Blood pressure
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Randomized Controlled Trial Multicenter Study Clinical Trial
Reductions in the risks of recurrent stroke in patients with and without diabetes: the PROGRESS Trial.
Analyses of the risks of stroke were conducted for subjects with and without diabetes, participating in a randomized, double-blind, placebo-controlled trial of a perindopril-based blood pressure lowering regimen in 6105 people with prior stroke or transient ischaemic attack (TIA), followed for a median of 3.9 years. ⋯ Diabetes is an important risk factor for stroke in patients with established cerebrovascular disease. Treatment with the ACE inhibitor perindopril with discretionary use of the diuretic indapamide produced reductions in the risk of recurrent stroke in patients with diabetes that were at least as great as those achieved in patients without diabetes.
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The 2003 European Society of Hypertension/European Society of Cardiology (ESH-ESC) guidelines have recently proposed a new risk stratification scheme for estimating absolute risk for cardiovascular disease. At variance from the previous 1999 World Health Organization-International Society of Hypertension (WHO/ISH) guidelines, the new criteria include some additional risk factors such as obesity, abnormal high-density (HDL) or low-density lipoprotein (LDL) cholesterol levels and define a slight increase in creatinine and microalbuminuria as signs of target organ damage (TOD). ⋯ Our findings show that: (i) more than one-third of uncomplicated grade 1 and 2 hypertensives seen in a outpatient hypertension hospital clinic have a high added risk according to the ESH-ESC scheme; (ii) classification of the patients in the high stratum is mainly influenced by the presence of TOD; (iii) the routine diagnostic work-up is a highly insensitive approach for the detection of TOD; (iv) the 2003 ESH-ESC guidelines stratify a higher proportion of hypertensive patients in the medium and high-risk groups than do the 1999 WHO/ISH guidelines.
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To assess the effect of a real life mental stress situation on blood pressure (BP) and heart rate (HR) in students undergoing a medical licensing examination. ⋯ Only DBP increased during medical licensing examination, albeit within a small range. SBP did not change significantly and HR decreased during the exam. Male students showed a higher SBP compared to female students.
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Comparative Study
Clinical, haemodynamic, anthropometric, metabolic and insulin profile of men with high-stage and high-grade clinical prostate cancer.
Previous studies have shown that non-insulin-dependent diabetes mellitus (NIDDM), hypertension, atherosclerotic disease manifestations, tallness, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high alanine aminotransferase (ALAT) levels are risk factors for development of benign prostatic hyperplasia (BPH). This indicates that BPH is a component of the metabolic syndrome. In a subsequent study, we found that there was an association between the BPH growth rate and the development of clinical prostate cancer. These findings generated a hypothesis that clinical prostate cancer also was a component of the metabolic syndrome. In the present study, this hypothesis was tested on 299 patients with recently diagnosed clinical prostate cancer. If this hypothesis is true, patients with clinical prostate cancer of high stage and grade would have a larger prostate gland volume, a faster BPH growth rate and a more pronounced clinical, haemodynamic, anthropometric, metabolic and insulin profile than patients with clinical prostate cancer of low stage and grade have. ⋯ The results of the present study suggest that the prostate gland volume, the BPH growth rate, hypertension, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high ALAT levels are risk factors for the development of clinical prostate cancer. Thus, our results support the hypothesis that clinical prostate cancer is a component of the metabolic syndrome. Patients with clinical prostate cancer may have the same metabolic abnormality of a defective insulin-stimulated glucose uptake and secondary hyperinsulinaemia as patients with the metabolic syndrome. Our data also support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer.