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BackgroundThe purpose of the Finnish Cardiovascular Study (FINCAVAS) is to construct a risk profile – using genetic, haemodynamic and electrocardiographic (ECG) markers – of individuals at high risk of cardiovascular diseases, events and deaths.Methods and designAll patients scheduled for an exercise stress test at Tampere University Hospital and willing to participate have been and will be recruited between October 2001 and December 2007. The final number of participants is estimated to reach 5,000. Technically successful data on exercise tests using a bicycle ergometer have been collected of 2,212 patients (1,400 men and 812 women) by the end of 2004. In addition to repeated measurement of heart rate and blood pressure, digital high-resolution ECG at 500 Hz is recorded continuously during the entire exercise test, including the resting and recovery phases. About 20% of the patients are examined with coronary angiography. Genetic variations known or suspected to alter cardiovascular function or pathophysiology are analysed to elucidate the effects and interactions of these candidate genes, exercise and commonly used cardiovascular medications.DiscussionFINCAVAS compiles an extensive set of data on patient history, genetic variation, cardiovascular parameters, ECG markers as well as follow-up data on clinical events, hospitalisations and deaths. The data enables the development of new diagnostic and prognostic tools as well as assessments of the importance of existing markers.

The diagnostic performance of heart rate variability (HRV) analysis from exercise ECG in the detection of coronary artery disease (CAD) is unknown. Bicycle exercise ECG recordings from The Finnish Cardiovascular Study (FINCAVAS) of angiography-proofed CAD patients (n = 112) and a patient group with a low likelihood of CAD (n = 114) were analyzed. HRV parameters (SDNN, RMSSD, Poincaré SD1 and SD2) were calculated from 1 min segments before exercise, during exercise and after exercise. All the parameters were in addition calculated from heart rate (HR)-corrected RR-interval segments. The ST-segment depressions in each stage were also determined. The diagnostic performance of the parameters was evaluated with the area under the receiver operating characteristic (ROC) curve method. The uncorrected HRV parameters showed the best diagnostic performance in the recovery segments but the correlation with HR was also high (SDNN: 0.758/-0.64, RMSSD: 0.747/-0.60; area under the ROC/correlation coefficient). The HR correction decreased the correlation and the diagnostic performance in recovery segments (SDNN: 0.515/-0.12, RMSSD: 0.609/0.20). The diagnostic performance of ST-level at its best was higher than any of HRV parameters (ST-level: 0.795/0.36). According to the results, the HR correction decreased the diagnostic performance of the recovery phase. The HRV parameters calculated from 1 min segments of exercise test ECG were not as capable as traditional ST-segment analysis. In conclusion, the HRV analysis from exercise or recovery phase seems to be inadequate in the detection of CAD.

The effects of guar gum (GG) and microcrystalline cellulose (MC) on metabolic control and serum lipids were compared in a double-blind, cross-over trial in 18 poorly controlled Type 2 diabetic patients. There were two 12 week treatment periods separated by a 4 week wash-out period. A significant reduction in fasting BG was found after 6 weeks treatment with GG, but the initial level was regained after further 6 weeks, at the end of the treatment period. No statistically significant change in fasting BG was observed with MC. Serum cholesterol was lowered by 10% during GG treatment. Microcrystalline cellulose had no effect on serum lipids. The results suggest, that during 12 weeks supplementation with guar gum, the improvement in glycemic control was not sustained, but that it might reduce the risk of macrovascular disease in diabetic patients.

Although many studies have shown an increased risk of death from cancer in subjects with low plasma cholesterol concentrations, the underlying mechanism between low blood cholesterol and cancer is unclear. Apolipoprotein E is a central regulatory protein in cholesterol metabolism, and recent studies have shown that apolipoprotein E is a potent inhibitor of angiogenesis and tumour cell growth.1 Apolipoprotein E has three common isoforms, E2, E3, and E4, which are coded by the alleles e2, e3 and e4, respectively. The e4 allele is associated with high serum total and low density lipoprotein cholesterol concentrations. Recently, it was suggested that the apolipoprotein E e4 allele may protect from carcinoma and adenoma of the colon. 3 We hypothesised that the apolipoprotein E polymorphism could also be associated with other cancer types. The main question of this study was whether the apolipoprotein E allele distribution is diVerent in patients with cancer of the breast or prostate compared with patients with benign breast disease (BBD) or benign prostate hyperplasia (BPH) and a random population. The possible abnormalities in serum cholesterol and its fractions in patients with cancer of the breast or prostate in comparison with non-cancer patients were also investigated. MethodsTwo hundred and eleven consecutive women undergoing surgery for breast carcinoma, 299 women treated for BBD, 130 consecutive men undergoing treatment for prostate cancer, and 201 men treated for BPH in Oulu University Hospital between January 1996 and December 1997 were studied. To compare the apolipoprotein E phenotype distributions in our patient and control groups with a populationbased cohort in northern Finland, 267 women and 259 men aged 54-61 years were randomly selected by age stratification from the social insurance register covering the whole population of Oulu. All the patients gave informed consent for the investigations, which were approved by the Ethical Committee of the University of Oulu.Venous blood samples were drawn into EDTA tubes after an overnight fast. The plasma low density and high density lipoprotein cholesterol concentrations were estimated as described in the Lipid Research Clinics Manual of Laboratory Operations. 4 Cholesterol and triglycerides were analysed enzymatically with kits of Boehringer Diagnostica, Mannheim GmbH, Germany. The apolipoprotein E phenotype was determined from the plasma with the isoelectric focusing and immunoblotting techniques.The results were expressed as means (95% confidence intervals). The diVerences in the means were calculated with the analysis of variance. For triglycerides, which did not follow a normal distribution, the analysis was performed after logarithmic transformation. The distribution of allele frequencies was assessed with the 2 test. ResultsThe allelic frequencies of apolipoprotein E did not diVer between the patients with breast cancer (with frequencies of 0.040, 0.784, and 0.175 for the e2, e3 and e4 alleles, respectively), the patients with BBD, (0.036, 0.780 and 0....