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Atrial fibrillation is the most common sustained cardiac arrhythmia and is associated with significant morbidity and mortality. Coronary artery disease frequently coexists with AF, and management of these associated conditions can be challenging. Endurance veteran athletes are a population at high risk to have episodes of paroxysmal atrial fibrillation. Herewith the author describes an original case of induced atrial fibrillation and myocardial ischemia during an Ex-ECG stress test in a veteran amateur runner.

Background in liver cirrhosis, a marked splanchnic vasodilation causes an increase in portal blood flow, contributing to the development of portal hypertension. Aim To evaluate if, in experimental cirrhosis, a different vascular reactivity exists between splenic and mesenteric components of the splanchnic circulation. Methods Liver cirrhosis was induced in Sprague Dawley rats by common bile duct ligation. in sections of splenic and superior mesenteric arteries, cumulative dose-response curves were obtained. mRNA expression of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and prostaglandin I-2 synthase (PTGIS) was evaluated. Results in cirrhotic rats, mesenteric but not splenic arteries showed a significant increase in endothelium-dependent relaxation to acetylcholine. in control and cirrhotic rats, COX inhibition alone did not significantly change the response of mesenteric arteries to acetylcholine; after inhibiting also NOS, the relaxation was completely abolished in control but only partially decreased in cirrhotic rats. After the inhibition of COX and NOS, the relaxation to acetylcholine was similarly decreased in splenic arteries from control and cirrhotic animals. the contraction induced by phenylephrine of both mesenteric and splenic arteries was decreased in cirrhotic rats. PTGIS mRNA expression did not differ in splenic and mesenteric arteries from control and cirrhotic rats; in cirrhotic rats, eNOS and iNOS mRNA expression was increased in mesenteric but not in splenic vascular bed. Conclusion in cirrhotic rats, a decreased splenic arterial response to vasoconstrictors, rather than an increased response to vasodilators, contributes to splanchnic vasodilation, while in mesenteric arteries also an increased response to vasodilators secondary to, but not only, eNOS and iNOS overexpression, plays a role.

In liver cirrhosis, oxidative stress plays a major role in promoting liver inflammation and fibrosis. Mitochondria dysregulation is responsible for excessive reactive oxygen species production. Therefore, in an experimental model of cirrhosis, we investigated the effect of mitochondria-targeted antioxidant mitoquinone. Liver cirrhosis was induced in Spraque-Dawley rats by common bile duct ligation (CBDL). Mitoquinone (10 mg·kg−1·day−1, oral gavage) or vehicle was administered from 3rd to 28th day after CBDL, when animals were euthanized; liver oxidative stress, inflammation, fibrosis, mitophagy were evaluated; and in vivo and ex vivo hemodynamic studies were performed. In cirrhotic rats, mitoquinone prevented liver inflammation, hepatocyte necrosis, and fibrosis at histological examination; decreased circulating TNF-α, gene expression of transforming growth factor-β1, collagen type 1a1, TNF-α, IL-6, IL-1β, tissue inhibitor of metalloproteinase-1, matrix metalloproteinase (MMP)-2, and MMP-13; and reduced hepatic oxidative stress, as shown by reduced oxidative carbonylation of the proteins, by modulating antioxidants catalase, Mn superoxide dismutase, and Cu/Zn superoxide dismutase. Furthermore, mitoquinone attenuated apoptosis by reducing hepatic protein expression of cleaved caspase-3. A selective removal of dysfunctional mitochondria was improved by mitoquinone, as shown by the increase in Parkin translocation to mitochondria. Treatment with mitoquinone normalized the weight of the spleen; however, it increased portal blood flow and reduced splenic artery intrahepatic resistance, suggesting an effect on resistance index. Mitochondria-targeted antioxidant mitoquinone improves liver inflammation and fibrosis in cirrhotic rats by reducing hepatic oxidative stress, preventing apoptosis, and promoting removal of dysfunctional mitochondria. Therefore, it may represent a promising strategy for the prevention and treatment of liver cirrhosis.

Ascites has been classified according to quantity and response to medical therapy. Despite its precise definitions, little is known about the effects of grade 1 ascites or recurrent ascites (i.e. ascites that recurs at least on 3 occasions within a 12-month period despite dietary sodium restriction and adequate diuretic dosage) on patient outcome. We studied progression of grade 1 ascites and recurrent ascites in a large cohort of outpatients with cirrhosis.We performed a post-hoc analysis of data from 547 outpatients with cirrhosis (259 without ascites, 54 patients with grade 1 ascites, 234 with grade 2 or 3 ascites) who participated a care management program study in Italy from March 2003 through September 2017. We collected demographic, clinical, and laboratory data and patients were evaluated at least every 6 months. Patients received abdominal ultrasound analysis at study inclusion and at least twice a year. Number and volume of paracentesis were collected, when available. Patients were followed until death, liver transplantation, or March 2018. The median follow-up time was 29 months. Primary outcomes were mortality and development of complications of cirrhosis.There was no significant difference in 60-month transplant-free survival between patients with grade 1 vs grade 2 or 3 ascites (36% vs 43%) but survival was significantly lower when both groups were compared with patients without ascites (68%; P.001 for both comparisons). However, the grade of systemic inflammation and the rate of complications were significantly greater in patients with grade 1 ascites than in patients without ascites, but significantly lower than in patients with grade 2 or 3 ascites. Development of grade 2 or 3 ascites did not differ significantly between patients with no ascites vs grade 1 ascites (10% vs 14%). There was no significant difference in 36-month transplant-free survival between patients with ascites responsive to medical treatment vs recurrent ascites (78% vs 62%), whereas patients with refractory ascites had significantly lower survival than patients with responsive or recurrent ascites (23%; responsive vs refractory ascites P.001; recurrent vs refractory ascites P = .022).In an analysis of data from a large cohort of outpatients with cirrhosis, we found that grade 1 ascites is associated with systemic inflammation, more complications, and increased mortality compared with no ascites. Mortality does not differ significantly between patients with recurrent ascites vs ascites responsive to medical treatment.

