CARDIAC HYPERTROPHY: A REVIEW ON PATHOGENESIS AND TREATMENT
Abstract
Cardiac hypertrophy has been considered as an important risk factor for cardiac morbidity and mortality whose prevalence has increased during the last few decades. Cardiac hypertrophy, a disease associated with the myocardium, is characterized by thickening of ventricle wall of heart and consequent reduction in the contracting ability of heart to pump the blood. Cardiac hypertrophy has been divided into two types, i.e. physiological and pathological hypertrophy. The exercise-induced increase in the ability of pumping blood leads to thickening of ventricle wall, referred to as physiological hypertrophy. On the other hand, reduced ability of pumping blood as a result of hypertension and volume overload on heart denotes pathological hypertrophy. Numerous mediators have been found to be involved in the pathogenesis of cardiac hypertrophy that include mitogen-activated protein kinase (MAPK), protein kinase C (PKC) insulin-like growth factor-I (IGF-I), phosphatidylinositol 3-kinase (PI3K)-AKT/PKB, calcinurin-nuclear factor of activated T cells (NFAT) and mammalian target of rapamycin (mTOR). The prevention strategy for cardiac hypertrophy involve thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin (Ang) II receptor blockers, beta blockers and calcium channel blockers. The present review article highlights the signaling mechanisms involved and the approaches required in the treatment of cardiac hypertrophy.
Keywords:
Cardiac hypertrophy, Ventricle, Physiological, PathologicalDOI
https://doi.org/10.25004/IJPSDR.2012.040301References
1. Akhter SA, Luttrel LM, Rockman HA, Lacirino G, Lefkowitz RJ, Koch WJ. Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy. Science 1998; 280: 574-577.
2. Marian AJ. Genetic determinants of cardiac hypertrophy. Curr Opin Cardiol. 2008; 23: 199-205.
3. Kee HJ, Kook H. Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy. J Biomed Biotech. 2011; 2011: 928326.
4. Tikhonoff V, Casiglia E. Evolving concepts of left ventricular hypertrophy. Eur Heart J. 2008; 29: 846-848.
5. Ojamaa K. Signaling Mechanisms in Thyroid Hormone-Induced Cardiac Hypertrophy. Vascul Pharmacol. 2010; 52: 113-119.
6. Dillmann W. Cardiac hypertrophy and thyroid hormone signaling. Heart Fail Rev. 2010; 15: 125-132.
7. McMullen JR, Jennings GL. Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure. Clin Exp Pharmacol Physiol. 2007; 34: 255-262.
8. Buss SJ, Riffel JH, Malekar P, Hagenmueller M, Asel C, Zhang M, et al. Chronic Akt blockade aggravates pathological hypertrophy and inhibits physiological hypertrophy. Am J Physiol Heart Circ Physiol. 2012; 302: H420-H430.
9. Diwan A, Dorn GW. Decompensation of cardiac hypertrophy: cellular mechanisms and novel therapeutic targets. Physiology. 2007; 22: 56-64.
10. Oka T, Komuro I. Molecular mechanisms underlying the transition of cardiac hypertrophy to heart failure. Circ J. 2008; 72: A13-A16.
11. Soesanto W, Lin HY, Hu E, Lefler S, Litwin SE, Sena S, et al. Mammalian target of rapamycin is a critical regulator of cardiac hypertrophy in spontaneously hypertensive rats. Hypertension. 2009; 54: 1321-1327.
12. Balakumar P, Jagadeesh G. Multifarious molecular signaling cascades of cardiac hypertrophy: can the muddy waters be cleared. Pharmacol Res. 2010; 62: 365-383.
13. Aoyagi T, Matsui T. Phosphoinositide-3 kinase signaling in cardiac hypertrophy and heart failure. Curr Pharm Des. 2011; 17: 1818-1824.
14. Van Zwieten PA. The influence of antihypertensive drug treatment on the prevention and regression of left ventricular hypertrophy. Cardiovasc Res. 2000; 45: 82-91.
