Reversibly injured, postischemic canine myocardium retains normal contractile reserve.

Abstract

Transient coronary occlusion (15 minutes) does not result in irreversible myocardial injury but is associated with a depression of contractile function sustained for several hours to days ("stunned myocardium"). The defect in the contractile process responsible for this phenomenon has been suggested to be causally related to a reduced energetic state, altered excitation or excitation-contraction coupling, or damaged contractile filaments. The purpose of this study was to attempt to exclude one or more of these hypotheses by evaluating the contractile reserve of reperfused myocardium. Regional subendocardial segment function was measured (sonomicrometry) in a control region and in an area (treatment region) perfused by a carotid artery to anterior descending coronary artery bypass in 13 chloralose-anesthetized dogs. Dose-response curves were constructed from changes in segment shortening (%SS) in response to intracoronary calcium infusion before ischemia and following 5 or 15 minutes of occlusion and reperfusion (30 minutes). Calcium infusion before ischemia resulted in dose-dependent increases in %SS in the treatment area to a maximum value of 36.6% from a preinfusion value of 25.5% (p less than 0.01), in the absence of changes in control region shortening (23.7%). After 15 minutes of occlusion and reperfusion, treatment area %SS had fallen to a depressed but stable level (46% of preischemic values; p less than 0.01). Subsequent calcium infusion at the same doses as in the preischemic trial produced increases in treatment segment function with return of shortening to control levels at an intermediate dose. At the highest dose, %SS was 35.4%, which was not different from the maximal value found in the preischemic trial. Alterations in heart rate and left ventricular systolic and diastolic pressures during calcium infusion were minor and similar before and after ischemia. Calcium-induced increases in regional segment shortening above control levels (113% of control) in reperfused myocardium were sustained with continuous infusion (30 minutes) without deleterious effects on subsequent function. These results demonstrate that stunned myocardium in this model retains a normal contractile reserve in response to calcium, suggesting that the mechanism responsible for postischemic contractile dysfunction involves calcium.

Noninvasive Quantification of the Contractile Reserve of Stunned Myocardium by Ultrasonic Strain Rate and Strain

“…[3][4][5][6][7] For the first time, however, this study has quantified, by use of SR and ⑀, the response of stunned myocardium to an incremental dobutamine infusion in a closed-chest animal model that mimics the clinical setting.…”

“…For stunned myocardium, all previous reports have investigated the regional magnitude of deformation (ie, strain) by use of microcrystals 3,[5][6][7] or echocardiography. 4 Systolic strain values, however, not only are influenced by the regional contractile function but also are modified by changes in heart rate ( Figure 3).…”

“…1,2 Stunned myocardium has been shown to retain significant contractile reserve in response to a variety of positive inotropic stimuli and pharmacological agents. [3][4][5][6][7] The response of dysfunctional myocardium to dobutamine is widely used to identify viable myocardium during clinical stress testing monitored by echocardiography. 8,9 Clinically relevant stress-induced changes in regional function, however, might occur below the threshold of visual detection.…”

A depressão miocárdica pós-isquemia/reperfusão não altera a resposta cardíaca à elevação da freqüência de contrações

“…Therefore, postischemia/reperfusion stunned myocardium has been proven not to reduce the intracellular content of the ion 3,4,7 and to preserve the physiological and pharmacological maneuvers that stimulate inotropism by increasing the intracellular content of calcium ([Ca] i ): beta-adrenergic agonists [8][9][10][11] , milrinone 8,12 , calcium administration 5,13 , postpause potentiation 14 , and postextrasystolic potentiation 9,13 . However, the positive inotropic effect depending on heart rate elevation studied in myocardial segments of dogs undergoing regional ischemia has been reported to transform into negative inotropic action after myocardial ischemia/reperfusion 12 .…”

Does Preconditioning Affect Recovery in Stunned Myocardium?

“…In previous studies, stunned myocardiumwas induced by transient brief total occlusion or prolonged severe stenosis of a coronary artery (supply ischemia) (6)(7)(8). This phenomenon was characterized by prolonged contractile dysfunction without a decrease in coronary blood flow after reperfusion of the coronary artery.…”