The Pickelhaube Sign is today recognized as a novel Echocardiographic Risk Marker for Malignant Mitral Valve Prolapse Syndrome. Mitral Valve Prolapse (MVP) has long been recognized to be a relatively common valve abnormality in the general population. Patients with relatively non-specific symptoms and asymptomatic athletes who have MVP still represent an important clinical conundrum for any physician involved in preventive medicine and sports screening. Although cardiac arrhythmias and/or cardiac death are an undesirable problem in MVP patients, when these subjects were studied with Holter Electrocardiogram (ECG) monitoring a prevalence of ventricular arrhythmias up to 34% was observed, with premature ventricular contractions as the most common pattern (66% of cases). At this regard a paper by Anders et al. described a series of cases that suggest that even clinically considered benign cases of MVP in young adults may cause sudden and unexpected death. However, cardiac arrest and Sudden Arrhythmic Cardiac Death (SCD) resulted in rare events only in patients with MVP based on data from a community study. A middle-aged athletic male who has been practicing competitive cycling for about 20 years came to our Sports Medicine Centre to undergo screening of sports preparation for competitive cycling and the related renewal of certification for participation in sports competitions. This athlete was always considered suitable in previous competitive fitness assessments performed in other sports medicine centers. His family history was unremarkable, as well as his recent and remote pathological anamnesis. The physical examination revealed a 3/6 regurgitation heart murmur with a click in the mid late systole. Previous echocardiographic examinations revealed a MVP which was considered benign with mild not relevant mitral regurgitation. He did not complain of symptoms such as dyspnoea or heart palpitations during physical activity. The resting ECG showed negative T waves in the inferior limb leads, and the stress test showed sporadic premature ventricular beats (a couple) with right bundle branch block morphology. An echocardiogram confirmed the presence of a classic mitral valve prolapse with billowing of both mitral leaflets, associated with a mild to moderate valve regurgitation. The TDI exam at the level of the lateral mitral annulus showed a high-velocity mid-systolic spike like a Pickelhaube sign, i.e. spiked German military helmet morphology. Consequently, an in-depth diagnostic imaging with cardiac magnetic resonance imaging was proposed, but the athlete refused it, both because he was totally asymptomatic and above all because he would be forced to pay a considerable amount of money as the examination is not guaranteed by the Italian National Health Service. In conclusion, the athlete remained sub judice as for competitive suitability, Finally, the question is: does MVP really cause sudden death? Is it enough to detect the Pickelhaube signal by echocardiography to stop this athlete? Let us bear in mind that this athlete was asymptomatic, and he had not had any trouble during exercise and maximal effort for many years. Why must we declare him unsuitable to do competitive sports?

Background & aims In patients with cirrhosis, the clinical benefit of the treatment with human albumin for ascites is debated, and no data are available regarding refractory ascites. In this study, in patients with cirrhosis and refractory ascites, we assessed the effect of long-term albumin administration on emergent hospitalization and mortality. Methods Seventy patients with cirrhosis and refractory ascites, followed at the Unit of Internal Medicine and Hepatology, University and General Hospital of Padova, Italy, were included into the study. Forty-five patients were non-randomly assigned to receive long-term administration of human albumin at the doses of 20 g twice per week (n = 45), in addition to standard medical of care (SOC), and compared to those followed according to SOC. Patients were followed up to the end of the study, liver transplantation or death. Results The cumulative incidence of 24-month mortality was significantly lower in patients treated with albumin than in the group of patients treated with SOC (41.6% vs 65.5%; P = 0.032). The period free of emergent hospitalization was significantly longer in patients treated with long-term administration of albumin (P = 0.008). Analysing separately the causes of inpatient admission, patients treated with albumin showed a reduction in the incidence of overt hepatic encephalopathy, ascites, spontaneous bacterial peritonitis (SBP) and non-SBP infections. In addition, a non-significant trend towards a reduced probability of hepatorenal syndrome was observed. Conclusion In patients with cirrhosis and refractory ascites, long-term treatment with albumin improves survival and reduces the probability of emergent hospitalizations.

Cardiorenal syndrome type 1 (CRS-1) is the acute kidney disfunction caused by an acute worsening of cardiac function. CRS-1 is the consequence of renal vasoconstriction secondary to renin-angiotensin system (RAS) activation. No animal models of CRS-1 are described in literature.To characterize a murine model of CRS-1 by using a high-resolution ultrasound echo-color Doppler system (VEVO2100).Post-ischemic heart failure was induced by coronary artery ligation (LAD) in seven CD1 mice. Fifteen and thirty days after surgery, mice underwent cardiac and renal echo-color Doppler. Serum creatinine and plasma renin activity were measured after killing. Animals were compared to seven CD1 control mice.Heart failure with left ventricle dilatation (end diastolic area, p 0.05 vs. controls) and significantly reduced ejection fraction (EF; p 0.01 vs. controls) was evident 15 days after LAD. We measured a significant renal vasoconstriction in infarcted mice characterized by increased renal pulsatility index (PI; p 0.05 vs. controls) associated to increased creatinine and renin levels (p 0.05 vs. controls).The mice model of LAD is a good model of CRS-1 evaluable by Doppler sonography and characterized by renal vasoconstriction due to the activation of the renin-angiotensin system secondary to heart failure.Per sindrome cardiorenale tipo-1 (SCR-1) si intende il peggioramento acuto della funzione renale dovuto alla riduzione della funzione cardiaca. La SCR-1 è conseguenza della vasocostrizione renale dovuta all’attivazione del sistema renina-angiotensina. In letteratura non sono descritti modelli animali che riproducono tale patologia. Obiettivo di questo studio è caratterizzare mediante l’utilizzo di un sistema ecografico ad alta risoluzione (VEVO2100) un modello murino di CRS-1.lo scompenso cardiaco post ischemico è stato indotto in 7 topi CD1 mediante legatura dell’arteria coronaria sinistra discendente anteriore. 15 e 30 giorni dopo la procedura chirurgica gli animali sono stati valutati mediante ecografia ed ecoDoppler cardiaco e renale. Gli animali sono stati sacrificati il trentesimo giorno e sono stati effettuati il dosaggio della creatinina sierica e dell’attività reninica plasmatica. I risultati sono stati confrontati con quelli ottenuti da 7 topi CD1 di controllo.la presenza di scompenso cardiaco, valutato mediante misurazione ecocardiografica dell’area telediastolica del ventricolo sinistro (EDA) e della frazione di eiezione (FE), è risultata evidente già 15 giorni dopo la LAD (rispettivamenteil modello murino di legatura di coronaria è un buon modello di SCR valutabile mediante ecoDoppler e caratterizzato da vasocostrizione renale e attivazione del sistema renina angiotensina.

Herein, we report a case of classical Hodgkin’s lymphoma (HL) in an otherwise healthy 27- year-old female who came to the office of her general practitioner with flu-like illness and left supraclavicular swelling of uncertain nature, without other symptoms. An ultrasound of the neck detected many enlarged lymph nodes in the left supraclavicular region, and a chest X-ray showed left mediastinal enlargement. Subsequent Computed Tomography scan of the chest and abdomen confirmed the presence of many enlarged lymph nodes in the neck, mediastinum and liver, and a FDG-PET/CT scan showed multiple scattered consolidation lesions involving also the bones. The diagnosis of classical Hodgkin’s lymphoma, nodular sclerosis subtype, was made on a subsequent cervical lymph node biopsy.