15. Liao Y, Asakura M, Takashima S, Ogai A, Asano Y, Shintani Y, et al. Celiprolol, a vasodilatory beta-blocker, inhibits pressure overload-induced cardiac hypertrophy and prevents the transition to heart failure via nitric oxide-dependent mechanisms in mice. Circulation 2004; 110: 692-629.
16. Horiba M, Muto T, Ueda N, Opthof T, Miwa K, Hojo M, et al. T-type Ca2+ channel blockers prevent cardiac cell hypertrophy through an inhibition of calcinurin-NFAT3 activation as well as L-type Ca2+ channel blockers. Life Sci. 2008; 82: 554-560.
17. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. 1975; 56: 56-64.
18. Pluim BM, Zwinderman AH, Van Der Laarse A, Van Der Wall EE. The athlete’s heart. A meta-analysis of cardiac structure and function. Circulation 2000; 101: 336-344.
19. Mone SM, Sanders SP, Colan SD. Control mechanisms for physiological hypertrophy of pregnancy. Circulation 1996; 94: 667-672.
20. Iemitsu M, Miyauchi T, Maeda S, Sakai S, Kobayashi T, Fujii N, et al. Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat. AJP - Regu Physiol. 2001; 281: R2029-R2036.
21. Sagara S, Osanai T, Itoh T, Izumiyama K, Shibutani S, Hanada K, et al. Over expression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by inhibiting PI3K/Akt signaling in mice. J Hypertension. 2012; 30: 778-786.
22. Zak R. Growth of the Heart in Health and Disease. Raven Press, New York. 1984.
23. Finsen AV, Lunde IG, Sjaastad I, Ostli EK, Lyngra M, Jarstadmarken HO, et al. Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcinurin-NFAT pathway. PLOS One. 2011; 6: e28302.
24. Usui S, Maejima Y, Pain J, Hong C, Cho J, Park JY, et al. Endogenous muscle atrophy F-box mediates pressure overload-induced cardiac hypertrophy through regulation of nuclear factor-kappa B. Circ Res. 2011; 109: 161-171.
25. Fagard RH. Impact of different sports and training on cardiac structure and function. Cardiol Clin. 1997; 15: 397-412.
26. Barry SP, Davidson SM, Townsend PA. Molecular regulation of cardiac hypertrophy. Int J Biochem. Cell Biol. 2008; 40: 2023-2039.
27. Rohini A, Agrawal N, Koyani CN, Singh R. Molecular targets and regulators of cardiac hypertrophy. Pharmacol Res. 2010; 61: 269-280.
28. Force T, Pombo CM, Avruch JA, Bonventre JV, Kyriakis JM. Stress-activated protein kinases in cardiovascular disease. Circ Res. 1996; 78: 947-953.
29. Carreno JE, Apablaza F, Ocaranza MP, Jalil JE. Cardiac hypertrophy: molecular and cellular events. Rev Esp Cardiol. 2006; 59: 473-486.
30. Wang Y, Huang S, Sah VP, Ross J Jr, Brown JH, Han J, Chien KR. Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. J Biol Chem. 1998; 273: 2161-2168.
31. Ramirez MT, Sah VP, Zhao XL, Hunter JJ, Chien KR, Brown JH. The MEKK-JNK pathway is stimulated by alpha1-adrenergic receptor and ras activation and is associated with in vitro and in vivo cardiac hypertrophy. J Biol Chem. 1997; 272: 14057-14061.
32. Dorn GW, Brown JH. Gq signaling in cardiac adaptation and maladaptation. Trends Cardiovasc Med. 1999; 9: 26-34.
33. Molkentin JD. Calcinurin-NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs. Cardiovasc Res. 2004; 63: 467-475.
34. Kim J, Wende AR, Sena S, Theobald HA, Soto J, Sloan C, et al. Insulin-like growth factor I receptor signaling is required for exercise-induced cardiac hypertrophy. Mol Endocrinol. 2008; 22: 2531-2543.
35. McMullen JR, Izumo S. Role of the insulin-like growth factor 1 (IGF1)/phosphoinositide-3-kinase (PI3K) pathway mediating physiological cardiac hypertrophy. Novartis Found Symp. 2006; 274: 90-111.
