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Precocious virulent coronary atherosclerosis in the very young

Published online by Cambridge University Press:  31 August 2011

Robert Chait*
Affiliation:
Internal Medicine and Cardiology, JFK Medical Center, Miller School of Medicine, University of Miami, Atlantis, Florida, United States of America
Rajesh Ramineni*
Affiliation:
Internal Medicine and Cardiology, University of Texas Galveston, Galveston, Texas, United States of America
Erin A. Fender
Affiliation:
Internal Medicine, School of Medicine, University of Miami, Miami, Florida, United States of America
*
Correspondence to: Dr R. Chait, MD, 2413 Embassy Drive, West Palm Beach, Florida 33401, United States of America. Tel: 561 301 4633, Fax: 561 478 9505; E-mail: [email protected]

Abstract

Background

The incidence of Myocardial Infarction (MI) in patients under the age of 30 has been rarely addressed. Moreover, it is not understood why these patients develop symptomatic Coronary Artery Disease (CAD) at such an early age. Traditional risk factor assessment has not been successful in identifying these patients before they present with MI.

Methods

Retrospective, single cohort, observational study of 14,704 cardiac catheterizations performed in a community hospital between January 2006–January 2010 identified 12 cases age <30 with MI secondary to a fixed atherosclerotic lesion requiring angioplasty and stenting. The angiograms and charts were reviewed to assess the incidence and frequency of traditional risk factors such as smoking, dyslipidemia and diabetes and family history.

Results

All the patients had single vessel disease. Many of the patients were noted to have traditional CAD risk factors. 2 patients had an intervention and then months later sustained another acute MI secondary to a new culprit lesion despite aggressive risk factor modification.

Conclusion

Evaluating patients for premature CAD by screening for traditional risk factors has not effectively identified at risk patients prior to presentation with MI. There is a role for studies evaluating new and novel risk factors and imaging modalities so that these patients can be identified prior to experiencing MI.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2011

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References

1.Heron, M, Hoyert, DL, Murphy, SL, Xu, J, Kochanek, KD, Tejada-Betzaida, B. Deaths: final data for 2006. Natl Vital Stat Rep 2009; 57: 1134.Google ScholarPubMed
2.Eagle, KM, Ginsburg, GS, Musunuru, K, et al. Identifying patients at high risk of a cardiovascular event in the near future Current status and future directions: report of a National Heart, Lung and Blood Institute worining group. Circ 2010; 121: 14471454.CrossRefGoogle ScholarPubMed
3.Doughty, M, Mehta, R, Bruckman, D, et al. Acute myocardial infarction in the young – the University of Michigan experience. Am Heart J 2002; 143: 5662.CrossRefGoogle Scholar
4.Holman, RL, McGill, HC Jr, Strong, JP, Greer, JC. Observations on the natural history of atherosclerosis. J La State Med Soc 1958; 110: 361369.Google ScholarPubMed
5.Joseph, A, Ackerman, D, Talley, JD, Johnstone, J, Kupersmith, J. Manifestations of coronary atherosclerosis in young trauma victims – an autopsy study. J Am Coll Cardiol 1993; 22: 459467.CrossRefGoogle ScholarPubMed
6.Lange, R, Hillis, L. Cardiovascular complications of cocaine use. NEJM 2001; 345: 351359.CrossRefGoogle ScholarPubMed
7.Kolodgie, FD, Virmani, R, Cornhill, JF, Herderick, EE, Smialek Kolodgie, J. Increase in atherosclerosis and adventitial mast cells in cocaine abusers: an alternative mechanism of cocaine-associated coronary vasospasm and thrombosis. J Am Coll Cardiol 1991; 17: 15531560.CrossRefGoogle ScholarPubMed
8.Schoenenberger, AW, Radovanovic, D, Stauffer, JC, et al. Acute coronary syndromes in young patients: presentation, treatment and outcome. Int J Cardiol 2011; 148: 300304.CrossRefGoogle ScholarPubMed
9.Cohn, JN, Duprez, DA, Grandits, GA. Arterial elasticity as part of a comprehensive assessment of cardiovascular risk and drug treatment. Hypertension 2005; 46: 217220.CrossRefGoogle ScholarPubMed
10.Kaufmann, BA, Sanders, JM, Davis, C, et al. Molecular imaging of inflammation in atherosclerosis with targeted ultrasound detection of vascular cell adhesion molecule-1. Circulation 2007; 116: 276284.CrossRefGoogle Scholar
11.Tahara, N, Hisashi, K, Hiroyuki, N, et al. The prevalence of inflammation in carotid atherosclerosis: analysis with fluorodeoxyglucose-positron emission tomography. Eur Heart J 2007; 28: 22432248.CrossRefGoogle Scholar
12.Kaul, S, Lindner, JR. Visualizing coronary atherosclerosis in vivo: thinking big, imaging small. J Am Coll Cardiol 2004; 43: 461463.CrossRefGoogle ScholarPubMed
13.Roberts, R. Genetics of premature myocardial infarction. Curr Atheroscler Rep 2008; 10: 186193.CrossRefGoogle ScholarPubMed
14.Abdullah, KG. Phenotypes, genotypes, and the 9p21 locus for prediction of cardiovascular events. JACC Cardiovasc Interv 2010; 3: 260261.CrossRefGoogle ScholarPubMed
15.Yabushita, H, Bouma, BE, Houser, SL, et al. Characterization of human atherosclerosis by optical coherence tomography. Circulation 2002; 106: 16401645.CrossRefGoogle ScholarPubMed
16.de Kleijn, DPV, Moll, FL, Hellings, HE. Local atherosclerotic plaques are a source of prognostic biomarkers for adverse cardiovascular events. Arterioscler Thromb Vasc Biol 2010; 30: 612619.CrossRefGoogle ScholarPubMed