Background: Silent myocardial ischemia is defined as objective documentation of myocardial ischemia in the absence of angina or anginal equivalents. There are a number of reports of exercise-related sudden deaths and myocardial infarctions in aerobically trained athletes suffering from exercise induced silent myocardial ischemia. The most appropriate and used method to discover silent myocardial ischemia is the exercise stress testing. Case Reports: In this article the authors describe three emblematic cases of silent myocardial ischemia detected in master marathon runners during systematic prepartecipation screening. These marathon runners were asymptomatic but suffering from a severe coronary artery disease that only thanks to exercise treadmill stress test was detected and properly treated. Conclusions: Silent myocardial ischemia is not such a rare event in athletes, indeed quite the opposite. In fact, even though athletes are asymptomatic this does not exclude the possibility that they are suffering from severe coronary artery disease.

Background: Misdiagnosis of angina pectoris is not uncommon in athletes. Physicians can fail to make a correct clinical diagnosis if they don’t have the skills and experience needed to recognize this disease. Case Report: This case report describes an exertional angina misdiagnosis due to a severe coronary artery disease in a 50-year-old male athlete initially examined by both a general practitioner and a cardiologist. The athlete subsequently underwent physical examination in a sports cardiology medicine center where diagnosis of angina pectoris caused by severe mono-vessel coronary artery disease was made, requiring an angioplasty with stenting. Conclusions: Although most of the severe symptoms in a heart attack are hard to miss, sometimes in athletes angina pectoris is not readily recognized. However, this is dangerous and can lead to the sudden death of the athlete. Diagnosis must be timely and accurate, in order for the patient to receive the best prognosis.

Background: In clinical practice and setting of general practice it is common to see patients with leg edema. To correctly identify the etiology of the edema and then properly manage the cause is not always easy. The unilateral lymphedema of the lower limb has rarely been reported as an initial presentation for lymphoma, especially in females, usually without classic signs or symptoms, but often with inguinal lymphadenopathy or abdominal masses. Case Report: In this article, we report a rare case of unilateral lower limb edema in a healthy obese woman who complained about the appearance of the disease for several months and for whom deep vein thrombosis and other diseases had been excluded. The histological examination of the biopsy of an enlarged lymph node in the right groin, which was compressing the iliac and femoral vein, revealed the presence of B cell non-Hodgkin lymphoma with high-grade malignancy. Conclusions: A common challenge for primary care physicians is to determine the cause and find an effective treatment for leg edema of unclear etiology. Non-Hodgkin’s B-cell Lymphoma should be considered in the differential diagnosis in patients with unilateral leg edema when the swelling is chronic and deep venous thrombosis is promptly excluded.

Patient: Male, 0 Final Diagnosis: Tetralogy of Fallot Symptoms: — Medication: — Clinical Procedure: — Specialty: Cardiology Objective: Unusual or unexpected effect of treatment Background: Tetralogy of Fallot (ToF) is the most common form of cyanotic congenital defect. Adult subjects with results of repair of tetralogy of Fallot may present post-surgical consequences that limit their physical capacity and thus their ability to compete in sports. Conversely, adults with excellent repair of congenital heart disease may have a chance to participate in competitive sports. Case Report: This case report illustrates the clinical course of a teenager with an outcome of surgical repair for TOF and demonstrates the boy’s excellent physical capacity that ensures his ability to play soccer. Conclusions: This case report raises the question of the possible revision of the criteria of the Italian COCIS protocol in terms of corrected congenital heart disease.

Measurement of portal pressure is pivotal in the evaluation of patients with liver cirrhosis. The measurement of the hepatic venous pressure gradient represents the reference method by which portal pressure is estimated. However, it is an invasive procedure that requires significant hospital resources, including experienced staff, and is associated with considerable cost. Non-invasive methods that can be reliably used to estimate the presence and the degree of portal hypertension are urgently needed in clinical practice. Biochemical and morphological parameters have been proposed for this purpose, but have shown disappointing results overall. Splanchnic Doppler ultrasonography and the analysis of microbubble contrast agent kinetics with contrast-enhanced ultrasonography have shown better accuracy for the evaluation of patients with portal hypertension. A key advancement in the non-invasive evaluation of portal hypertension has been the introduction in clinical practice of methods able to measure stiffness in the liver, as well as stiffness/congestion in the spleen. According to the data published to date, it appears to be possible to rule out clinically significant portal hypertension in patients with cirrhosis (i.e., hepatic venous pressure gradient ≥ 10 mmHg) with a level of clinically-acceptable accuracy by combining measurements of liver stiffness and spleen stiffness along with Doppler ultrasound evaluation. It is probable that the combination of these methods may also allow for the identification of patients with the most serious degree of portal hypertension, and ongoing research is helping to ensure progress in this field.

BACKGROUND & AIMS: Sleep preparation/onset are associated with peripheral vasodilatation and a decrease in body temperature. The hyperdynamic syndrome exhibited by patients with cirrhosis may impinge on sleep preparation, thus contributing to their difficulties falling asleep. The aim of this study was the assessment of skin temperature, in relation to sleep-wake patterns, in patients with cirrhosis. METHODS: Fifty three subjects were initially recruited, and 46 completed the study. Of the final 46, twelve were outpatients with cirrhosis, 13 inpatients with cirrhosis, 11 inpatients without cirrhosis and 10 healthy volunteers. All underwent baseline sleep-wake evaluation and blood sampling for inflammatory markers and morning melatonin levels. Proximal/distal skin temperature and their gradient (DPG) were recorded for 24 hours by a wireless device. Over this period subjects kept a sleep-wake diary. RESULTS: Inpatients with cirrhosis slept significantly less well than the other groups. Inpatients and outpatients with cirrhosis had higher proximal temperature and blunted rhythmicity compared to the other groups. Inpatients with/without cirrhosis had higher distal temperature values and blunted rhythmicity compared to the other groups. Inpatients and outpatients with cirrhosis had significantly lower DPG values compared to the other groups, and DPG reached near-zero values several hours later. Significant correlations were observed between temperature and sleep-wake variables and inflammatory markers. CONCLUSIONS: Alterations of distal/proximal skin temperature, their gradient and their time-course were observed in patients with cirrhosis, which may contribute to their sleep disturbances. This article is protected by copyright. All rights reserved.

