Association of central blood pressure with an exaggerated blood pressure response to exercise among elite athletes.

PURPOSE: The systolic blood pressure/workload (SBP/MET) slope was recently reported to be a reliable parameter to identify an exaggerated blood pressure response (eBPR) in the normal population and in athletes. However, it is unclear whether an eBPR correlates with central blood pressure (CBP) and vascular function in elite athletes. METHODS: We examined 618 healthy male elite athletes (age 25.8 ± 5.1 years) of mixed sports with a standardized maximum exercise test. CBP and vascular function were measured non-invasively with a validated oscillometric device. The SBP/MET slope was calculated and the threshold for an eBPR was set at > 6.2 mmHg/MET. Two groups were defined according to ≤ 6.2 and > 6.2 mmHg/MET, and associations of CBP and vascular function with the SBP/MET slope were compared for each group. RESULTS: Athletes with an eBPR (n = 180, 29%) displayed a significantly higher systolic CBP (102.9 ± 7.5 vs. 100 ± 7.7 mmHg, p = 0.001) but a lower absolute (295 ± 58 vs. 384 ± 68 W, p < 0.001) and relative workload (3.14 ± 0.54 vs. 4.27 ± 1.1 W/kg, p < 0.001) compared with athletes with a normal SBP/MET slope (n = 438, 71%). Systolic CBP was positively associated with the SBP/MET slope (r = 0.243, p < 0.001). In multiple logistic regression analyses, systolic CBP (odds ratio [OR] 1.099, 95% confidence interval [CI] 1.045-1.155, p < 0.001) and left atrial volume index (LAVI) (OR 1.282, CI 1.095-1.501, p = 0.002) were independent predictors of an eBPR. CONCLUSION: Systolic CBP and LAVI were independent predictors of an eBPR. An eBPR was further associated with a lower performance level, highlighting the influence of vascular function on the BPR and performance of male elite athletes.

Sex differences in workload-indexed blood pressure response and vascular function among professional athletes and their utility for clinical exercise testing.

PURPOSE: Sex differences in blood pressure (BP) regulation at rest have been attributed to differences in vascular function. Further, arterial stiffness predicts an exaggerated blood pressure response to exercise (BPR) in healthy young adults. However, the relationship of vascular function to the workload-indexed BPR and potential sex differences in athletes are unknown. METHODS: We examined 47 male (21.6 ± 1.7 years) and 25 female (21.1 ± 2 years) athletes in this single-center pilot study. We assessed vascular function at rest, including systolic blood pressure (SBP). Further, we determined the SBP/W slope, the SBP/MET slope, and the SBP/W ratio at peak exercise during cycling ergometry. RESULTS: Male athletes had a lower central diastolic blood pressure (57 ± 9.5 vs. 67 ± 9.5 mmHg, p < 0.001) but a higher central pulse pressure (37 ± 6.5 vs. 29 ± 4.7 mmHg, p < 0.001), maximum SBP (202 ± 20 vs. 177 ± 15 mmHg, p < 0.001), and ΔSBP (78 ± 19 vs. 58 ± 14 mmHg, p < 0.001) than females. Total vascular resistance (1293 ± 318 vs. 1218 ± 341 dyn*s/cm5, p = 0.369), pulse wave velocity (6.2 ± 0.85 vs. 5.9 ± 0.58 m/s, p = 0.079), BP at rest (125 ± 10/76 ± 7 vs. 120 ± 11/73.5 ± 8 mmHg, p > 0.05), and the SBP/MET slope (5.7 ± 1.8 vs. 5.1 ± 1.6 mmHg/MET, p = 0.158) were not different. The SBP/W slope (0.34 ± 0.12 vs. 0.53 ± 0.19 mmHg/W) and the peak SBP/W ratio (0.61 ± 0.12 vs. 0.95 ± 0.17 mmHg/W) were markedly lower in males than in females (p < 0.001). CONCLUSION: Male athletes displayed a lower SBP/W slope and peak SBP/W ratio than females, whereas the SBP/MET slope was not different between the sexes. Vascular functional parameters were not able to predict the workload-indexed BPR in males and females.

