Myocardial dysfunction

CHF or Ml - Use cautiously in patients with a history of CHF or myocardial dysfunction (see Warnings). 

Cardiovascular effects Limit use of levorphanol in acute Ml or in cardiac patients with myocardial dysfunction or coronary insufficiency because the effects of levorphanol on the heart are unknown. 

Bax JJ, Cornel JH, Visser FC, Fioretti PM, van LA, Reijs AE et al. Prediction of recovery of myocardial dysfunction after revascularization. Comparison of fluorine-18 fluorodeoxyglucose/thalhum-201 SPECT, thaUium-201 stress-reinjection SPECT and dobutamine echocardiography. J Am Coll Cardiol 1996 28 558-564... 

Stenestrand U, Tabriz F, Lindback J, England A, Rosenqvist M, Wallentin L. Comorbidity and myocardial dysfunction are the main explanations for the higher 1-year mortality in acute myocardial infarction with left bundle-branch block. Circulation 2004 110 1896-902. 

Cardiovascular disease. The hypotensive effects of thiopentone are exaggerated in patients with myocardial dysfunction, fixed cardiac output (valvular stenosis, constrictive pericarditis), and in the hypovolaemic... 

Chen H, Mohuczy D, Li D, et al. Protection against ischemia/reperfusion injury and myocardial dysfunction by anti-sense-oligodeoxynucleotide directed at angiotensin-converting enzyme mRNA. Gene Ther 2001 8 804-810. 

Rajnoch C, ChachquesJC, Berrebi A, et al. Cellular therapy reverses myocardial dysfunction. J Thorac Cardiovasc Surg 2001 121 871-878. 

Skeletal myoblast intramyocardial injection for ischemic myocardial dysfunction... 

In acute or chronic ischemia patients, angiogenic potential of transplanted cells is of the greatest importance. The patients with chronic nonviable scar and myocardial dysfunction are more likely to benefit from the cells that, either directly or indirectly (via paracrine effect) (47), improve the contractility of the treated myocardium (9). Autologous skeletal myoblasts have been successfully expanded in vitro and implanted in the myocardia of animals. Although they do not contract synchronously with the rest of the myocardium and do not integrate into it, they have been shown to improve contractility... 

Baneijee, A., Locke-Winter, C., Rogers, K., Mitchell, M.B., Brew, E.C., Cairns, C., Bensard, D., and Harken, A.H. 1993. Preconditioning against myocardial dysfunction after ischemia and reperfusion by an alpha-adrenergic mechanism. Circ. Res. 73 656-670. 

Frances, C., Nazeyrollas, P., Prevost, A., Moreau, F., Pisani, J., Davani, S., Kantelip, J.P., and Millart, H. 2003. Role of beta 1- and beta 2-adrenoceptor subtypes in preconditioning against myocardial dysfunction after ischemia and reperfusion. J. Cardiovasc. Pharmacol. 41 396 105. 

Myocardial dysfunction may arise from Al loading, but this is not substantiated as yet. Al levels have been found markedly increased in the heart in patients with chronic dialysis encephalopathy [15]. It is presumed that sudden cardiac death may practically be due to Al cardiotoxicity [27, 106]. At pathology evaluation patients Nos. 7-9 showed signs of pulmonary edema. 

Deficiency—may result in neuromuscular dysfunction. Excess—may cause myocardial dysfunction. 

Among other cardiovascular complications, cardiac dysrhythmias were reported in 6-10% of patients, angina pectoris or documented myocardial infarction in 3-4%, and mortality due to myocardial infarction in 1-2% (4). Severe myocardial dysfunction, myocarditis, and cardiomyopathy have been seldom reported (SED-13, 1103) (SEDA-20, 334) (SEDA-22, 406). 

