BACKGROUND: Coronary artery disease (CAD) has turned into a prevalent cause of morbi-mortality contributing some polymorphisms in the recurrence of major adverse cardiac events (MACE). METHODS: Three hundred and fifty six patients with first myocardial infarction (MI) were followed up during a 60-month period to find out if ACE I/D, AT1R A1166C, PAI-I 4G/5G and GPIIIa a1/a2 polymorphisms, in combination with other classical cardiovascular risk factors, can contribute to the relapse of MACE. RESULTS: Two hundred and eighty five (80.1%) men and 71 (19.9%) women were followed up after first MI. The primary clinical endpoint, a composite of MACE, was reached in 106 (29.8%) patients. In the Cox univariate survival analysis those risk factors influencing a poorer prognosis were age (p = 0.004), a positive family history of CAD (p = 0.007), diabetes (p = 0.004), smoking (p = 0.024), fibrinolytic therapy (p = 0.012) and having 2 or 3 vessels CAD (p = 0.046). Cox proportional hazards regression model showed that patients with the DD genotype had a 1.5 increased risk of having an unfavorable outcome when compared with No-DD genotype patients (RR 1.561, 95% CI 1.048-2.326, p = 0.028) and that patients with the ACE DD genotype plus the AT1R No-AA genotype, the GPIIIa No-a1a1 genotype or a combination of both, had a twice higher risk than any other genotype of MACE in the follow-up (RR 1.978, 95% CI 1.286-3.043, p = 0.002). CONCLUSIONS: Patients with the ACE DD genotype plus 1 or 2 unfavorable genotypes, the AT1R No-AA, the GPIIIa No-a1a1 or a combination of both, have twice higher the risk of MACE during their clinical follow-up.
BACKGROUND:Coronary artery disease (CAD) has turned into a prevalent cause of morbi-mortality contributing some polymorphisms in the recurrence of major adverse cardiac events (MACE). METHODS: Three hundred and fifty six patients with first myocardial infarction (MI) were followed up during a 60-month period to find out if ACE I/D, AT1RA1166C, PAI-I 4G/5G and GPIIIa a1/a2 polymorphisms, in combination with other classical cardiovascular risk factors, can contribute to the relapse of MACE. RESULTS: Two hundred and eighty five (80.1%) men and 71 (19.9%) women were followed up after first MI. The primary clinical endpoint, a composite of MACE, was reached in 106 (29.8%) patients. In the Cox univariate survival analysis those risk factors influencing a poorer prognosis were age (p = 0.004), a positive family history of CAD (p = 0.007), diabetes (p = 0.004), smoking (p = 0.024), fibrinolytic therapy (p = 0.012) and having 2 or 3 vessels CAD (p = 0.046). Cox proportional hazards regression model showed that patients with the DD genotype had a 1.5 increased risk of having an unfavorable outcome when compared with No-DD genotype patients (RR 1.561, 95% CI 1.048-2.326, p = 0.028) and that patients with the ACE DD genotype plus the AT1R No-AA genotype, the GPIIIa No-a1a1 genotype or a combination of both, had a twice higher risk than any other genotype of MACE in the follow-up (RR 1.978, 95% CI 1.286-3.043, p = 0.002). CONCLUSIONS:Patients with the ACE DD genotype plus 1 or 2 unfavorable genotypes, the AT1R No-AA, the GPIIIa No-a1a1 or a combination of both, have twice higher the risk of MACE during their clinical follow-up.
Authors: Nguyen T Nguyen; Xiaolin Zhang; Cathy Wu; Richard A Lange; Robert J Chilton; Merry L Lindsey; Yu-Fang Jin Journal: PLoS Comput Biol Date: 2014-03-20 Impact factor: 4.475