Summary:Five groups of 20 patients each were studied to analyze the vascular dynamics and structure of the elastic arteries. Group I consisted of healthy young individuals (27 f 4 years); Group II of healthy adults (46 f 9 years); Group IU of normotensive hypercholesterolemic adults (45 f 12 years and serum cholesterol >239 mg/dl); Group IV of hypertensive normocholesterolemic adults (56 f 13 years); and Group V of hypertensive hypercholesterolemic adults (56 f 9 years). The differential arterial pressure was estimated and divided by the volume change (delta P/delta V) of the aorta and the carotid and brachial arteries. The volume change was calculated using the "cylinder formula," measuring the radius from the ultrasonographic vessel image and assigning the cylinder a height of 1 cm. The A/E index of the Doppler transmitral spechum and the maximum velocity flow using Doppler in the above arteries were calculated. The presence of carotid atherosclerosis was observed and given an arbitrary scoring grade of 0, 1 , or 2. A higher arterial and ventricular stiffness was found in the hypertensive patients regardless of the presence of hypercholesterolemia. A higher fall in Doppler velocity and an increase in atherosclerosis lesions were found in Group V. Based on the results of this study, it was concluded that vascular and left ventricular stiffness have a close relationship with arterial hypertension but not with hypercholesterolemia. The hypercholesterolemic patients had a higher prevalence of carotid atherosclerosis and a higher scoring grade of severity.

Summary:With a growing elderly population, the incidence ol' isolated systolic hypertension (ISH) has increased. This study characterizes dynamic vascular changes that occur with achnnced age and with ISH. Fifty-the healthy individuals and seven with ISH were distributed in seven age groups from the second to the seventh decade. An index of aortic stiffness (AWAV) was derived using a mercury sphygmomanometer to oht;lin pulse pressure, and ultrasonographic measurements were iiaed to estimate aortic volumes applying the "cylinder formula." The mathematic derivation of this formula is explairied in detail. Pulse pressure showed no significant change with age, but showed a significant increase with ISH. A decretisc in volume change from systole to diastole was found with advanced age. Norinotensive subjects aged 6.5 -t 2 years hut1 ;I %-fold increase in aortic stiffness compared with young individuals. Elderly patients with ISH had a 7-fold increase in aoilic stiffness compared with Group 1 (15 -t 2 years) (p <: 0.001 ) rind a 2.7-fold increase compared with Group 6 (normotensive subjects aged 65 -t 2 years). A strong correlation between systolic pressure and arterial stiffness was observed (r = 0.953) (p < 0.001 ). The proposed stiffness index was compared with the one described by Hirai, obtaining a high correlation, that is. r = 0.989 (p < 0.001 ). When compared with Stefanadis's index of distensibility, our index showed a coi-rclation ofr = 0.932 (p < 0,003). It is concluded that while systolic pressure is a main detenninant of arterial stiffness, the AWAV is a more sensitive method to estimate dynamic chnnges in elastic arteries such as the aorta.

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Aldosterone has been associated with the development of cardiac hypertrophy and a correlation has been found between levels of aldosterone and the degree of cardiac hypertrophy in hypertensive patients. Our study aimed to test the relation between physiologic cardiac hypertrophy and serum aldosterone in a group of highly trained cyclists. Determination of the left ventricular mass index (LVMI) was performed in a group of 40 professional cyclists by using Devereux's formula with correction for body surface area. After an overnight fast, blood samples were collected and serum aldosterone levels were measured using RIA. LVMI and serum aldosterone were intercorrelated using linear regression analysis. Twenty-three of the 40 cyclists (58%) presented an LVMI > 130 g.m-1 and the other 17 subjects (42%) presented an LVMI < 130 g.m-1. Serum aldosterone levels did not correlate with LVMI in either of the groups (LVMI > 130 g.m-1, r = -0.089; LVMI < 130 g.m-1, r = 0.146). The lack of correlation of this hypertrophy with serum aldosterone levels suggests that physiologic hypertrophy of the athlete's heart could be caused by a different stimulus to that seen in pathologic hypertrophy of hypertensives.

BackgroundSystemic sclerosis is an autoimmune disease characterized by microvascular damage and fibrosis. There are several studies that shown macrovascular damage with arterial stiffness (AS) and the risk of cardiovascular complications. Carotid-femoral pulse wave velocity (CF-PWV) and augmentation index (AIx) are two competent methods to determine AS and predictors of cardiovascular disease. Association between AS and microvascular damage is unknown in systemic sclerosis patients.ObjectivesTo determine the frequency of arterial stiffness in patients with systemic sclerosis and its association with clinical manifestations.MethodsWe performed a cross-sectional study; patients with diagnosis of systemic sclerosis according to ACR/EULAR 2013 criteria were included and the control group was selected from a database of mechanical vascular service. AS was non-invasively assessed by Pulse pen device and AIx was evaluated by tonometry. Statistical analysis was done with SPSS v22 software, we calculated mean and standard deviation, for continuous variables we used Student t test, categorical variables were analyzed by using chi-square or Fisher's exact test. The correlation of AS and clinical variables was assessed with Spearman's correlation.ResultsForty seven patients were included and compared with 39 healthy subjects; mean age of study group was 48±14. vs control group 47±13.7 (p=0.08) 93% were female. Prevalence of AS was 11% vs 3% p=0.039. AS was more frequent in limited systemic sclerosis sub-group and we found correlation with abnormal capillaroscopy, Rho 0.292 p=0.04.ConclusionsArterial stiffness is more prevalent in patients with limited systemic sclerosis and association with abnormal caillaroscopy suggest that both macro and microvascular damage is present in these patients and could explain the presence of early atherosclerosis and increased risk of cardiovascular disease.References Vargas John, Lafyatis Robert. Etiology and pathogenesis of systemic sclerosis. Marc Hochberg. Texbook of Rheumatology (Sixth Edit). Elsevier, 2015. 1177–1245.Ngian G.-S., Sahhar J., Wicks I., Van Doornum, S. Arterial stiffness is increased in systemic sclerosis: A cross-sectional comparison with matched controls. Arthritis and Rheumatism 2012. 64, S301.Colaci M., Giuggioli D., Manfredi A., Sebastiani M. Aortic pulse wave velocity measurement in systemic sclerosis patients, Rheumatism 2012. 64(6), 360–367.Man A., Zhu Y., Zhang Y., Dubreuil M., Rho Y. H., Peloquin C. Choi, H. K. The risk of cardiovascular disease in systemic sclerosis: a population-based cohort study. Annals of the Rheumatic Diseases 2013. 72(7), 1188–93. Disclosure of InterestNone declared