Dismantling Anti-Ageing Medicine: Why Age-Relatedness of Cardiovascular Disease is Proof of Robustness Rather Than of Ageing-Associated Vulnerability.

Ageing is perceived to be the common culprit behind the most prevalent noncommunicable chronic diseases (NCD) such as cardiovascular disease (CVD). Treating ageing as a means to prevent its downstream pathologies has become the logical extension of this idea, and the defining criterion of anti-ageing medicine (evidence-based early detection, prevention, and treatment of age-related diseases). Challenging the underlying rationale, we here argue that the disease's late-in-life occurrence is proof of a genetically conserved robustness that helps us resist disease long enough for it to masquerade as a consequence of living long rather than of living wrong. Robustness is an acknowledged hallmark phenomenon of all complex systems (while there exists no universally adopted definition, a hallmark of complex systems is that they consist of many networked components whose interactions may give rise to system behaviours which cannot be derived or predicted from a reductionist knowledge of the interacting parts, even if this knowledge is complete) and a key concept in the complexity sciences (a relatively new branch of science that attempts to find and understand the common mechanisms and patterns shared by all complex systems). To reconceptualise the age-relatedness of chronic diseases in this sense has important implications for medical research and practice. The goal of our essay is to open a discussion that may enhance the overall understanding of robustness and prevent a misguided redirection of funding away from established disease specific research and towards anti-ageing medicine. This essay is timely, as the forthcoming 11th version of the International Classification of Diseases (ICD) will be the first to recognise ageing as a condition, thereby legitimising anti-ageing medical research. On a more pragmatic note, and for the benefit of people alive today, we propose a practical strategy to remedy the mismatch between heritable robustness and the lifestyle challenges that gradually overwhelm it.

Association of 25-hydroxy vitamin D level with the blood pressure response to a maximum exercise test among professional indoor athletes.

PURPOSE: Low vitamin D levels have been associated with elevated blood pressure (BP) in the general population. However, whether there is an association of vitamin D insufficiency with BP changes during maximum exercise in athletes is currently unclear. METHODS: A total of 120 male professional indoor athletes (age 26 ± 5 years) were examined. BP was measured at rest and during a graded cycling test. We assessed the BP response (BPR) during maximum exercise and the respective load. BP and BPR (peak-baseline BP) were analysed with respect to 25-OH vitamin D levels, with levels < 30 ng/mL defining vitamin D insufficiency. RESULTS: 35 athletes were classified as being vitamin D insufficient. BP was not different between sufficient and insufficient vitamin D groups (122 ± 10/75 ± 7 vs. 120 ± 12/77 ± 9 mmHg). At maximum exercise, however, systolic BP (198 ± 17 vs. 189 ± 19, p = 0.026) and the pulse pressure (118 ± 18 vs. 109 ± 21 mmHg, p = 0.021) were higher in the sufficient group; the BPR was not different between groups (76 ± 20/5 ± 6 vs. 69 ± 22/3 ± 6 mmHg, p = 0.103). Athletes with sufficient levels had a higher maximum power output (3.99 ± 0.82 vs. 3.58 ± 0.78 W/kg, p = 0.015) and achieved higher workloads (367 ± 78 vs. 333 ± 80 W, p = 0.003). The workload-adjusted BPR (maximum systolic BP/MPO) was not different between athletes with sufficient and insufficient vitamin D levels (51 ± 10 vs. 56 ± 14 mmHg × kg/W, p = 0.079). CONCLUSION: Athletes with sufficient vitamin D achieved a higher maximum systolic BP and a higher maximum power output. The workload-adjusted BPR was not different between groups, which suggests that this finding reflects a better performance of athletes with sufficient vitamin D.

Elite athletes as research model: vitamin D insufficiency associates with elevated central blood pressure in professional handball athletes.