Background: Many patients are affected by idiopathicbronchiolitis obliterans organizing pneumonia (BOOP). There are several known causes of BOOP, and several systemic disorders have BOOP as an associated primary pulmonary lesion. Numerous agents including cytotoxic and noncytotoxic drugs have the potential to cause pulmonary toxicity. Descriptions of amiodaronerelated BOOP continue to be reported throughout the world. Case Report: We reported a patient with original clinical presentation who developed recurrent sustained ventricular tachycardia (SVT) despite the presence of implantable cardioverter-defibrillator (ICD), hypoxaemia and interstitial pneumonitis in both lung bases. After percutaneous transluminal coronary angioplasty, he developed bronchiolitis obliterans organizing pneumonia (BOOP). Conclusions: To our knowledge, such complications after percutaneous coronary procedure in patients with amiodarone therapy for arrhythmia prophylaxis, are not very frequent in literature.

Patient: Male, 58 Final Diagnosis: Myopericarditis Symptoms: Retrosternal thoracic pain Medication: — Clinical Procedure: MRI Specialty: Cardiology Objective: Challenging differential diagnosis Background: Patients with acute cardiac symptoms, elevated cardiac troponin, and culprit-free angiograms are a consistent proportion of patients admitted with presumed acute coronary syndromes (ACS). Current literature on this population of patients justifies the diagnostic importance of cardiovascular magnetic resonance (CMR) imaging. Case Report: This report describes the case of a 58-year-old cyclist in which CMR allowed us to perform a diagnosis of myopericarditis mimicking acute STEMI against other evidence. There are several such reports in literature because the clinical presentation of myocarditis is quite variable. Conclusions: This case report emphasizes the importance of cardiovascular magnetic resonance imaging in the differential diagnosis of the etiology of acute coronary syndromes. This is especially important because the signs and symptoms presented are ambiguous and equivalent to those of other diseases, such as myopericarditis, which affects mainly young athletes but also middle-aged athletes.

In liver cirrhosis, portal hypertension is a consequence of enhanced intrahepatic vascular resistance and portal blood flow. Significant vasodilation in the arterial splanchnic district is crucial for an increase in portal flow. In this pathological condition, increased levels of circulating endogenous vasodilators, including nitric oxide, prostacyclin, carbon monoxide, epoxyeicosatrienoic acids, glucagon, endogenous cannabinoids, and adrenomedullin, and a decreased vascular response to vasoconstrictors are the main mechanisms underlying splanchnic vasodilation. In this review, the molecular pathways leading to splanchnic vasodilation will be discussed in detail.

The relationship between hepatic encephalopathy (HE) and the sleep-wake disturbances exhibited by patients with cirrhosis remains debated. The aim of this study was to examine the usefulness of sleep-wake interview within the context of HE assessment. One-hundred-and-six cirrhotic patients were asked three yes/no questions investigating the presence of difficulty falling asleep, night awakenings and daytime sleepiness. All underwent formal HE assessment, quantitative electroencephalography and standardised psychometry. Fifty-eight were monitored for 8 ± 6 months in relation to the occurrence of HE. Patients complaining of daytime sleepiness (n = 75, 71 %) had slower EEGs than those who did not report it (relative alpha power: 37 ± 19 vs. 48 ± 17 %, p

The hyperdynamic circulation of cirrhosis participates in the pathophysiology of portal hypertension. P450-dependent epoxyeicosatrienoic acids (EET) are potent vasodilators. We evaluated plasma levels of EETs in cirrhotic patients and the effect of epoxygenase and nitric oxide synthase (NOS) inhibition on skin blood flow, measured by laser Doppler flowmetry, in normal subjects and cirrhotic patients with and without ascites. Free plasma EETs were increased in cirrhotic patients compared to normal subjects, while the ratio between 8,9-, 11,12-, and 14-15-EET was the same. In cirrhotic patients without ascites, skin blood flow was significantly increased compared to normal subjects. In patients with ascites skin blood flow was significantly reduced compared to control subjects and patients without ascites. Inhibition of epoxygenase with miconazole and of NOS with l -NG-Nitroarginine methyl ester ( l -NAME) decreased basal skin flow in normal subjects and in cirrhotic patients, the effect being higher in cirrhotic patients. Miconazole caused a further decrease in flow when administered with l -NAME, both in normal subjects and in cirrhotic patients. In conclusion, EETs participate in the control of peripheral circulation of normal subjects and in the pathophysiology of peripheral vasodilatation of cirrhotic patients with ascites.

Splenic Doppler impedance indices are measurements of splenic congestion in chronic liver disease. It is not known whether they can also assess splenic congestion in patients affected by right-sided or congestive heart failure. We analyzed splanchnic hemodynamics with Doppler ultrasound and systemic hemodynamics with right-sided heart catheterization in patients with heart failure. Splenic pulsatility index (PI) was higher in patients with heart failure (48 patients) compared with healthy subjects (39 patients) (1.19 ± 0.41 vs. 0.73 ± 0.11, p0.0001) and was related to hepatic vein diameter (p = 0.02). Splenic PI was not related to systemic arterial pressure, cardiac output, systemic vascular resistance or splenic arterial resistance, whereas it was related to right atrial mean pressure (p = 0.0003) and to right ventricle end-diastolic pressure (p = 0.011) (34 patients). In conclusion, splenic PI is a measurement of splenic congestion caused by an increase in venous outflow resistance. It can estimate splenic congestion in patients with right-sided or congestive heart failure.

Portal hypertension is primarily caused by the increase in resistance to portal outflow and secondly by an increase in splanchnic blood flow, which worsens and maintains the increased portal pressure. Increased portal inflow plays a role in the hyperdynamic circulatory syndrome, a characteristic feature of portal hypertensive patients. Almost all the known vasoactive systems/substances are activated in portal hypertension, but most authors stress the pathogenetic role of endothelial factors, such as COX-derivatives, nitric oxide, carbon monoxide. Endothelial dysfunction is differentially involved in different vascular beds and consists in alteration in response both to vasodilators and to vasoconstrictors. Understanding the pathogenesis of portal hypertension could be of great utility in preventing and curing the complications of portal hypertension, such as esophageal varices, hepatic encephalopathy, ascites.