36. Teos LY, Zhao A, Alvin Z, Laurence GG, Li C, Haddad GE. Basal and IGF-I-dependent regulation of potassium channels by MAP kinases and PI3-kinase during eccentric cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2008; 295: H1834-H1845.
37. Oudit GY, Sun H, Kerfant BG, Crackower MA, Penninger JM, Backx PH. The role of phosphoinositide-3 kinase and PTEN in cardiovascular physiology and disease. J Mol Cell Cardiol. 2004; 37: 449-471.
38. Cantley LC. The phosphoinositide 3-kinase pathway. Science. 2002; 296: 1655-1657.
39. DeBosch B, Treskov I, Lupu TS, Weinheimer C, Kovacs A, Courtois M, et al. Akt1 is required for physiological cardiac growth. Circulation. 2006; 113: 2097-2104.
40. Shioi T, McMullen JR, Kang PM, Douglas PS, Obata T, Franke TF, et al. Akt/protein kinase B promotes organ growth in transgenic mice. Mol Cell Biol. 2002; 22: 2799-2809.
41. Heineke J, Molkentin JD. Regulation of cardiac hypertrophy by intracellular signaling pathways. Mol Cel Biol. 2006; 7: 589-600.
42. Kurdi M, Booz GW. Three 4-letter words of hypertension-related cardiac hypertrophy: TRPC, mTOR, and HDAC. J Mol Cell Cardiol. 2011; 50: 964-971.
43. Lim JY, Park SJ, Hwang HY, Park EJ, Nam JH, Kim J, et al. TGF-beta1 induces cardiac hypertrophic responses via PKC-dependent ATF-2 activation. J Mol Cell Cardiol. 2005; 39: 627-636.
44. Mariappan N, Soorappan RN, Haque M, Sriramula S, Francis J. TNF-alpha-induced mitochondrial oxidative stress and cardiac dysfunction: restoration by superoxide dismutase mimetic Tempol. Am J Physiol Heart Circ Physiol. 2007; 293: H2726-H2737.
45. Molkentin JD, Dorn GW 2nd. Cytoplasmic signaling pathways that regulate cardiac hypertrophy. Annu Rev Physiol. 2001; 63: 391-426.
46. Zhang P, Mende U. Regulators of G-protein signaling in the heart and their potential as therapeutic targets. Circ Res. 2011; 109: 320-333.
47. Fu Y, Xiao H, Zhang Y. Beta-adrenoceptor signaling pathways mediate cardiac pathological remodeling. Front Biosci. 2012; 4: 1625-1637.
48. Finckenberg P, Mervaala E. Novel regulators and drug targets of cardiac hypertrophy. J Hypertens. 2010; 1: S33-S38.
49. Juliano N, Wong SC, Naidu SS. Alcohol septal ablation for failed surgical myectomy. J Invasive Cardiol. 2005; 17: 569-571.
50. Teare D. Asymmetrical Hypertrophy of the heart in young adults. Br heart J. 1958; 20: 1-8.
51. Ommen SR, Maron BJ, Olivotto I, Maron MS, Cecchi F, Betocchi S, et al. Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 2005; 46: 470-476.
52. Brown ML, Schaff HV, Dearani JA, Li Z, Nishimura RA, Ommen SR. Relationship between left ventricular mass, wall thickness, and survival after subaortic septal myectomy for hypertrophic obstructive cardiomyopathy. J Thorac Cardiovasc Surg. 2011; 141: 439-443.
53. Prinz C, Hering D, Bitter T, Horstkotte D, Faber L. Left atrial size and left ventricular hypertrophy correlate with myocardial fibrosis in patients with hypertrophic cardiomyopathy. Acta Cardiol. 2011; 66:153-157.
54. Ralph-Edwards A, Woo A, McCrindle BW, Shapero JL, Schwartz L, Rakowski H, et al. Hypertrophic obstructive cardiomyopathy: comparison of outcomes after myectomy or alcohol ablation adjusted by propensity score. J Thorac Cardiovasc Surg. 2005; 129: 351-358.
