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Background Parental history of cardiovascular disease (CVD) is an established risk factor for the development of CVD in offspring. Several studies have suggested that a maternal transmission of CVD is more important for the development of CVD than paternal transmission. Method A systematic search and meta-analysis were conducted, using the Medline and Embase databases. Included were cohort, case-control and cross-sectional studies (n = 26) focusing on the relation between paternal and maternal histories of cardiovascular disease and offspring CVD (myocardial infarction, stroke or cardiovascular mortality). The pooled estimates were calculated using a random-effects model. Results The pooled OR of CVD in offspring having a positive paternal history of CVD compared to not having a positive parental history was 1.91 (95% CI 1.56-2.34; I² 53%), the RR1.54 (95% CI 1.33-1.77; I² 96%). The OR of a maternal history was 2.16 (95% CI 1.71-2.74; I² 50%), RR1.59 (95% CI 1.38-1.84; I² 90%). Regarding different age limits, a maternal history < 50 years (3.15, 95% CI 2.18-4.55) and paternal history < 55 years (2.82, 95% CI 2.25-3.54) were associated with the highest cardiovascular risk. Additional analyses for sons demonstrated an estimate for a positive paternal history of 1.55 (95% CI 1.39-1.71; I² 74%) and 1.56 (95% CI 1.46-1.67; I² 16%) for maternal history. For daughters, the estimate for paternal history was 1.48 (95% CI 1.26-1.74; I² 73%) and 1.79 (95% CI 1.50-2.13; I² 68%) for maternal history . Conclusions The conferred risk of CVD in offspring was not substantially different between positive paternal and maternal histories of CVD, the highest risk was observed for maternal history < 50 years. Since a positive parental history of CVD involves an increased cardiovascular risk, parental history inquiry is useful in clinical practice. No distinction has to be made whether the affected parent is the mother or the father. [ABSTRACT FROM AUTHOR]

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. [Copyright &y& Elsevier]