Juonala M, Jarvisalo MJ, Maki-Torkko N, et al.: Risk factors identified in childhood and decreased carotid artery elasticity in adulthood. Juonola M, Viikari J, Rasanen L, et al.: Young adults with family history of coronary heart disease have increased arterial vulnerability to metabolic risk factors. Jomini V, Oppliger-Pasquali S, Wietlisbach V, et al.: Combination of major cardiovascular risk factors to familial premature coronary artery disease. Schiff I, Bell WR, Davis V, et al.: Oral contraceptives and smoking current recommendations of a consensus panel. Evidence of reduced coronary flow in spite of normal coronary arteries. N Engl J Med 2003, 349:2407вЂ“2415.Д®ngel H, Hundershagen H, Lichtlen P: Transmural myocardial infarction in young women taking oral contraceptives. J Am Coll Cardiol 2007, 50:e1вЂ“e157.ДЄsanuma Y, Oeser A, Shintani A, et al.: Premature coronary artery atherosclerosis in systemic lupus erythematosus. Clin Rheumatol 2007, 26:695вЂ“699.ДЄnderson JL, Adams C, Antman EM, et al.: ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. Karadag O, Calquneri M, Atalar E, et al.: Novel cardiovascular risk factors and cardiac event predictors in female inactive lupus erythematosus patients. Goldstein JL, Brown MS: Regulation of low density lipoprotein receptors: implications for pathogenesis and therapy for hypercholesterolemia and atherosclerosis. Trans Am Climatol Assoc 2004, 115:99вЂ“114.Д«arton M, Dubez R, Traupe T, et al.: Oral contraceptives and the risk of thrombosis and atherosclerosis. Woodward Award: cardiovascular complications of cocaine abuse. Lange R, Cigarroa J, Hills D, et al.: Theodore E. Michos E, Vasamreddy C, Becker D, et al.: Women with a low Framingham risk score and a family history of premature coronary heart disease have a high prevalence of subclinical atherosclerosis. Wilson PW, DвЂ™Agostino RB, Levy D, et al.: Prediction of coronary heart disease using risk factor categories. A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Rosamond W, Flegal K, Furie K, et al.: Heart disease and stroke statistics 2008 update. The confirmation and replication of these associations through further study will lead to earlier detection of P-CAD in at-risk patients and a better understanding of the underlying pathologic mechanisms, thereby influencing the development of preventive therapies. The chromosome 9p21.3 locus, which is the most replicated to date, has provided some insight into the pathologic mechanism of coronary disease. With the use of genome-wide association analysis, several chromosome loci have been identified as being linked to the development of coronary atherosclerosis and risk factors. Patients with primary P-CAD usually have a family history of coronary disease, suggesting a strong genetic component. Most cases of P-CAD, however, are the result of primary causes involving more complex interactions among genetic, metabolic, and environmental risk factors. It is important to evaluate young patients for acquired P-CAD because in many instances treatment may be tailored to the underlying medical condition. Acquired P-CAD is associated with an underlying medical condition or influencing factor, such as systemic lupus erythematosus or cocaine use, that directly contributes to the rapid progression of coronary atherosclerosis. P-CAD refers to the accelerated development of coronary atherosclerosis before age 55 in men and 65 in women, which may be the result of acquired or primary causes. In identifying patients at risk for a cardiovascular event, global risk models often fail to assess family history, an important risk factor in patients with premature coronary artery disease (P-CAD).

Although cardiovascular disease is commonly recognized as a disease of the elderly, young patients are also at risk for coronary atherosclerosis, which has a devastating impact on their more active lifestyle.

How to use pcad 2006 reports