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Objective: Acute SarsCoV2 infection is associated with endothelial dysfunction and endothelitis which might explain systemic microvascular impairment. The presence of endothelial damage can promote vasoconstriction with consequent organ ischemia, inflammation, tissue edema and a procoagulant state resulting in an increase in the incidence of cardio-and cerebrovascular events. Microvascular thrombosis has been demonstrated in post-mortem autopsy of COVID19 patients;however no data are available about skin capillary alterations in these patients. Design and method: We evaluated skin microvascular alterations in 14 patients admitted to our hospital with SarsCov2 infection. Basal capillary density was performed by capillaroscopy bedside in the nailfold and in the dorsum of the 4th finger. Results: Fourteen patients (9 males, 5 females) were evaluated: average age was 66±1 years, BMI 26±3. Nine patients were hypertensive (64%), 4 diabetic (29%), 3 were dyslipidemic (21%), 3 with cerebrovascular or cardiovascular disease history (21%). Seven patients were treated with ev steroid (50%), 3 with tocilizumab (21%) and 7 were treated with non-invasive ventilation (50%). During the hospitalisation all patients presented interstitial pneumonia SarsCov2 associated whereas vascular complication (ischaemic stroke or pulmonary embolism) were observed in 3 patients (21%) with SarsCov2 infection. Nine patients showed skin capillary alterations (5 thrombosis, 5 haemorrhage/ microbleeding, 4 neoangiogenesis). Interestingly, capillary alterations were present only in patients treated with non-invasive ventilation and/or with cardio-or cerebrovascular complications. These alterations were not detected after 2 month from the discharge. Conclusions: This is the first in vivo evidence of skin capillary thrombosis, microhaemorragia and angiogenesis in patients with acute SARS-CoV2 infection which support the presence of endothelial dysfunction and inflammation. Capillary alterations might reflect systemic vascular effects of viral infection.

Objective:Non-alcoholic fatty liver disease (NAFLD) may be detected in nearly 40% of subjects with a body mass index > 25, with a dramatic increase over time. Aim of the present observational study was to evaluate the prevalence of cardiovascular risk factors in a selected population of patients wit

Objective:Immune system (in particular T lymphocytes) is involved in the pathogenesis of arterial hypertension and microvascular remodelling. It has also been recently suggested a crucial role for spleen in the development and onset of hypertension, through a neuroimmune mechanism mediated by a sple

Objective: Wall-to-lumen ratio of retinal arterioles might serve as an in-vivo parameter of vascular damage. Previous studies have shown a correlation between retinal arteriolar structure and blood pressure values, measured both in the clinic and during 24 hours ambulatory monitoring. We analyzed the impact of brachial clinic blood pressure (BP), of central BP and of 24 hours BP values on wall-to-lumen ratio of retinal arterioles. Methods: In 267 subjects (129 males, age range 20–72 years; mean 54±7 years) wall-to-lumen ratio of retinal arterioles was assessed in vivo using scanning laser doppler flowmetry (Heidelberg retina flowmeter, Heidelberg Engineering). In addition clinic and 24 hours BP values were measured. Central hemodynamics and augmentation index (Ai) were assessed by pulse wave analysis. Results: In never treated patients with essential hypertension (n=56) a higher wall-to-lumen ratio (0.37±0.19 vs. 0.30±0.13, P=0.05) was observed in comparison with normotensive individuals (n=115); no significant differences were observed between treated (n=96) and untreated hypertensive patients. Wall to lumen ratio and wall cross sectional area of retinal arterioles were significantly related to clinic systolic BP(r=0.23, P=0.005) and PP(r=0.18, P=0.005), to 24 hours systolic BP(r=0.28, P=0.0001) and PP(r=0.19, P=0.003) and to central systolic BP(r=0.20, P=0.01) and central PP(r=0.21, P=0.001). Multiple regression analysis including all BP indices revealed that only mean systolic 24 hours BP is independently associated with an increased wall-to-lumen ratio of retinal arterioles. Conclusion: in this quite large group of hypertensive patients and normotensive individuals 24 hours systolic BP seems to be the strongest determinant of increased WLR of retinal arterioles.