PURPOSE: Low vitamin D levels have been associated with elevated blood pressure in the general population. Prospective studies, however, have produced conflicting evidence about the blood pressure-lowering effects of vitamin D supplementation. Cardiorespiratory fitness may modulate the vitamin D-blood pressure association. We therefore examined this association in professional athletes, whose high training load serves as a biological control for physical fitness. METHODS: 50 male professional handball players (age 26 ± 5 years) were examined. We assessed the central aortic pressure parameters using transfer function-based analysis of oscillometrically obtained peripheral arterial waveforms. Serum 25-OH vitamin D concentrations were determined by chemiluminescent immunoassay. The threshold for insufficiency was set at values of < 30 ng/mL. RESULTS: Central blood pressure (cBP) was 98 ± 7/60 ± 10 mmHg. The aortic pulse wave velocity (PWV) was 6.3 ± 1.0 m/s. Nine athletes (18%) displayed insufficient 25-OH vitamin D levels and had a significantly (p < 0.01) higher cBP compared with the 41 (82%) athletes with sufficient 25-OH vitamin D levels (106 ± 5/68 ± 8 vs. 97 ± 7/58 ± 9 mmHg). Central systolic blood pressure (cSBP) in vitamin D-sufficient athletes was significantly lower in comparison to the healthy reference population (97 mmHg vs. 103 mmHg, p < 0.001). This significance of difference was lost in vitamin D-insufficient athletes (106 mmHg vs. 103 mmHg, p = 0.12). CONCLUSION: Significantly raised central systolic and diastolic blood pressure in vitamin D-insufficient elite athletes implicates vitamin D as a potential modifier of vascular functional health.

Web-enabled feedback control over energy balance promotes an increase in physical activity and a reduction of body weight and disease risk in overweight sedentary adults.

This study aims to investigate whether a Web-based tool will facilitate the adoption of feedback control over calorie balance in overweight individuals, thereby promoting an increase of physical activity and a reduction of body weight and cardiovascular risk factors. This is a prospective exercise intervention study, commencing with a minimum weekly 3 × 20-min requirement of high-intensity interval training and requirement for Web-based self-monitoring and self-reporting of exercise and body weight. Subjects of this study include 83 overweight, sedentary, otherwise healthy adults aged 26-68 years. Anthropometric parameters, body fat, peak oxygen consumption, self-reported physical activity, frequency of use of the Web-based tool are among the characters measured in this study. This 24-week intervention substantially increased time spent for exercise (mean and median of 135 and 170 min/week, respectively) among the 72 % of participants who had adopted cognitive feedback control vs. no increase in the remaining participants of nonadopters. Adopters witnessed significantly improved peak oxygen consumption of >1 metabolic equivalent vs. no improvement among nonadopters. Adopters also reduced body mass index, body weight, and body fat by 1.6 kg/m(2), 4.8 kg, and 3.6 kg, respectively vs. 0.4 kg/m(2), 1.4 kg, and 1.1 kg in the control group. The increase in physical activity came at virtually no intervention effort of the investigators. This study demonstrates for the first time that adoption of cognitive feedback control over energy balance is possible with the help of a simple Web-based tool and that overweight adopters self-regulate exercise volume to significantly reduce body weight and improve biomarkers of fitness and cardiovascular risk.

Normative values of non-invasively assessed RV function and pulmonary circulation coupling for pre-participation screening derived from 497 male elite athletes.

