González-Márquez TN, López-Quijano JM, Carrillo-Calvillo J, Leiva- Pons JL, Mejía-Argüelles O

Language: Spanish
References: 15
Page: 634-638
PDF size: 794.85 Kb.

ABSTRACT

In patients admitted for ACS (acute coronary syndrome) usually only a coronary lesion is the cause of the symptoms; however, many broken or unstable plaques have been observed in patients presenting or die by ACS. We report the case of a 68-year-old male patient admitted to our hospital with the diagnosis of ST segment elevation ACS in anterior segments not reperfused. In Intensive Cardiovascular Unit Care, the patient underwent hemodynamic stability without recurrence of angina; in electrocardiographic monitoring was observed subepicardial lesion in the inferior segment without clinical expression. Angiography reported anterior descending artery with an important proximal eccentric lesion and proximal ulcerated lesion in right coronary artery; a stent was placed in both arteries with a TIMI 3 flow as a final result. The patient evolved without complications and was discharged to continue outpatient handling. This case exemplifies the utility of electrocardiographic monitoring in patients with ACS, also demonstrates coexistence of multiple vulnerable plaques.

REFERENCES

1. Akkerhuis KM, Klootwijk PA, Lindeboom W, Umans M, et al. Recurrent ischaemia during continuous multilead ST-segment monitoring identifies patients with acute coronary síndromes at high risk of adverse cardiac events. Eur Heart J 2001;22:1997-2006.

2. Morrison LJ, Brooks S, Sawadsky B, et al. Prehospital 12-lead electrocardiography impact on acute myocardial infarction treatment times and mortality: A systematic review. Acad Emerg Med 2006:13:84.

3. Holmvang L, Andersen K, Dellborg M, et al. Relative contributions of a single-admission 12-lead electrocardiogram and early 24 hour continuous electrocardiographic monitoring for early risk stratification in patients with unstable coronary artery disease. Am J Cardiol 1999;83:667-674.

4. Buffon A, Biasicci L, Liuzzo G, et al. Widespread coronary inflammation in unstable angina. N Engl J Med 2002;346:2047-2052.

5. Masanori A, Yasunori U, et al. Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: An angioscopic study. J Am Coll Cardiol 2001;37:1284-1288.

6. Gaxiola E. Detección y tratamiento de la placa vulnerable. Arch Cardiol Méx 2007;77:S4,178-184.

7. Falk E. Pathogenesis of atherosclerosis. J Am Coll Cardiol 2006;47:C7-C12.

8. Bonow RO, Mann DL, Zipes DP, et al. Braunwald’s Heart Disease: A textbook of cardiovascular medicine. 9th ed. Philadelphia: Elsevier Saunders, 2011.

9. Libby P. Inflammation in atherosclerosis. Nature 2002;420:868-874.

10. Berry C, L’Allier PL, Grégoire J, Tardif JC. Comparison of intravascular ultrasound and quantitative coronary angiography for the assessment of coronary artery disease progression. Circulation 2007;115:1851.

11. Rishi P, Worthely M, Nicholis SP. Intravascular imaging of vulnerable coronary plaque: current and future concepts. Nat Rev Cardiol 2011;8:131-139.

12. Barlis P, Serruys PW, Devries A, Regar E. Optical coherence tomography assessment of vulnerable plaque rupture: Predilection for the plaque ‘shoulder’. Eur Heart J 2008;29:2023.

13. Achenbach S. Can CT detect the vulnerable coronary plaque? Int J Cardiovasc Imaging 2008;24:311.

14. Mauriello A, Sangiorgi G, Fratoni S, Palmieri G, Bonanno E, et al. Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree. J Am Coll Cardiol 2005;45:1585-1593.

15. Ramcharitar S, Gonzalo N, Jan Van Geuns R, Garcia H, et al. First case of stenting of a vulnerable plaque in the SECRITT I trial- the dawn of a new era? Nat Rev Cardiol 2009;6:374-378.