Increased morning blood pressure surge and coronary microvascular dysfunction in patient with early stage hypertension

Çalışkan, Mustafa; Çalışkan, Zuhal; Güllü, Hakan; Keleş, Nurşen; Bulur, Serkan; Turan, Yaşar; Köstek, Osman; Çiftçi, Özgür; Güven, Aytekin; Aung, Soe Moe; Müderrisoğlu, Haldun

doi:10.1016/j.jash.2014.05.010

Cited by 21 publications

(10 citation statements)

References 44 publications

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“…Circadian variations in relevant risk factors for CVD such as insulin sensitivity, blood pressure, renal function, heart rate, platelet aggregability, fibrinolytic markers and levels, hormone concentrations etc. [ 9 , 16 , 17 , 56 – 58 ] may explain the morning onset of myocardial infarction, stroke and other CVD clinical events [ 17 , 18 , 23 ]. These circadian variations may be more important in T2D patients and their dysregulation contributing to a higher CVD (mainly stroke) incidence in more susceptible individuals such as CLOCK -rs4580704 CC homozygous subjects (for whom our results suggest a lower flexibility).…”

Section: Discussionmentioning

confidence: 99%

“…In humans, this circadian timing coordinates virtually all physiological processes encompassing the states of sleep and wakefulness, endocrine functions and cardiovascular activity [ 15 , 17 ]. It has been shown that several aspects of the cardiovascular physiopathology and incidence of CVD events, such as myocardial infarction, ischemic and hemorrhagic stroke, have diurnal variation, peaking in the early morning hours [ 18 – 23 ]. Moreover, a higher risk of obesity, metabolic alterations and T2D has been found in shift workers [ 24 – 27 ] and adverse cardiometabolic effects (including postprandial glucose in a range typical of a prediabetes state) have been detected in subjects who underwent forced circadian misalignment [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

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CLOCK gene variation is associated with incidence of type-2 diabetes and cardiovascular diseases in type-2 diabetic subjects: dietary modulation in the PREDIMED randomized trial

Corella

Asensio

Coltell

et al. 2016

Cardiovasc Diabetol

114

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Background Circadian rhythms regulate key biological processes influencing metabolic pathways. Disregulation is associated with type 2 diabetes (T2D) and cardiovascular diseases (CVD). Circadian rhythms are generated by a transcriptional autoregulatory feedback loop involving core clock genes. CLOCK (circadian locomotor output cycles protein kaput), one of those core genes, is known to regulate glucose metabolism in rodent models. Cross-sectional studies in humans have reported associations between this locus and obesity, plasma glucose, hypertension and T2D prevalence, supporting its role in cardiovascular risk. However, no longitudinal study has investigated the association between CLOCK gene variation and T2D or CVD incidence. Moreover, although in a previous work we detected a gene-diet interaction between the CLOCK-rs4580704 (C > G) single nucleotide polymorphism (SNP) and monounsaturated (MUFA) intake on insulin resistance, no interventional study has analyzed gene-diet interactions on T2D or CVD outcomes.Methods We analyzed the association between the CLOCK-rs4580704 SNP and incidence of T2D and CVD longitudinally in 7098 PREDIMED trial (ISRCTN35739639) participants after a median 4.8-year follow-up. We also examined modulation by Mediterranean diet (MedDiet) intervention (high in MUFA) on these associations.ResultsWe observed a significant association between the CLOCK-rs4580704 SNP and T2D incidence in n = 3671 non-T2D PREDIMED participants, with variant allele (G) carriers showing decreased incidence (dominant model) compared with CC homozygotes (HR: 0.69; 95 % CI 0.54–0.87; P = 0.002). This protection was more significant in the MedDiet intervention group (HR: 0.58; 95 % CI 0.43–0.78; P < 0.001) than in the control group (HR: 0.95; 95 % CI 0.63–1.44; P = 0.818). Moreover, we detected a statistically significant interaction (P = 0.018) between CLOCK-rs4580704 SNP and T2D status on stroke. Thus, only in T2D subjects was CLOCK-rs4580704 SNP associated with stroke risk, G-carriers having decreased risk (HR: 0.61; 95 % CI 0.40–0.94; P = 0.024 versus CC) in the multivariable-adjusted model.ConclusionsIn agreement with our previous results showing a protective effect of the G-allele against hyperglycemia, we extended our findings by reporting a novel association with lower T2D incidence and also suggesting a dietary modulation. Moreover, we report for the first time an association between a CLOCK polymorphism and stroke in T2D subjects, suggesting that core clock genes may significantly contribute to increased CVD risk in T2D.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-015-0327-8) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CLOCK gene variation is associated with incidence of type-2 diabetes and cardiovascular diseases in type-2 diabetic subjects: dietary modulation in the PREDIMED randomized trial

Corella

Asensio

Coltell

et al. 2016

Cardiovasc Diabetol

114

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“…18 even in well-controlled hypertensive patients with 24-hour Bp values <130/80 mm Hg, MBps was significantly associated with left ventricular hypertrophy and an increase in carotid intimamedia thickness. 19 Hypertensive patients with exaggerated MBps had increased values of carotid intima-media thickness and urinary catecholamine excretion, as well as higher levels of inflammatory markers, such as C-reactive protein, interleukin-6, interleukin-18 (P<0.001), and uric acid compared with those without MBps.…”

Section: Associated Organ Damage and Risk Factorsmentioning

confidence: 74%

Prognosis in Relation to Blood Pressure Variability

Kario

2015

Hypertension

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“…The patient was placed in the left lateral position, and the acoustic window was around the mid‐clavicular line in the fourth and fifth intercostal spaces. Coronary blood flow velocities were evaluated both at rest and after hyperemia induced by dipyridamole infusion (0.56 mg/kg over 4 minutes) . If the increase in heart rate was insufficient (<10% increase from the baseline), an additional infusion of dipyridamole (0.28 mg/kg over a 2‐minute period) was administered.…”

Section: Methodsmentioning

confidence: 99%

“…Coronary blood flow velocities were evaluated both at rest and after hyperemia induced by dipyridamole infusion (0.56 mg/kg over 4 minutes). [17][18][19] If the increase in heart rate was insufficient (<10% increase from the baseline), an additional infusion of dipyridamole (0.28 mg/kg over a 2-minute period) was administered. Heart rate and blood pressure were followed every 4 minutes.…”

Section: Cfr Measurementmentioning

confidence: 99%