Cardiomyocyte injury

Padua RR, Fandrich RR, Kardami E Increased basic fibroblast growth factor accumulation and distinct pattern of localization in isoproterenol-induced cardiomyocytes injury. Growth Factors 1993 8 291-306. 

Esfandiarei, M., Suarez, A., Amaral, A., Si, X., Rahmani, M., Dedhar, S., and McManus, B.M. (2006). Novel role for integrin-linked kinase in modulation of coxsackievirus B3 replication and virus-induced cardiomyocyte injury. Circ Res 99, 354-361. 

R.R. Padua, and E. Kardami, Increased basic fibroblast growth factor (bFGF) accumulation and distinct patterns of localization in isoproterenol-induced cardiomyocyte injury, Growth Factors 8, 291-306 (1993). 

Shneyvays V, Leshem D, Zinman T, Mamedova LK, Jacobson KA, Shainberg A (2005) Role of adenosine A and A, receptors in regulation of cardiomyocyte homeostasis after mitochondrial respiratory chain injury. Am J Physiol Heart Circ Physiol 288(6) H2792-H2801... 

Terai, K., Hiramoto, Y., Masaki, M., Sugiyama, S., Kuroda, T., Hoti, M., Kawase, I., and Hirota, H. 2005. AMP-activated protein kinase protects cardiomyocytes against hypoxic injury through attenuation of endoplasmic reticulum stress. Mol Cell Biol 25 9554-9575. 

Studies in various animal models and in human hearts suggest that apoptosis does occur in ischemia/reperfusion injury of the heart, though the relative contribution of apoptosis in comparison with necrosis to cell loss in ischemia/ reperfusion injury is still controversial. Cardiomyocyte apoptosis was first reported by Gottlieb et al. [107], who studied the ischemia/reperfusion in rabbit hearts and found the hallmark of apoptosis in ischemic/reperfused hearts but not in the normal or ischemic-only rabbit hearts. Identification of apoptosis was based on the presence of fragmented DNA in electrophoretic gels, on in situ nick end-labeling assays, and on electron microscopy. They concluded that apoptosis may be a specific feature of reperfusion injury in cardiac myocytes. Subsequent studies have shown that apoptosis probably occurs both in ischemia and reperfusion [108], It appears that apoptosis is more prominent after ischemia followed by reperfusion than after ischemia alone [109, 110],... 

Although several potential therapeutic agents have been tested in animal models of ischemia/reperfusion heart injury with some success, nearly none of the specific antiapoptotic agents have reached the stage of clinical research [172]. The studies which have examined the effect of caspase inhibitors on ischemia/reperfusion models are summarized in Table 2. Broad-spectrum caspase inhibitors have been shown in many studies to reduce cardiomyo-cyte apoptosis, to reduce the size of MI, and to preserve heart function after MI [173-175, 178, 181]. The protective effect of caspase inhibitors can be seen when these agents are administered before or after the onset of ischemia but are most prominent when introduced before the onset of reperfusion [172, 175, 178]. Selective caspase inhibitors, on the other hand, have been reported to have varying effect they have been found to reduce cardiomyocytes apoptosis, but the infarct size remained unchanged [177, 178, 181],... 

Date T, Mochizuki S, Belanger AJ, Yamakawa M, Luo Z, Vincent KA, et al. Differential effects of membrane and soluble Fas ligand on cardiomyocytes Role in ischemia/reperfusion injury. J Mol Cell Cardiol 2003 35 811-821. 

Gottlieb RA, Burleson KO, Kloner RA, Babior BM, Engler RL. Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest 1994 94 1621-1628. 

There are causes of infarctions other than acute atherothrombotic coronary occlusion. For example, prolonged vasospasm can induce infarction, and spontaneous dissection is becoming more commonly appreciated, especially in pregnant females. Other conditions (Box 44-1) can also cause the death of cardiomyocytes and lead to a biochemical signal of myocyte damage, but these entities should not be confused with myocardial infarction. Some of these injurious stimuli include (1) trauma that may precip-... 

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