Is "stunned myocardium" a protective mechanism? Effect of acute recruitment and acute β-blockade on recovery of contractile function and high-energy phosphate stores at 1 day post-reperfusion

There is little doubt that the "stunned myocardium" is amenable to therapeutic intervention, as a host of diverse pharmacologic agents have all been shown to improve short-term contractile function of viable, previously ischemic myocardium. However, few studies have addressed the question: Should the stunned myocardium be forced to contract? If the stunned myocardium is a protective mechanism, then acute recruitment could have later deleterious consequences on recovery of contractile function and high-energy phosphate stores. Conversely, acutely "resting" the heart (i.e., by β-adrenergic blockade) could conceivably enhance or accelerate recovery of the stunned, postischemic tissue. We therefore sought to assess the immediate and longer-term effects of acute recruitment and acute β-blockade on regional wall thickening (WT: using two-dimensional echocardiography) and adenosine triphosphate (ATP) content in the canine model of the stunned myocardium. Anesthetized open-chest dogs underwent 15 minutes of transient coronary artery occlusion. At 30 minutes following reperfusion, the dogs acutely received either: the ultrashort-acting β-blocker esmolol, the afterload reducing and cardiostimulatory agent hydralazine, or saline. As anticipated, hydralazine enhanced contractile function of the stunned tissue in the short term: WT at 2 hours after treatment was 53.7 ± 6.9% versus 7.1 ± 6.5% in treated versus saline controls (p < 0.01). This short-term recruitment did not, however, cause later deterioration of contractile function or exacerbate ATP depletion: WT averaged 7.5 ± 5.1% versus 15.4 ± 10.6% at 1 day after treatment (p = NS), and ATP content in the previously ischemic endocardium was 31.5 ± 1.5 versus 29.6 ± 2.1 nmol/mg protein (p = NS) in animals treated with hydralazine versus saline controls. In contrast, acute β-blockade with esmolol had no significant beneficial effect: WT averaged 5% to 10% both for the short term and at 1 day after treatment (p = NS versus controls), and endocardial ATP content was 27.1 ± 2.5 nmol/mg protein (p = NS versus controls). As acute recruitment and acute β-blockade had neither beneficial nor deleterious effects on regional contractile function or high-energy phosphate stores at 1 day after reperfusion and treatment, we conclude that the stunned myocardium may not be an essential protective mechanism.