J Cardiovasc Ultrasound.  2010 Sep;18(3):77-83. 10.4250/jcu.2010.18.3.77.

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

• Kim SS
• Jeon HK
• Cho GM
• Lee JH
• Kim SJ
• Park MY
• Lee SJ
• Shim BJ
• Lee DH
• Shin WS
• Lee JM
• Youn HJ

• KMID: 2177303
• DOI: http://doi.org/10.4250/jcu.2010.18.3.77

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 +/- 71.3 msec, 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.

Keyword

Angiotensin II type 1 receptor blockers; Percutaneous transluminal coronary angioplasty; Myocardial infarction

MeSH Terms

Angioplasty, Balloon, Coronary
Angiotensin II Type 1 Receptor Blockers
Deceleration
Echocardiography
Follow-Up Studies
Humans
Myocardial Infarction
Myocardium
Percutaneous Coronary Intervention
Tetrazoles
Valine
Valsartan
Angiotensin II Type 1 Receptor Blockers
Tetrazoles
Valine

Figure

• 

  Fig. 1 Study design. STEMI: ST-segment elevation myocardial infarction, PCI: percutaneous coronary intervention, BP: blood pressure, TTE: transthoracic echocardiography.

• 

  Fig. 2 Comparison of the percent of patients according to improvement of wall motion in the injured myocardium between low- and high-dose valsartan groups

Reference

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

2. St John Sutton M, Pfeffer MA, Plappert T, Rouleau JL, Moyé LA, Dagenais GR, Lamas GA, Klein M, Sussex B, Goldman S, et al. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril. Circulation. 1994. 89:68–75.

3. Francis GS. Pathophysiology of chronic heart failure. Am J Med. 2001. 110:Suppl 7A. 37S–46S.

4. Gaudron P, Eilles C, Kugler I, Ertl G. Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors. Circulation. 1993. 87:755–763.

5. Pfeffer MA, Braunwald E, Moyé LA, Basta L, Brown EJ Jr, Cuddy TE, Davis BR, Geltman EM, Goldman S, Flaker GC, et al. The SAVE Investigators. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. N Engl J Med. 1992. 327:669–677.

6. Harada K, Sugaya T, Murakami K, Yazaki Y, Komuro I. Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction. Circulation. 1999. 100:2093–2099.

7. Patel AR, Konstam MA. Recent advances in the treatment of heart failure. Circ J. 2002. 66:117–121.

8. Dickstein K, Kjekshus J. 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. 2002. 360:752–760.

9. Pfeffer MA, McMurray JJ, Velazquez EJ, Rouleau JL, Køber L, Maggioni AP, Solomon SD, Swedberg K, Van de Werf F, White H, Leimberger JD, Henis M, Edwards S, Zelenkofske S, Sellers MA, Califf RM. 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. 2003. 349:1893–1906.

10. Kim YS, Cho HK, Chung IM, Park SH, Park SH, Shin GJ. Changes in LV mass, LV morphology and diastolic function of LV in response to antihypertensive treatment. J Korean Soc Echocardiogr. 1997. 5:154–163.

11. Tani S, Nagao K, Anazawa T, Kawamata H, Furuya S, Takahashi H, Iida K, Matsumoto M, Kumabe N, Onikura M, Hirayama A. 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. 2009. 48:877–882.

12. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. 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. 1995. 345:669–685.

13. Gruppo Italiano per lo Studio della Sopravvivenza nell'infarto Miocardico. GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction. Lancet. 1994. 343:1115–1122.

14. Solomon SD, Skali H, Anavekar NS, Bourgoun M, Barvik S, Ghali JK, Warnica JW, Khrakovskaya M, Arnold JM, Schwartz Y, Velazquez EJ, Califf RM, McMurray JV, Pfeffer MA. Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction. Circulation. 2005. 111:3411–3419.

15. Rim SJ, Chung NS, Lee NH, Goh CW, Ha JW, Kim JY, Oh EK, Ahn SK, Kim TY, Lee MH, Jang YS, Shim WH, Cho SY, Kim SS. Dobutamine echocardiography in the prediction of left ventricular remodeling after acute myocardial infarction. J Korean Soc Echocardiogr. 1997. 5:85–93.

16. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res. 2002. 53:31–47.

17. Anzai T, Yoshikawa T, Shiraki H, Asakura Y, Akaishi M, Mitamura H, Ogawa S. C-reactive protein as a predictor of infarct expansion and cardiac rupture after a first Q-wave acute myocardial infarction. Circulation. 1997. 96:778–784.

18. Maekawa Y, Anzai T, Yoshikawa T, Sugano Y, Mahara K, Kohno T, Takahashi T, Ogawa S. Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction. J Am Coll Cardiol. 2004. 44:1510–1520.

19. Kumar AG, Ballantyne CM, Michael LH, Kukielka GL, Youker KA, Lindsey ML, Hawkins HK, Birdsall HH, MacKay CR, LaRosa GJ, Rossen RD, Smith CW, Entman ML. Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. Circulation. 1997. 95:693–700.

20. Hayasaki T, Kaikita K, Okuma T, Yamamoto E, Kuziel WA, Ogawa H, Takeya M. CC chemokine receptor-2 deficiency attenuates oxidative stress and infarct size caused by myocardial ischemia-reperfusion in mice. Circ J. 2006. 70:342–351.

21. Hayashidani S, Tsutsui H, Shiomi T, Ikeuchi M, Matsusaka H, Suematsu N, Wen J, Egashira K, Takeshita A. Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation. 2003. 108:2134–2140.

22. Dewald O, Zymek P, Winkelmann K, Koerting A, Ren G, Abou-Khamis T, Michael LH, Rollins BJ, Entman ML, Frangogiannis NG. CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts. Circ Res. 2005. 96:881–889.

23. Kohno T, Anzai T, Naito K, Sugano Y, Maekawa Y, Takahashi T, Yoshikawa T, Ogawa S. Angiotensin-receptor blockade reduces border zone myocardial monocyte chemoattractant protein-1 expression and macrophage infiltration in post-infarction ventricular remodeling. Circ J. 2008. 72:1685–1692.