests, a beneficial effect on ventricular function with even short-term clinical use during a single episode of cardiopulmonary bypass.12Kramer CM Nicol PD Rogers WJ et al.Beta-blockade improves adjacent regional sympathetic innervation during postinfarction remodeling.Am J Physiol. 1999; 277: H1429-H1434PubMed Google Scholar, 13Foody JM Farrell MH Krumholz HM Beta-blocker therapy in heart failure: Scientific review.JAMA. 2002; 287: 883-889Crossref PubMed Scopus (278) Google Scholar, 14Zaugg M Schaub MC Pasch T Spahn DR Modulation of beta-adrenergic receptor subtype activities in perioperative medicine: Mechanisms and sites of action.Br J Anaesth. 2002; 88: 101-123Crossref PubMed Scopus (93) Google Scholar, 15Booth JV Spahn DR McRae RL et al.Esmolol improves left ventricular function via enhanced beta-adrenergic receptor signaling in a canine model of coronary revascularization.Anesthesiology. 2002; 97: 162-169Crossref PubMed Scopus (22) Google Scholar This is likely due to prevention of translocation of agonist-induced β-adrenergic-receptor kinase, which binds the inhibitor protein, β-arrestin, responsible for acute left ventricular dysfunction via dampened myocardial β-adrenergic-receptor signaling.15Booth JV Spahn DR McRae RL et al.Esmolol improves left ventricular function via enhanced beta-adrenergic receptor signaling in a canine model of coronary revascularization.Anesthesiology. 2002; 97: 162-169Crossref PubMed Scopus (22) Google Scholar The underlying molecular pharmacology of the adrenergic receptor has been reviewed in this journal and is rapidly coming to the forefront of clinical practice.16Smiley RM Kwatra MM Schwinn DA New developments in cardiovascular adrenergic receptor pharmacology: Molecular mechanisms and clinical relevance.J Cardiothorac Vasc Anesth. 1998; 12: 80-95Abstract Full Text PDF PubMed Scopus (32) Google Scholar Genetic polymorphisms in the β2-receptor are recognized to modulate vascular reactivity and hemodynamic responses to noxious clinical stimuli (eg, intubation) and may in the not-too-distant future influence the clinician's choice of a particular β-adrenergic-receptor blocker on a patient level.17Kim NS Lee IO Lee MK et al.The effects of beta2-adrenoceptor gene polymorphisms on pressor response during laryngoscopy and tracheal intubation.Anaesthesia. 2002; 57: 227-232Crossref PubMed Scopus (26) Google Scholar, 18Cockcroft JR Gazis AG Cross DJ et al.Beta2-adrenoceptor polymorphism determines vascular reactivity in humans.Hypertension. 2000; 36: 371-375Crossref PubMed Scopus (142) Google Scholar, 19Schwinn DA Booth JV Genetics infuses new life into human physiology: Implications of the human genome project for anesthesiology and perioperative medicine.Anesthesiology. 2002; 96: 261-263Crossref PubMed Scopus (17) Google Scholar A critical variable to be considered on the supply side is the status of the collateral circulation. As evidenced by the isoflurane controversy and by the daily decisions of the cardiac surgeon to attempt revascularization of a particular coronary lesion, the degree of collateral flow can significantly attenuate the amount of ischemia and the size of an infarct and mitigate adverse effects on ventricular function during ischemia. Striking species-specific differences in the ability to form collateral vessels (dogs>humans>pigs) must be considered, especially in studies of acute ischemia. Adrenergic receptor types and subtypes vary by location in the coronary circulation with β1 predominant in epicardial vessels, β2 in arterioles, and a mixed population in collateral vessels. β-Adrenergic-receptor blockers may antagonize β-mediated vasodilation in these vessels, causing vasoconstriction and reduction in flow to ischemic zones. Although α-receptors are not present in collaterals, they are present in the precollateral circulation and as such likewise can reduce flow. Clinical and laboratory studies are inconclusive in this regard, although the weight of evidence suggests a reduction in collateral flow, offset by a reduction in myocardial oxygen demand.20Kyriakides ZS Kolettis T Antoniadis A et al.Beta-adrenergic blockade decreases coronary collateral blood flow in patients with coronary artery disease.Cardiovasc Drugs Ther. 1998; 12: 551-559Crossref PubMed Scopus (10) Google Scholar Earlier animal and human studies for the most part reported a reduction in coronary blood flow associated with decreased myocardial oxygen consumption causing an increase in coronary vascular resistance. Their effects on coronary flow reserve (flow during maximal vasodilation from ischemia or a potent vasodilator such as adenosine divided by resting flow) are less well studied. In this regard, in vivo studies using newer methods for assessing flow reserve, such as intracoronary Doppler flow velocity and positron emission tomography, show greater flow reserve with β-adrenergic-receptor blockers as a result of enhanced flow with maximal vasodilatory stimuli.21Bottcher M Czernin J Sun K et al.Effect of beta1-adrenergic receptor blockade on myocardial blood flow and vasodilatory capacity.J Nucl Med. 1997; 38: 442-446PubMed Google Scholar, 22Billinger M Seiler C Fleisch M et al.Do beta-adrenergic blocking agents increase coronary flow reserve?.J Am Coll Cardiol. 2001; 38: 1866-1871Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar Even if resting flow is reduced, a greater increase in flow with maximal vasodilation (eg, in response to ischemia) will increase coronary flow reserve and lessen the potential for development of ischemia or infarction during stress. The effects of β-adrenergic-receptor blockers on the function of nonischemic adjacent segments have received some attention given the well-recognized clinical finding of compensatory hyperkinesis. Limited clinical data suggest a small but measurable effect of acute β-adrenergic-receptor blocker administration to decrease the latter and improve function in the infarct zone (most notable with dyskinetic segments).23Grines CL Booth DC Nissen SE et al.Acute effects of parenteral beta-blockade on regional ventricular function of infarct and noninfarct zones after reperfusion therapy in humans.J Am Coll Cardiol. 1991; 17: 1382-1387Abstract Full Text PDF PubMed Scopus (21) Google Scholar Although compensatory hyperkinesis is thought to be a helpful reflex, this acute effect may be protective against the relatively rare event of cardiac rupture (which is supported by larger scale epidemiologic studies).24Freemantle N Cleland J Young P et al.Beta-blockade after myocardial infarction: Systematic review and meta regression analysis.BMJ (Clin Res Ed). 1999; 318: 1730-1737Crossref PubMed Google Scholar The controversy over perioperative β-blockade for the prophylaxis of short-term and long-term cardiac morbidity and mortality in patients with coronary artery disease or known risk factors undergoing noncardiac surgery has been well reviewed.25Auerbach AD Goldman L Beta-blockers and reduction of cardiac events in noncardiac surgery: scientific review.JAMA. 2002; 287: 1435-1444Crossref PubMed Google Scholar, 26Auerbach AD Goldman L Beta-blockers and reduction of cardiac events in noncardiac surgery: clinical applications.JAMA. 2002; 287: 1445-1447Crossref PubMed Google Scholar The revised guidelines of the American College of Cardiology/American Heart Association Committee on Perioperative Cardiovascular Evaluation address this topic using the limited number of randomized, controlled trials available, granting class I and IIa recommendations for their use in high-risk and moderate-risk patients undergoing vascular and other noncardiac procedures, although the optimal timing, dose, duration, and class of β-blocker are not well delineated.27Eagle KA Berger PB Calkins H et al.ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery—executive summary a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery).Circulation. 2002; 105: 1257-1267Crossref PubMed Scopus (77) Google Scholar It seems that many clinicians are awaiting larger scale epidemiologic studies to better evaluate clinical effectiveness, some of which have started or are in planning stages (in Canada and the Department of Veterans Affairs). Substantial logistical issues are required for the institution and monitoring of perioperative β-blockade, factors not previously well considered.28Schmidt M Lindenauer PK Fitzgerald JL Benjamin EM Forecasting the impact of a clinical practice guideline for perioperative beta-blockers to reduce cardiovascular morbidity and mortality.Arch Intern Med. 2002; 162: 