UNLABELLED In cirrhosis, 11,12-epoxyeicosatrienoic acid (EET) induces mesenteric arterial vasodilation, which contributes to the onset of portal hypertension. We evaluated the hemodynamic effects of in vivo inhibition of EET production in experimental cirrhosis. Sixteen control rats and 16 rats with carbon tetrachloride-induced cirrhosis were studied. Eight controls and eight rats with cirrhosis were treated with the specific epoxygenase inhibitor N-(methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide (MS-PPOH; 20 mg/kg/day) for 3 consecutive days. Portal blood flow and renal and splenic resistive indexes were calculated through echographic measurements, while portal and systemic pressures were measured through polyethylene-50 catheters. Small resistance mesenteric arteries were connected to a pressure servo controller in a video-monitored perfusion system, and concentration-response curves to phenylephrine and acetylcholine were evaluated. EET levels were measured in tissue homogenates of rat liver, kidney, and aorta, using an enzyme-linked immunosorbent assay. Urinary Na(+) excretion function was also evaluated. In rats with cirrhosis, treatment with MS-PPOH significantly reduced portal blood flow and portal pressure compared to vehicle (13.6 ± 5.7 versus 25.3 ± 7.1 mL/min/100 g body weight, P < 0.05; 9.6 ± 1.1 versus 12.2 ± 2.3 mm Hg, P < 0.05; respectively) without effects on systemic pressure. An increased response to acetylcholine of mesenteric arteries from rats with cirrhosis (50% effect concentration -7.083 ± 0.197 versus -6.517 ± 0.73 in control rats, P < 0.05) was reversed after inhibition of EET production (-6.388 ± 0.263, P < 0.05). In liver, kidney, and aorta from animals with cirrhosis, treatment with MS-PPOH reversed the increase in EET levels. In both controls and rats with cirrhosis, MS-PPOH increased urinary Na(+) excretion. CONCLUSION In rats with cirrhosis, in vivo inhibition of EET production normalizes the response of mesenteric arteries to vasodilators, with beneficial effects on portal hypertension. (Hepatology 2016;64:923-930).

Figure 1: Old ECG. Figure 2: Last ECG. Figure 3: Focused 2D TT echocardiogram. Herewith the author describes the history of a healthy 60-year-old amateur rider who came to our sports cardiology medicine center for sports pre-participation screening. His family history was unremarkable and physical examination was normal. He claimed he felt fit and that he was taking regular physical activity by cycling. His old ECG was normal (Figure 1) while the last ECG (Figure 2) was abnormal for findings of recent anterior myocardial infarction. A subsequent focused 2D TT echocardiogram through classical and magnified apical 4 chamber view showed left ventricular apical akinesis with small apical thrombus (Figure 3 - see arrow) protruding into the left ventricular cavity and demonstrates mobility in real-time imaging. The athlete was admitted to cath lab for revascularization procedure and anticoagulation therapy was started. The risk of cardioembolic stroke was very high.

Background We investigated the effect of green tea extract (GTE) in arterial hypertension with high oxidative stress. Angiotensin (Ang) II induces endothelial dysfunction (ED) that is crucial for the development of atherosclerosis and hypertension. Methods Male Sprague-Dawley rats, 13 weeks old, randomly assigned to drinking water with or without GTE (6 mg/mL) received a vehicle, a high (700 μg/kg/d) or a low (350 μg/kg/d) Ang II dose for 13 days, by osmotic mini-pumps. Blood pressure (BP) was measured with telemetry. After sacrifice, left ventricular (LV) mass index, small mesenteric artery media-to-lumen ratio, and concentration–response curves of phenylephrine-precontracted arteries to acetylcholine were evaluated. The effect of the superoxide dismutase (SOD-1) analog tempol on artery responses to acetylcholine was assessed. Oxidative stress was measured by plasma hydroperoxides and nitrotyrosine levels. The mRNA of heme oxygenase 1 (HO-1), NADPH oxidase endothelial p22phox subunit, and SOD-1 was also measured in the aorta. Results Compared with vehicle high Ang II increased BP, LV mass index, media-to-lumen ratio, and hydroperoxide radicals. The GTE blunted these increases, prevented the increase in HO-1, p22phox, and SOD-1 mRNA in aorta caused by Ang II, and reduced them below baseline levels. Low Ang II dose increased BP values and plasma hydroperoxides only during the first week. Both Ang II doses shifted rightward the curves to acetylcholine; this was prevented in vivo by GTE and abolished in vitro by tempol. Conclusions The GTE prevented hypertension and target organ damage induced by a high Ang II dose, likely by prevention or scavenging of superoxide anion generation.

Increased resistance to portal flow and increased portal inflow due to mesenteric vasodilatation represent the main factors causing portal hypertension in cirrhosis. Endothelial cell dysfunction, defined as an imbalance between the synthesis, release, and effect of endothelial mediators of vascular tone, inflammation, thrombosis, and angiogenesis, plays a major role in the increase of resistance in portal circulation, in the decrease in the mesenteric one, in the development of collateral circulation. Reduced response to vasodilators in liver sinusoids and increased response in the mesenteric arterioles, and, viceversa, increased response to vasoconstrictors in the portal-sinusoidal circulation and decreased response in the mesenteric arterioles are also relevant to the pathophysiology of portal hypertension. Arachidonic acid (AA) metabolites through the three pathways, cyclooxygenase (COX), lipoxygenase, and cytochrome P450 monooxygenase and epoxygenase, are involved in endothelial dysfunction of portal hypertension. Increased thromboxane-A2 production by liver sinusoidal endothelial cells (LSECs) via increased COX-1 activity/expression, increased leukotriens, increased epoxyeicosatrienoic acids (EETs) (dilators of the peripheral arterial circulation, but vasoconstrictors of the portal-sinusoidal circulation), represent a major component in the increased portal resistance, in the decreased portal response to vasodilators and in the hyper-response to vasoconstrictors. Increased prostacyclin (PGI2) via COX-1 and COX-2 overexpression, and increased EETs/heme-oxygenase-1/K channels/gap junctions (endothelial derived hyperpolarizing factor system) play a major role in mesenteric vasodilatation, hyporeactivity to vasoconstrictors, and hyper-response to vasodilators. EETs, mediators of liver regeneration after hepatectomy and of angiogenesis, may play a role in the development of regenerative nodules and collateral circulation, through stimulation of vascular endothelial growth factor (VEGF) inside the liver and in the portal circulation. Pharmacological manipulation of AA metabolites may be beneficial for cirrhotic portal hypertension.

Background: There is an alarming prevalence of obesity and sedentariness in Western countries. An ideal context for health promotion and preventive medicine seems to be the setting of primary care provided by the general practitioner (GP).Purpose: Therefore, this study evaluated the impact of GPs’brief physical activity counseling for overweight and obese patients.Methods: Individuals recruited during routine physician visits were randomly split into an experimental (n = 48) group that received the Patient-centered Assessment and Counseling for Exercise (PACE) protocol, and a usual-care control (n = 48) group. Body mass index (BMI) and abdominal girth were assessed as objective biometrical parameters. Patients in the experimental group self-reported their readiness for physical activity and self-efficacy.Results: The experimental group had significantly better BMI and abdominal girth compared with the control group after a 5- to 6-month follow-up. Furthermore, the experimental group progressed in their stage of physical activity readiness and increased their self-efficacy.Conclusions: The GPs’counseling for physical activity using the PACE protocol influenced mediators and biometrical outcomes in an Italian primary care context.

