Search

Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver condition with significant risk of progression to steatohepatitis and cirrhosis. Therapeutic strategies in NAFLD include lifestyle changes mainly related to dietary interventions and use of drugs or nutritional components that could improve plasma lipid profiles and insulin sensitivity and decrease the local inflammatory response. In this study, we tested the effects of monacolin K, an inhibitor of HMCoA reductase. In a prospective, uncontrolled, open study, we treated 24 patients with NAFLD and mild hypercholesterolemia with 10 mg/day of monacolin K. At baseline and after 26 weeks, we measured in plasma liver tests, lipids, malondialdehyde, and oxidized glutathione, and assessed biochemical steatosis scores, liver elastography, and body composition with bioimpedance analysis. Monacolin K significantly reduced plasma alanine aminotransferase, cholesterol, triglycerides and the homeostatic model assessment (HOMA) index that indicated improved insulin sensitivity. No significant changes were found in body fat mass and visceral fat, nor in liver elastography, while the fatty liver index (FLI) was significantly decreased. Plasma levels of both malondialdehyde and oxidized glutathione were markedly reduced by monacolin K treatment, suggesting a reduction in oxidative stress and lipid peroxidation. In summary, this pilot study suggests possible benefits of monacolin K use in NAFLD patients that could be linked to a reduction in oxidative stress. This hypothesis should be further investigated in future studies.

Alcoholic beverages are common components of diets worldwide and understanding their effects on humans’ health is crucial. Because hypertension is the leading risk factor for cardiovascular diseases and all-cause mortality, the relationship of alcohol consumption with blood pressure (BP) has been the subject of extensive investigation. For the purpose of this review, we searched the terms “alcohol”, “ethanol”, and “arterial hypertension” on Pubmed MeSH and selected the most relevant studies. Short-term studies showed a biphasic BP response after ingestion of high doses of alcohol, and sustained alcohol consumption above 30 g/day, significantly, and dose-dependently, increased the risk for hypertension. These untoward effects of alcoholic beverages on BP can be mediated by a multiplicity of neurohormonal mechanisms. In addition to the effects on BP, excess alcohol intake might contribute to cardiac and renal hypertensive organ damage, although some studies suggest possible benefits of moderate alcohol consumption on additional cardiovascular risk factors, such as diabetes and lipoprotein(a). Some intervention studies and cumulative analyses support the evidence of a benefit of the reduction/withdrawal of alcohol consumption on BP and cardiovascular outcomes. This is why guidelines of scientific societies recommend avoidance or limitation of alcohol intake below one unit/day for women and two units/day for men. This narrative article overviews all these topics, providing an update of the current knowledge on the relationship between alcohol and BP.

Non-healing diabetic foot ulcers (DFU) are the most notable and striking complications of diabetes mellitus. More than 25% of nonhealing DFU can ultimately lead to amputation of the lower extremity within 6-18 mo after the first manifestation of the wound. Although wound healing is complex, nutritional status is crucial in soft tissue repair. Malnutrition is highly prevalent and overlooked in patients with diabetes and chronic wounds. Moreover, to date, we do not have clear recommendations or evidence about the use of nutritional supplements for improving wound healing in patients with DFU. In this article the authors briefly analyzed the current evidence on the use of nutritional supplements of proteins or amino acids, fatty acids, probiotics, vitamins, and trace elements in the wound healing process in patients with DFU.