63-69Crossref PubMed Scopus (47) Google Scholar Data suggest a more aggressive role for β-blockers in coronary artery bypass graft surgery, although similar to the noncardiac surgery studies, methodologic limitations limit immediate generalization of results. In particular, the large Society of Thoracic Surgeons database analysis showed extremely small differences in outcomes and suggested an adverse effect in patients with a preoperative ejection fraction of <0.35.29Ferguson Jr, TB Coombs LP Peterson ED Preoperative beta-blocker use and mortality and morbidity following CABG surgery in North America.JAMA. 2002; 287: 2221-2227Crossref PubMed Scopus (216) Google Scholar The growth of off-pump coronary artery bypass graft surgery, with reduction in use of cardiopulmonary bypass and growing appreciation of pharmacologic preconditioning effects of volatile anesthetics via modulation of the mitochondrial ATP-sensitive potassium (KATP) channel are factors that may temper β-adrenergic-receptor blocker use.30DeHert SG tenBroecke PW Mertens E et al.Sevoflurane but not propofol preserves myocardial function in coronary surgery patients.Anesthesiology. 2002; 97: 42-49Crossref PubMed Scopus (295) Google Scholar The news for clinicians interested in expanding their own (and perhaps more importantly their surgeons' and internists') use of β-adrenergic-receptor blockers perioperatively—the porcine data of Coetzee and Coetzee, new-generation cardiac catheterization studies using Doppler velocity and intravascular ultrasound to assess coronary vascular resistance more accurately, molecular pharmacology studies documenting salutary effects on the toxic effects of catecholamines on signal transduction pathways, and the emerging role of pharmacogenomics in clinical practice—is good. β-Adrenergic-receptor blockers have multiple salutary effects, and new information such as presented in this issue of the Journal of Cardiothoracic and Vascular Anesthesia continues to expand the knowledge base. The biggest task for the clinician is how to evaluate clinical efficacy among other therapies appreciated to be of value (eg, angiotensin-converting enzyme inhibition, statin use) or those on the horizon (eg, modulation of endothelial function and the inflammatory response, sodium/hydrogen ion inhibitor therapy). Despite this contention, it is likely that β-adrenergic-receptor blockers will remain one of the primary weapons in the armamentarium for treating ischemia for many years to come.31Freemantle N Urdahl H Eastaugh J Hobbs FD What is the place of beta-blockade in patients who have experienced a myocardial infarction with preserved left ventricular function? Evidence and (mis)interpretation.Prog Cardiovasc Dis. 2002; 44: 243-250Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar" @default.
• W2146242058 created "2016-06-24" @default.
• W2146242058 creator A5065411611 @default.
• W2146242058 date "2002-12-01" @default.
• W2146242058 modified "2023-10-05" @default.
• W2146242058 title "β-adrenergic-receptor blockade and myocardial ischemia: Something old, something new" @default.
• W2146242058 cites W1969663663 @default.
• W2146242058 cites W1986874790 @default.
• W2146242058 cites W1987353626 @default.
• W2146242058 cites W1989225005 @default.
• W2146242058 cites W1994230402 @default.
• W2146242058 cites W1994724092 @default.
• W2146242058 cites W1999543448 @default.
• W2146242058 cites W2001911519 @default.
• W2146242058 cites W2006756434 @default.
• W2146242058 cites W2008234569 @default.
• W2146242058 cites W2013162676 @default.
• W2146242058 cites W2017306262 @default.
• W2146242058 cites W2053296636 @default.
• W2146242058 cites W2061158982 @default.
• W2146242058 cites W2062311377 @default.
• W2146242058 cites W2070568974 @default.
• W2146242058 cites W2080376663 @default.
• W2146242058 cites W2087216753 @default.
• W2146242058 cites W2098882610 @default.
• W2146242058 cites W2105790269 @default.
• W2146242058 cites W2106722354 @default.
• W2146242058 cites W2112021997 @default.
• W2146242058 cites W2118402599 @default.
• W2146242058 cites W2119791714 @default.
• W2146242058 cites W2134325937 @default.
• W2146242058 cites W2139595288 @default.
• W2146242058 cites W2172146634 @default.
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