Summary Background : The acute effects of β-blockers may be different from chronic; mechanisms underlying this difference are poorly elucidated. Aim : To assess portal pressure and its pathophysiological determinants after acute and chronic administration of nadolol. Methods : In 24 patients with cirrhosis and portal hypertension hepatic venous pressure gradient, portal blood flow and resistance to portal blood flow were measured before, 60–90 min after acute administration of nadolol, and after 1 month. Patients were good-responders if hepatic venous pressure gradient was ≤12 mmHg, or decreased by at least 20%. Results : Eleven and 13 patients were good- and poor-responders to acute administration, respectively. Acute poor-responders showed a lower decrease in portal blood flow (P = 0.04) and a less evident decrease in mean arterial pressure (P

Sedentary habits and obesity are important problems in public health. The main objective of this study has been to increase motivation level and physical activity practice in overweight and obese patients, through a counseling intervention made from primary care physicians (MMG). The counseling model has been taken from the program PACE (Patient-centered Assessment and Counseling for Exercise and Nutrition). In the period May-April 2002–2003, 145 patients, with a BMI≥27, underwent a physical activity counseling administered by 10 primary care physicians (MMG). The main measures of outcome were the change of physical activity level and the state of change score and their related improvements; secondary measures: BMI and abdominal circumference. The median follow-up was 7 months. 103 of 145 (71%) agreed to the project; afterwards their motivation level and physical activity increased. BMI and abdominal circumference were reduced. There were no differences between subjects about studied features (sex, age, instruction, work, health). The counseling, following PACE’s model, positively influenced the increase of physical activity and motivational level correlated in the patients who participated in the study project. It is necessary to do further studies to evaluate the real efficacy and to understand how this problem influences public health.

Notoriously, the valvular disease of the right heart have always received less attention than the left heart valvular disease both by echocardiographers and by researchers, probably due to the long period of latent asymptomatic and for the intrinsic difficulties of examination. However, it is increasingly recognized that right-sided valve disease is not a benign lesion and has a significant and independent impact on morbidity and mortality. Pulmonary regurgitation (PR) is common after surgical or percutaneous relief of pulmonary stenosis and following repair of tetralogy of Fallot. This case report describes the natural history of an adult patient with grown-up congenital heart (GUCH) who became competitive athlete and who showed signs of extreme morphological and functional adaptation of the right heart resulting in the outcome of a previous run surgical valvotomy at the age of 5 years for a congenital pulmonary stenosis. These anatomic changes of the right ventricle and pulmonary circulation have requested the replacement of the pulmonary valve for the symptomatic pulmonary hypertension, with subsequent gradual return to sports activity.

Introduction Liver cirrhosis is characterized by structural and hemodynamic changes that affect mainly the liver, the kidney and the vascular system. Cytochrome P-450 (CYP) is a variegated family of enzymes that, among many other activities, metabolize arachidonic acid to the vasoactive epoxyeicosatrienoic acids (EETs). Aim To investigate in an animal model of cirrhosis the m-RNA expression of CYPs in liver, kidney and aorta and to evaluate the effect of epoxygenase inhibition by N -(methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide (MS-PPOH). Methods In aorta, liver and kidney from 3 control, 3 cirrhotic and 6 cirrhotic rats treated with MS-PPOH, quantitative real-time PCR reactions were performed and the m-RNA expression of CYP2J3, CYP2J4, CYP2J10, CYP2C11, CYP2C12 and CYP2C23 was calculated. Results In cirrhotic rats, the gene expression of hepatic CYP2C11 and CYP2J10 was increased, of aortic CYP2J4 was increased, of aortic CYP2C12 was reduced and of renal CYP2C11 was increased. In cirrhotic rats, MS-PPOH reduced CYP2J10 hepatic and CYP2C11 renal gene expression to levels similar to the ones of control rats. Conclusions Changes in CYPs gene expression may contribute to the hemodynamic alterations typical of cirrhosis. The altered gene expression of CYPs can, in some cases, be reversed by epoxygenase inhibition.

The author reports on the history of a middle-aged male athlete who had sudden acute left pure motor hemiparesis due to a ischemic stroke 7 days after prolonged and strenuous exercise with severe physical fatigue. No chest pain or fever had been reported at that time, only a general feeling of weakness. In hospital all the examinations carried out led to the exclusion of paradoxical embolism via Patent Foramen Ovale. No other investigation was carried out and no anomalies were detected, therefore the patient was discharged with a diagnosis of cryptogenic stroke and neurologic follow up. Two years later the athlete underwent further investigations such as echocardiographic examination which showed a clear left ventricular apical akinesis. On suspicion, therefore, of coronary artery disease a coronary angiography was performed for suspected critical narrowing of the left coronary descending artery branch. However, the coronary angiogram showed patent coronary artery. Assuming that the left ventricular apical akinesia was probably the genesis of ischemic stroke for the formation ofapical thrombus that has migrated into the cerebral circulation occluding the anterior cerebral artery, other examinationswere performed to visualize the cardiovascular findings of the damaged left ventricle apical A cardiac CMR showed a akinetic and thinned left ventricular apex. The LGE showed an aspect of LV apical transmural fibrosis most probably to be attributed to an inflammatory event, that is, to an extended myocarditis, even if the morphological and functional pattern of CMR appears suggestive for an ischemic event. A contemporary coronary computed tomography showed patent coronary arteries as well as profound myocardial bridging at the middle segment of the anterior interventricular artery. The dilemma is thus: the athlete had had extensive myocarditis that had affected the function of the LV apex or he had had a heart attack caused by underlying but hemodynamically significant myocardial bridge?

The detection and diagnosis of Gestational Diabetes Mellitus (GDM) follow different recommendations according to the various groups, in particular for what concerns the endorsement of screening practices and diagnostic threshold recommended by the International Association of Diabetes and Pregnancy Study Groups (IADPSG). This paper draws attention to the overdiagnosis of gestational diabetes mellitus, when the doctor adheres to the criteria set out in the various international recommendations and also wants to present a case study that explains how easily a poor diagnosis can be made. Here the author describes a recent case report of a 36-year-old pregnant woman with overdiagnosis of gestational diabetes.