Background: Left ventricular (LV) abnormalities were reported in patients with overt and subclinical Cushing syndrome. The aim of this study was to investigate the relationships of daily plasma cortisol profile and cortisol response to an overnight suppression test with cardiac changes in patients with hypertension. Methods: In a cross-sectional study, we included 136 nondiabetic, patients with essential hypertension who were free of cardiovascular and renal complications. Plasma cortisol was measured at 8 am , 3 pm , and 12 am and at 8 am after overnight suppression with 1 mg dexamethasone (dexamethasone suppression test [DST]). Echocardiography was performed with standard B-mode and tissue-Doppler imaging. Results: LV hypertrophy was present in 30% and LV diastolic dysfunction in 51% of patients who were older and had significantly higher body mass index, systolic blood pressure, duration of hypertension, and 12 am and DST cortisol. LV mass index and relative wall thickness increased progressively across tertiles of DST cortisol, together with progressive worsening of diastolic function. LV mass index was directly related to age, systolic blood pressure, duration of hypertension, and 12 am and DST cortisol, and inversely to creatinine clearance. Multivariate regression analysis showed independent correlation of LV mass index with body mass index, systolic blood pressure, and 12 am and DST cortisol. Logistic regression showed that DST cortisol independently predicted LV hypertrophy. Conclusions: Midnight and DST plasma cortisol levels are independent determinants of LV mass and geometry in patients with essential hypertension suggesting that even minor changes in regulation of cortisol secretion could contribute to cardiac abnormalities in these patients.

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), including alpha-linolenic acid (ALA) and its derivatives eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are “essential” fatty acids mainly obtained from diet sources comprising plant oils, marine blue fish, and commercially available fish oil supplements. Many epidemiological and retrospective studies suggested that ω-3 PUFA consumption decreases the risk of cardiovascular disease, but results of early intervention trials have not consistently confirmed this effect. In recent years, some large-scale randomized controlled trials have shed new light on the potential role of ω-3 PUFAs, particularly high-dose EPA-only formulations, in cardiovascular prevention, making them an attractive tool for the treatment of “residual” cardiovascular risk. ω-3 PUFAs' beneficial effects on cardiovascular outcomes go far beyond the reduction in triglyceride levels and are thought to be mediated by their broadly documented “pleiotropic” actions, most of which are directed to vascular protection. A considerable number of clinical studies and meta-analyses suggest the beneficial effects of ω-3 PUFAs in the regulation of blood pressure in hypertensive and normotensive subjects. These effects occur mostly through regulation of the vascular tone that could be mediated by both endothelium-dependent and independent mechanisms. In this narrative review, we summarize the results of both experimental and clinical studies that evaluated the effect of ω-3 PUFAs on blood pressure, highlighting the mechanisms of their action on the vascular system and their possible impact on hypertension, hypertension-related vascular damage, and, ultimately, cardiovascular outcomes.

Background: Takayasu Arteritis (TAK) increases vascular stiffness and arterial resistance. Hypertension and atherosclerosis lead to similar changes. We investigated possible differences in cardiovascular remodeling between these diseases and whether the differences are correlated with immune cell expression. Methods: Patients with active TAK arteritis were compared with age- and sex-matched hypertensive and atherosclerotic patients. In a subpopulation of TAK patients, Treg/Th17 cells were measured before (T0) and after 18 months (T18) of infliximab treatment. Echocardiogram, supraaortic Doppler ultrasound, and lymphocytogram were performed in all patients. Histological and immunohistochemical evaluation of the vessel wall was performed to compare the in vivo results. Results: TAK patients have increased aortic valve dysfunction and diastolic dysfunction. These data have been associated with uric acid levels. A significant increase in aortic stiffness was also noted and associated with peripheral T lymphocyte levels. CD3+CD4+ cell infiltrates were detected in the vessel wall samples of these patients. They had a lower mean percentage of Tregs at T0 than controls, but levels increased significantly at T18. Opposite results were found in Th17 cells. Finally, TAK patients were found to have an increased risk of atherosclerotic cardiovascular disease (ASCVD). Conclusion: Our data suggest that different pathogenic mechanisms of vessel damage, including atherosclerosis, underlie TAK patients compared with control subjects. The increased risk of ASCVD in TAK patients correlates directly with the degree of inflammatory cell infiltration in the vessel wall. Infliximab restores the normal frequency of Tregs/Th17 in TAK patients and allows a possible reduction of steroids and immunosuppressants.

No abstract present.

