The early diagnosis and appropriate treatment of subclinical atherosclerosis before the onset of life-threatening cardiovascular (CV) diseases are major unmet medical needs in current clinical ...practice. Noninvasive arterial stiffness indices, the arterial velocity–pulse index (AVI) and the arterial pressure–volume index (API) have been associated with CV risks, conventional arterial stiffness indices, and the severity of coronary atherosclerosis. However, few studies have examined the relationship between these indices and the occurrence of CV events. We measured the AVI and API in 113 consecutive patients admitted to Yokohama City University Hospital for cardiac catheterization between June 2015 and March 2016. Patients were followed until September 2022, and the occurrence of CV events was assessed. The mean age was 71.2 ± 10.7 years, and 83 patients (73.5%) were male. In total, 80 patients (70.8%) had hypertension, 87 (77.0%) had dyslipidemia, and 91 (80.5%) had a history of ischemic heart disease (IHD). The mean follow-up duration was 1752 ± 819 days. Patients who received elective percutaneous coronary intervention (PCI) based on the results of coronary angiography (CAG) at the time of enrollment had significantly higher API than those who did not (38.5 ± 12.6, n = 17 vs. 31.3 ± 7.4, n = 96, p = 0.001). The API was independently associated with the risk of elective PCI in multiple logistic regression analysis. In conclusion, the API could be a useful indicator for estimating the need for coronary interventional treatment in patients with a high CV risk.
Objective: In the present study, a photoplethysmographic (PPG) waveform analysis for assessing differences in autonomic reactivity to mental stress between patients with Major Depressive ...Disorder (MDD) and healthy control (HC) subjects is presented. Methods: PPG recordings of 40 MDD and 40 HC subjects were acquired at basal conditions, during the execution of cognitive tasks, and at the post-task relaxation period. PPG pulses are decomposed into three waves (a main wave and two reflected waves) using a pulse decomposition analysis. Pulse waveform characteristics such as the time delay between the position of the main wave and reflected waves, the percentage of amplitude loss in the reflected waves, and the heart rate (HR) are calculated among others. The intra-subject difference of a feature value between two conditions is used as an index of autonomic reactivity. Results: Statistically significant individual differences from stress to recovery were found for HR and the percentage of amplitude loss in the second reflected wave (<inline-formula><tex-math notation="LaTeX">A_{13}</tex-math></inline-formula>) in both HC and MDD group. However, autonomic reactivity indices related to <inline-formula><tex-math notation="LaTeX">A_{13}</tex-math></inline-formula> reached higher values in HC than in MDD subjects (Cohen's <inline-formula><tex-math notation="LaTeX">{d=\!-0.81},{\,\text {AUC}=0.74}</tex-math></inline-formula>), implying that the stress response in depressed patients is reduced. A statistically significant (<inline-formula><tex-math notation="LaTeX">p \,<\, 0.001</tex-math></inline-formula>) negative correlation (<inline-formula><tex-math notation="LaTeX">r=-0.5</tex-math></inline-formula>) between depression severity scores and <inline-formula><tex-math notation="LaTeX">A_{13}</tex-math></inline-formula> was found. Conclusion: A decreased autonomic reactivity is associated with higher degree of depression. Significance: Stress response quantification by dynamic changes in PPG waveform morphology can be an aid for the diagnosis and monitoring of depression.