55. Heldman AW, Wu KC, Abraham TP, Cameron DE. Myectomy or alcohol septal ablation surgery and percutaneous intervention go another round. J Am Coll Cardiol. 2007; 49: 358-360.
56. Alam M, Dokainish H, Lakkis N. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: a systematic review of published studies. J Interv Cardiol. 2006; 19: 319-327.
57. Gimeno JR, Tomé MT, McKenna WJ. Alcohol Septal Ablation in Hypertrophic Cardiomyopathy: An Opportunity to Be Taken. Rev Esp Cardiol. 2012; 65: 314-318.
2. Marian AJ. Genetic determinants of cardiac hypertrophy. Curr Opin Cardiol. 2008; 23: 199-205.
3. Kee HJ, Kook H. Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy. J Biomed Biotech. 2011; 2011: 928326.
4. Tikhonoff V, Casiglia E. Evolving concepts of left ventricular hypertrophy. Eur Heart J. 2008; 29: 846-848.
5. Ojamaa K. Signaling Mechanisms in Thyroid Hormone-Induced Cardiac Hypertrophy. Vascul Pharmacol. 2010; 52: 113-119.
6. Dillmann W. Cardiac hypertrophy and thyroid hormone signaling. Heart Fail Rev. 2010; 15: 125-132.
7. McMullen JR, Jennings GL. Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure. Clin Exp Pharmacol Physiol. 2007; 34: 255-262.
8. Buss SJ, Riffel JH, Malekar P, Hagenmueller M, Asel C, Zhang M, et al. Chronic Akt blockade aggravates pathological hypertrophy and inhibits physiological hypertrophy. Am J Physiol Heart Circ Physiol. 2012; 302: H420-H430.
9. Diwan A, Dorn GW. Decompensation of cardiac hypertrophy: cellular mechanisms and novel therapeutic targets. Physiology. 2007; 22: 56-64.
10. Oka T, Komuro I. Molecular mechanisms underlying the transition of cardiac hypertrophy to heart failure. Circ J. 2008; 72: A13-A16.
11. Soesanto W, Lin HY, Hu E, Lefler S, Litwin SE, Sena S, et al. Mammalian target of rapamycin is a critical regulator of cardiac hypertrophy in spontaneously hypertensive rats. Hypertension. 2009; 54: 1321-1327.
12. Balakumar P, Jagadeesh G. Multifarious molecular signaling cascades of cardiac hypertrophy: can the muddy waters be cleared. Pharmacol Res. 2010; 62: 365-383.
13. Aoyagi T, Matsui T. Phosphoinositide-3 kinase signaling in cardiac hypertrophy and heart failure. Curr Pharm Des. 2011; 17: 1818-1824.
14. Van Zwieten PA. The influence of antihypertensive drug treatment on the prevention and regression of left ventricular hypertrophy. Cardiovasc Res. 2000; 45: 82-91.
15. Liao Y, Asakura M, Takashima S, Ogai A, Asano Y, Shintani Y, et al. Celiprolol, a vasodilatory beta-blocker, inhibits pressure overload-induced cardiac hypertrophy and prevents the transition to heart failure via nitric oxide-dependent mechanisms in mice. Circulation 2004; 110: 692-629.
16. Horiba M, Muto T, Ueda N, Opthof T, Miwa K, Hojo M, et al. T-type Ca2+ channel blockers prevent cardiac cell hypertrophy through an inhibition of calcinurin-NFAT3 activation as well as L-type Ca2+ channel blockers. Life Sci. 2008; 82: 554-560.
17. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. 1975; 56: 56-64.
18. Pluim BM, Zwinderman AH, Van Der Laarse A, Van Der Wall EE. The athlete’s heart. A meta-analysis of cardiac structure and function. Circulation 2000; 101: 336-344.
19. Mone SM, Sanders SP, Colan SD. Control mechanisms for physiological hypertrophy of pregnancy. Circulation 1996; 94: 667-672.
20. Iemitsu M, Miyauchi T, Maeda S, Sakai S, Kobayashi T, Fujii N, et al. Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat. AJP - Regu Physiol. 2001; 281: R2029-R2036.
