Contractile dysfunction

Bolli, R., Jeroudi, M.O., Patel, B.S., Aruoma, O.I., Halliwell, B., Lai, E.K. and McCay, P.B. (1989). Marked reduction of free radical generation and contractile dysfunction by antioxidant therapy begun at the time of reperfiision. Circ. Res. 65, 607-622. 

Lawson, C.S. (1993). Ischaemic preconditioning, arrhythmias and post-ischaemic contractile dysfunction in rat hearts in vitro and in vivo. M.D. thesis. University of London. 

For example, Ide et al. [43] demonstrated the involvement of oxygen radicals produced by mitochondria in heart failure myocytes from adult mongrel dogs, which could be responsible for contractile dysfunction and structural damage to the myocardium. In a subsequent study... 

Skeletal muscle dysfunction can cause myalgia, bone pain, weakness, and potentially fatal rhabdomyolysis. Respiratory muscle weakness and diaphragmatic contractile dysfunction can cause acute respiratory failure. 

The value of PET for predicting contractile function after revascularization depends on whether perfusion or metabolic imaging is performed, or both. For perfusion imaging alone, if regional blood flow is preserved to more than 50% of normal, contractile dysfunction will likely recover with an average positive and negative predictive value of 63% (range... 

Schooner H, Campos R, Outtake T, Hoh CK, Moon DH, Czerny J et al. Blood flow-metabolism imaging with positron emission tomography in patients with diabetes mellitus for the assessment of reversible left ventricular contractile dysfunction. J Am Coll Cardiol 1999 33 1328-1337... 

Young ME, Laws FA, Goodwin GW, et al. Reactivation of peroxisome proliferator-activated receptor alpha is associated with contractile dysfunction in hypertrophied rat heart. J Biol Chem. Nov 30 2001 276(48) 44390 4395. 

Tsuji, T., Ohga, Y., Yoshikawa, Y., et al., 2001, Rat cardiac contractile dysfunction induced by Ca2+ overload possible link to the proteolysis of alpha-fodrin, Am. J. Physiol. Heart. Circ. Physiol., 281, 1286-1294... 

Bers, D. M., Pogwizd, S. M., and Schlotthauer, K. (2002b). Upregulated Na/Ca Exchange is Involved in both Contractile Dysfunction and Arrhythmogenesis in Heart Failure. Basic Res Cardiol 97 Suppl 1 136-42. 

Sun, H., Gaspo, R., Eeblanc, N., and Nattel, S. (1998). Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia. Circulation 98(7) 719—27. 

Zhong, Y., Ahmed, S., Grupp, I. L., and Matlib, M. A. (2001). Altered SR Protein Expression Associated with Contractile Dysfunction in Diabetic Rat Hearts. Am J Physiol Heart Circ Physiol 281(3) HI 137 17. 

Pogwizd, S.M., Schlotthauer, K., Li, L., et al., 2001, Arrhythmogenesis and contractile dysfunction in heart failure Roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness. Circ Res., 88(11), pp 1159—67. 

Asimakis, G.K., Inners-McBride, K., Conti, V.R., and Yang, C.J. 1994. Transient beta adrenergic stimulation can precondition the rat heart against post-ischaemic contractile dysfunction. Cardiovasc. Res. 28 1726-1734. 

Hintz, K. K., Aberle, N. S., and Ren, J. 2003. Insulin resistance induces hyperleptinemia, cardiac contractile dysfunction but not cardiac leptin resistance in ventricular myocytes. Int. J. Obes. Relat. Metab. Disord. 27 1196-1203. 

Rogers JH, Tsirka A, Kovacs A, Blumer KJ, Dorn GW 2nd, Muslin AJ. RGS4 reduces contractile dysfunction and hypertrophic gene induction in G(ltt overexpressing mice. J Mol Cell Cardiol 2001 33 209-218. 

Stunning is related to decreased availability of adenosine triphosphate (ATP) to the myofibrils injury of the contractile apparatus alterations in calcium homeostasis with calcium overload and burst of free radicals. The earliest consequence of severe ischemia is contractile dysfunction, occurring within 6-10 s of ischemia. Loss of tetrazolium staining after ischemic injury occurs due to loss of cofactor NADH and reflects lack of dehydrogenase enzymatic activity. The total NAD and NADH contents are relatively stable in the early phases of ischemia but decrease after irreversible myocardial injury. 

Z.Q. Zhao, C.D. Morris, J.M. Budde, N.P. Wang, S. Muraki, H.Y. Sun and R.A. Guyton, Inhibition of myocardial apoptosis reduces infarct size and improves regional contractile dysfunction during reperfusion, Cardiovasc Res. 59(1), 132-142 (2003). 

W.R. Ford, A.S. Clanachan, C.R. Hiley and B.I. Jugdutt, Angiotensin II reduces infarct size and has no effect on post-ischemic contractile dysfunction in isolated rat hearts, Br. J. Pharmacol. 134, 38-45 (2001). 

This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features - arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve -, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein Ilb/IIIa antagonism. 

Clearly, inflammation is important for the contractile dysfunction that develops after coronary microembolization. Whether or not the therapeutic use of cortisone can be exploited in patients who have possibly suffered coronary microembolization during a coronary intervention remains to be studied. 

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