Markers of risk in young offspring with paternal history of myocardial infarction

• Published in: International journal of cardiology Vol. 89; no. 2; pp. 287 - 293
• Main Authors: Makris, Thomas K., Hatzizacharias, Antonios N., Krespi, Panagiota G., Chronakis, Emmanuel V., Vythoulkas, John S., Maria, Kouli, Tsoukala, Caterina G., Votteas, Vassilios V.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.06.2003; Elsevier Science
• Subjects: Adolescent; Adult; Age Factors; Biological and medical sciences; Biomarkers; Cardiology. Vascular system; Coronary artery disease; Coronary Disease - genetics; Coronary Disease - metabolism; Coronary heart disease; Female; Genetic Predisposition to Disease; Heart; Humans; Male; Medical sciences; Models, Cardiovascular; Myocardial Infarction - genetics; Myocardial Infarction - metabolism; Offspring; Paternal history; Risk; Risk Factors; Sex Factors; Offspring; Coronary artery disease; Risk factors; Paternal history; Human; Infarct; Risk factor; Myocardium; Cardiovascular disease; Coronary heart disease; Myocardial disease; Genetic determinism
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/S0167-5273(02)00480-1

Coronary heart disease clusters within families, but there may be several reasons for this phenomenon to occur. A possible way to elucidate this is to study biological relatives of affected individuals. The aim of our study was thus to compare a number of clinical, metabolic, clotting and immunologic factors between offspring with paternal history of premature myocardial infarction and controls and to propose a model which could safely allow to identify the high risk subgroup among them. Sixty-nine offspring of both sexes mean age 18.1 years old (cases) and thirty-two frequency matched relative to age and gender controls were studied. Cases compared to controls had significantly increased diastolic blood pressure levels (74.0±9.9 vs. 67.4±8.3 mmHg, P=0.002), leptin plasma levels (11.8±10.8 vs. 6.8±3 ng/ml, P=0.046) and fibrinogen, plasminogen, fibrin degradation products and plasminogen activator inhibitor-1 plasma levels (306.6±52.5 vs. 280.6±28.9 mg%, P=0.03, 97.4±23.5 vs. 83.6±15 mg%, P=0.0007, 292.0±148.5 vs. 219.2±69.4 ng/ml, P=0.036, 14.7±5.3 vs. 8.7±3.1 I.U./ml, P=0.0001, respectively), while cases had significantly decreased HDL-cholesterol serum levels (45.9±12.5 vs. 50.5±8.8 mg%, P=0.03) and protein S plasma levels (89.9±17.5 vs. 101.3±13.7%, P=0.001). Our findings suggest that offspring of affected individuals may be considered as a high risk group for cardiovascular disease.