A systematic literature review was conducted using PubMed, Embase and the Cochrane Library to determine the effect of acute, chronic and passive smoking on arterial stiffness and to determine whether these effects are reversible after smoking cessation. A total of 39 relevant studies were identified and included. Acute smoking was found to cause an acute increase in arterial stiffness. Similarly, passive smoking increased arterial stiffness acutely and chronically. The majority of studies identified chronic smoking as a risk factor for increasing arterial stiffness. However, some studies found no statistical difference in arterial stiffness between nonsmokers and long-term smokers, although chronic smoking seems to sensitize the arterial response to acute smoking. In addition, whether arterial stiffness is reversed after smoking cessation and the timeline in which this may occur could not be determined from the identified literature. The effect of smoking discontinuation on arterial stiffness remains to be established by prospective smoking cessation trials.

A systematic review and meta-analysis was conducted using MEDLINE, EMBASE, and the Cochrane Library to investigate the association between preeclampsia and arterial stiffness. Twenty-three relevant studies were included. A significant increase in all arterial stiffness indices combined was observed in women with preeclampsia vs. women with normotensive pregnancies [standardized mean difference 1.62, 95% confidence interval (CI) 0.73-2.50]; carotid-femoral pulse wave velocity (cfPWV) and augmentation index (AIx) were also significantly increased (weighted mean difference, WMDcfPWV 1.04, 95% CI 0.34-1.74; WMDAIx 15.10, 95% CI 5.08-25.11), whereas carotid-radial PWV (crPWV) increase did not reach significance (WMDcrPWV 0.99, 95% CI -0.07 to 2.05). Significant increases in arterial stiffness measurements were noted in women with preeclampsia compared with those with gestational hypertension. Arterial stiffness measurements may also be useful in predicting preeclampsia and may play a role in the increased risk of future cardiovascular complications seen in women with a history of preeclampsia.

Obstructive sleep apnea is a prevalent disease that is associated with significant morbidity and mortality, particularly due to cardiovascular disease. An emerging cardiovascular risk factor, arterial stiffness, may also be involved in the cardiovascular complications of obstructive sleep apnea. The purpose of this review was to summarize the current literature regarding the effect of obstructive sleep apnea on arterial stiffness. We conducted a systematic literature review using PubMed, Embase and the Cochrane Library. We identified 24 studies that met search criteria investigating the effect of obstructive sleep apnea on arterial stiffness. Arterial stiffness was found to be increased in obstructive sleep apnea patients compared with controls or increased in severe compared with mild sleep apnea. In some studies, a positive correlation was identified between the degree of arterial stiffness and sleep apnea severity. In the two randomized, controlled trials and the two nonrandomized trials identified, treatment of obstructive sleep apnea with continuous positive airway pressure led to significant decreases in arterial stiffness. Obstructive sleep apnea appears to have an independent effect on arterial stiffness, which may be one of the mechanisms accounting for sleep apnea-associated cardiovascular risk.

BackgroundStudies showed that long-standing smokers have stiffer arteries at rest. However, the effect of smoking on the ability of the vascular system to respond to increased demands (physical stress) has not been studied. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals.Methods/ResultsHealthy light smokers (n = 24, pack-years = 2.9) and non-smokers (n = 53) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest, and 2, 5, 10, and 15 minutes following an exercise test to exhaustion. Smokers were tested, 1) after 12h abstinence from smoking (chronic condition) and 2) immediately after smoking one cigarette (acute condition). At rest, chronic smokers had higher augmentation index and lower aortic pulse pressure than non-smokers, while subendocardial viability ratio was not significantly different. Acute smoking increased resting augmentation index and decreased subendocardial viability ratio compared with non-smokers, and decreased subendocardial viability ratio compared with the chronic condition. After exercise, subendocardial viability ratio was lower, and augmentation index and aortic pulse pressure were higher in non-smokers than smokers in the chronic and acute conditions. cfPWV rate of recovery of was greater in non-smokers than chronic smokers after exercise. Non-smokers were also able to achieve higher workloads than smokers in both conditions.ConclusionChronic and acute smoking appears to diminish the vascular response to physical stress. This can be seen as an impaired ‘vascular reserve’ or a blunted ability of the blood vessels to accommodate the changes required to achieve higher workloads. These changes were noted before changes in arterial stiffness or subendocardial viability ratio occurred at rest. Even light smoking in young healthy individuals appears to have harmful effects on vascular function, affecting the ability of the vascular bed to respond to increased demands.

Three-dimensional MALDI imaging MS (IMS) is a growing branch of IMS still requiring developments in methodology and technology to make the technique routinely accessible. Many challenges are simply a matter of producing 3D reconstructions and interpreting them in a timely fashion. In this aim and using analysis of lipids from atherosclerotic plaques from a human carotid and mouse aortic sinuses, we describe 3D reconstruction methods using open-source software that provides high-quality visualization and rapid interpretation through multivariate segmentation of the 3D IMS data. Multiple datasets were generated for each sample and we provide insight into simple means to correlate the separate datasets.