Myocardial infarction ventricular remodeling

Ventricular Remodeling Following an Acute Myocardial Infarction... 

Parissis JT, Adamopoulos S, Venetsanou KF, Mentzikof DG, Karas SM, Kremastinos DT. Serum profiles of C-C chemokines in acute myocardial infarction possible implication in postinfarction left ventricular remodeling. J Interferon Cytokine Res 2002 22(2) 223-229. 

ACE-inhibitors are known to cause regression of left ventricular and vascular hypertrophy. This phenomenon is important in the long-term treatment of hypertension, where cardiac hypertrophy is known to be an important, virtually independent risk factor. Data that are beginning to emerge, which indicate that ACE-inhibitors may be beneficial as secondary prevention in postinfarct patients, especially if signs of heart failure occur. This favourable influence of the ACE-inhibitors may be the result of haemodynamic effects, a favourable effect on neuroendocrine mechanisms, and also a beneficial influence on the process of remodeling of the heart, secondary to a myocardial infarction. 

Pfeffer JM, Pfeffer MA, Fletcher PJ, Braunwald E. Progressive ventricular remodelling in rat myocardial infarction. Am J Physiol 1991 260 H 14106-H1414. 

St. John Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction. Pathophysiology and therapy. Circulation 2000 101 2981-2988. 

Jain M, DerSimonian H, Brenner DA, et al. Cell therapy attenuates deleterious ventricular remodeling and improves cardiac performance after myocardial infarction. Circulation 2001 ... 

Matsushima, S., Ide, T., Yamato, M., Matsusaka, H., Hattori, F., Ikeuchi, M., Kubota, T., Sunagawa, K., Hasegawa, Y., Kurihara, T., Oikawa, S., Kinugawa, S., and Tsutsui, H. 2006. Overexpression of mitochondrial peroxiredoxin-3 prevents left ventricular remodeling and failure after myocardial infarction in mice. Circulation 113 1779-1786. 

Chareonthaitawee, P., Christian, T.F., Hirose, K., Gibbons, R.J., and Rumberger, J.A. 1995. Relation of initial infarct size to extent of left ventricular remodeling in the year after acute myocardial infarction. J. Am. Coll. Cardiol. 25 567-573. 

Pfeffer, J.M., Pfeffer, M.A., Fletcher, P.J., and Braunwald, E. 1991. Progressive ventricular remodeling in rat with myocardial infarction. Am. J. Physiol. 260 H1406-H1414. 

Pfeffer, J.M., Fischer, T.A., and Pfeffer, M.A. 1995. Angiotensin-converting enzyme inhibition and ventricular remodeling after myocardial infarction. Amur Rev. Physiol. 57 805-826. 

Abbate A, Biondi-Zoccai GG, Bussani R, Dobrina A, Camilot D, Feroce F, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. J Am Coll Cardiol 2003 41 753-760. 

Sam F, Sawyer DB, Chang DL, Eberli FR, Ngoy S, Jain M, et al. Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart. Am J Physiol Heart Circ Physiol 2000 279 H422-H428. 

Palojoki E, Saraste A, Eriksson A, Pulkki K, Kallajoki M, Voipio-Pulkki LM, et al. Cardiomyocyte apoptosis and ventricular remodeling after myocardial infarction in rats. Am J Physiol Heart Circ Physiol 2001 280 H2726-H2731. 

Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation 1990 81 1161-1172. 

Anversa P, Olivetti G, Capasso JM. Cellular basis of ventricular remodeling after myocardial infarction. Am J Cardiol 1991 68 7D-16D. 

Yarbrough WM, Mukherjee R, Escobar GP, Sample JA, McLean JE, Dowdy KB, et al. Pharmacologic inhibition of intracellular caspases after myocardial infarction attenuates left ventricular remodeling A potentially novel pathway. J Thorac Cardiovasc Surg 2003 126 1892-1899. 

Chandrashekhar Y, Sen S, Anway R, Shuros A, Anand I. Long-term caspase inhibition ameliorates apoptosis, reduces myocardial troponin-1 cleavage, protects left ventricular function, and attenuates remodeling in rats with myocardial infarction. J Am Coll Cardiol 2004 43 295-301. 

Saitoh T, Nakajima T, Takahashi T, Kawahara K. Changes in cardiovascular function on treatment of inhibitors of apoptotic signal transduction pathway in left ventricular remodeling after myocardial infarction. Cardiovasc Pathol 2006 15 130-138. 

Antagonistic effects of cyclo-oxygenase inhibitors (indo-metacin or aspirin) have been repeatedly reported both in hypertension and in heart failure, strongly suggesting that there may be prostaglandin participation in the clinical response to ACE inhibitors (103,104). In animals, although not in all experimental models, aspirin can attenuate the beneficial effects of ACE inhibitors on ventricular remodelling after myocardial infarction. 

McKay RG, Pfeffer MA, Pasternak RC, Markis JE, Come PC, Nakao S, Alderman JD, Ferguson JJ, Safian RD, Grossman W (1986) Left ventricular remodeling after myocardial infarction a corollary to infarct expansion. Circulation 74 693-702... 

V. Marangelli, C. Memmola, M.S. Brigiani, L. Boni, M.G. Biasco, D. Scrutinio, S. Iliceto and P. Riz-zon, Early administration of verapamil after thrombolysis in acute anterior myocardial infarction. Effect on left ventricular remodeling and clinical outcome. VAMI Study Group. Verapamil Acute Myocardial Infarction, Ital Heart J. 1(5), 336-343 (2000). 

A beneficial effect of thyroid hormone on left ventricular remodeling is also reported. In an experimental model of acute myocardial infarction in rats, a decline in serum T3 was observed associated with left ventricular dysfunction and changes in T3 responsive genes. Treatment with high doses of T3 for three weeks resulted in improved cardiac function with normalization of most of the changes in gene expression.89 Similarly, administration of DITPA (a thyroid analogue) after myocardial infarction in rabbits was associated with improved cardiac function.90... 

K. W. Mahaffey, T.E. Raya, G.D. Pennock, E. Morkin and S. Goldman, Left ventricular performance and remodeling in rabbits after myocardial infarction effects of a thyroid hormone analogue, Circulation 91(3), 794-801 (1995). 

M.A. Pfeffer, Left ventricular remodeling after acute myocardial infarction, Anna Rev Med 46,455-466 (1995). 

FIGURE 14-4. Key components of the pathophysiology of cardiac remodeling. Myocardial injury (e.g., myocardial infarction) results in the activation of a number of hemodynamic and neurohormonal compensatory responses in an attempt to maintain circulatory homeostasis. Chronic activation of the neurohormonal systems results in a cascade of events that affect the myocardium at the molecular and cellular levels. These events lead to the changes in ventricular size, shape, structure, and function known as ventricular remodeling. The alterations in ventricular function result in further deterioration in cardiac systolic and diastolic function, which further promotes the remodeling process. 

St John Sutton M, Ferrari VA. Prevention of left ventricular remodeling after myocardial infarction. Curr Treat Options Cardiovasc Med 2002 4 97-108. 

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