Pressure-dependence of arterial stiffness: potential clinical implications

BACKGROUND: Arterial stiffness measures such as pulse wave velocity (PWV) have a known dependence on actual blood pressure, requiring consideration in cardiovascular risk assessment and management. Given the impact of ageing on arterial wall structure, the pressure-dependence of PWV may vary with age. METHODS: Using a noninvasive model-based approach, combining carotid artery echo-tracking and tonometry waveforms, we obtained pressure-area curves in 23 hypertensive patients at baseline and after 3 months of antihypertensive treatment. We predicted the follow-up PWV decrease using modelled baseline curves and follow-up pressures. In addition, on the basis of these curves, we estimated PWV values for two age groups (mean ages 41 and 64 years) at predefined hypertensive (160/90 mmHg) and normotensive (120/80 mmHg) pressure ranges. RESULTS: Follow-up measurements showed a near 1 m/s decrease in carotid PWV when compared with baseline, which fully agreed with our model-prediction given the roughly 10 mmHg decrease in diastolic pressure. The stiffness-blood pressure-age pattern was in close agreement with corresponding data from the 'Reference Values for Arterial Stiffness' study, linking the physical and empirical bases of our findings. CONCLUSION: Our study demonstrates that the innate pressure-dependence of arterial stiffness may have implications for the clinical use of arterial stiffness measurements, both in risk assessment and in treatment monitoring of individual patients. We propose a number of clinically feasible approaches to account for the blood pressure effect on PWV measurements

Pressure-dependence of arterial stiffness:potential clinical implications

BACKGROUND: \u3cbr/\u3eArterial stiffness measures such as pulse wave velocity (PWV) have a known dependence on actual blood pressure, requiring consideration in cardiovascular risk assessment and management. Given the impact of ageing on arterial wall structure, the pressure-dependence of PWV may vary with age.\u3cbr/\u3eMETHODS: \u3cbr/\u3eUsing a noninvasive model-based approach, combining carotid artery echo-tracking and tonometry waveforms, we obtained pressure-area curves in 23 hypertensive patients at baseline and after 3 months of antihypertensive treatment. We predicted the follow-up PWV decrease using modelled baseline curves and follow-up pressures. In addition, on the basis of these curves, we estimated PWV values for two age groups (mean ages 41 and 64 years) at predefined hypertensive (160/90 mmHg) and normotensive (120/80 mmHg) pressure ranges.\u3cbr/\u3eRESULTS: \u3cbr/\u3eFollow-up measurements showed a near 1 m/s decrease in carotid PWV when compared with baseline, which fully agreed with our model-prediction given the roughly 10 mmHg decrease in diastolic pressure. The stiffness-blood pressure-age pattern was in close agreement with corresponding data from the 'Reference Values for Arterial Stiffness' study, linking the physical and empirical bases of our findings.\u3cbr/\u3eCONCLUSION: \u3cbr/\u3eOur study demonstrates that the innate pressure-dependence of arterial stiffness may have implications for the clinical use of arterial stiffness measurements, both in risk assessment and in treatment monitoring of individual patients. We propose a number of clinically feasible approaches to account for the blood pressure effect on PWV measurements.\u3cbr/\u3

Arterial stiffness in patients with COPD: the role of systemic inflammation and the effects of pulmonary rehabilitation

Clear evidence for an association between systemic inflammation and increased arterial stiffness in patients with COPD is lacking. Moreover, the effects of pulmonary rehabilitation (PR) on arterial stiffness are not well studied.We aimed 1. to confirm increased arterial stiffness in COPD; 2. to evaluate its correlates including systemic inflammation; and 3. to study whether or not it is influenced by PR.Aortic pulse wave velocity (APWV) was determined in 168 healthy volunteers and APWV and inflammatory markers in 162 COPD patients during baseline evaluation of a PR-program. A complete post-PR dataset was collected in 129 patients.APWV was increased in COPD patients compared to controls. Blood pressure and age predicted baseline APWV. Systemic inflammatory markers were not independently related to APWV. Although baseline APWV was predictive for the change in APWV after PR (r= -0.77), on average APWV did not change (10.7+/-2.7 vs. 10.9+/-2.5 m.s-1; p=0.339).Arterial stiffness in COPD is not related to systemic inflammation and does not respond to state-of-the-art PR. These results emphasize the complexity of cardiovascular risk and its management in COPD