BACKGROUND: Reference values for right ventricular function and pulmonary circulation coupling were recently established for the general population. However, normative values for elite athletes are missing, even though exercise-related right ventricular enlargement is frequent in competitive athletes. METHODS: We examined 497 healthy male elite athletes (age 26.1 ± 5.2 years) of mixed sports with a standardized transthoracic echocardiographic examination. Tricuspid annular plane excursion (TAPSE) and systolic pulmonary artery pressure (SPAP) were measured. Pulmonary circulation coupling was calculated as TAPSE/SPAP ratio. Two age groups were defined (18-29 years and 30-39 years) and associations of clinical parameters with the TAPSE/SPAP ratio were determined and compared for each group. RESULTS: Athletes aged 18-29 (n = 349, 23.8 ± 3.5 years) displayed a significantly lower TAPSE/SPAP ratio (1.23 ± 0.3 vs. 1.31 ± 0.33 mm/mmHg, p = 0.039), TAPSE/SPAP to body surface area (BSA) ratio (0.56 ± 0.14 vs. 0.6 ± 0.16 mm*m2/mmHg, p = 0.017), diastolic blood pressure (75.6 ± 7.9 vs. 78.8 ± 10.7 mmHg, p < 0.001), septal wall thickness (10.2 ± 1.1 vs. 10.7 ± 1.1 mm, p = 0.013) and left atrial volume index (27.5 ± 4.5 vs. 30.8 ± 4.1 ml/m2, p < 0.001), but a higher SPAP (24.2 ± 4.5 vs. 23.2 ± 4.4 mmHg, p = 0.035) compared to athletes aged 30-39 (n = 148, 33.1 ± 3.4 years). TAPSE was not different between the age groups. The TAPSE/SPAP ratio was positively correlated with left ventricular stroke volume (r = 0.133, p = 0.018) and training amount per week (r = 0.154, p = 0.001) and negatively correlated with E/E' lat. (r = -0.152, p = 0.005). CONCLUSION: The reference values for pulmonary circulation coupling determined in this study could be used to interpret and distinguish physiological from pathological cardiac remodeling in male elite athletes.

Vascular alterations among male elite athletes recovering from SARS-CoV-2 infection.

SARS-CoV-2 may affect the cardiovascular system and vascular impairment has been reported in healthy young adults recovering from COVID-19. However, the impact of SARS-CoV-2 infection on the vascular function of elite athletes is unknown. We examined 30 healthy male elite athletes (age 25.8 ± 4.6 years) pre-season and at a 6-month follow-up (182 ± 10 days). Vascular function and central blood pressure were calculated using transfer function-based analysis of peripheral arterial waveforms obtained by oscillometry. We performed a two-way repeated-measures ANOVA on the biomarker data, with SARS-CoV-2 status as the between-groups factor and time as the within-groups factor. Subjects who tested positive for SARS-CoV-2 were studied 18 ± 4 days after their positive testing date at follow-up. Of 30 athletes, 15 tested positive for SARS-CoV-2 after the first examination and prior to the follow-up. None had severe COVID-19 or reported any persisting symptoms. The results of the two-way repeated measures ANOVA revealed that there was no significant main effect of COVID-19 on any of the investigated biomarkers. However, there was a significant interaction between the effects of SARS-CoV-2 exposure and time on augmentation index (Aix) (p = 0.006) and augmentation index normalized to a heart rate of 75 beats per minute (Aix@75), (p = 0.0018). The observation of an interaction effect on Aix and Aix@75 in the absence of any main effect indicates a cross-over interaction. Significant vascular alterations in male elite athletes recovering from COVID-19 were observed that suggest vascular impairment. Whether these alterations affect athletic performance should be evaluated in future studies.

Workload-indexed blood pressure response to a maximum exercise test among professional indoor athletes.

BACKGROUND: Exercise testing is performed regularly in professional athletes. However, the blood pressure response (BPR) to exercise is rarely investigated in this cohort, and normative upper thresholds are lacking. Recently, a workload-indexed BPR (increase in systolic blood pressure per increase in metabolic equivalent of task (SBP/MET slope)) was evaluated in a general population and was compared with mortality. We sought to evaluate the SBP/MET slope in professional athletes and compare it with performance. DESIGN: This was a cross-sectional study. METHODS: A total of 142 male professional indoor athletes (age 26 ± 5 years) were examined. Blood pressure was measured at rest and during a standardized, graded cycle ergometer test. We assessed the BPR during exercise, the workload, and the metabolic equivalent of task (MET). Athletes were divided into groups according to their SBP/MET slope quartiles (I <4.3; II 4.3-6.2; III >6.2-9; IV >9 mmHg/MET) and compared regarding systolic BP (sBP) and workload achieved. RESULTS: Athletes in group I (n = 42) had the lowest maximum sBP (180 ± 13 mmHg) but achieved the highest relative workload (4.2 ± 1 W/kg). With increasing SBP/MET slope, the maximum sBP increased (II (n = 56): 195 ± 15 mmHg; III (n = 44): 216 ± 16 mmHg) and the workload achieved decreased (II: 3.9 ± 0.7 W/kg; III: 3.3 ± 0.5 W/kg). The differences in sBP between these groups were significant (p < 0.001). None of the athletes were assigned to group IV (>9 mmHg/MET). CONCLUSION: Athletes in the lowest SBP/MET slope quartile displayed the lowest maximum sBP but achieved a higher workload than athletes classified into the other SBP/MET slope groups. This simple, novel metric might help to distinguish a normal from an exaggerated BPR to exercise, to identify athletes at risk of developing hypertension.