Background COVID-19 has caused considerable morbidity and mortality worldwide and cardiac involvement has been reported during infection. The short-term cardiac outcome in survivors of COVID-19 is not known. Objective To examine the heart of patients who survived COVID-19 and to compare the cardiac outcome between patients who recovered from mild-to-moderate or severe illness. Methods With use of ECG and echocardiography, we examined the heart of 105 patients who had been hospitalized with COVID-19 and were consecutively recruited after hospital discharge while attending follow-up visits. Survivors of COVID-19 were compared with 105 matched controls. We also compared the cardiac outcome and lung ultrasound scan between COVID-19 patients who had mild-to-moderate or severe illness. Results Cardiac data were collected a median of 41 days from the first detection of COVID-19. Symptoms were present in a low percentage of patients. In comparison with matched controls, no considerable structural or functional differences were observed in the heart of survivors of COVID-19. Lung ultrasound scan detected significantly greater residual pulmonary involvement in COVID-19 patients who had recovered from severe than mild-to-moderate illness. No significant differences were detected in ECG tracings nor were found in the left and right ventricular function of patients who had recovered from mild-to-moderate or severe illness. Conclusions In a short-term follow-up, no abnormalities were identified in the heart of survivors of COVID-19, nor cardiac differences were detected between patients who had different severity of illness. With the limitations of a cross-sectional study, these findings suggest that patients who recover from COVID-19 do not have considerable cardiac sequelae. Graphic abstract

Atrial fibrillation (AF) is the most common type of arrhythmia in the general population with a prevalence that reaches one third of patients with arterial hypertension. Several risk factors frequently associated with hypertension predispose the myocardium to AF by inducing atrial inflammation and fibrosis and altering atrial electrical and mechanical characteristics. AF influences the quality of life of hypertensive patients since it increases incidence of stroke and other thromboembolic events, and mortality. Polyunsaturated fatty acids of the ω-3 family (ω-3 PUFA) have been demonstrated to be beneficial in cardiovascular disease prevention by reducing plasma lipids and blood pressure levels and decreasing the risk of sudden death. These fatty acids can act as potent anti-inflammatory and anti-arrhythmic agents. Many studies have investigated a possible preventive effect of ω-3 PUFA on incident AF reporting contradictory results. This article overviews the evidence currently available on this important topic and provides some conclusive remarks on the possibility that these fatty acids could be beneficial in hypertensive patients.

Background: Takotsubo syndrome (TTS) is an acute heart syndrome characterised by reversible ventricular dysfunction with the absence of significant coronary occlusion, which typically occurs in pos...

Objectives: Recent studies suggest an association between vitamin D deficiency and prevalence of cardiovascular disease in the general population. However, the evidence of a relationship between vitamin D status and vascular functional changes in hypertension is currently controversial. We aimed to investigate if the presence of low serum vitamin D levels is associated with an increased arterial stiffness in essential hypertension. Design and Method: In 151 essential hypertensive patients (53±13 y, 71 males) we measured serum 25(OH)-vitamin D levels and performed a carotid ultrasound examination to determine variables of carotid stiffness, such as distensibility, compliance, Young elastic modulus and beta-stiffness. Furthermore, in a subgroup of 86 subjects we evaluated the augmentation index and the pulse wave velocity. The patients were subdivided into two groups according to the 25(OH)-vitamin D levels, lower or higher than 30 nmol/L. Results: A plasma vitamin D level lower than 30 nmol/L was found in 83 (55%) of 151 patients. Patients with low vitamin D levels were significantly older than those with a normal value of serum vitamin D. No significant differences in carotid artery distensibility, compliance, Young elastic modulus, and beta-stiffness were observed between patients with plasma vitamin D below or above 30 nmol/L. Also, the augmentation index and the pulse wave velocity were comparable in hypertensive patients with lower or higher plasma vitamin D levels. Conclusions: This study does not support the hypothesis of an association between vitamin D deficiency and functional vascular changes in hypertensive patients.

