Creatine kinase was associated with blood pressure in this population.

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There was no indication of more seasonal variation of headache in a population of otherwise healthy people with migraine living in an extreme Arctic area with long periods of midnight sun and polar nights with complete darkness. The strength of conclusion, however, is significantly limited by a low response rate and small sample size.

2The correlation between creatine kinase (CK) and blood pressure (BP) was examined prospectively in 120 patients with persistent high CK and 130 individuals with normal CK. Hypertension was defined as systolic BP (SBP) ≥140 mm Hg or diastolic BP (DBP) ≥90 mm Hg or current use of antihypertensive medication. Baseline CK was weakly correlated with SBP (r=0.11, P=.07) and DBP (r=0.16, P=.01) at follow-up. Persons with persistent high CK had higher SBP (140.8 mm Hg vs 138.2 mm Hg) and DBP (83.2 mm Hg vs 81.0 mm Hg, P=.06) values and were more likely to have hypertension (66.7% vs 55.5%, P=.05) than individuals with normal CK. In age-and sex-adjusted analysis, a 1-unit change in logCK was associated with a 4.9-mm Hg higher SBP, a 3.3-mm Hg higher DBP, and a 2.2-higher odds for having hypertension at follow-up (P=.1, .07, and .06, respectively). When including body mass index (BMI) to the model, BMI was a strong and independent predictor for SBP, DBP, and hypertension at follow-up and the CK effect on blood pressure was substantially attenuated. This study showed that the CK effect on blood pressure is clearly modified by BMI. J Clin Hypertens (Greenwich). 2014;16:820-826. ª 2014 Wiley Periodicals, Inc.Hypertension is a global burden, affecting more than a quarter of the adult population worldwide, which often goes undiagnosed.1 It has been hypothesized, in a biological plausible manner, that high creatine kinase (CK) activity could be a genetic factor responsible for primary hypertension.2 Two large cross-sectional, population-based studies have demonstrated an independent dose-response association between CK and blood pressure (BP).3,4 High CK has also been associated with failure of antihypertensive therapy. 5 In addition, a low CK level was associated with lower BP and an increased prevalence of fainting.6 Cross-sectional studies, however, make causal inferences impossible because of the lack of temporality between exposure and outcome. Whether the observed relationship between CK and BP is causal or confounded is still unresolved. 7,8 In the present prospective study, we measured CK and BP simultaneously at two points in time and examined whether BP at follow-up was correlated with CK at baseline. In addition, we examined CK in persons with and without hypertension at follow-up and whether CK was a long-term predictor of hypertension. Figure 1 shows a diagram of the flow of participants. All study participants were recruited from the sixth survey of the Tromsø Study in [2007][2008]. 9 CK and BP were analyzed cross-sectionally in 12,828 participants aged 30 to 87 years (mean 58 years), 6834 women and 5994 men, 65% of those eligible. A total of 686 participants had high CK according to references given by the Nordic Reference Interval Project (NORIP) 10 and were invited to a second visit for CK control. Of the 686 persons with high CK, 562 attended the second visit (baseline), and CK was measured after 3 days of refraining from alcohol and muscular load, leisure physical activity, muscular training, physiotherapy, ...