Myocardial protection in normal and hypoxically stressed neonatal hearts: The superiority of hypocalcemic versus normocalcemic blood cardioplegia Kirk.

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Presentation transcript:

Myocardial protection in normal and hypoxically stressed neonatal hearts: The superiority of hypocalcemic versus normocalcemic blood cardioplegia Kirk Bolling, MD, Michael Kronon, MD*, Bradley S. Allen, MD, Shaik Ramon, MS, Tingrong Wang, MD, Renee S. Hartz, MD, Harold Feinberg, PhD The Journal of Thoracic and Cardiovascular Surgery Volume 112, Issue 5, Pages 1193-1201 (November 1996) DOI: 10.1016/S0022-5223(96)70132-0 Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 1 Left ventricular systolic function as measured by end-systolic elastance and expressed as a percentage of control. There is complete preservation of systolic function independent of cardioplegic calcium concentration in noninjured (nonhypoxic) hearts. In hypoxic hearts low-calcium blood cardioplegia solution allows cellular repair of the hypoxic reoxygenation injury, with complete return of systolic function. In contrast, there is diminished systolic function in hypoxic hearts protected with a normocalcemic (NL) cardioplegia solution. *p < 0.05. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1193-1201DOI: (10.1016/S0022-5223(96)70132-0) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 2 Left ventricular diastolic compliance as measured by the end-diastolic pressure-volume relationship and expressed as a percentage of stiffness compared with control determinations. There is only a minimal increase in diastolic stiffness in noninjured hearts independent of cardioplegia calcium concentration. In hypoxic hearts hypocalcemic blood cardioplegia solution allows cellular repair of the hypoxic reoxygenation injury, resulting in only a mild increase in diastolic stiffness, which is not statistically different from noninjured hearts. Conversely, there was a marked increase in diastolic stiffness in hypoxic hearts protected with a normocalcemic (NL) cardioplegic solution. *p < 0.05. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1193-1201DOI: (10.1016/S0022-5223(96)70132-0) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 3 Overall left ventricular myocardial function as measured by preload recruitable stroke work and expressed as a percentage of control. There is complete preservation of global myocardial function independent of cardioplegia calcium concentration in noninjured (nonhypoxic) hearts. In hypoxic hearts hypocalcemic cardioplegia solution allowed cellular repair of the hypoxic reoxygenation injury, with complete preservation of global myocardial function. In contrast, global myocardial function is depressed in hypoxic hearts protected with a normocalcemic (NL) cardioplegia solution, indicating cellular damage. *p < 0.05. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1193-1201DOI: (10.1016/S0022-5223(96)70132-0) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 4 Coronary vascular resistance (CVR) measured during each cardioplegic infusion. Cardioplegia infusions 1 and 4 were during warm (37º C) induction and reperfusion, respectively, and 2 and 3 were during cold (4º C) multidose infusions. There is no difference in CVR in noninjured (nonhypoxic) hearts independent of cardioplegia calcium concentration, indicating that both solutions preserve vascular endothelial cell function. In hypoxic hearts, a hypocalcemic blood cardioplegia solution resulted in CVRs that were similar to nonhypoxic hearts, indicating avoidance of a vascular injury. Conversely, there was a marked rise in CVR when a normocalcemic (NL) cardioplegic solution was infused in hypoxic hearts, indicating that high calcium caused a vascular injury. *p < 0.05. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1193-1201DOI: (10.1016/S0022-5223(96)70132-0) Copyright © 1996 Mosby, Inc. Terms and Conditions