Objective: It has been previously demonstrated that T lymphocytes may be involved in the development of hypertension and microvascular remodeling, and that circulating T effector lymphocytes may be increased in hypertension. In particular, Th1 and Th17 lymphocytes may contribute to the progression of hypertension and microvascular damage while TREG lymphocytes seem to be protective. However, no data is available about patients with severe obesity, in which pronounced microvascular alterations were observed. Methods: We have investigated 32 severely obese patients undergoing bariatric surgery, 24 normotensive lean subjects and 11 hypertensive lean subjects undergoing an election surgical intervention. No sign of local or systemic inflammation was present in any subject or patient. A peripheral blood sample was obtained before surgery for assessment of CD4+ T lymphocyte subpopulations. Lymphocyte phenotype was evaluated by flow cytometry after 5 hour in vitro activation in order to assess T-effector and T-regulatory (TREG) lymphocytes. Subsets of TREGS were defined as follows: −TREGS recent thymic emigrants (RTE), directly derived from thymus: CD31+; −TREGS naïve: CCR7+CD45RA+; −TREGS central memory (CM): CCR7+CD45RA−; −TREGS effector memory (EM): CCR7−CD45RA−; −TREGS terminal differentiated effector memory (TDEM): CCR7−CD45RA+. Results: The results are summarized in the Table (*p < 0.05, **p < 0.01, ***p < 0.001 vs. lean normotensives; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. lean hypertensives). A marked reduction of several TREG subpopulations was observed in obese patients compared with controls, together with an increased in some T-effector cells. Lean normotensives Lean hypertensives Obese patients TREGs (%) 4.11 ± 1.60 4.64 ± 1.66 2.69 ± 1.81**## TREGs (abs number) 45.4 ± 24.3 45.4 ± 23.8 27.3 ± 21.1**# TREGs naíve (%) 22.1 ± 10.1 18.1 ± 13.1 13.34 ± 12.9** TREGs naíve (abs number) 10.6 ± 7.75 9.71 ± 8.87 3.87 ± 5.28***## TREG CM (%) 32.3 ± 13.8 32.8 ± 17.8 22.7 ± 15.2*# TREGs CM (abs number) 14.7 ± 10.2 14.2 ± 9.08 6.10 ± 8.08***## CD4+ EM (%) 24.4 ± 9.96 26.8 ± 12.5 34.1 ± 13.3** CD161+CD28+ (%) 86.2 ± 28.5 94.9 ± 5.63 97.2 ± 5.39* Conclusion: TREG lymphocytes are clearly reduced in severely obese patients, possibly contributing to the development of marked microvascular alterations previously observed in such a population.

Objective: Primary aldosteronism is a relatively common condition in hypertensive patients. Only few studies, in small groups of patients, have evaluated large arteries alterations. In some, but not in all studies, positive relationship with vascular damage was observed. Objective: Aim of the study: To compare the prevalence of cardiac and large arteries vascular organ damage in patients with essential hypertension (EH) or primary aldosteronism (PA). Design and method: In 243 consecutive patients with no interfering therapy (147 M, mean age 48 ± 11 years) a routine blood sample, including measurement of aldosterone/renin ratio (ARR) and saline load if ARR>30, was obtained. Echocardiography, carotid ultrasound and measurement of pulse wave velocity (PWV) were performed. We considered 3 groups: 48 patients with EH (ARR 100ng/ml)(51 % with adrenal adenoma). Results: No differences between groups were observed in age, gender, BMI, BP values (clinic and 24 hours), glucose, lipids and renal function. LVMI was greater in PA vs both IA and EH (PA 45 ± 18, IA 39 ± 12, EH 39 ± 10 gr/m2.7, p Conclusions: A greater prevalence of cardiac, but not of large arteries damage is observed in PA as compared to EH when a simultaneous assessment of cardiac and vascular OD is performed.

