OBJECTIVES: This study was designed to assess the prevalence of major cardiovascular risk factors in familial premature coronary artery disease (P-CAD), affecting two or more siblings within one sibship. BACKGROUND: Premature CAD has a genetic component. It remains to be established whether familial P-CAD is due to genes acting independently from major cardiovascular risk factors. METHODS: We recruited 213 P-CAD survivors from 103 sibships diagnosed before age <or=50 (men) or <or=55 (women) years old. Hypertension, hypercholesterolemia, obesity, and smoking were documented at the time of the event in 163 patients (145 men and 18 women). Each patient was compared with two individuals of the same age and gender, diagnosed with sporadic (nonfamilial) P-CAD, and three individuals randomly sampled from the general population. RESULTS: Compared with the general population, patients with sporadic P-CAD had a higher prevalence of hypertension (29% vs. 14%, p < 0.001), hypercholesterolemia (54% vs. 33%, p < 0.001), obesity (20% vs. 13%, p < 0.01), and smoking (76% vs. 39%, p < 0.001). These risk factors were equally or even more prevalent in patients with familial P-CAD (43% [p < 0.05 vs. sporadic P-CAD], 58% [p = 0.07], 21% and 72%, respectively). Overall, only 7 (4%) of 163 of patients with familial P-CAD and 22 (7%) of 326 of patients with sporadic P-CAD had none of these conditions, as compared with 167 (34%) of 489 patients in the general population. CONCLUSIONS: Classic, remediable risk factors are highly prevalent in patients with familial P-CAD. Accordingly, a major contribution of genes acting in the absence of these risk factors is unlikely.
OBJECTIVES: This study was designed to assess the prevalence of major cardiovascular risk factors in familial premature coronary artery disease (P-CAD), affecting two or more siblings within one sibship. BACKGROUND: Premature CAD has a genetic component. It remains to be established whether familial P-CAD is due to genes acting independently from major cardiovascular risk factors. METHODS: We recruited 213 P-CAD survivors from 103 sibships diagnosed before age <or=50 (men) or <or=55 (women) years old. Hypertension, hypercholesterolemia, obesity, and smoking were documented at the time of the event in 163 patients (145 men and 18 women). Each patient was compared with two individuals of the same age and gender, diagnosed with sporadic (nonfamilial) P-CAD, and three individuals randomly sampled from the general population. RESULTS: Compared with the general population, patients with sporadic P-CAD had a higher prevalence of hypertension (29% vs. 14%, p < 0.001), hypercholesterolemia (54% vs. 33%, p < 0.001), obesity (20% vs. 13%, p < 0.01), and smoking (76% vs. 39%, p < 0.001). These risk factors were equally or even more prevalent in patients with familial P-CAD (43% [p < 0.05 vs. sporadic P-CAD], 58% [p = 0.07], 21% and 72%, respectively). Overall, only 7 (4%) of 163 of patients with familial P-CAD and 22 (7%) of 326 of patients with sporadic P-CAD had none of these conditions, as compared with 167 (34%) of 489 patients in the general population. CONCLUSIONS: Classic, remediable risk factors are highly prevalent in patients with familial P-CAD. Accordingly, a major contribution of genes acting in the absence of these risk factors is unlikely.
Authors: Daniel E Platt; Michella Ghassibe-Sabbagh; Sonia Youhanna; Jörg Hager; Jean-Baptiste Cazier; Yoichiro Kamatani; Angelique K Salloum; Marc Haber; Jihane Romanos; Bouchra Doueihy; Francis Mouzaya; Samer Kibbani; Hana Sbeite; Mary E Deeb; Elie Chammas; Hamid El Bayeh; Georges Khazen; Dominique Gauguier; Pierre A Zalloua; Antoine B Abchee Journal: J Thromb Thrombolysis Date: 2015-01 Impact factor: 2.300
Authors: Elizabeth R Hauser; David C Crossman; Christopher B Granger; Jonathan L Haines; Christopher J H Jones; Vincent Mooser; Brendan McAdam; Bernhard R Winkelmann; Alan H Wiseman; J Brent Muhlestein; Alan G Bartel; Charles A Dennis; Elaine Dowdy; Susan Estabrooks; Karen Eggleston; Sheila Francis; Kath Roche; Paula W Clevenger; Liling Huang; Bonnie Pedersen; Svati Shah; Silke Schmidt; Carol Haynes; Sandra West; Donny Asper; Michael Booze; Sanjay Sharma; Scott Sundseth; Lefkos Middleton; Allen D Roses; Michael A Hauser; Jeffery M Vance; Margaret A Pericak-Vance; William E Kraus Journal: Am J Hum Genet Date: 2004-07-22 Impact factor: 11.025
Authors: Paul N Hopkins; M Nazeem Nanjee; Lily L Wu; Michael G McGinty; Eliot A Brinton; Steven C Hunt; Jeffrey L Anderson Journal: Atherosclerosis Date: 2009-05-22 Impact factor: 5.162
Authors: Raja Babu Panwar; Rajeev Gupta; Bal Kishan Gupta; Sadiq Raja; Jaishree Vaishnav; Meenakshi Khatri; Aachu Agrawal Journal: Indian J Med Res Date: 2011-07 Impact factor: 2.375
Authors: Marie-Louise Gander; Joachim E Fischer; Friedrich E Maly; Roland von Känel Journal: BMC Cardiovasc Disord Date: 2004-10-14 Impact factor: 2.298