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Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis
International Journal of Cardiology 119 (2007) 124 – 125 www.elsevier.com/locate/ijcard
Letter to the Editor
Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis Hasan Turhan ⁎, Yuksel Aksoy, Ertan Yetkin, Feridun Kosar Inonu University Medical Faculty, Department of Cardiology, Malatya, Turkey Received 16 March 2006; accepted 15 July 2006 Available online 16 October 2006
Keywords: Ventricular remodeling; Myocardial infarction; Collagen homeostasis
Dear Editor, Ventricular remodeling following myocardial infarction, characterized by detrimental changes on ventricular size, shape and function, is considered to be one of the most powerful predictors of adverse outcomes after myocardial infarction [1,2]. Recently, McGavigan et al. [3] have evaluated the role of impaired collagen homeostasis in predicting the development of early ventricular remodeling following acute myocardial infarction. Fifty-one patients with acute myocardial infarction have been included in this study. Twenty-three of these patients had normal left ventricular wall motion index and 28 have had abnormal wall motion index. C-propeptide for type-I collagen (PICP) and C-telopeptide for type-I collagen (CITP) have been measured as the markers of collagen synthesis and degradation, respectively. Patients who manifested early left ventricular remodeling following acute myocardial infarction have increased degradation and reduced synthesis of collagen, favoring net collagen breakdown. Both groups with normal and abnormal wall motion index have shown to have increased in PICP and CITP over time. However mean admission of CITP levels, indicating collagen degradation, has been detected to be significantly higher in patients with abnormal wall motion index. In contrary, admission of PICP levels, indicating collagen synthesis, has been shown to be significantly lower in abnormal wall motion index group. In addition admission of CITP levels had a positive correlation with wall motion index. CITP N 3.2 ng/ml has been reported to ⁎ Corresponding author. Tel.: +90 422 3410660/4503. E-mail address: [email protected] (H. Turhan). 0167-5273/$ - see front matter © 2006 Published by Elsevier Ireland Ltd. doi:10.1016/j.ijcard.2006.07.101
have 74% positive predictive value and 65% negative predictive value for abnormal wall motion index. It has been well established that matrix metalloproteinases play a significant role in collagen degradation, cardiac extracellular matrix remodeling and subsequent development of ventricular dysfunction [4–6]. Previously, Matsunaga et al. [7] and Nakaya et al. [8] have evaluated the impact of matrix metalloproteinases on the development of ventricular remodeling following myocardial infarction. They have suggested that matrix metalloproteinase-2 is likely to play role in ventricular remodeling following acute myocardial infarction. Moreover, Nakaya et al. [8] have also shown the beneficial effects of provastatin in preventing ventricular remodeling by decreasing the levels of matrix metalloproteinase-2. Recently, Zhou et al. [9] have reported that phenytoin can attenuate the adverse ventricular remodeling after myocardial infarction in rat, possibly by facilitating and strengthen extracellular matrix deposition. The findings of McGavigan et al. [3] may be considered to be compatible with these previously reported data. Although the subject of McGavigan et al.'s [3] article is original and the obtained data are exciting, there a some methodologic weaknesses, limiting the reliability of the findings. The most important one is the heterogeneous study groups regarding the localization of myocardial infarction. It is reasonable to observe abnormal wall motion index, prominent ventricular remodeling and higher CITP levels after extensive anterior myocardial infarction compared with inferior myocardial infarction with limited infarct size. The second issue is the definition of first group as having normal wall motion index. All patients included within this group have been reported to have acute myocardial infarction (78%
H. Turhan et al. / International Journal of Cardiology 119 (2007) 124–125
inferior myocardial infarction, 18% anterior myocardial infarction and 4% left bundle branch block) and the CK levels are comparable with the abnormal wall motion index group. Theoretically, it is not possible to see normal wall motion index in all patients included in this group. Nevertheless, altered collagen homeostasis seems to be a potential explanation and its serum markers as CITP and PICP are likely the predictors of early ventricular remodeling following acute myocardial infarction. Further studies including larger series and more homogeneous groups (including only patients with anterior myocardial infarction) should be performed to well establish this association. References [1] Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation 1990;81:1161–72.
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[2] Mahon NG, O'rorke C, Codd MB, McCann HA, McGarry K, Sugrue DD. Hospital mortality of acute myocardial infarction in the thrombolytic era. Heart 1999;81:478–82. [3] McGavigan AD, Maxwell PR, Dunn FG. Serological evidence of altered collagen homeostasis reflects early ventricular remodeling following acute myocardial infarction. Int J Cardiol 2006;111:267–74. [4] Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002;53:31–47. [5] Creemers EE, Cleutjens JP, Smits JF, Daemen MJ. Matrix metalloproteinase inhibition after myocardial infarction: a new approach to prevent heart failure? Circ Res 2001;89:201–10. [6] Birkedal-Hansen H, Moore WG, Bodden MK, et al. Matrix metalloproteinases: a review. Crit Rev Oral Biol Med 1993;4:197–250. [7] Matsunaga T, Abe N, Kameda K, et al. Circulating level of gelatinase activity predicts ventricular remodeling in patients with acute myocardial infarction. Int J Cardiol 2005;105:203–8. [8] Nakaya R, Uzui H, Shimizu H, et al. Pravastatin suppresses the increase in matrix metalloproteinase-2 levels after acute myocardial infarction. Int J Cardiol 2005;105:67–73. [9] Zhou X, Li YM, Ji WJ, et al. Phenytoin can accelerate the healing process after experimental myocardial infarction? Int J Cardiol 2006;107:21–9.
