Ankle blood pressure as a predictor of total and cardiovascular mortality

<p>Abstract</p> <p>Background</p> <p>The ankle blood pressure is commonly used as a ratio to the brachial blood pressure, called ankle-brachial index (ABI). Very few studies have considered the independent value of the ankle blood pressure without indexing it to the brachial blood pressure. We examined the value of ankle blood pressure, together with the exercise blood pressure, as a predictor of cardiovascular (CVD) and total mortality.</p> <p>Methods</p> <p>A prospective follow-up study of 3,858 consecutive ambulatory patients (mean age 51 years, 65,9% male) referred to a symptom-limited exercise test between August 1989 and December 1995. The cohort was followed up for all-cause and CVD mortality until December 31, 2004, by record linkage with the National Causes-of-Death Register. The independent value of ankle blood pressure as a predictor of cardiovascular and total mortality was assessed using Cox proportional hazards modelling.</p> <p>Results</p> <p>The average follow-up time was 14 years, during which 346 persons died, 108 of them due to CVD. Persons with normal (<140 mmHg) resting brachial blood pressure, ankle blood pressure < 175 mmHg and exercise blood pressure at moderate exercise level ≤215 mmHg at baseline investigation, had the best prognosis and were taken as the reference category. Among persons with elevated ankle blood pressure (≥175 mmHg) but normal or borderline resting brachial pressure and normal exercise blood pressure (≤215 mmHg) at moderate exercise level the multivariate-adjusted hazard ratios (HR, 95% confidence interval) for CVD and total mortality were 2.70 (1.52 – 4.80) and 2.13 (1.58 – 2.85), respectively. Similar and equally significant HRs were observed in persons with both elevated ankle blood pressure and elevated exercise blood pressure, as well as in those persons with elevated exercise blood pressure but ankle blood pressure < 175 mmHg.</p> <p>Conclusion</p> <p>These results suggest that the ankle blood pressure has an independent value as a marker of arterial stiffness or subclinical atherosclerosis and a risk of future mortality in middle-aged, asymptomatic persons.</p

Is Brain-Derived Neurotrophic Factor Associated With Smoking Initiation? Replication Using a Large Finnish Population Sample : Replication Using a Large Finnish Population Sample

Introduction: Brain-derived neurotrophic factor (BDNF) is a growth factor in the central nervous system. There is evidence for the involvement of BDNF in addictions and mental disorders. We aimed to replicate the earlier reported association of a functional genetic variant of BDNF with smoking initiation (SI) using a large population-based sample and to test whether the association is independent of depression. Methods: Our sample was drawn from the Finnish population-based FINRISK surveys conducted in 1992, 1997, 2002, and 2007. We had nonmissing data on the genotype BDNF Val66Met (G/A) variant (rs6265) and self-reported never (n = 10 619) versus ever (n = 16 028) smoking among 26 647 adults aged 25-74 years. The association between BDNF Val66Met and SI was modeled using logistic regression adjusted for age and sex, and in secondary analyses also for depression. Depression was defined as self-reported depression diagnosed or treated by physician during the past year. Results:The sex- and age-adjusted analysis confirmed that the major (Val) allele increased the risk of being a lifetime ever smoker (per allele odds ratio [OR] = 1.07; 95% CI = 1.01 to 1.12; p =.01). When depression, which itself was significantly associated with SI (OR = 1.58; 95% CI = 1.37 to 1.82; p Conclusions: In a Finnish population sample, we replicated the earlier reported association of BDNF Val66Met with SI. Our data further suggest that this association is independent of depression.Peer reviewe

Oral health : a neglected aspect of diabetes care

Non peer reviewe

Association of the DBH Polymorphism rs3025343 With Smoking Cessation in a Large Population-Based Sample

Introduction: Genetic variations in DBH-gene and its surroundings have been shown to associate with smoking behavior including smoking cessation in several studies. In this study we replicate and measure the effect size for association between DBH polymorphism rs3025343 and smoking cessation in a large population-based sample while examining environmental factors that could relate to the association. Methods: We studied 11 926 adult subjects from four surveys of the National FINRISK Study. The analysis was restricted to either current or former smokers. Logistic and linear regression analyses were conducted to investigate the relationships of the single nucleotide polymorphism (SNP), covariates, smoking cessation, and smoking severity (cotinine, CPD). Gene-environment interactions were tested by likelihood-ratio test. Results: The association between rs3025343 and smoking cessation (prevalence odds ratio, OR = 1.12, p = .094, 95% CI = 0.98-1.30) was replicated identically with the GWAS study of The Tobacco and Genetics Consortium (OR = 1.12, 95% CI = 1.08-1.18). None of our tested phenotypes significantly influenced the association between rs3025343 and smoking cessation. Overall, marital status, education, depression, alcohol use, self-rated health, and chronic obstructive pulmonary disease (COPD) showed phenotypic associations with smoking cessation, but the association of various phenotypes with smoking cessation did not vary by genotype. Conclusions: The current study replicates the effect size for the association between rs3025343 and smoking cessation despite lack of overall significance due to smaller sample size. We could not show environmental influences on the association of rs3025343 with smoking cessation. Implications: Our study replicates the direction and strength of the association of DBH polymorphism rs3025343 with smoking cessation. We could not detect environmental influences on the strength of the association of rs3025343 with smoking cessation, but the limited power of our analysis needs to be taken into account.Peer reviewe

Cause-specific mortality of 1-year survivors of subarachnoid hemorrhage

OBJECTIVE: To assess long-term, cause-specific mortality rates and rate ratios of the patients alive at 1 year after subarachnoid hemorrhage (SAH). METHODS: The population-based, prospective, cohort study with a nested case-control design consisted of 64,349 persons (aged 25-74 years at enrollment) who participated in the National FINRISK Study between 1972 and 2007. Four hundred thirty-seven SAH cases, 233 one-year SAH survivors, and their matched intrinsic controls were identified and followed up until the end of 2009 through the nationwide Finnish Causes of Death Register. All-cause mortality rates and rate ratios of the 1-year SAH survivors and controls were the main outcome measures. RESULTS: Eighty-eight (37.8%) of 233 one-year SAH survivors died during the total follow-up time of 2,487 person-years (median 8.6 years, range 0.1-35.8 years). The 1-year SAH survivors had a hazard ratio of 1.96 (95% confidence interval 1.57-2.47) for death compared with the matched general population with 10 controls for each SAH survivor. One-year SAH survivors had up to 31 additional deaths per 1,000 person-years compared with controls with minimal cerebrovascular risk factors. The higher long-term risk of death among SAH survivors was attributed solely to cerebrovascular diseases, and most important modifiable risk factors for death were smoking, high systolic blood pressure (≥159 mm Hg), and high cholesterol levels (≥7.07 mmol/L). CONCLUSION: One-year SAH survivors have excess mortality, which is attributed to an exceptional risk of deadly cerebrovascular events. Aggressive post-SAH cerebrovascular risk factor intervention strategies are highly warranted.Peer reviewe