21. Sagara S, Osanai T, Itoh T, Izumiyama K, Shibutani S, Hanada K, et al. Over expression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by inhibiting PI3K/Akt signaling in mice. J Hypertension. 2012; 30: 778-786.
22. Zak R. Growth of the Heart in Health and Disease. Raven Press, New York. 1984.
23. Finsen AV, Lunde IG, Sjaastad I, Ostli EK, Lyngra M, Jarstadmarken HO, et al. Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcinurin-NFAT pathway. PLOS One. 2011; 6: e28302.
24. Usui S, Maejima Y, Pain J, Hong C, Cho J, Park JY, et al. Endogenous muscle atrophy F-box mediates pressure overload-induced cardiac hypertrophy through regulation of nuclear factor-kappa B. Circ Res. 2011; 109: 161-171.
25. Fagard RH. Impact of different sports and training on cardiac structure and function. Cardiol Clin. 1997; 15: 397-412.
26. Barry SP, Davidson SM, Townsend PA. Molecular regulation of cardiac hypertrophy. Int J Biochem. Cell Biol. 2008; 40: 2023-2039.
27. Rohini A, Agrawal N, Koyani CN, Singh R. Molecular targets and regulators of cardiac hypertrophy. Pharmacol Res. 2010; 61: 269-280.
28. Force T, Pombo CM, Avruch JA, Bonventre JV, Kyriakis JM. Stress-activated protein kinases in cardiovascular disease. Circ Res. 1996; 78: 947-953.
29. Carreno JE, Apablaza F, Ocaranza MP, Jalil JE. Cardiac hypertrophy: molecular and cellular events. Rev Esp Cardiol. 2006; 59: 473-486.
30. Wang Y, Huang S, Sah VP, Ross J Jr, Brown JH, Han J, Chien KR. Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. J Biol Chem. 1998; 273: 2161-2168.
31. Ramirez MT, Sah VP, Zhao XL, Hunter JJ, Chien KR, Brown JH. The MEKK-JNK pathway is stimulated by alpha1-adrenergic receptor and ras activation and is associated with in vitro and in vivo cardiac hypertrophy. J Biol Chem. 1997; 272: 14057-14061.
32. Dorn GW, Brown JH. Gq signaling in cardiac adaptation and maladaptation. Trends Cardiovasc Med. 1999; 9: 26-34.
33. Molkentin JD. Calcinurin-NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs. Cardiovasc Res. 2004; 63: 467-475.
34. Kim J, Wende AR, Sena S, Theobald HA, Soto J, Sloan C, et al. Insulin-like growth factor I receptor signaling is required for exercise-induced cardiac hypertrophy. Mol Endocrinol. 2008; 22: 2531-2543.
35. McMullen JR, Izumo S. Role of the insulin-like growth factor 1 (IGF1)/phosphoinositide-3-kinase (PI3K) pathway mediating physiological cardiac hypertrophy. Novartis Found Symp. 2006; 274: 90-111.
36. Teos LY, Zhao A, Alvin Z, Laurence GG, Li C, Haddad GE. Basal and IGF-I-dependent regulation of potassium channels by MAP kinases and PI3-kinase during eccentric cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2008; 295: H1834-H1845.
37. Oudit GY, Sun H, Kerfant BG, Crackower MA, Penninger JM, Backx PH. The role of phosphoinositide-3 kinase and PTEN in cardiovascular physiology and disease. J Mol Cell Cardiol. 2004; 37: 449-471.
38. Cantley LC. The phosphoinositide 3-kinase pathway. Science. 2002; 296: 1655-1657.
39. DeBosch B, Treskov I, Lupu TS, Weinheimer C, Kovacs A, Courtois M, et al. Akt1 is required for physiological cardiac growth. Circulation. 2006; 113: 2097-2104.
40. Shioi T, McMullen JR, Kang PM, Douglas PS, Obata T, Franke TF, et al. Akt/protein kinase B promotes organ growth in transgenic mice. Mol Cell Biol. 2002; 22: 2799-2809.
41. Heineke J, Molkentin JD. Regulation of cardiac hypertrophy by intracellular signaling pathways. Mol Cel Biol. 2006; 7: 589-600.