Blood Pressure Response and Vascular Function of Professional Athletes and Controls.

Workload-indexed blood pressure response (wiBPR) to exercise has been shown to be superior to peak systolic blood pressure (SBP) in predicting mortality in healthy men. Thus far, however, markers of wiBPR have not been evaluated for athletes and the association with vascular function is unclear. We examined 95 male professional athletes (26±5 y) and 30 male controls (26±4 y). We assessed vascular functional parameters at rest and wiBPR with a graded bicycle ergometer test and compared values for athletes with those of controls. Athletes had a lower pulse wave velocity (6.4±0.9 vs. 7.2±1.5 m/s, p=0.001) compared to controls. SBP/Watt slope (0.34±0.13 vs. 0.44±0.12 mmHg/W), SBP/MET slope (6.2±1.8 vs. 7.85±1.8 mmHg/MET) and peak SBP/Watt ratio (0.61±0.12 vs. 0.95±0.17 mmHg/W) were lower in athletes than in controls (p<0.001). The SBP/Watt and SBP/MET slope in athletes were comparable to the reference values, whereas the peak SBP/Watt-ratio was lower. All vascular functional parameters measured were not significantly correlated to the wiBPR in either athletes or controls. In conclusion, our findings indicate the potential use of the SBP/Watt and SBP/MET slope in pre-participation screening of athletes. Further, vascular functional parameters, measured at rest, were unrelated to the wiBPR in athletes and controls.

Are we losing the battle against cardiometabolic disease? The case for a paradigm shift in primary prevention.

BACKGROUND: Cardiovascular and diabetic disease are the leading and preventable causes of death worldwide. The currently prognosticated dramatic increase in disease burden over the next two decades, however, bespeaks a low confidence in our prevention ability. This conflicts with the almost enthusiastic reporting of study results, which demonstrate substantial risk reductions secondary to simple lifestyle changes. DISCUSSION: There is a case to be made for a disregard of the difference between statistical significance and clinical relevance of the reported data. Nevertheless, lifestyle change remains the main weapon in our battle against the epidemic of cardiometabolic disease. But along the way from risk screening to intervention to maintenance the compound inefficiencies of current primary preventive strategies marginalize their impact. SUMMARY: Unless we dramatically change the ways in which we deploy preventive interventions we will inevitably lose the battle. In this paper we will argue for three provocative strategy changes, namely (a) the disbanding of screening in favor of population-wide enrollment into preventive interventions, (b) the substitution of the current cost utility analysis for a return-on-investment centered appraisal of interventions, and (c) the replacement of standardized programs modeled around acute care by individualized and perpetual interventions.

Impact of Vascular Function on Maximum Power Output in Elite Handball Athletes.