Erythromycin has antidysrhythmic properties similar to those of Class lA antidysrhythmic drugs, and causes an increase in atrial and ventricular refractory periods. This is only likely to be a problem in patients with heart disease or in those who are receiving drugs that delay ventricular repolarization (5). High-doses intravenously have caused ventricular fibrillation and torsade de pointes (6). Each episode of dysrhythmia, QT interval prolongation, and myocardial dysfunction occurred 1-1.5 hours after erythromycin infusion and resolved after withdrawal. 

Myocardial dysfunction can completely reverse after withdrawal of interferon alfa and does not exclude further treatment with lower doses (28). 

In one patient, mycophenolate mofetil was putatively involved in a constellation of symptoms that included fever, exudative pharyngitis, adynamic ileus, electrolytic abnormalities, and myocardial dysfunction, which resolved on withdrawal (SEDA-20, 346). 

Severe hypophosphatemia with myocardial dysfunction was noted in patients receiving tumor necrosis factor alfa by continuous hepatic arterial infusion (SEDA-17, 433). 

Prostacyclin is increased in response to ischemia and reperfusion through activation of the cyclooxygenase-2 pathway. Inhibition of cyclooxygenase-2 by celecoxib or meloxicam resulted in a concentration dependent exacerbation of the myocardial dysfunction and damage in a perfused rabbit heart model of ischemia and reperfusion, indicating a cardioprotective role for prostacyclin.104... 

M. Thielmann, H. Dorge, C. Martin, S. Belosjorow, U. Schwanke, A. van De Sand, I. Konietzka, A. Buchcrt, A. Kruger, R. Schulz and Heusch G, Myocardial dysfunction with coronary microembolization signal transduction through a sequence of nitric oxide, tumor necrosis factor-alpha, and sphingosine, Circ. Res. 90(7), 807-813 (2002). 

C. Pantos, I. Mourouzis, S. Tzeis, P. Moraitis, V. Malliopoulou, D.D. Cokkinos, H. Carageorgiou, D. Varonos, D.V. Cokkinos, Dobutamine administration exacerbates postischemic myocardial dysfunction in isolated rat hearts An effect reversed by thyroxine pre-treatment, Eur J Pharmacol 460,155-161 (2003). 

G. Rossoni, M.N. Muscara, G. Cirino, J.L. Wallace, Inhibition of cyclo-oxygenase -2 exacerbates ischemia -induced acute myocardial dysfunction in the rabbit, Br. J. Pharmacol. 135, 1540-1546 (2002). 

T. Asahi, M. Shimabukuro, Y. Oshiro, H. Yoshida and N. Takasu, Cilazapril prevents cardiac hypertrophy and postischemic myocardial dysfunction in hyperthyroid rats, Thyroid 11(11), 1009-1015 (2001). 

A. Banerjce, C. Locke-Wintcr, K. B. Rogers, M. B. Mitchell, E. C. Brew, C.B. Cairns, D. D. Bensard and A. H. Harken, Preconditioning against myocardial dysfunction after ischemia and reperfusion by an al-adrenergic mechanism, Circ Res 73, 656-670, (1993). 

A. Skyschally, M. Haude, H. Dorge, M. Thielmann, A. Duschin, A. van de Sand, I. Konietzka, A. Bochert, S. Aker, P. Massoudy, R. Schulz, R. Erbel and G. Heusch, Glucocorticoid treatment prevents progressive myocardial dysfunction resulting from experimental coronary microembolization, Circulation 109,2337-2342 (2004). 

S.L. House, C. Bolte, M. Zhou, T. Doetschman, R. Klevitsky, G. Newman, and J. Schultz Jel, Cardiac-specific overexpression of fibroblast growth factor-2 protects against myocardial dysfunction and infarction in a murine model of low-flow ischemia, Circulation 108,3140-3148 (2003). 

C. I. Pantos, C. H. Davos, H. C. Carageorgiou, D. V. Varonos, D. V. Cokkinos, Ischemic preconditioning protects against myocardial dysfunction caused by ishaemia in isolated hypertrophied rat hearts, Basic Res Cardiol 91, 444-449 (1996). 

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