Strategia di ricerca e sviluppo

Flow-mediated dilation is aimed at normalization of local wall shear stress under varying blood flow conditions. Blood flow velocity and vessel diameter are continuous and opposing influences that modulate wall shear stress. We derived an index FMDv to quantify wall shear stress normalization performance by flow-mediated dilation in the brachial artery. In 22 fasting presumed healthy men, we first assessed intra-and inter-session reproducibilities of two indices pFMD(v) and mFMD(v), which consider the relative peak and relative mean hyperemic change in flow velocity, respectively. Second, utilizing oral glucose loading, we evaluated the tracking performance of both FMDv indices, in comparison with existing indices [i.e., the relative peak diameter increase (%FMD), the peak to baseline diameter ratio (D-peak/D-base), and the relative peak diameter increase normalized to the full area under the curve of blood flow velocity with hyperemia (FMD/shear(AUC)) or with area integrated to peak hyperemia (FMD/shear(AUC_peak))]. Inter-session and intra-session reproducibilities for pFMD(v), mFMD(v) and %FMD were comparable (intra-class correlation coefficients within 0.521-0.677 range). Both pFMD(v) and mFMD(v) showed more clearly a reduction after glucose loading (reduction of similar to 45%, p = 0.074); D-peak/D-base (similar to 11%, p >= 0.074); FMD/shear(AUC_peak) (similar to 20%, p >= 0.016) and FMD/shear(AUC) (similar to 38%,

Acute Effects of Cocoa Flavanols on Blood Pressure and Peripheral Vascular Reactivity in Type 2 Diabetes Mellitus and Essential Hypertension

Background: Type 2 diabetes mellitus (T2DM) is associated with a high risk of vascular complications. Interestingly, cocoa flavanols (CF) can exert beneficial vascular effects in non-diabetic subjects. However, these effects have only been scarcely studied in T2DM. Therefore, we performed a study to assess the effects on vascular reactivity of a single dose of CF (790 mg) in T2DM and whether certain antihypertensive drugs may modulate these effects. Methods: 24 non-diabetic and 11 T2DM subjects were studied in a cross-over design. Fasting blood samples, blood pressure (BP), and arterial vasoreactivity (flow-mediated dilation) were assessed before and 70 min after capsule ingestion. Muscle microvascular reactivity was only assessed after capsule ingestion. Age, waist-to-hip ratio, BP at baseline, and the use of antihypertensive drugs were regarded as covariates in a mixed models analysis. Results: CF ingestion did not affect any parameter. However, independent of the type of capsules ingested, a decrease in diastolic BP by 3 mmHg (95% CI: -4.0; -2.0) and an increase in the change in brachial artery diameter (pre vs. post occlusion) by 0.06 mm (95% CI: 0.01; 0.12) were detected in the non-diabetic group, while they remained unchanged in the T2DM group. Conclusion: No beneficial effects of CF were detected on vascular reactivity parameters in T2DM and non-diabetic participants

Acute Effects of Cocoa Flavanols on Blood Pressure and Peripheral Vascular Reactivity in Type 2 Diabetes Mellitus and Essential Hypertension

Background: Type 2 diabetes mellitus (T2DM) is associated with a high risk of vascular complications. Interestingly, cocoa flavanols (CF) can exert beneficial vascular effects in non-diabetic subjects. However, these effects have only been scarcely studied in T2DM. Therefore, we performed a study to assess the effects on vascular reactivity of a single dose of CF (790 mg) in T2DM and whether certain antihypertensive drugs may modulate these effects. Methods: 24 non-diabetic and 11 T2DM subjects were studied in a cross-over design. Fasting blood samples, blood pressure (BP), and arterial vasoreactivity (flow-mediated dilation) were assessed before and 70 min after capsule ingestion. Muscle microvascular reactivity was only assessed after capsule ingestion. Age, waist-to-hip ratio, BP at baseline, and the use of antihypertensive drugs were regarded as covariates in a mixed models analysis. Results: CF ingestion did not affect any parameter. However, independent of the type of capsules ingested, a decrease in diastolic BP by 3 mmHg (95% CI: -4.0; -2.0) and an increase in the change in brachial artery diameter (pre vs. post occlusion) by 0.06 mm (95% CI: 0.01; 0.12) were detected in the non-diabetic group, while they remained unchanged in the T2DM group. Conclusion: No beneficial effects of CF were detected on vascular reactivity parameters in T2DM and non-diabetic participants