title: Determinants of contractile reserve in viable, chronically dysfunctional myocardium.
abstract: There is considerable variability in the sensitivity of inotropic reserve to identify viability in chronically dysfunctional myocardium. This is partially related to the underlying pathophysiology, with more frequent contractile reserve in chronically stunned (with normal resting perfusion) than hibernating myocardium (with reduced flow). This study was undertaken to determine the physiological responses to transient and graded stimulation in chronically stunned and hibernating myocardium to define the relative roles of acute catecholamine desensitization and biphasic responses. Pigs were chronically instrumented with a fixed left anterior descending artery stenosis that resulted in chronically stunned myocardium after 2 mo. One month later, hibernating myocardium was confirmed by regional dysfunction (wall thickening, 3.2 +/- 0.3 vs. 5.5 +/- 5 mm in remote, P=0.01) with reduced resting flow (0.70 +/- 0.07 vs. 0.92 +/- 0.09 ml x min(-1) x g(-1) in remote, P=0.01) without infarction. Wall thickening in dysfunctional regions significantly increased during both graded and transient epinephrine stimulation in chronically stunned (from 3.6 +/- 0.3 to 5.6 +/- 0.5 and 4.9 +/- 0.5 mm, respectively) and hibernating myocardium (from 3.3 +/- 0.3 to 5.4 +/- 0.6 and 5.0 +/- 0.7 mm, respectively) and returned to baseline within 15 min. Although a biphasic response during graded stimulation was common, the subsequent decrement in function was small and similar in both groups (stunned, 0.7 +/- 0.2 mm; hibernating, 1.1 +/- 0.3 mm, P=0.25). We conclude that 1) the extent of contractile reserve during beta-adrenergic stimulation is similar in chronically stunned and hibernating myocardium, 2) there are no significant differences between the responses to transient compared with graded catecholamine stimulation, and 3) submaximal catecholamine stimulation does not induce additional stunning in either chronically stunned or hibernating myocardium.
authors.affiliation: Veterans Affairs Western New York Health Care System, Buffalo, NY, USA.
authors.forename: Michael D
authors.initials: MD
authors.lastname: Banas
authors.forename: Sunil
authors.initials: S
authors.lastname: Baldwa
authors.forename: Gen
authors.initials: G
authors.lastname: Suzuki
authors.forename: John M
authors.initials: JM
authors.lastname: Canty
authors.forename: James A
authors.initials: JA
authors.lastname: Fallavollita
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D002470:Cell Survival; D002908:Chronic Disease; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects; D017682:Myocardial Stunning / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology*; D012107:Research Design; D013552:Swine; D016276:Ventricular Function / Q000187:drug effects
chemical_list: D000318:Adrenergic beta-Agonists; D002316:Cardiotonic Agents; D004837:Epinephrine