Background. Despite the global trend towards a decrease in mortality from cardiovascular pathology of atherosclerotic genesis, this group of diseases continues to occupy a leading position in the ...structure of disability and mortality among the population of many countries. Aim. Identification of noninvasive markers of arterial wall lesions associated with the presence of arterial hypertension (AH) and coronary heart disease (CHD) in persons younger than 55 years. Materials and methods. The study included 81 people. Three groups were distinguished from them: 1st (n=31) – a control group of practically healthy individuals, average age – 43 (40; 48) years; 2nd group (n=21) – patients with coronary heart disease without a history of cardiovascular diseases (CVD), average age – 45,5±6,1; group 3 (n=29) – patients with AH without CHD, average age – 47 (35; 50) years. The parameters of a biochemical blood test were determined, volumetric sphygmography and a sample with post-occlusive reactive hyperemia were performed. Results. In groups of patients with CHD and AH, negative changes in the lipid profile and higher glucose levels were recorded compared to healthy individuals. According to the results of volumetric sphygmography, the pulse wave velocity in arteries of predominantly elastic type (R/L-PWV) in group 1 was 10.1±1.7 m/s, in group 2 – 12.9±1.8 m/s, in group 3 – 13.1 (12; 14) m/s (р1–2=0.029; р1–30.001); cardio-ankle vascular index (CAVI) – 6.5±0.7, 7.7 (7; 8.7) and 7.8 (7.3; 8.4), respectively (р1–20.001; р1–30.001). According to the data of the test with post-occlusive reactive hyperemia, a comparably high frequency of pathological values of flow-dependent vasodilation (FDV) and reactivity index (RI) was demonstrated in patients with CHD and AH (р1–20.05; р1–30.05). A multifactorial model of noninvasive diagnosis of CHD in individuals without a history of CVD, including non-high-density lipoprotein cholesterol, R/L-PWV, and FDV, has been developed. For patients with AH, glucose, lipid metabolism, R/L-PWV, pulse wave velocity in muscle-type arteries (B-PWV), augmentation index (AI), biological age, CAVI, FDV, RI were the risk factors for the presence of the disease in the anamnesis. Conclusion. The results obtained confirm the importance of an integrated approach in the screening diagnosis of CVD.
In the last decades, the search for mechanisms underlying progressive arterial stiffening and for interventions to avoid or reverse this process has gained much attention. In general, arterial ...stiffening displays regional variation and is, for example, during aging more prominent in elastic than in muscular arteries. We hypothesize that besides passive also active regulators of arterial compliance i.e., endothelial and vascular smooth muscle cell (VSMC) function differ between these arteries. Hence, it is conceivable that these vessel types will display different time frames of stiffening. To investigate this hypothesis segments of muscular arteries such as femoral and mesenteric arteries and elastic arteries such as the aorta and carotid artery were isolated from female C57Bl6 mice (5-6 months of age, n = 8). Both microscopy and passive stretching of the segments in a myograph confirmed that passive mechanical properties (elastin, collagen) of elastic and muscular arteries were significantly different. Endothelial function, more specifically basal nitric oxide (NO) efficacy, and VSMC function, more specifically L-type voltage-gated Ca(2+) channel (VGCC)-mediated contractions, were determined by α1-adrenoceptor stimulation with phenylephrine (PE) and by gradual depolarization with elevated extracellular K(+) in the absence and presence of eNOS inhibition with L-NAME. PE-mediated isometric contractions significantly increased after inhibition of NO release with L-NAME in elastic, but not in muscular vessel segments. This high basal eNOS activity in elastic vessels was also responsible for shifts of K(+) concentration-contraction curves to higher external K(+). VGCC-mediated contractions were similarly affected by depolarization with elevated K(+) in muscular artery segments or in elastic artery segments in the absence of basal NO. However, K(+)-induced contractions were inhibited by the VGCC blocker diltiazem with significantly higher sensitivity in the muscular arteries, suggestive of different populations of VGCC isoforms in both vessel types. The results from the present study demonstrate that, besides passive arterial wall components, also active functional components contribute to the heterogeneity of arterial compliance along the vascular tree. This crucially facilitates the search for (patho) physiological mechanisms and potential therapeutic targets to treat or reverse large artery stiffening as occurring in aging-induced arterial stiffening.
Abstract
Aims
To determine the impact of smoking and alcohol exposure during adolescence on arterial stiffness at 17 years.
Methods and results
Smoking and alcohol use were assessed by questionnaires ...at 13, 15, and 17 years in 1266 participants (425 males and 841 females) from the ALSPAC study. Smoking status (smokers and non-smoker) and intensity (‘high’ ≥100, ‘moderate’ 20–99, and ‘low or never’ <20 cigarettes in lifetime) were ascertained. Participants were classified by frequency (low or high) and intensity of drinking light (LI <2), medium (MI 3–9), and heavy (HI >10 drinks on a typical drinking day). Carotid to femoral pulse wave velocity (PWV) was assessed at 17 years mean ± standard deviation and/or mean difference (95% confidence intervals). Current smokers had higher PWV compared with non-smokers (P = 0.003). Higher smoking exposure was associated with higher PWV compared with non-smokers 5.81 ± 0.725 vs. 5.71 ± 0.677 m/s, mean adjusted difference 0.211 (0.087–0.334) m/s, P = 0.001. Participants who stopped smoking had similar PWV to never smokers (P = 0.160). High-intensity drinkers had increased PWV HI 5.85 ± 0.8 vs. LI 5.67 ± 0.604 m/s, mean adjusted difference 0.266 (0.055–0.476) m/s, P = 0.013. There was an additive effect of smoking intensity and alcohol intensity, so that ‘high’ smokers who were also HI drinkers had higher PWV compared with never-smokers and LI drinkers mean adjusted increase 0.603 (0.229–0.978) m/s, P = 0.002.