Purpose: To evaluate vascular function and its relationship to cardiorespiratory fitness in professional handball athletes. Method: We examined 30 male professional handball athletes (age 27 ± 4 y) and 10 male sedentary controls (age 26 ± 5 y) at rest. The workup included exercise testing via ergometry. To assess vascular function, a validated electronic model of the arterial tree (vasc assist 2®) was used. It replicates noninvasively acquired pulse pressure waves by modulating the relevant functional parameters of compliance, resistance, inertia, pressure, and flow. The maximum oxygen uptake (VO2max) was estimated using the validated heart rate ratio method. Results: Athletes had a significantly lower systolic and diastolic central blood pressure (cBP) compared to controls (102 ± 9/60 ± 9 vs. 110 ± 8/74 ± 9 mmHg, p < .01), whereas aortic pulse wave velocity (PWV) (6.2 ± 0.8 vs. 6.3 ± 0.5 m/s, p = .45) and augmentation index at a heart rate of 75 (Aix@75) (-4 ± 12 vs. -13 ± 16%, p = .06) were not different. Resistance index (R) (15.9 ± 4.4 vs. 10.6 ± 0.6, p = .001) and maximum power output (MPO) (3.55 ± 0.54 vs. 2.46 ± 0.55 Watt/kg, p < .001) were significantly higher in athletes compared to controls. We found no relevant correlation between MPO, resting heart rate, PWV, Aix@75, and cBP. A higher VO2max (p = .02) and a lower R (p < .01) were significant predictors of a higher MPO in athletes. Conclusion: R had an independent and strong correlation to MPO in athletes, which might help to disentangle the contribution of aerobic capacity and arterial function to physical power.

Vascular robustness: The missing parameter in cardiovascular risk prediction.

Undetected high risk for premature death of cardiovascular disease (CVD) among individuals with low-to-moderate risk factor scores is an acknowledged obstacle to CVD prevention. The vasculature's functional robustness against risk factor derailment may serve as a novel discriminator of mortality risk under similar risk factor loads. To test this assumption, we hypothesized that the expected inverse robustness-mortality association is verifiable as a significant trend along the age spectrum of risk factor-challenged cohorts. This is a retrospective cohort study of 372 adults (mean age 56.1 years, range 21-92; 45% female) with a variety of CV risk factors. An arterial model (VascAssist 2, iSYMED GmbH, Germany) was used to derive global parameters of arterial function from non-invasively acquired pulse pressure waves. Participants were stratified by health status: apparently healthy (AH; n = 221); with hypertension and/or hypercholesterolemia (CC; n = 61); with history of CV event(s) (CVE; n = 90). Multivariate linear regression was used to derive a robustness score which was calibrated against the CVD mortality hazard rate of a sub-cohort of the LURIC study (n = 1369; mean age 59.1 years, range 20-75; 37% female). Robustness correlated linearly with calendar age in CC (F(1, 59) = 10.42; p < 0.01) and CVE (F(1, 88) = 40.34; p < 0.0001) but not in the AH strata, supporting the hypothesis of preferential elimination of less robust individuals along the aging trajectory under risk factor challenges. Vascular robustness may serve as a biomarker of vulnerability to CVD risk factor challenges, prognosticating otherwise undetectable elevated risk for premature CVD mortality.

A novel principled method for the measurement of vascular robustness uncovers hidden risk for premature CVD death.

The detection of high risk for premature death of cardiovascular disease (CVD) among individuals with low-to-moderate risk factor scores is a major challenge. Systems biology suggests that the vasculature's functional robustness against risk factor challenges may serve as a novel discriminator of mortality risk under similar risk factor loads. However, principled methods to measure vascular robustness are not available. To develop a score for the vasculature's functional robustness we used a recently presented method that applies computational physiological modeling to the quantitation of vascular function. We hypothesized that the expected inverse robustness-mortality association is verifiable as a significant robustness-calendar age trend in a cross-sectional investigation of a population cohort of risk factor-challenged individuals. Using only functional parameters of the cardiovascular system we applied multivariate linear regression to derive from our study population of 372 adults gender-specific multivariate robustness scoring algorithms. For any individual, the deviation of his/her robustness score from the value of the regression function characterizes the deviation of the individual's fatal CVD event probability from its age-appropriate fatal CVD event probability. Robustness correlated linearly with calendar age in our risk factor-challenged but not in our unchallenged cohorts. This observation supports the hypothesis of preferential elimination of less robust individuals along the aging trajectory under risk factor challenges. We conclude that physiologically principled scoring for vascular robustness may serve as a biomarker of vulnerability to CVD risk factor challenges, prognosticating otherwise undetectable elevated risk for premature CVD mortality. NEW & NOTEWORTHY We developed a principled method for the derivation of a vascular robustness score that we translated into a correction factor for calendar age. We demonstrated the score's potential to uncover risk for premature cardiovascular death in apparently healthy young adults whose risk elevation remains hidden in conventional risk factor models.

