arterial stiffness

Platelet vesiculation is common factor contributing in coagulation and thromboembolism in patients with atrial fibrillation (AF). Platelet-derived vesicles are involved in the coagulation, thromboembolism, microvascular inflammation, arterial stiffness, vascular calcification, atherosclerotic plaque shaping and rupture, endothelial dysfunction, cardiac remodelling, and kidney dysfunction. Recent clinical studies have revealed elevated concentrations of platelet-derived vesicles in peripheral blood of patients with current AF and history of AF. The aim of the mini review is to discuss the role of platelet-derived micro vesicles as predictive biomarker in AF. Serial measures of circulating levels of platelet-derived vesicules are discussed to be useful in stratification of AF patients at risk of thromboembolic complications, but there is limiting evidence regarding their predictive value that requires further investigations in large clinical trials.

Background: Arterial stiffness has been considered an independent predictor of cardiovascular disease in addition to the traditionally known cardiovascular risk factors. Objectives: This study aimed to investigate the associations between arterial stiffness with left ventricular mass index and carotid intima-media thickness in the hypertensives. Methods: A descriptive cross-sectional study compared a control group in 210 study subjects (105 hypertensives and 105 normotensives). Measuring left ventricular mass index by echocardiography and carotid intima-media thickness by carotid doppler ultrasonography. Pulse wave velocity was measured using the Agedio B900 device and the Agedio K520 application. The manual method was measured by the ankle-brachial index.Results: There was a statistically significant positive correlation between pulse wave velocity and age (r = 0.922, p < 0.001). The ankle-brachial index had a statistically significant positive correlation at a weak level with left ventricular mass index and carotid intima-media thickness, in which the coefficient r was equal to 0.219 (p < 0.05) and 0.250 (p < 0,001), respectively. Pulse wave velocity also had a statistically significant positive correlation at a weak level with left ventricular mass index and carotid intima-media thickness, in which the coefficient r was equal to 0.188 (p < 0.05) and 0.289 (p < 0,001), respectively. Pulse wave velocity had a multivariable linear correlation with gender, pulse, mean blood pressure, and ankle-brachial index with statistical significance; and they were written in the form of the following equation: Pulse wave velocity (R2: 41.3%) = 0.641*(Gender) – 0.027*(Pulse) + 0.043*(Mean blood pressure) + 8.378*(Ankle-brachial index) – 3.254.Conclusion: Arterial stiffness was statistically correlated with left ventricular mass index and carotid intima-media thickness in the hypertensives. Through the above research results, we suggest that the hypertensives should be combined with the evaluation of hemodynamic parameters and arterial stiffness for contributing to the diagnosis and detection of cardiovascular complications, thereby improving the quality of monitoring and treatment in hypertensive patients.

Background: Absence of nocturnal decrease in Blood Pressure (BP) (“non-dipping”) has been shown to be a strong and independent predictor of cardiovascular events, target organ damage, cardiovascular sequela and cardiovascular mortality. Obstructive Sleep Apnea (OSA) has been associated with non-dipping with an estimated prevalence of approximately 50%, but factors associated with non-dipping in OSA patients remain poorly understood. In this study, we examined clinically relevant variables associated with non-dipping in OSA.Methods: Patients (n = 35) undergoing overnight valuation for OSA, laboratory-based polysomnography, structured clinical interviews, and comprehensive metabolic and anthropometric evaluations, and ambulatory BP monitoring for 24 hours. Patients were classified into a) dipping BP group or b) non-dipping BP group, based on (a) a nocturnal systolic BP decrease of 10% - 20% or (b) a systolic BP decrease of < 10%. Results: Patients had moderate and severe OSA (AHI = 34.8 ± 29.1), and 42.9% demonstrated a non-dipping BP pattern. The severity of OSA measures did not differ between dipping group and non-dipping group. However, Wake after Sleep Onset (WASO) and chronicity of insomnia predicts non-dipping BP independent of demographics, sleep stages, anthropometrics, metabolic measures, or arterial stiffness. Conclusion: These findings contribute to a better understanding of the cardiovascular impacts of OSA and indicate that sleep quality should be incorporated into clinical assessments and management of OSA patients.