Letter to the Editor
Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis Hasan Turhan ⁎, Yuksel Aksoy, Ertan Yetkin, Feridun Kosar Inonu University Medical Faculty, Department of Cardiology, Malatya, Turkey Received 16 March 2006; accepted 15 July 2006 Available online 16 October 2006
Keywords: Ventricular remodeling; Myocardial infarction; Collagen homeostasis
Dear Editor, Ventricular remodeling following myocardial infarction, characterized by detrimental changes on ventricular size, shape and function, is considered to be one of the most powerful predictors of adverse outcomes after myocardial infarction [1,2]. Recently, McGavigan et al. [3] have evaluated the role of impaired collagen homeostasis in predicting the development of early ventricular remodeling following acute myocardial infarction. Fifty-one patients with acute myocardial infarction have been included in this study. Twenty-three of these patients had normal left ventricular wall motion index and 28 have had abnormal wall motion index. C-propeptide for type-I collagen (PICP) and C-telopeptide for type-I collagen (CITP) have been measured as the markers of collagen synthesis and degradation, respectively. Patients who manifested early left ventricular remodeling following acute myocardial infarction have increased degradation and reduced synthesis of collagen, favoring net collagen breakdown. Both groups with normal and abnormal wall motion index have shown to have increased in PICP and CITP over time. However mean admission of CITP levels, indicating collagen degradation, has been detected to be significantly higher in patients with abnormal wall motion index. In contrary, admission of PICP levels, indicating collagen synthesis, has been shown to be significantly lower in abnormal wall motion index group. In addition admission of CITP levels had a positive correlation with wall motion index. CITP N 3.2 ng/ml has been reported to ⁎ Corresponding author. Tel.: +90 422 3410660/4503. E-mail address: [email protected] (H. Turhan). 0167-5273/$ - see front matter © 2006 Published by Elsevier Ireland Ltd. doi:10.1016/j.ijcard.2006.07.101
have 74% positive predictive value and 65% negative predictive value for abnormal wall motion index. It has been well established that matrix metalloproteinases play a significant role in collagen degradation, cardiac extracellular matrix remodeling and subsequent development of ventricular dysfunction [4–6]. Previously, Matsunaga et al. [7] and Nakaya et al. [8] have evaluated the impact of matrix metalloproteinases on the development of ventricular remodeling following myocardial infarction. They have suggested that matrix metalloproteinase-2 is likely to play role in ventricular remodeling following acute myocardial infarction. Moreover, Nakaya et al. [8] have also shown the beneficial effects of provastatin in preventing ventricular remodeling by decreasing the levels of matrix metalloproteinase-2. Recently, Zhou et al. [9] have reported that phenytoin can attenuate the adverse ventricular remodeling after myocardial infarction in rat, possibly by facilitating and strengthen extracellular matrix deposition. The findings of McGavigan et al. [3] may be considered to be compatible with these previously reported data. Although the subject of McGavigan et al.'s [3] article is original and the obtained data are exciting, there a some methodologic weaknesses, limiting the reliability of the findings. The most important one is the heterogeneous study groups regarding the localization of myocardial infarction. It is reasonable to observe abnormal wall motion index, prominent ventricular remodeling and higher CITP levels after extensive anterior myocardial infarction compared with inferior myocardial infarction with limited infarct size. The second issue is the definition of first group as having normal wall motion index. All patients included within this group have been reported to have acute myocardial infarction (78%
H. Turhan et al. / International Journal of Cardiology 119 (2007) 124–125
inferior myocardial infarction, 18% anterior myocardial infarction and 4% left bundle branch block) and the CK levels are comparable with the abnormal wall motion index group. Theoretically, it is not possible to see normal wall motion index in all patients included in this group. Nevertheless, altered collagen homeostasis seems to be a potential explanation and its serum markers as CITP and PICP are likely the predictors of early ventricular remodeling following acute myocardial infarction. Further studies including larger series and more homogeneous groups (including only patients with anterior myocardial infarction) should be performed to well establish this association. References [1] Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation 1990;81:1161–72.
125
[2] Mahon NG, O'rorke C, Codd MB, McCann HA, McGarry K, Sugrue DD. Hospital mortality of acute myocardial infarction in the thrombolytic era. Heart 1999;81:478–82. [3] McGavigan AD, Maxwell PR, Dunn FG. Serological evidence of altered collagen homeostasis reflects early ventricular remodeling following acute myocardial infarction. Int J Cardiol 2006;111:267–74. [4] Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002;53:31–47. [5] Creemers EE, Cleutjens JP, Smits JF, Daemen MJ. Matrix metalloproteinase inhibition after myocardial infarction: a new approach to prevent heart failure? Circ Res 2001;89:201–10. [6] Birkedal-Hansen H, Moore WG, Bodden MK, et al. Matrix metalloproteinases: a review. Crit Rev Oral Biol Med 1993;4:197–250. [7] Matsunaga T, Abe N, Kameda K, et al. Circulating level of gelatinase activity predicts ventricular remodeling in patients with acute myocardial infarction. Int J Cardiol 2005;105:203–8. [8] Nakaya R, Uzui H, Shimizu H, et al. Pravastatin suppresses the increase in matrix metalloproteinase-2 levels after acute myocardial infarction. Int J Cardiol 2005;105:67–73. [9] Zhou X, Li YM, Ji WJ, et al. Phenytoin can accelerate the healing process after experimental myocardial infarction? Int J Cardiol 2006;107:21–9.