Patients with premature cardiovascular disease and a positive family history for cardiovascular disease are prone to recurrent events

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• 作者：Ties A. Mulders^a ;   ; ^b ;   ; ^c ; Zainna Meyer^a ; Christel van der Donk^a ; Abraham A. Kroon^a ;   ; ^c ; Isabel Ferreira^a ;   ; ^d ; Coen D.A. Stehouwer^a ;   ; ^c ; Sara-Joan Pinto-Sietsma^b ;   ; ^e ;   ; ^{s.j.pinto@amc.nl}
• 关键词：Premature cardiovascular disease ; Positive family history
• 刊名：International Journal of Cardiology
• 出版年：2011
• 出版时间：17 November 2011
• 年：2011
• 卷：153
• 期：1
• 页码：64-67
• 全文大小：200 K

文摘

Background: Premature cardiovascular disease (CVD) is treated in the same way as CVD of advanced age. However, in patients with premature CVD and a family history of CVD, different ¡ªpossibly genetic?mechanisms may underlie this disease, which current medical treatment is not targeted to. This suggests that subjects with a genetic predisposition to CVD are more likely to have recurrent cardiovascular events.

Methods: We retrospectively investigated 291 patients with premature CVD and assessed the amount of recurrent events according to family history in a follow-up period of 31 years. Premature CVD was defined as an event < 51 years for men or < 56 for women. We used a Cox proportional hazards model to estimate the relationship between a positive family history and recurrence of cardiovascular events.

Results: Patients with recurrent events had more often a positive family history (60.0 % vs. 47.1 % ; p < 0.05), were more often smokers (85.2 % vs. 70.7 % ; p < 0.05), had more often hypertension (36.3 % vs. 23.6 % ; p < 0.05) and had a longer follow-up period (10.0 years vs. 5.4 years; p < 0.001) than patients without recurrent events. After adjusting for these differences and modelling time to events, a positive family history was independently associated with recurrent events (Hazard ratio 1.31 (95 % confidence intervals (CI) 1.01-1.72; p < 0.05)).

Conclusions: Patients with a genetic predisposition for CVD are at risk for recurrent events, after adjusting for risk factors and other confounders. This might imply that in subjects with a genetic predisposition for CVD different pathophysiological mechanisms are active, leading to recurrent events.