Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmö Preventive Project)

Aims Orthostatic hypotension (OH) has been linked to increased mortality and incidence of cardiovascular disease in various risk groups, but determinants and consequences of OH in the general population are poorly studied. Methods and results Prospective data of the Swedish 'Malmö Preventive Project' (n = 33 346, 67.3% men, mean age 45.7 +/- 7.4 years, mean follow-up 22.7 +/- 6.0 years) were analysed. Orthostatic hypotension was found in 6.2% of study participants and was associated with age, female gender, hypertension, antihypertensive treatment, increased heart rate, diabetes, low BMI, and current smoking. In Cox regression analysis, individuals with OH had significantly increased all-cause mortality (in particular those aged less than 42 years) and coronary event (CE) risk. Mortality and CE risk were distinctly higher in those with systolic blood pressure (BP) fall >/=30 mmHg [hazard ratio (HR): 1.6, 95% CI 1.3-1.9, P /=15 mmHg (HR: 1.4, 95% CI 1.1-1.9, P = 0.024 and 1.7, 95% CI 1.1-2.5, P = 0.01). In addition, impaired diastolic BP response had relatively greater impact (per mmHg) on CE incidence than systolic reaction. Conclusion Orthostatic hypotension can be detected in approximately 6% of middle-aged individuals and is often associated with such comorbidities as hypertension or diabetes. Presence of OH increases mortality and CE risk, independently of traditional risk factors. Although both impaired systolic and diastolic responses predict adverse events, the diastolic impairment shows stronger association with coronary disease

[OP.7C.09] COFFEE, SMOKING HABITS AND BLOOD PRESSURE IN THE LIGHT OF A SINGLE NUCLEOTIDE POLIMORPHYSM OF CYP1A1/1A2 GENE

OBJECTIVE: Between genetic variants pinpointed in genome wide association study there is the rs1378942 near the CYP1A1/CYP1A2 locus. Coffee consumption has been associated with blood pressure (BP) but with sometimes contrasting evidences. A part of BP-coffee relationship could be mediated by genetic mechanisms: that is single nucleotide polymorphisms (SNPs) nearby the CYP1A2 gene, which metabolize caffeine, could influence BP. Indeed, smoking habit induces the expression of the CYP1A2 enzyme whereas coffee consumption itself could increase CYP1A2 activity. The aim of the present study was to explore if coffee consumption and/or smoking habit may affect BP and BP change over time (delta-BP), considering the rs1378942A\u200a>\u200aC polimorphysm. DESIGN AND METHOD: Coffee intake was collected by a modified diet history method and the rs1378942 was genotyped by Taqman in\u200a>\u200a28,000 participant of the Malmo Diet and Cancer (MDC). We performed a replication in 3381 participants that were rescreened after a period (13-20 years) of follow-up (MDC-FU) and in the Malmo Preventive Project (MPP; n\u200a>\u200a17,000). RESULTS: In MDC, both systolic and diastolic BP were positively associated with the rs1378942A\u200a>\u200aC, suggesting that carrying the C variant could increase BP (for SBP beta\u200a=\u200a0.397\u200a\ub1\u200a0.185, p\u200a=\u200a0.031; for DBP beta\u200a=\u200a0.220\u200a\ub1\u200a0.100, p\u200a=\u200a0.028). Coffee consumption as well as smoking were negatively associated with both SBP and DBP (p\u200a\u200aC (pinteraction\u200a\u200aC and smoking (pinteraction\u200a<\u200a0.05; data on coffe consumption not available). CONCLUSIONS: This study demonstrates that the effect of some genetic loci on BP could be highly influenced by voluptuary habits. In particular, coffee and smoke could influence the effect of the CYP1A1/CYP1A2 locus probably due to the metabolic action of the CYP1A2