Objective: In patients with primary hypertension, plasma aldosterone levels are significantly decreased by an intravenous saline load (IVSL), but this response is variable among patients and related to the ability of salt to modulate aldosterone production. Previous studies have reported that activity of the renin-angiotensin-aldosterone system is related with age. The aim of this study was to investigate whether age might affect the aldosterone response to an IVSL. Design and Method: In 124 hypertensive patients (48±13 y, 71 males) who were washed-out of antihypertensive drugs for 2 weeks, we measured renin and PA levels before and after an IVSL (2 lt. saline in 4 h). In all patients secondary causes of hypertension were excluded. For statistical purposes patients were subdivided into two groups based on age (< or > 60 y). Results: Twenty-three of 124 patients (18%) were had 60 y of age or more (range 61-77) and the remaining were younger than 60 y (19-60 y). No differences were found between the two groups for gender, body mass index, serum potassium and creatinine clearance. Urinary sodium excretion was comparable in patients older (159±83) or younger (159±66) than 60 y. Baseline PA (76 [49-121] pg/ml) and renin (5.0 [1.9-9.8] mcIU/ml) levels were significantly lower in patients older than 60 y than in those younger than 60 y (115 [77-162] pg/ml, P=0.019; 10.7 [5.1-20.8] mcIU/ml, P=0.026). As expected IVSL decreased significantly (P Conclusions: PA levels are lower in hypertensive patients older than 60 y. This difference becomes more relevant after IVSL suggesting greater response of the renin-angiotensin system to volume expansion. This should be taken into account in the diagnostic work-out of hypertensive patients.

International audience; Arterial stiffness and compliance parameters from two adjacent elastic arteries [aorta and common carotid artery (CCA)] were compared and their relationship with left ventricular (LV) structure and function and clinical parameters was assessed. 584 healthy subjects were prospectively enrolled [mean age 47.8 ± 18.4 years, range 16-94; 318 (54.4%) men]. They underwent comprehensive transthoracic echocardiography; M-mode diameters were measured at the level of the ascending aorta in systole and diastole and by echo-tracking at the level of the left CCA. The β-stiffness, pressure-strain elastic modulus, arterial compliance and one-point pulse wave velocity were derived. A significant correlation was observed between aortic and CCA stiffness and compliance parameters (p

Background Both hyperuricaemia and left ventricular (LV) hypertrophy are associated with the metabolic syndrome and increased cardiovascular risk. The relationship between uric acid levels and left ventricular mass in hypertension, however, is unclear. In this study, we have investigated this relationship in hypertensive patients without the metabolic syndrome. Materials and methods In a cross-sectional study, 367 nondiabetic, essential hypertensive patients (age 52 ± 14; 194 males and 173 females) free of clinically relevant cardiovascular complications and without the metabolic syndrome were consecutively recruited at a university hypertension clinic. In these patients, we measured plasma levels of uric acid, lipids, glucose and insulin at fast and after an oral glucose load (OGTT), renal function and performed both conventional and tissue Doppler echocardiography. Results Hypertensive patients with LV hypertrophy had higher uric acid levels and greater prevalence of hyperuricemia than patients with normal left ventricular mass. Uric acid levels were directly related with fasting and post-OGTT plasma insulin and with the HOMA index and inversely with 24-h creatinine clearance. Uric acid was also significantly and directly related with the left ventricular mass and multivariate regression analysis showed that this relationship was independent from components of the metabolic syndrome and renal function in women, but not in men. Conclusions Elevated uric acid levels are independently related to the left ventricular mass in hypertensive women without the metabolic syndrome. In these patients with a low cardiovascular risk profile, uric acid might contribute to the development of subclinical cardiac damage.

Objectives:Cushing syndrome and subclinical hypercortisolism are associated with changes in left ventricular (LV) structure. No data are available on the relationship between cortisol production and LV mass and geometry in essential hypertension (EH).Methods:In 103 EH patients, we evaluated clinical

Experimental and clinical evidence obtained in the last 2 decades clearly indicates that protracted exposure to inappropriately elevated aldosterone levels causes significant changes in left ventricular structure and function. Animal studies have demonstrated that aldosterone induces myocardial inflammatory changes and fibrosis in the presence of a high salt diet. Moreover, the effects of aldosterone on the heart have been investigated in different clinical conditions. These conditions include systolic and diastolic heart failure, essential hypertension, and primary aldosteronism that offers a unique clinical model to study the cardiac effects of excess aldosterone because these effects are isolated from those of the renin-angiotensin axis. A relatively clear picture is emerging from these studies with regard to aldosterone-related changes in left ventricular mass and geometry. Conversely, no direct effect of aldosterone on left ventricular diastolic function can be demonstrated and improvement of diastolic function obtained in some studies that have employed mineralocorticoid receptor blockers could result from left ventricular mass reduction. Animal experiments demonstrate that effects of aldosterone on the left ventricle require high salt intake to occur, but the evidence of this contribution of salt to aldosterone-induced cardiac changes in humans remains weaker and needs further research. The article reviews the results of clinical studies addressing the role of aldosterone in regulation of LV remodeling and diastolic function, and focuses on the possible relevance of salt intake.

Introduction: Imidapril data are favorable, showing that presents an appropriate metabolic profile in patients with metabolic syndrome or glucose intolerance. However, there are few data in real-life treatments with imidapril compared with other angiotensin-converting enzyme inhibitors (ACE I). In this paper, we compared a group of diabetic hypertensive patients receiving imidapril with another group receiving enalapril for the treatment of hypertension and value the impact on glycosylated haemoglobin (Hb A1c) over several months. Objectives: To study the effect on glycaemic control and renal function following the treatment with imidapril or enalapril in hypertensive diabetic patients (PHD). Materials and Methods: We studied 56 PHD (68 5 years, 36 women and 25 men) who were treated with imidapril (30 P) or enalapril (26P) in addition to the usual treatment their doctor considered it necessary to maintain BP 120 / 80 controls on the office. All underwent a A1cHb and glycaemic control at the beginning, first, two and 6 months, end of the study with a 24 hr, microalbuminuria (Mcalb).,at the beginning and the end to the study. The results were compared and shown in the following table

AIM A prothrombotic state is associated with organ damage in hypertensive patients. Carotid intima-media thickness (IMT) is an early marker of vascular damage that anticipates the development of atherosclerotic plaques. The aim of the present study was to investigate the relationships between subclinical carotid damage and markers of the prothrombotic state in hypertension. METHODS In 258 essential hypertensive patients who were consecutively recruited at a hypertension clinic an ultrasound carotid scan was performed with assessment of the IMT and plasma levels of C-reactive protein, fibrinogen, fibrin D-dimer, prothrombin fragment 1+2, homocysteine, and lipoprotein(a) were measured. RESULTS Patients with an IMT above the median of the distribution (800 µm) were older and had greater BMI, pulse pressure, duration of hypertension, and prevalence of coronary heart disease than patients with an IMT below the median. Patients with higher IMT had also greater levels of C-reactive protein, fibrinogen, fibrin D-dimer, and homocysteine. Regression analysis showed a direct relationship of IMT with age, waist circumference, pulse pressure, fibrinogen, fibrin D-dimer, and number of cigarettes smoked per day, and an inverse relationship with creatinine clearance. On multivariate analysis, age, pulse pressure, and fibrin D-dimer were independently related with IMT. CONCLUSION In hypertensive patients, subclinical carotid damage is related with evidence of activated coagulation system suggesting a prothrombotic state. This might contribute to the development of hypertensive arterial damage even in the earliest stages.

Experimental and clinical studies indicate that exposure to high aldosterone concentrations causes cardiac damage independent of the blood pressure level. In recent years, it has become clear that the effects of aldosterone on the heart are mediated by actions on a variety of cell types and intracellular mechanisms that contribute to regulation of specific tissue responses, leading to hypertrophy and fibrosis. Most cardiac effects of aldosterone are mediated by activation of mineralocorticoid receptors that are detected in cardiac myocytes and fibroblasts. Clinical evidence of the unfavorable cardiac effects of aldosterone has been established in landmark studies that have tested the benefits of aldosterone antagonists in patients with heart failure and decreased ejection fraction. However, evidence of benefits of aldosterone antagonists occurring independent of the renal effects of these agents is not limited to patients with systolic heart failure. In this article, we briefly summarize the current knowledge on the effects of aldosterone antagonists on cardiac protection and highlight the most recent findings that have been obtained in different cardiac conditions with use of these drugs.