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The interaction between the heart and large arteries represent a not fully understood process, which results from the integration of pressure wave generation, flow ejection, wave travel and reflection, and geometric mismatch between structures. Left ventricular (LV) mass and geometry, two independent predictors of worse cardiac outcomes, are modelled by changes in cardiac afterload. Central pulse pressure (cPP) itself, a marker of LV afterload, is generated from heart contraction and pressure/flow propagation into the arterial system. As such, increased cPP may be viewed as both the cause and the consequence of an increased LV work. Our research group first described an inverse, age-dependent, relationship between aortic PWV, relative wall thickness, and the velocity of LV circumferential fiber shortening. We also showed that the relationship between cPP and stroke volume is progressively lost at increasing age. Finally, we found, in a cohort of untreated hypertensives, a pressure-independent relationship between aortic characteristic impedance, LV mass and geometry. Taken together, these results suggest that changes in LV structure and function occur as part of the compensatory response of the LV to unfavourable ventricular-vascular coupling and increased aortic stiffness. Heart rate (HR) is another relevant effect-modifier of the interconnection between cardiac and arterial function. HR is independently associated with cardiac index, PP amplification, and aortic stiffness. Pharmacological BP-lowering interventions combined with HR-lowering effect, such as beta-blockers, are ineffective in reducing LV mass. Moreover, HR changes are positively related to DBP changes. Therefore, anti-hypertensive drugs with associated HR-lowering effect only spuriously affect the ventricular-vascular coupling. More research is needed in order to find new targets of treatment able to prevent the occurrence of structural LV remodeling.

Hypothesis: increased arterial stiffness has been reported in subjects with systemic lupus erythematosus (SLE) compared with healthy controls. In SLE, indexes of organ damage are related to a poor clinical status and worse prognosis independently from the activity of the disease. Data are controversial about the association between SLE-related organ damage and arterial stiffness. Methods: 40 subjects with history of SLE (mean age 45±12 years, 90% women) and a median disease duration of 12 years (IQR 5–19), underwent assessment of carotid-femoral pulse wave velocity (cf-PWV) by means of applanation tonometry (SphygmoCor). A comprehensive clinical, metabolic and immunological assessment was performed. Irreversible organ damage, not related to active inflammation, was assessed through the Systemic Lupus International Collaborating Clinics (SLICC) damage index. Results: mean BP was 128/75±16/10 mmHg. 9 subjects (23%) were on anti-hypertensive treatment, 4 (10%) had had previous cardiovascular events, 17 (42%) were treated with steroids, 29 (71%) with hydroxychloroquine, 15 (37%) with other immunosuppressants. Median SLICC index was 2 (IQR 1–3), average cf-PWV was 7.5±1.9 m/s. cf-PWV significantly increased across SLICC damage index categories (F=3.141, p

Objective: Pulse pressure (PP) is a complex physiologic trait affected by many variables, including LV contractility (reflected by stroke volume), arterial stiffness, and central-to-brachial amplification.The impact of age on the relationship between stroke volume and central or brachial PP has not been investigated. Methods: 3765 untreated hypertensive adults (men 56%, age 50 ± 12 years) underwent 24-hour ambulatory BP monitoring (SpaceLabs) and M-mode echocardiography. In a subset of 982 subjects in whom central PP was measured by applying a transfer function to radial pulse wave (SphygmoCor), we also estimated central office (or 24 h) PP by regression equations based on office (or 24 h) PP and MAP, heart rate, age, height and sex (R2 = 0.92 between estimated and measured central PP).The same equations were then applied to the original population to obtain estimated central PP. Results: Stroke volume had a significant direct association with both brachial and central 24 h PP up to the age of 39 years. The above relationship weakened with age and became mostly non-significant after the age of 40 (all r < 0.10). Similar, although weaker, trends were observed for office PP (both brachial and central). Conclusions: 24-h PP has a strong direct association with LV stroke volume in the young only, and might more exclusively depend on arterial stiffness later in life. Since the above relationship was also observed with estimated central PP, it may not depend on PP amplification. The “young” and “old” pathophysiological patterns of PP may help to explain the increasingly adverse prognostic value of PP observed with advancing age.

The relation between carotid-femoral pulse wave velocity (cfPWV) and LV remodeling/dysfunction is confounded by the effect of blood pressure (BP). We evaluated the relationship between cardio-ankle vascular index (CAVI), a less BP-dependent measure of the stiffness constant (β) of the aorta, iliac, femoral and tibial arteries, and prognostically relevant measures of LV structure and systolic function. In 119 subjects with hypertension or high-normal BP (34% treated; 56±16 years, BP 144/89±21/12 mmHg), we measured CAVI and cfPWV, and LV mass and systolic function at echocardiography. cfPWV had a direct association with SBP/DBP (r=0.33/0.25, p0.1). Both CAVI and cfPWV had direct univariate relationships with LV mass index (r=0.38, p0.1). In a multivariate stepwise linear regression model, CAVI was an independent predictor of inappropriate LV mass (β=0.44, p

Pregnancy is associated with profound vascular adaptive changes. Cross-sectional studies show greater arterial stiffness in gestational diabetes than in normal pregnancy. However, the time course of maternal cardiovascular hemodynamics in normal and diabetic pregnancy can only be appreciated in longitudinal studies. Thirty-six women with gestational diabetes (34±5 years, BP 111/69±13/8 mmHg) and 36 with normal pregnancy (33±3 years, BP 111/68±10/8 mmHg) were examined 3 times, at a gestational age of 30 and 35 weeks, and 12 weeks after delivery. On each occasion, tonometry-based carotid-femoral pulse wave velocity (cfPWV) and heart-rate corrected aortic augmentation index (AIx@75) were obtained (SphygmoCor). Compared to women with normal pregnancies, women with gestational diabetes had a higher age- and mean arterial pressure-adjusted cfPWV (p

Background: Migraine is associated with an increased risk for ischemic stroke and other cardiovascular (CV) events, including angina, myocardial infarction, and CV death. However, the mechanisms which link migraine to CV disease remain uncertain. In the present case-control study, we hypothesized that aortic stiffness, a direct measure of pulse wave velocity and an independent predictor of stroke and CV disease, may be increased in young migraineurs with no overt CV disease or major CV risk factors. Methods and Results: We studied 41 individuals with migraine (age 31±8 years, 82% females, blood pressure 118/73±12/9 mmHg) and 41 age- and sex-matched healthy control subjects. In all participants, carotid-to-femoral pulse wave velocity was determined by applanation tonometry (SphygmoCor). Cases and controls were free from overt CV disease, diabetes, and major CV risk factors. Subjects with migraine had a higher aortic pulse wave velocity than matched control subjects (7.4±1.2 vs 6.5±1.1m×s−1, p=0.001). Age, mean arterial pressure as a measure of distending pressure and the presence of migraine (all p