Time rate of blood pressure variation: a new factor associated with coronary atherosclerosis

Manios, E.; Stamatelopoulos, Kimon; Tsivgoulis, Georgios; Barlas, Gerassimos; Koroboki, Eleni; Tsagalis, Georgios; Michas, F.; Vemmos, Konstantinos

doi:10.1097/hjh.0b013e3283454ff4

Cited by 42 publications

(30 citation statements)

References 30 publications

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“…Regarding the clinical setting, Manios et al [44] recently evaluated the association between the rate of blood pressure variation, derived from ambulatory blood pressure monitoring data analysis, and the severity and topography of coronary artery lesion in a cohort of normotensive patients with suspected coronary artery disease. Abrupt variations in blood pressure are related to atherosclerosis and enhance cardiac hypertrophy [45].…”

Section: Circadian Rhythms and Cardiovascular Diseasementioning

confidence: 99%

The Biological Clock and Vascular Disease: Application to Pregnancy

Karoutsos¹,

Karoutsos²,

Karoutsou³

2017

J Clin Epigenet

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In mammals, the components of the biological clock function peripherally in a complex network and modulate the transcription of specific target genes and their products, expressed rhythmically in a 24 h rhythm. The central biological clock includes the suprachiasmatic nucleus, which rhythmically 'tunes' peripheral clocks (Figure 1) [1][2][3][4][5][6][7][8].Having the molecular basis of SCN being clarified the so-called core clock genes such as per1-2, cry1-2, bmal1 [9,10] and the demonstration that these genes are rhythmically expressed in peripheral tissues, including the liver, adrenal and pituitary glands [11][12][13], this central clock model is reshaped [14][15][16].Clock/Bmal, formed by the product of the genes circadian locomotor output cycles kaput [Clock] and brain and muscle aryl hydrocarbon receptor nuclear translocator like-Arntl (Bmal) represents the transcription initiator of the feedback loops [17].Clock/Bmal binds to E-box in the promoter regions of target genes Period homolog 1, 2 and 3 genes (Per1, Per2, Per3), Cryptochrome genes (Cry1, Cry2), retinoic acid-related orphan receptor (Rora, Rorb, Rorc) and Rev-Erb nuclear orphan receptor(Rev-Erbα, RevErbβ) to activate their expression [18,19].Transcription of Pers and Crys is initiated during the day, while degradation during the night. PER and CRY proteins enter the nucleus, probably as a multimeric complex (PER/CRY), and inhibit Clock/Bmal-mediated transcription [20,21].As to the role of the PER/CRY complex, Cryptochrome (CRY) is a blue-light sensor, which regulates neuronal firing rate, that is AbstractThe creation of a biological clock adjusted to way of life synchronizers influences the function of peripheral clocks and by extension, all physiological processes as well as secretion of hormones. Further, disturbance of the function of the biological clock exerts a strong impact on the pathogenesis of several disorders, including diabetes mellitus, insomnia, depression, cardiovascular disease and cancer, linking the pathophysiology of many diseases to one molecular mechanism, the 'out of tune clock'.Keywords: Diabetes mellitus; Pathogenesis; Suprachiasmatic nucleus; Cryptochrome circadian entrainment in Drosophila melanogaster [22]. Light activates CRY. When CRY is activated TIM [timeless] degrades, tuning the clock daily. In the absence of cry, the clock can still be activated by light, though the mechanisms are unclear; possibly, there are two types of clock neurons having differential sensitivities to light and temperature [23].With regard to the remainder feedback loop, the ROR/Bmal/RevErb (RBR) frames the original shape [20]. ROR acts as an activator of Bmal and Rev-Erb as an inhibitor which results in tuning of Bmal transcription [24,25]. Suppression of Rev-Erbα expression resulted in elevated Clock mRNA expression consistent with RevErbα's role as a transcriptional repressor, adding a regulation role of the activity of the Bmal1/Clock heterodimer by regulation of the expression of both the Bmal1 and Clock genes directly (Figure 2) [26]...

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Section: Circadian Rhythms and Cardiovascular Diseasementioning

confidence: 99%

The Biological Clock and Vascular Disease: Application to Pregnancy

Karoutsos¹,

Karoutsos²,

Karoutsou³

2017

J Clin Epigenet

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“…In addition to the degree of short-term BPV, the rate of BP variation also contributes in the likelihood of development of early carotid atherosclerosis [44]. Steeper fluctuations in BP produce greater stress on the arterial wall and may have an additive role in the detection of the severity of coronary artery lesions in normotensive individuals with suspected coronary artery disease [44].…”

Section: Clinical Impact Of Short-term Bpv On Target Organ Damage Andmentioning

confidence: 99%

“…Steeper fluctuations in BP produce greater stress on the arterial wall and may have an additive role in the detection of the severity of coronary artery lesions in normotensive individuals with suspected coronary artery disease [44]. Although ample evidence establishes the existence of a positive relationship between short-term BPV and the severity and rate of progression of end-organ damage, cardiovascular events and mortality [45,46], a number of reports fail to demonstrate the prognostic relevance of BP fluctuations in hypertensive patients [47][48][49].…”

Section: Clinical Impact Of Short-term Bpv On Target Organ Damage Andmentioning

confidence: 99%

Blood Pressure Variability: Prognostic Value and Therapeutic Implications

Höcht

2013

ISRN Hypertension

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Blood pressure variability (BPV) is considered nowadays a novel risk factor for cardiovascular disease. Early findings in sinoaortic denervated rats have clearly shown that enhanced fluctuation of blood pressure induced left ventricular hypertrophy, vascular stiffness, and renal lesion. A large number of clinical trials confirm that short-term and long-term blood pressure variability independently contributes to target organ damage, cardiovascular events, and mortality not only in hypertensive patients but also in subjects with diabetes mellitus and chronic kidney disease. Therefore, amelioration of BPV has been suggested as an additional target of the treatment of cardiovascular diseases. Preliminary evidence obtained from meta-analysis and controlled clinical trials has shown that antihypertensive classes differ in their ability to control excessive BP fluctuations with an impact in the prevention of cardiovascular events. Calcium channel blockers seem to be more effective than other blood pressure lowering drugs for the reduction of short-term and long-term BPV. In order to increase actual knowledge regarding the prognostic value and therapeutic significance of BPV in cardiovascular disease, there is a need for additional clinical studies specifically designed for the study of the relevance of short-term and long-term BPV control by antihypertensive drugs.

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“…Although the main predictor of risk in arterial hypertension is an increase in mean blood pressure (BP) levels, which makes reduction of BP per se a primary goal in treatment of arterial hypertension, increased 24 h BP variability (BPV) is increasingly recognized as an additional marker for cardiovascular complications in hypertensive patients, being able to predict organ damage and cardiovascular events over and above an increase in mean BP levels [1][2][3][4][5][6]. This is the case also for residual long-term, visit-to-visit systolic BPV on treatment, an increase of which was found associated with a poor prognosis even when mean systolic BP was under control [7].…”

Section: Introductionmentioning

confidence: 99%