The differential diagnosis of intracardiac masses that involves the right atrial chamber include vegetation, thrombus or tumours, and anatomic normal variants such as crista terminalis. Size, shape,location, mobility and attachment of the mass combined with the clinical findings help differentiate etiology. Two Dimensional Trans Thoracic Echocardiography (TTE) became the gold standard test for the diagnosis of intracardiac masses and further examination such as transesophagealechocardiography (TEE) and Cardiac Magnetic Resonance (CMR) improved the accuracy. The cardiovascular imaging is crucial to establish a correct diagnosis for proper management and therapy. Here the author describes the case report of a healthy middle-aged athlete who underwent echocardiography for sports preparticipation screening which detected the presence of a peduncolated right atrial mass of uncertain nature. Because of the strong suspicion for small right atrial mixoma, he underwent CMR that showed a small enhancing mass adherent to the right atrial posterior wall typical of prominent crista terminalis. This report of rare Crista Terminalis muscular bridge that mimicks right atrial mixoma gives new information for the understanding of the aspect of complex and strange right atrial anatomy

Here the author shows two cardiac ultrasound images of otherwise healthy young athletes recorded during sports preparticipation screening. Figure 1 shows the typical aortic valve deformity called, “hockey stick”, of the bicuspid aortic valve magnified by parasternal long axis view, while Figure 2 shows the typical finding of type I supra-valvular pulmonic stenosis, involving main pulmonary artery, visualized by parasternal short axis view. Despite the congenital heart valvular anomalies, both athletes were considered fit to sports competition. Congenital cardiac anomalies are frequent in young athletes, however in most cases the physical fitness is not compromised. Echocardiography is the mainstay in the diagnosis and follow-up assessment of young athletes with congenital heart disease.

Information on changes in splanchnic hemodynamics after liver transplantation is incomplete. In particular, data on long-term changes are lacking, and the relationship between changes in arterial and portal parameters is still under debate. The effect of liver transplantation on splanchnic hemodynamics was analyzed with echo-Doppler in 41 patients with cirrhosis who were followed for up to 4 years. Doppler parameters were also evaluated in 7 patients transplanted for acute liver failure and in 35 controls. In cirrhotics, portal blood velocity and flow increased immediately after transplantation (from 9.1 plus minus 3.7 cm/sec to 38.3 plus minus 14.6 and from 808 plus minus 479 mL/min to 2,817 plus minus 1,153, respectively, P

The role of portal-systemic shunting and portal liver hypoperfusion in the pathophysiology of central nervous system dysfunction (CNSD) of cirrhosis is not yet well defined. It is well known that one of the most important collateral vessels (CVs) is a patent paraumbilical vein (PUV), but there is controversy regarding its clinical significance. We have evaluated the relationships between neuropsychological and EEG alterations, ammonia plasma level (NH4), hepatic function, and portal hemodynamics (Doppler Ultrasound) in 95 cirrhotic patients. Patency, diameter, or flow of PUV or the presence of other CVs were not related to an increased prevalence of neuropsychological or EEG abnormalities. Patients with effective portal flow (EPF = portal flow − PUV flow) lower than 692 mL/min (median) had a significantly higher risk of failing the neuropsychological test, or of having an altered EEG. Low EPF and prothrombin time (

The possibility of estimating portal hypertension combining splenic Doppler pulsatility index (PI), which has been shown strictly to be related to portal resistance, and portal blood flow (PBF) was evaluated. Hepatic venous pressure gradient, and splanchnic Doppler parameters were measured in 40 cirrhotic patients. A formula to assess the severity of portal hypertension from Doppler parameters was calculated in a training group of 19 patients, and then this formula was tested to prospectively predict the degree of portal pressure in 21 further patients. In the training group, the regression of portal resistance over splenic PI was calculated and individual values of estimated portal resistance were obtained for every patient of the test group. From them and from observed values of PBF, an estimated value of portal pressure was calculated. The following formula was obtained [(0.066*splenic PI -0.044)*PBF]. In the second group, predicted and observed portal pressure were well correlated (r = 0.71, p = .0003). A good accuracy for the prediction of mild or severe portal hypertension was obtained.

To evaluate the usefulness of routine ultrasonographic (US) evaluation of the hepatic arterial resistive and pulsatility indexes and of the direction of portal venous blood flow for the diagnosis of intrahepatic arterioportal fistulas (APFs) in patients with liver cirrhosis.In all patients with cirrhosis examined at one center over 4 years, the resistive (RI) and the pulsatility (PI) indexes in the right and left branches of the hepatic artery were evaluated with Doppler US. An APF was suspected when an RI decrease of at least 20% and a PI decrease of at least 30% were present in one hepatic lobe relative to values in the other lobe and portal blood flow in the lobe with the decreased values was reversed. The RI and PI in patients with an APF were compared with those in 75 patients with cirrhosis and without APFs at angiography.Seven patients with an APF were identified. APFs suspected at Doppler US were always confirmed with angiography. The percent differences +/- SD in the RI and the PI between the two intrahepatic branches of the hepatic artery in patients with versus in patients without an APF were as follows: RI, 35% +/- 6 (range, 27%-42%) versus 5% +/- 4 (range, 0%-15%) (P:.001); PI, 50% +/- 5 (range, 41%-58%) versus 11% +/- 7 (range, 0%-26%) (P:.001).The intrahepatic arterial resistive and pulsatility indexes and the direction of portal blood flow should be evaluated in routine screening for APFs in patients with liver cirrhosis.

We read with great interest the leading article by Rosselli et al 1 which offers a contemporary perspective to the clinical issue of interpreting progression (and regression) of chronic liver diseases (CLDs). We fully agree with the view that the histological scoring of fibrosis is a reductive approach to the assessment of CLDs, as it does not fully reflect the complex events involved in the progression to cirrhosis. As suggested by Rosselli et al , a more insightful morphological analysis of liver biopsy should consider other important factors contributing to disease progression/regression, and possibly to cancer development. Angiogenesis represents one of such key factors. Liver angiogenesis is a pathophysiological process characterised by changes in the phenotype of sinusoidal endothelial cells, which assume the features of capillary endothelial cells. This process, …

The regular practice of physical and sporting activities is one of the most important measures in cardiovascular prevention. It is to be recommended at all ages as it improves fitness and significantly reduces cardiovascular morbidity and mortality. However, exercise can become a trigger of Sudden Cardiac Death (SD) in patients with often, underlying cardiovascular disease.

The prevention of sudden death in athletes is one the greatest challenges in sports cardiology. Early identification of athletes at high risk of sudden death can lead to difficult decisions such as restriction of competitive sports activity, but also treatment with medications and implantable cardioverter-defibrillator. We report a case of a 41-year-old female triathlete who had recurrent syncope during exercise with documented polymorphic ventricular tachycardia and nonspecific abnormalities on endomyocardial biopsy. Against medical advice, she continued to participate in athletic events and subsequently had a sudden cardiac death during a cycling event.