BACKGROUND AND AIM: Increased vascular resistance is a hallmark of hypertension and involves structural alterations, which may entail smooth muscle cell hypertrophy or hyperplasia, or qualitative or quantitative changes in extracellular matrix (ECM) proteins. Since the renin-angiotensin-aldosterone system modulates these changes, we investigated the effects of 8 weeks of treatment with an angiotensin-converting enzyme (ACE) inhibitor, ramipril (RAM), or a dual ACE and neutral endopeptidase (NEP) inhibitor, MDL-100240 (MDL), on mesenteric small artery structure and ECM proteins in mRen2-transgenic rats (TGRs), an animal model of hypertension with severe cardiovascular damage. MATERIALS AND METHODS: Thirty-five 5-week-old rats were included in the study: six TGRs received RAM; five TGRs RAM + the bradykinin receptor inhibitor, icatibant; six TGRs, MDL; and five TGRs MDL + icatibant, while eight TGRs and five normotensive Sprague-Dawley controls were kept untreated. Mesenteric small arteries were dissected and mounted on a micromyograph. The media-to-lumen ratio (M/L) was then calculated. Vascular metalloproteinase (MMP) content was evaluated by zymography. RESULTS: In untreated TGRs severe hypertension was associated with inward eutrophic remodelling of small arteries. Both RAM and MDL prevented the increase in blood pressure and M/L and decreased MMPs. Icatibant blunted the effect of MDL on BP, M/L and MMPs. CONCLUSIONS: Changes in collagenase activity induced by ramipril and MDL are associated with prevention of small artery structural alterations in TGRs. Furthermore, MDL-induced enhancement of bradykinin could play a role in both the prevention of vascular structural alterations and in the stimulation of MMPs.

Calcitonin is a hormone secreted by thyroid C-cells. Its primary effect seems to be a direct inhibition of bone degradation, but the physiological function of calcitonin in humans is still uncertain. The role of this hormone in the development of osteoporosis is unknown, but few authors have shown bone mass reduction in thyroidectomy patients.To investigate the influence of calcitonin deficiency on bone turnover, 9 males (age 31 to 66 years) submitted to total thyroidectomy in 1996 for non-toxic goitre have been studied. These patients received thyroxine treatment at individual dose but never with suppressed TSH levels. Moreover 8 sex-, age- and Body Mass Index-matched normal subjects have also been studied as control group.Calcitonin was undetectable in thyroidectomized patients, while the mean value was 7.1+/-3.2 pg/ml in the control group. At bone ultrasonography 50% of patients showed osteopenia, while only 1 subject showed osteopenia in the control group. The mean calcium serum level of patients was significant lower than in the control group (p0.001). Calcium urinary level was increased in patients than controls. PTH serum levels were statistically decreased (p0.001) in patients more than in controls. Osteocalcin showed a significantly (p0.05) lower bone formation in patients than in controls, while the markers of resorption, deoxypyridinoline and N-terminal telopeptide of type I collagen, suggested an increased bone turnover in calcitonin-deficiency patients.The results of this study show that the chronic lack of calcitonin in total thyroidectomized patients may play a role in increased bone degradation and osteopenia with a higher risk of bone fracture.

OBJECTIVE To investigate changes in left ventricular (LV) performance, as evaluated by measurement of midwall LV fractional shortening (FS), after reduction of cardiac hypertrophy. DESIGN AND METHODS Echocardiographic evaluation of LV anatomy and function was performed by M-mode echocardiography at baseline, after long-term antihypertensive therapy, and after treatment withdrawal in 68 asymptomatic hypertensive patients (50 males, 18 females, age range 22-62 years). Patients were divided according to the presence of LV hypertrophy (LVH) at baseline (LV mass index, LVMI, > or = 51 g/m(2.7)). RESULTS At baseline patients with concentric (relative wall thickness > 0.44) LV hypertrophy (n = 38) or remodelling (n = 7) had reduced midwall shortening with respect to patients with normal LV geometry (n = 4) or eccentric LVH (n = 19); no differences were observed for endocardial FS. After long-term treatment (average 15 months), in 11 patients LV mass remained within normal limits, in 45 patients LVH reduction was obtained, while in 12 patients LV mass remained persistently elevated. Midwall FS was significantly increased in patients with reduction of LVH both during treatment and after withdrawal of treatment, while it remained significantly lower in patients with persistently elevated LV mass. Changes in midwall fractional shortening were independently associated with modifications in relative wall thickness (P < 0.00001), with changes in end-diastolic dimensions (P < 0.0001) and those of LVMI (P< 0.02) as shown by multivariate analysis. CONCLUSION LV midwall systolic performance significantly improved after reduction of LVH, even in the presence of high blood pressure values. Modifications in relative wall thickness are more independently associated with changes, in LV diastolic dimensions and mass, to midwall improvement