Conclusion
Smoking exposure even at low levels and intensity of alcohol use were associated individually and together with increased arterial stiffness. Public health strategies need to prevent adoption of these habits in adolescence to preserve or restore arterial health.
Deteriorated arterial function and high incidence of cardiovascular events characterise diabetes mellitus. Metformin and recent antidiabetic drugs, SGLT2 inhibitors, reduce cardiovascular events. We ...explored the possible effects of empagliflozin's effect on top of metformin treatment on endothelial function and arterial stiffness parameters in type 1 diabetes mellitus (T1DM) patients.
Forty T1DM patients were randomised into three treatment groups: (1) empagliflozin (25 mg daily), (2) metformin (2000 mg daily) and (3) empagliflozin/metformin (25 mg daily and 2000 mg daily, respectively). The fourth group received placebo. Arterial function was assessed at inclusion and after 12 weeks treatment by: endothelial function brachial artery flow-mediated dilation (FMD), reactive hyperaemia index (RHI), arterial stiffness pulse wave velocity (PWV) and common carotid artery stiffness (β-stiffness). For statistical analysis one-way analysis of variance with Bonferroni post-test was used.
Empagliflozin on top of metformin treatment significantly improved endothelial function as did metformin after 12 weeks of treatment: FMD 2.6-fold (P < 0.001) vs. 1.8-fold (P < 0.05) and RHI 1.4-fold (P < 0.01) vs. 1.3-fold (P < 0.05). Empagliflozin on top of metformin treatment was superior to metformin in improving arterial stiffness parameters; it significantly improved PWV and β-stiffness compared to metformin by 15.8% (P < 0.01) and by 36.6% (P < 0.05), respectively. Metformin alone did not influence arterial stiffness.
Empagliflozin on top of metformin treatment significantly improved arterial stiffness compared to metformin in T1DM patients. Endothelial function was similarly improved in all treatment groups. Empagliflozin seems to possess a specific capacity to decrease arterial stiffness, which could support its cardioprotective effects observed in large clinical studies. Trial registration Clinical trial registration: NCT03639545.
Background: Coronary slow flow may not only affect the coronary arteries, but it may also be a vascular problem affecting the rest of the arterial system. ＜br＞
Objective: The aim of this study was to ...determine peripheral arterial stiffness and the thickness of the choroid layer in patients with slow coronary flow. ＜br＞
Methods: Fifty consecutive patients (age, 54.3 ± 11.4 years, 38 male) with coronary slow flow and 25 consecutive patients (age, 50.5 ± 9.9 years, 16 male) with normal coronary arteries both documented by coronary angiography were included. Arterial stiffness parameters were measured noninvasively using a Mobil-O-Graph arteriography system. The choroidal thickness was assessed using the enhanced depth imaging optical coherence tomography method. ＜br＞
Results: The patients with coronary slow flow had significantly higher peripheral systolic blood pressure, peripheral pulse pressure, central pulse pressure, and pulse wave velocity (PWV) and significantly thinner choroidal thickness compared to the
Brachial blood pressure is predictive of cardiovascular outcome; however central pressure may better represent the load imposed on the coronary and cerebral arteries and thereby bear a stronger ...relationship to vascular damage and prognosis. Relations of brachial and central pressures to carotid artery hypertrophy (intimal-medial thickness and vascular mass), extent of atherosclerosis (plaque score), and incident cardiovascular events were examined in the Strong Heart Study. Central pressures were calculated using radial applanation tonometry. Among 3520 participants, central and brachial pulse pressures were more strongly related to vascular hypertrophy and extent of atherosclerosis than were systolic pressures. Central pulse pressure was more strongly related to all 3 arterial measures than was brachial pulse pressure (r=0.364 versus 0.309 for plaque score; P<0.001 for comparison of Spearman correlation coefficient; r=0.293 versus 0.249 for intimal-medial thickness; P<0.002; r=0.320 versus 0.289 for vascular mass; P<0.05). Among the 2403 participants free of clinical cardiovascular disease at baseline, 319 suffered fatal or nonfatal cardiovascular events during mean follow-up of 4.8±1.3 years. After adjustment for age, gender, current smoking, body mass index, cholesterol:HDL ratio, creatinine, fibrinogen, diabetes, and heart rate, central pulse pressure predicted cardiovascular events more strongly than brachial pulse pressure (hazards ratio=1.15 per 10 mm Hg, χ=13.4, P<0.001 versus hazards ratio=1.10, χ=6.9, P=0.008). In conclusion, noninvasively-determined central pulse pressure is more strongly related to vascular hypertrophy, extent of atherosclerosis, and cardiovascular events than is brachial blood pressure. These findings support prospective examination of use of central blood pressure as a treatment target in future trials.
