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1.
Minerva Cardioangiol ; 62(4): 335-41, 2014 Aug.
Article in English | MEDLINE | ID: mdl-24699549

ABSTRACT

AIM: Aim of this study was to better understand interactions between left ventricular (LV) and right ventricular (RV) systolic and diastolic function echocardiographic indexes in stable cardiovascular diseased patients and in subjects with cardiovascular risk factors. METHODS: The study enrolled 683 stable patients who were submitted to standard transthoracic echocardiography with evaluation of left ventricular ejection fraction (LVEF) (Simpson biplane method), LV and RV systolic peak on Doppler tissue imaging (LVSys and RVSys), tricuspid annulus plane systolic excursion (TAPSE), pulmonary artery systolic pressure (PASP), and multiparameter evaluation of LV and RV diastolic function utilizing E and A peak, their ratio, E peak deceleration time, E' and A' peak on Doppler tissue imaging, their ratio, and E/E' ratio. RESULTS: Part of the considered indexes had interactions but only LVEF and TAPSE were related to all the others (LVEF P<0.001 with all the considered parameters; TAPSE P<0.001 with all parameters except with PASP=0.003). Unexpectedly TAPSE seems to have, such as LVEF, a pivotal position among LV and RV function. CONCLUSION: The study demonstrates the existence of interactions between LV and RV function indexes; these results may be considered as a piece of evidence in favor of heart seen as a single structure.


Subject(s)
Cardiovascular Diseases/physiopathology , Ventricular Function, Left , Ventricular Function, Right , Aged , Aged, 80 and over , Echocardiography, Doppler, Pulsed/methods , Female , Humans , Male , Middle Aged , Retrospective Studies , Risk Factors
2.
Dig Dis ; 29(2): 202-10, 2011.
Article in English | MEDLINE | ID: mdl-21734385

ABSTRACT

Non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) have a similar pathogenesis and histopathology but a different etiology and epidemiology. NASH and ASH are advanced stages of non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD). NAFLD is characterized by excessive fat accumulation in the liver (steatosis), without any other evident causes of chronic liver diseases (viral, autoimmune, genetic, etc.), and with an alcohol consumption ≤20-30 g/day. On the contrary, AFLD is defined as the presence of steatosis and alcohol consumption >20-30 g/day. The most common phenotypic manifestations of primary NAFLD/NASH are overweight/obesity, visceral adiposity, type 2 diabetes, hypertriglyceridemia and hypertension. The prevalence of NAFLD in the general population in Western countries is estimated to be 25-30%. The prevalence and incidence of NASH and ASH are not known because of the impossibility of performing liver biopsy in the general population. Up to 90% of alcoholics have fatty liver, and 5-15% of these subjects will develop cirrhosis over 20 years. The risk of cirrhosis increases to 30-40% in those who continue to drink alcohol. About 10-35% of alcoholics exhibit changes on liver biopsy consistent with alcoholic hepatitis. Natural histories of NASH and ASH are not completely defined, even if patients with NASH have a reduced life expectancy due to liver-related death and cardiovascular diseases. The best treatment of AFLD/ASH is to stop drinking, and the most effective first-line therapeutic option for NAFLD/NASH is non-pharmacologic lifestyle interventions through a multidisciplinary approach including weight loss, dietary changes, physical exercise, and cognitive-behavior therapy.


Subject(s)
Fatty Liver, Alcoholic/pathology , Fatty Liver/pathology , Fatty Liver/diagnosis , Fatty Liver/epidemiology , Fatty Liver/etiology , Fatty Liver, Alcoholic/diagnosis , Fatty Liver, Alcoholic/epidemiology , Fatty Liver, Alcoholic/etiology , Humans , Non-alcoholic Fatty Liver Disease
3.
Dig Dis ; 28(6): 799-801, 2010.
Article in English | MEDLINE | ID: mdl-21525765

ABSTRACT

Population-based studies on the natural history of chronic viral liver disease that consider co-morbidity factors, such as alcohol or metabolic diseases, are lacking. We report here the contribution of ethanol intake and non-organ-specific autoantibodies (NOSA) to the course of chronic viral disease in the Dionysos cohort. As reported elsewhere, the Dionysos study was performed in two towns of Northern Italy, started in 1992 with 10 years of follow-up in 2002, and allowed us to quantify the burden of chronic liver disease in Northern Italy. We followed 139 subjects with chronic hepatitis C virus (HCV) infection and 61 with chronic hepatitis B virus (HBV) infection for a median (IQR) time of 8.4 (1.0) and 8.3 (0.9) years, respectively. The incidence and remission rates of steatosis were 9.0 and 29.7 per 1,000 person-years in the HCV cohort and 4.0 and 30.4 per 1,000 person-years in the HBV cohort. Progression to cirrhosis and hepatocarcinoma was more common in the HCV than in the HBV cohort. In the HCV cohort, ethanol intake was an independent predictor of liver cirrhosis and of death rate in both cohorts. We found no association between baseline NOSA and 8.4-year mortality. We conclude that morbidity and mortality rate of HBV and HCV infection in the general population is lower than that reported in secondary care populations, blood donors, or clinical series, and that ethanol intake >30 g/day is the most important and evitable risk factor for cirrhosis and death in patients with chronic HCV or HBV infection.


Subject(s)
Alcoholic Beverages/adverse effects , Hepacivirus/physiology , Hepatitis B virus/physiology , Cohort Studies , Humans , Liver Diseases/mortality , Liver Diseases/virology , Risk Factors
4.
Aliment Pharmacol Ther ; 22 Suppl 2: 64-70, 2005 Nov.
Article in English | MEDLINE | ID: mdl-16225477

ABSTRACT

Hepatic steatosis may be both an adaptive phenomenon and an example of lipotoxicity. Its prevalence ranks in the same order of magnitude of insulin resistance in the general population. Studies support the finding that hepatic steatosis is secondary to insulin resistance and not vice versa. A steatotic liver will further contribute to the development of insulin resistance through impaired clearance of insulin from the portal blood, creating a vicious cycle. Insulin resistance is the leading force in the pathogenesis and natural history of non-alcoholic fatty liver disease. Dysfunction of energetic homeostasis and the interaction of adiponectin, leptin and tumour necrosis factor-alpha are key events in the pathogenesis of steatosis and insulin resistance. Insulin resistance represents the frame within which hepatic and extrahepatic non-alcoholic fatty liver disease-related clinical manifestations are to be anticipated and interpreted.


Subject(s)
Fatty Liver/metabolism , Insulin Resistance/physiology , Adenosine Triphosphate/metabolism , Adipose Tissue/metabolism , Animals , Disease Models, Animal , