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Chapter 38: Molecular and Cellular Mechanisms of Myocardial Ischemia/Reperfusion Injury

Ravi Karra

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    AMA Citation
    Karra R. Karra R Karra, Ravi.Molecular and Cellular Mechanisms of Myocardial Ischemia/Reperfusion Injury. In: Eisenberg MJ, Afilalo J, Joza JE, Karra R, Lawler PR. Eisenberg M.J., & Afilalo J, & Joza J.E., & Karra R, & Lawler P.R.(Eds.),Eds. Mark J. Eisenberg, et al.eds. Cardiology Board Review and Self-Assessment: A Companion Guide to Hurst's the Heart, 14e. McGraw-Hill; Accessed July 14, 2020. https://accesscardiology.mhmedical.com/content.aspx?bookid=2459&sectionid=193145055
    APA Citation
    Karra R. Karra R Karra, Ravi. (2018). Molecular and cellular mechanisms of myocardial ischemia/reperfusion injury. Eisenberg MJ, Afilalo J, Joza JE, Karra R, Lawler PR. Eisenberg M.J., & Afilalo J, & Joza J.E., & Karra R, & Lawler P.R.(Eds.),Eds. Mark J. Eisenberg, et al. Cardiology Board Review and Self-Assessment: A Companion Guide to Hurst's the Heart, 14e. McGraw-Hill. https://accesscardiology.mhmedical.com/content.aspx?bookid=2459&sectionid=193145055
    MLA Citation
    Karra R. Karra R Karra, Ravi. "Molecular and Cellular Mechanisms of Myocardial Ischemia/Reperfusion Injury." Cardiology Board Review and Self-Assessment: A Companion Guide to Hurst's the Heart, 14e Eisenberg MJ, Afilalo J, Joza JE, Karra R, Lawler PR. Eisenberg M.J., & Afilalo J, & Joza J.E., & Karra R, & Lawler P.R.(Eds.),Eds. Mark J. Eisenberg, et al. McGraw-Hill, 2018, https://accesscardiology.mhmedical.com/content.aspx?bookid=2459&sectionid=193145055.

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Chapter 38: Molecular and Cellular Mechanisms of Myocardial Ischemia/Reperfusion Injury

Which of the following is not a determinant of infarct size?

A. Time to reperfusion

B. The presence of collaterals

C. Blood pressure

D. Temperature

E. Ischemia/reperfusion injury

The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 38) Shorter time to reperfusion and an increased number of collaterals are associated with smaller infarct sizes (options A and B). Lower temperatures and larger ischemia/reperfusion injury are associated with larger infarct sizes (options D and E). Blood pressure by itself is not directly associated with infarct size (option C).

Which of the following does not contribute to myocyte necrosis after reperfusion?

A. Sarcolemma disruption and calcium overload

B. ATP depletion and reversal of the Na+/Ca2+ exchanger, resulting in increased intracellular calcium

C. The no-reflow phenomenon

D. Tissue edema

E. Autophagy

The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 38) Calcium overload that results from disruption of the sarcolemma and reversal of the Na+/Ca2+ exchanger contribute to reperfusion injury (options A and B).1 Impairment of the microcirculation via the no-reflow phenomenon or by compression through tissue edema can exacerbate reperfusion injury (options C and D).2,3 Autophagy is not known to contribute to reperfusion injury (option E).

Which of the following is true about intracellular Ca2+ during ischemia-reperfusion injury?

A. The Na+/Ca2+ exchanger extrudes Ca2+ from the cytoplasm

B. Calpains are activated by increases in Ca2+

C. The RyR2 does not contribute to increased intracellular Ca2+

D. Sarcolemma membranes remain intact

E. Calpains are only active at low pH

The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 38) Altered Ca2+ handling is one of the most prominent and relevant aspects of cardiomyocyte reperfusion. Reperfusion causes further Ca2+ influx through the Na+/Ca2+ exchanger in response to Na+ overload (option A). An important consequence of increased Ca2+ is activation of the Ca2+-dependent proteases calpains. Calpains translocate to the sarcolemma during ischemia in response to Ca2+ overload but are activated ...

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