Left ventricular hypertrophy (LVH) and depressed left ventricular performance have been shown to be associated to an adverse prognosis in hypertensive patients. It has not been established, however, whether, during chronic antihypertensive treatment, the increased cardiovascular risk is more strictly related to the presence of LVH or of a low left ventricular performance.A total of 215 patients with uncomplicated hypertension (129 males, 86 females; age range 18-70 years, mean +/- SD 45 +/- 11) underwent an echocardiographic evaluation of left ventricular anatomy and function. In 151 patients (87 males, 64 females; age range 18-70 years, mean 45 +/- 10.4) the echocardiogram was repeated on average 10 +/- 1 years after the initial study. The presence of LVH (left ventricular mass index134 g/m2 in males and 110 g/m2 in females) and the midwall left ventricular shortening/end-systolic stress relationship were prospectively analysed as predictors of cardiovascular non-fatal events (n = 23) in patients who were seen at follow-up.The incidence of non-fatal cardiovascular events was greater in patients with LVH (n = 17, P0.0001) and in those with a lower midwall performance (n = 14, P0.01) at baseline. At follow-up, the incidence of non-fatal cardiovascular events was significantly greater in patients without a reduction in the left ventricular mass index, after adjusting for traditional risk factors (relative risk 3.52 versus 1.38 in patients with persistence and regression of LVH, respectively; P0.01). The baseline midwall fractional shortening was lower in patients with both persistence or regression of LVH (analysis of variance, P0.0001) than in patients with a normal left ventricular mass index. In logistic analysis, the left ventricular mass index at follow-up and age were independent determinants of non-fatal cardiovascular events (P0.001); without the left ventricular mass index at follow-up, this analysis showed that age, systolic blood pressure at follow-up and baseline midwall fractional shortening were independent determinants of non-fatal cardiovascular events.Our results suggest that lack of regression of LVH is a stronger indicator of cardiovascular risk than a depressed baseline midwall left ventricular performance.

Regression of cardiovascular structural changes is a main goal of antihypertensive treatment. Two recent meta-analyses of relatively small noncomparative studies have suggested that angiotensin-converting enzyme (ACE) inhibitors may be more effective than other classes of drugs in inducing regression of left ventricular hypertrophy (LVH). The effect of different antihypertensive drugs on arteriolar structural changes has not yet been properly investigated. The aim of this study was to evaluate the effect of 6 months of treatment with amlodipine (5-10 mg o.d.) or enalapril (10-20 mg o.d.) on blood pressure (BP) (ambulatory monitoring), heart rate (HR), LV mass and function (M-mode echo, two-dimensionally guided), forearm minimal vascular resistance (min VR = BP/max blood flow-venous occlusion plethysmography, taken as an index of vascular structural changes) in 24 hypertensive patients in a comparative single-blind, randomized study, with blind reading of echocardiograms and plethysmographic tracings. After 6 months of treatment with amlodipine 5-10 mg o.d., significant reductions in LV mass index (p = 0.004) and forearm min VR (p = 0.02) were observed. Before and during treatment, LV systolic function, both at rest and during stress (handgrip test), evaluated by fractional shortening as related to end-systolic stress, was in every case within 95% confidence limits calculated in normal subjects. Similar results were observed with enalapril. No significant differences were observed for Doppler indices of diastolic filling after 6 months of treatment with either drug. These results indicate that a significant regression of structural changes in the heart and in the small resistance vessels can be observed after long-term treatment with amlodipine in essential hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)