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ICVTS on-line discussion A Coronary artery spasm: chest drainage or something else

University Hospital Sestre Milosrdnice, Zagreb 10000, Croatia

Coronary artery spasm following aortic valve replacement

eComment: I read with great interest the article of Pinho et al. [1] in which they speculate that the coronary artery spasm should be considered as a cause of unexplained electrical or hemodynamic instability. Be that as it may, there are some physiological issues that cause one to pause regarding the findings in this case report.

Ischemic or myocardial preconditioning [IPC] is a phenomenon whereby brief intervals of sublethal ischemia either delay or reduce the extent of necrosis following a subsequent more prolonged episode of ischemia. Coronary vasospasm may be provoked by a supersensitivity of the vascular smooth muscle cells. In the vasculature, ATP-sensitive potassium [KATP] channels regulate vascular tone. The channel is composed of a pore-forming unit [Kir6.x] and a regulatory subunit, the sulfonylurea receptor [SURalternatively spliced form SUR2]. In the cardiovascular system, Kir6 and SUR2 constitute the major KATP channels of the heart [2]. There is evidence that the pathways involved in the protection mediated by acute IPC may depend on the stimulus used to elicit IPC and the end point of injury used to demonstrate the protective effect, i.e., infarct size, stunning, and arrhythmias [3]. Experimental study findings indicated that coronary artery vascular spasm associated with global loss of SUR2-Kir6.1 KATP channels arises from a vascular smooth muscle cell-extrinsic process. There is evidence to support a role for endothelial KATP channels in vascular function and, potentially, in the regulation of vascular tone and vascular spasm. This finding suggests that the loss of KATP channels in an organ system in close interaction with the coronary vasculature is vital for normal coronary function as studies in isolated hearts showed evidence of abnormal vascular reactivity, eliminating more distant regulators of vascular tone. It is possible that the normal, KATP-mediated regulation of cardiovascular function may also be controlled though multi-organ systems or a proximal paracrine effect mediated by the neuronal or endothelial crosstalk to vascular smooth muscle. Until today, a variety of ‘triggers’ have been identified that are activated and/or released during the preconditioning stimulus, including adenosine, cathecolamines, bradykinin, opioids, and nitric oxide. These triggers may be dependent on the severity and length of the preconditioning stimulus. Considerable evidence suggests that the KATP channel is intimately involved as either a trigger or end effectors in IPC, and have potential mechanisms responsible for the cardioprotection. For the purposes of further discussions of coronary artery spasm it could be advised that we are bearing on our minds the possibility that the spontaneous coronary vasospasm could arise, not only from mechanical damage, but from a coronary artery vascular smooth muscle-extrinsic process.

Maybe, if we introduce these facts in the article of Pinho et al., we could shift it from negative to positive content of paper.

	References

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1. Pinho T, Almeida J, Garcia M, Pinho P. Coronary artery spasm following aortic valve replacement. Interact CardioVasc Thorac Surg 2007; 6:387–389.[Abstract/Free Full Text]
2. Noma A. ATP-regulated Kq channels in cardiac muscle. Nature 1983; 305:147–148.[CrossRef][Medline]
3. Seino S, Miki T. Physiological and pathophysiological roles of ATPsensitive K channels. Prog Biophys Mol Biol 2003; 81:133–176.[CrossRef][Medline]

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