Evaluation of Cardiac Function by Transthoracic Echocardiography in Subjects with ST-Segment Elevation Myocardial Infarction Following Primary Percutaneous Coronary Intervention according to Valsartan Dose: The Valsartan One Center Trial
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Background: The aim of this study was to evaluate the mid-term changes in cardiac function by transthoracic echocardiogram (TTE) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) according to valsartan dose. Methods: Between April 2006 and February 2009, 78 subjects (mean age: 57 ± 12 years, M : F = 74 : 4) with STEMI who underwent primary PCI were enrolled. Fifty three patients received low dose valsartan (40 or 80 mg) and 25 patients received high dose valsartan (160 or 320 mg). Follow-up TTE was done approximately 2 years later. We evaluated the changes in left ventricular (LV) function between initial and final TTE after primary PCI and compared the changes between low and high dose valsartan group. Results: The mean follow-up TTE duration was 24 ± 8 months. Deceleration time (188.6 ± 56.3 msec vs. 221.5 ± 71.3msec, p = 0.01), E/e’ (12.24 ± 5.2 vs. 10.1 ± 4.9, p = 0.002), ejection fraction (52.7 ± 8% vs. 55.2 ± 8.4%, p < 0.01), and wall motion score index (1.45 ± 0.30 vs. 1.33 ± 0.32, p < 0.01) showed significant changes during the follow-up period. Wall motion improvement in injured myocardial segments was more frequently observed in the high-dose valsartan group compared to the low-dose group [18/25 (72%) vs. 24/53 (43.7%), p = 0.03]. There was no significant difference in the changes in cardiac dimensions and function between the low and high dose valsartan group. Conclusion: In patients with STEMI who undergoing primary PCI, high-dose valsartan treatment may be more helpful than low-dose in improving wall motion in the injured myocardium.
Abstract
Background: The aim of this study was to evaluate the mid-term changes in cardiac function by transthoracic echocardiogram (TTE) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) according to valsartan dose. Methods: Between April 2006 and February 2009, 78 subjects (mean age: 57 ± 12 years, M : F = 74 : 4) with STEMI who underwent primary PCI were enrolled. Fifty three patients received low dose valsartan (40 or 80 mg) and 25 patients received high dose valsartan (160 or 320 mg). Follow-up TTE was done approximately 2 years later. We evaluated the changes in left ventricular (LV) function between initial and final TTE after primary PCI and compared the changes between low and high dose valsartan group. Results: The mean follow-up TTE duration was 24 ± 8 months. Deceleration time (188.6 ± 56.3 msec vs. 221.5 ± 71.3msec, p = 0.01), E/e’ (12.24 ± 5.2 vs. 10.1 ± 4.9, p = 0.002), ejection fraction (52.7 ± 8% vs. 55.2 ± 8.4%, p < 0.01), and wall motion score index (1.45 ± 0.30 vs. 1.33 ± 0.32, p < 0.01) showed significant changes during the follow-up period. Wall motion improvement in injured myocardial segments was more frequently observed in the high-dose valsartan group compared to the low-dose group [18/25 (72%) vs. 24/53 (43.7%), p = 0.03]. There was no significant difference in the changes in cardiac dimensions and function between the low and high dose valsartan group. Conclusion: In patients with STEMI who undergoing primary PCI, high-dose valsartan treatment may be more helpful than low-dose in improving wall motion in the injured myocardium.
참고문헌 (23)
- Pfeffer MA, "Ventricular remodeling after myocardial infarction, Experimental observations and clinical implications", Circulation, 81, pp.1161~1172 (1990)
- St John Sutton M, "Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril", Circulation, 89, pp.68~75 (1994)
- Francis GS, "Pathophysiology of chronic heart failure", Am J Med, 110(Suppl 7A), pp.37S~46S (2001)
- Gaudron P, "Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors", Circulation, 87, pp.755~763 (1993)
- Pfeffer MA, "Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators", N Engl J Med, 327, pp.669~677 (1992)
- Harada K, "Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction", Circulation, 100, pp.2093~2099 (1999)
- Patel AR, "Recent advances in the treatment of heart failure", Circ J, 66, pp.117~121 (2002)
- Dickstein K, "OPTIMAAL Steering Committee of the OPTIMAAL Study Group. Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the OPTIMAAL randomised trial. Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan", Lancet, 360, pp.752~760 (2002)
- Pfeffer MA, "Valsartan in Acute Myocardial Infarction Trial Investigators. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both", N Engl J Med, 349, pp.1893~1906 (2003)
- Kim YS, "Changes in LV mass, LV morphology and diastolic function of LV in response to antihypertensive treatment", J Korean Soc Echocardiogr, 5, pp.154~163 (1997)
- Tani S, "Effects of enalapril and losartan in left ventricular remodeling after acute myocardial infarction: a possible mechanism of prevention of cardiac events by angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high-risk myocardial infarction", Intern Med, 48, pp.877~882 (2009)
- ISIS-4, "a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction", Lancet, 345, pp.669~685 (1995), ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group
- GISSI-3, "effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction. Gruppo Italiano per lo Studio della Sopravvivenza nell’infarto Miocardico", Lancet, 343, pp.1115~11122 (1994)
- Solomon SD, "Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction", Circulation, 111, pp.3411~3419 (2005)
- Rim SJ, "Dobutamine echocardiography in the prediction of left ventricular remodeling after acute myocardial infarction", J Korean Soc Echocardiogr, 5, pp.85~93 (1997)
- Frangogiannis NG, "The inflammatory response in myocardial infarction", Cardiovasc Res, 53, pp.31~47 (2002)
- Anzai T, "C-reactive protein as a predictor of infarct expansion and cardiac rupture after a first Q-wave acute myocardial infarction", Circulation, 96, pp.778~784 (1997)
- Maekawa Y, "Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction", J Am Coll Cardiol, 44, pp.1510~1520 (2004)
- Kumar AG, "Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium", Circulation, 95, pp.693~700 (1997)
- Hayasaki T, "CC chemokine receptor-2 deficiency attenuates oxidative stress and infarct size caused by myocardial ischemia-reperfusion in mice", Circ J, 70, pp.342~351 (2006)
- Hayashidani S, "Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction", Circulation, 108, pp.2134~2140 (2003)
- Dewald O, "CCL2", Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts, 2005, pp.96, 881~889
- Kohno T, "Angiotensin-receptor blockade reduces border zone myocardial monocyte chemoattractant protein-1 expression and macrophage infiltration in post-infarction ventricular remodeling", Circ J, 72, pp.1685~1692 (2008)