Background: Primary cancer may occur synchronously in two different organs.The presence of a renal primary cancer discovered by chance during staging prior to surgery of another cancer (caecum-colon) is not as rare an event as is believed. In this case report the authors report an interesting case of double malignancy in which a patient was struck by two separate carcinomas, carcinoma of the caecum and renal cell carcinoma. Case report: A 59-year-old male underwent screening with faecal occult blood test (FOBT) for colorectal cancer. The resulting positive test of which required a colonoscopy indicated the malignancy of the caecum-colon. Renal cell carcinoma was detected incidentally through Computed Tomography (CT) during preliminary investigations for the staging of the disease prior to surgery. The patient subsequently underwent simultaneous, radical, right nephrectomy and hemicolectomy. Both tumours were confirmed in pathologic evaluation, revealing chromophobe renal cell carcinoma and caecum- right colon adenocarcinoma. Conclusion: In conclusion, the elevated frequency of coexisting synchronous renal and colonic carcinomas, recommends routine use of preoperative imaging studies, in order to rule out coexistent, asymptomatic malignant lesions in patients with colorectal cancer.

The association beta-blockers plus isosorbide-5-mononitrate (I5M) has been proposed for the treatment of portal hypertension in patients with insufficient response to beta-blockers alone, according to hemodynamic criteria. The mechanism of action in these patients is not clearly defined. Fifteen patients with cirrhosis and esophageal varices were evaluated by hepatic venous pressure gradient (HVPG) measurement and duplex-Doppler ultrasonography before and after 1 month of treatment with nadolol. Nine patients who did not exhibit a decrease in HVPG to 12 mm Hg or a percent decrease greater than 20% were classified as poor responders, and were studied again with the same methodology after 3 months of chronic administration of nadolol + I5M 20 mg twice per day. In poor responders, mean HVPG decrease after nadolol was 8.9% +/- 2.8%, and after the combination, it was 25.7% +/- 1.7% (P = .004). All patients except one became good responders to the association. Portal blood flow (PBF) decreased significantly after nadolol (P = .004), and remained unchanged after the addition of nitrates. Resistance to portal blood flow (RPBF) increased after nadolol (P = .02) and returned to baseline values during combined treatment (P = .03). In good responders, an adequate decrease in HVPG was associated with a decrease in PBF (P = .06) but no change in RPBF. A wide spectrum of combined changes in PBF and in RPBF after nadolol was observed in poor responders, ranging from no change in either parameter to a marked decrease in PBF counterbalanced by a marked increase in RPBF. The addition of I5M was followed in most cases by larger effects on resistance than on flow. Doppler parameters were not significantly correlated with the HVPG response to nadolol alone or associated with I5M. It is concluded that good hemodynamic responders to nadolol differ from poor responders in the lack of increase in RPBF after the drug. The addition of nitrates to nadolol is effective in decreasing portal pressure in most poor responders to nadolol alone. A decrease in outflow resistance is the main mechanism involved.

To evaluate the prevalence, severity, and hemodynamic features of nonalcoholic fatty liver disease (NAFLD) in nonobese diabetics.We studied 100 consecutive nonobese (body mass index [BMI] 30) patients with type 1 (n = 17) or type 2 (n = 83) diabetes and no known causes of liver disease. Steatosis was diagnosed and graded with ultrasonography. Digital sonographic images of the liver and right kidney were analyzed with dedicated software (HDI-Lab), and the liver/kidney ratio of grey-scale intensity was calculated as an index of the severity of the steatosis. Severity scores ranging from 0 (none) to 5 (severe) were compared with sonographic and Doppler findings (right liver size, portal vein diameter and flow velocity, hepatic and splenic arterial pulsatility indices, hepatic-vein flow profile and A- and S-wave velocities).The prevalence of steatosis was 24% in type I and 80% in type II diabetes (grade 1 in 17%, grade 2 in 34%, grade 3 in 33%, grade 4 in 9%, grade 5 in 7%). In patients with steatosis (especially those with grades 4-5 disease), hepatic volume was increased (p 0.005). Portal vein diameter was increased in grade 5 steatosis. The hepatic artery pulsatility index was significantly increased, particularly in grades 4 and 5 (p 0.0001); portal and A-wave velocities were significantly reduced in grades 3-5 (p 0.001); and the hepatic vein flow profile was altered in 27% (biphasic: 20%, flat: 7%) patients with steatosis, although there was no correlation with severity.NAFLD is very frequent in nonobese diabetics with type 2 but not type 1 disease, and it is associated with hepatomegaly and liver hemodynamic alterations only when it is severe.Sommario SCOPO: Valutare la prevalenza e la gravità della steatosi nei pazienti diabetici non-obesi e le alterazioni emodinamiche epatiche associate. METODI: Sono stati studiati 100 pazienti diabetici non-obesi (BMI 30 kg/m), 17 di tipo I e 83 di tipo II, privi di cause note di epatopatia. Mediante eco-color-Doppler sono stati valutati: un'immagine digitale di confronto tra fegato e corticale del rene destro, analizzata tramite un programma dedicato per la valutazione del grado di steatosi (rapporto fegato/rene dell'intensità dei grigi), le dimensioni del lobo epatico destro, il calibro della vena porta (PV), la velocità della vena porta (PBV), gli indici di pulsatilità arteriosa epatica (PI-L) e splenica (PI-S), il profilo flussimetrico e la velocità delle onde a (HV-a) e s (HV-s) delle vene sovraepatiche. RISULTATI: La prevalenza di steatosi è stata del 24% nel diabete di tipo I e dell'80% nel tipo II ed è risultata prevalentemente di grado lieve-moderato. Nella steatosi il volume epatico è risultato aumentato (p 0,005), in particolare nei gradi superiori a 3, e il diametro della vena porta è risultato aumentato nel grado 5. Il PI-L è risultato aumentato in tutti i gradi di steatosi, in particolare in quelli di grado 4 e 5 (p 0,0001); la PBV è risultata ridotta nei gradi 3, 4 e 5 (p 0,001); la HV-a è risultata ridotta nei pazienti con grado 3, 4 e 5. Il profilo flussimetrico delle vene sovraepatiche è risultato alterato nel 27% (20% bifasico, 7% appiattito). CONCLUSIONI: La steatosi epatica è un reperto molto frequente nel diabete di tipo II senza obesità ed è associata a epatomegalia e alterazioni emodinamiche epatiche nelle forme più gravi.