Increased Plasma Plasminogen Activator Inhibitor-1 Levels: A Possible Marker of Hypertensive Target Organ Damage

• Published in: Clinical and experimental hypertension (1993) Vol. 25; no. 1; pp. 1 - 9
• Main Authors: Diamantopoulos, Emmanuel J., Andreadis, Emmanuel A., Vassilopoulos, Charalambos V., Theodorides, Theodoros G., Giannakopoulos, Nikolaos S., Chatzis, Nikolaos A., Christopoulou-Kokkinou, Vana D.
• Format: Journal Article
• Language: English
• Published: Colchester Informa UK Ltd 2003; Taylor & Francis
• Subjects: Adult; Aged; Albuminuria - urine; Antihypertensive agents; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Biomarkers - blood; Blood and lymphatic vessels; Cardiology. Vascular system; Cardiovascular system; Carotid Arteries - diagnostic imaging; Carotid intima-media thickness; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Echocardiography; Female; Humans; Hypertension - blood; Hypertension - complications; Hypertension - diagnostic imaging; Hypertension - urine; Hypertrophy, Left Ventricular - diagnostic imaging; Hypertrophy, Left Ventricular - etiology; Left ventricular mass; Male; Medical sciences; Microalbuminuria; Middle Aged; Pharmacology. Drug treatments; Plasminogen Activator Inhibitor 1 - blood; Plasminogen activator inhibitor-1; Tunica Intima - diagnostic imaging; Tunica Media - diagnostic imaging; Human; Hypertension; Nervous system diseases; Stroke; Urinary system disease; Target organ; Albumin; Biological marker; Cardiovascular disease; Left ventricular mass; Plasminogen activator inhibitor-1; Coronary heart disease; Carotid intima- media thickness; Left ventricle; Cerebral disorder; Vascular disease; Plasminogen activator inhibitor 1; Chemotherapy; Carotid; Central nervous system disease; Antihypertensive agent; Cerebrovascular disease; Microalbuminuria; Proteinuria
• DOI: 10.1081/CEH-120017736
• ISSN: 1064-1963

High plasma plasminogen-activator inhibitor-1 (PAI-1) concentrations have been reported in coronary artery disease and stroke. We therefore, prospectively studied the association of PAI-1 with early target organ damage in patients with arterial hypertension has not been clearly established. We therefore investigated 136 subjects, 64 males and 72 females, mean age 50.0 ± 12.3 years, with newly diagnosed essential hypertension who were free of cardiovascular events and were not receiving any antihypertensive medication. Plasma PAI-1 levels were measured by an ELISA method (STAGO). The study population was divided into two groups, group A with PAI-1 levels below 40 ng mL and group B with more than 40 ng mL. The left ventricular mass was calculated according to the formula of Devereux and was normalized by the individual's body surface area (LVM BSA). Carotid intima-media thickness (IMT) was determined by ultrasonography. Microalbuminuria was assessed by an immunoturbidimetric method (SERA-PAK). Group A consisted of 89 individuals with hypertension (65.4%), 41 males and 48 females and group B of 47 individuals with hypertension (34.6%), 21 males and 26 females. Individuals in group B exhibited significantly higher LVM BSA than individuals in group A (155.9 ± 23.1 g m2 vs. 129.7 ± 32.2 g m2, respectively, p = 0.004) and increased IMT (0.97 ± 0.20 mm vs. 0.87 ± 0.21 mm, respectively, p < 0.001). Microalbumin excretion rate was greater in group B than group A (70.9 ± 84.4 mg 24 hrs vs. 20.9 ± 45.1 mg 24 hrs, respectively, p = 0.002). In conclusion, elevated PAI-1 levels are associated with target organ damage in subjects with newly diagnosed arterial hypertension. Thus, it can be postulated that this fibrinolytic inhibitor may characterize hypertensives in the early stages of the atherothrombotic process.