The cardiovascular robustness hypothesis: Unmasking young adults' hidden risk for premature cardiovascular death.

An undetected high risk for premature death of cardiovascular disease (CVD) among individuals with low-to-moderate risk factor levels is an acknowledged obstacle to CVD prevention. In this paper, we present the hypothesis that the vasculature's robustness against risk factor load will complement conventional risk factor models as a novel stratifier of risk. Figuratively speaking, mortality risk prediction without robustness scoring is akin to predicting the breaking risk of a lake's ice sheet considering load only while disregarding the sheet's bearing strength. Taking the cue from systems biology, which defines robustness as the ability to maintain function against internal and external challenges, we develop a robustness score from the physical parameters that comprehensively quantitate cardiovascular function. We derive the functional parameters using a recently introduced novel system, VascAssist 2 (iSYMED GmbH, Butzbach, Germany). VascAssist 2 (VA) applies the electronic-hydraulic analogy to a digital model of the arterial tree, replicating non-invasively acquired pule pressure waves by modulating the electronic equivalents of the physical parameters that describe in vivo arterial hemodynamics. As the latter is also subject to aging-associated degeneration which (a) progresses at inter-individually different rates, and which (b) affects the biomarker-mortality association, we express the robustness score as a correction factor to calendar age (CA), the dominant risk factor in all CVD risk factor models. We then propose a method for the validation of the score against known time-to-event data in reference populations. Our conceptualization of robustness implies that risk factor-challenged individuals with low robustness scores will face preferential elimination from the population resulting in a significant robustness-CA correlation in this strata absent in the unchallenged stratum. Hence, we also present an outline of a cross-sectional study design suitable to test this hypothesis. We finally discuss the objections that may validly be raised against our robustness hypothesis, and how available evidence encourages us to refute these objections.

Automated oscillometric blood pressure and pulse-wave acquisition for evaluation of vascular stiffness in atherosclerosis.

OBJECTIVE: Evaluation of diagnostic accuracy of an oscillometry-based device (VascAssist) combining fully automated ankle-brachial index (ABI) and pulse-wave velocity (PWV) assessment for detection of peripheral arterial disease (PAD). SUBJECTS AND METHODS: 110 consecutive subjects including symptomatic PAD patients (n = 41) and healthy PAD-free participants (n = 69) were recruited. All subjects underwent standard manual Doppler-based ABI (sABI) and oscillometry-based automated ABI (aABI) measurements (VascAssist). Oscillometry by the VascAssist included central and peripheral PWV assessment. Additionally, arterial stiffness (AS) was evaluated by flow-mediated vasodilation (FMD) of the brachial artery in all patients. All symptomatic PAD patients underwent catheter angiography for endovascular intervention and post-interventional acquisition of sABI, aABI, PWV and FMD. RESULTS: Sensitivity, specificity, PPV and NPV of aABI for detecting PAD was 73%, 100%, 100%, and 86% as compared to 80%, 96%, 92%, and 89% for sABI. Pearson-correlation for diabetics was r = 0.81; (P < .001) and for non-diabetics r = 0.77; (P < .001). Bland-Altman-analysis revealed a difference (95% CI) for diabetics of 0.09 (-0.22-0.4] and non-diabetics 0.022 [-0.25-0.295]. Weak correlation exists for FMD/AS analysis (pre-interventional R = 0.386, P = .043; post-interventional R = -0.06; P = .76) and significant increase of pre-/post-interventional PWV analysis (P < .001). CONCLUSION: Combined automatic ABI and PWV acquisition with the VascAssist device showed excellent diagnostic accuracy for detection of PAD. Compared to FMD, AS analysis may serve as an investigator-independent (screening) tool for determination of functional vascular damage in atherosclerosis.