Vitamin K deficiency is common among kidney transplant recipients (KTRs) and likely contributes to progressive vascular calcification and stiffness. In this single-center, randomized, double-blind, ...placebo-controlled trial, we aimed to investigate the effects of vitamin K supplementation on the primary end point, serum calcification propensity (calciprotein particle maturation time, T50), and secondary end points arterial stiffness (pulse wave velocity PWV) and vitamin K status in 40 vitamin K-deficient KTRs (plasma dephosphorylated uncarboxylated matrix Gla protein dp-ucMGP ≥500 pmol/L). Participants (35% female; age, 57 ± 13 years) were randomized 1:1 to vitamin K2 (menaquinone-7, 360 μg/day) or placebo for 12 weeks. Vitamin K supplementation had no effect on calcification propensity (change in T50 vs baseline +2.3 ± 27.4 minutes) compared with placebo (+0.8 ± 34.4 minutes; Pbetween group = .88) but prevented progression of PWV (change vs baseline −0.06 ± 0.26 m/s) compared with placebo (+0.27 ± 0.43 m/s; Pbetween group = .010). Vitamin K supplementation strongly improved vitamin K status (change in dp-ucMGP vs baseline −385 −631 to −269 pmol/L) compared with placebo (+39 −188 to +183 pmol/L; Pbetween group < .001), although most patients remained vitamin K-deficient. In conclusion, vitamin K supplementation did not alter serum calcification propensity but prevented progression of arterial stiffness, suggesting that vitamin K has vascular effects independent of calciprotein particles. These results set the stage for longer-term intervention studies with vitamin K supplementation in KTRs.
EU Clinical Trials Register (EudraCT Number: 2019-004906-88) and the Dutch Trial Register (NTR number: NL7687).
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Certain exposures and risk factors during the first 1,000 days of life are known to influence future cardiovascular disease (CVD) risk. Pulse wave velocity (PWV) is a measure of arterial stiffness ...and a recognised surrogate marker of CVD. We performed a systematic review and meta-analyses to investigate whether early life exposures were associated with increased PWV compared with controls in youth.
Databases AMED, MEDLINE, EMBASE, CINAHL and Scopus were searched from inception until February 2022. Eligibility criteria: observational controlled studies in youth aged <20 years with risk factors/exposure during the first 1,000 days and PWV measurement. This review is registered with PROSPERO (CRD42019137559). Outcome data were pooled using random-effects meta-analysis. Meta-regression was used to investigate potential confounders.
We identified 24 eligible studies. Age of participants ranged from 1-day to 19-years at time of PWV assessment. Exposures included pre-term birth, small for gestational age (SGA), maternal diabetes and assisted reproductive technologies, none of which were significantly associated with PWV in meta-analysis. Sub-group analysis by age demonstrated increased PWV in childhood and adolescence in those exposed to maternal diabetes or born SGA. In meta-regression of pre-term studies, higher prevalence of SGA was associated with increased PWV compared with controls (p = 0.034, R2 = 1).
We found limited evidence that youth exposed to maternal diabetes or born SGA have increased PWV, consistent with increased future CVD risk. These changes in PWV appear to manifest in later childhood and adolescence. Further research is required to better understand the observed relationships.
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•This is the first review to investigate pulse wave velocity in youth and exposure to early life risks.•Limited evidence supports increased pulse wave velocity when exposed to maternal diabetes or born small for gestational age.•These changes in pulse wave velocity appear to manifest in childhood and adolescence.•Further research is required to better understand the observed associations.
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