Resistance to activated protein C and FV Leiden mutation in patients with a history of acute myocardial infarction or primary hypertension

• Published in: American journal of hypertension Vol. 13; no. 1; pp. 61 - 65
• Main Authors: Makris, Thomas K, Krespi, Panagiota G, Hatzizacharias, Anthony N, Gialeraki, Argyri E, Anastasiadis, George, Triposkiadis, Filippos K, Mandalaki, Titika, Kyriakidis, Michael K
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 2000; Oxford University Press; Elsevier Science
• Subjects: Activated Protein C Resistance - genetics; Activated Protein C Resistance - physiopathology; Acute Disease; Anticoagulants - pharmacology; Biological and medical sciences; Blood Pressure - physiology; Cardiology. Vascular system; Coronary heart disease; Drug Resistance; Factor V - genetics; Female; genetics; Heart; Humans; hypertension; Hypertension - genetics; Hypertension - physiopathology; Male; Medical sciences; Middle Aged; Mutation, Missense - genetics; Mutation, Missense - physiology; Myocardial infarction; Myocardial Infarction - genetics; Myocardial Infarction - physiopathology; thrombosis; Myocardial infarction; genetics; thrombosis; hypertension; Human; Hypertension; Factor V Leiden; Infarct; Pathogenesis; Cardiovascular disease; Exploration; Protein C; Coronary heart disease; Myocardial disease; Genetic determinism; Thrombosis; Genetic disease; Incidence; Vascular disease; Resistance; Concomitant disease; Gene; Risk factor; Myocardium; Mutation; Coagulopathy
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/S0895-7061(99)00140-5

This study was designed to investigate both resistance to activated protein C (APC-R) and the factor FV Q506 mutation incidence in patients with a history of acute myocardial infarction (AMI) and patients with primary hypertension (PH), a high-risk group for arterial thrombosis. Eighty patients with a history of AMI (group A), 160 patients with a history of PH (group B), and 124 age-matched controls without arterial disease (group C) were studied. APC-R was determined using the Coatest APC Resistance Kit of Chromagenix, Sweden. The prevalence of the FV Q506 mutation was estimated by DNA analysis (Bertina method). The prevalence of the FV Q506 mutation was 20%, 13.75%, and 8% in groups A, B, and C, respectively (A
v C
P
= .0466). The prevalence of APC-R was 47.5% in group A
v 13% in group C (
P
< .0001) and 36.25% in group B
v 13% in group C (
P
< .0001). The response to activated protein C expressed as mean value
± SD was 2.05
± 0.33 in group A
v 2.56
± 0.46 in group C (
P
< .05) and 2
± 0.22 in group B
v 2.56
± 0.46 in group C (
P
< .05). These findings suggest that patients with a history of AMI or PH have a significantly increased incidence of both APC-R and FV Q506 mutation compared with the control group. These findings support the hypothesis that these anticoagulant defects may be risk factors for arterial thrombosis.