42. Kurdi M, Booz GW. Three 4-letter words of hypertension-related cardiac hypertrophy: TRPC, mTOR, and HDAC. J Mol Cell Cardiol. 2011; 50: 964-971.
43. Lim JY, Park SJ, Hwang HY, Park EJ, Nam JH, Kim J, et al. TGF-beta1 induces cardiac hypertrophic responses via PKC-dependent ATF-2 activation. J Mol Cell Cardiol. 2005; 39: 627-636.
44. Mariappan N, Soorappan RN, Haque M, Sriramula S, Francis J. TNF-alpha-induced mitochondrial oxidative stress and cardiac dysfunction: restoration by superoxide dismutase mimetic Tempol. Am J Physiol Heart Circ Physiol. 2007; 293: H2726-H2737.
45. Molkentin JD, Dorn GW 2nd. Cytoplasmic signaling pathways that regulate cardiac hypertrophy. Annu Rev Physiol. 2001; 63: 391-426.
46. Zhang P, Mende U. Regulators of G-protein signaling in the heart and their potential as therapeutic targets. Circ Res. 2011; 109: 320-333.
47. Fu Y, Xiao H, Zhang Y. Beta-adrenoceptor signaling pathways mediate cardiac pathological remodeling. Front Biosci. 2012; 4: 1625-1637.
48. Finckenberg P, Mervaala E. Novel regulators and drug targets of cardiac hypertrophy. J Hypertens. 2010; 1: S33-S38.
49. Juliano N, Wong SC, Naidu SS. Alcohol septal ablation for failed surgical myectomy. J Invasive Cardiol. 2005; 17: 569-571.
50. Teare D. Asymmetrical Hypertrophy of the heart in young adults. Br heart J. 1958; 20: 1-8.
51. Ommen SR, Maron BJ, Olivotto I, Maron MS, Cecchi F, Betocchi S, et al. Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 2005; 46: 470-476.
52. Brown ML, Schaff HV, Dearani JA, Li Z, Nishimura RA, Ommen SR. Relationship between left ventricular mass, wall thickness, and survival after subaortic septal myectomy for hypertrophic obstructive cardiomyopathy. J Thorac Cardiovasc Surg. 2011; 141: 439-443.
53. Prinz C, Hering D, Bitter T, Horstkotte D, Faber L. Left atrial size and left ventricular hypertrophy correlate with myocardial fibrosis in patients with hypertrophic cardiomyopathy. Acta Cardiol. 2011; 66:153-157.
54. Ralph-Edwards A, Woo A, McCrindle BW, Shapero JL, Schwartz L, Rakowski H, et al. Hypertrophic obstructive cardiomyopathy: comparison of outcomes after myectomy or alcohol ablation adjusted by propensity score. J Thorac Cardiovasc Surg. 2005; 129: 351-358.
55. Heldman AW, Wu KC, Abraham TP, Cameron DE. Myectomy or alcohol septal ablation surgery and percutaneous intervention go another round. J Am Coll Cardiol. 2007; 49: 358-360.
56. Alam M, Dokainish H, Lakkis N. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: a systematic review of published studies. J Interv Cardiol. 2006; 19: 319-327.
57. Gimeno JR, Tomé MT, McKenna WJ. Alcohol Septal Ablation in Hypertrophic Cardiomyopathy: An Opportunity to Be Taken. Rev Esp Cardiol. 2012; 65: 314-318.
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01-07-2012
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“CARDIAC HYPERTROPHY: A REVIEW ON PATHOGENESIS AND TREATMENT”. International Journal of Pharmaceutical Sciences and Drug Research, vol. 4, no. 3, July 2012, pp. 164-7, https://doi.org/10.25004/IJPSDR.2012.040301.
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How to Cite
“CARDIAC HYPERTROPHY: A REVIEW ON PATHOGENESIS AND TREATMENT”. International Journal of Pharmaceutical Sciences and Drug Research, vol. 4, no. 3, July 2012, pp. 164-7, https://doi.org/10.25004/IJPSDR.2012.040301.
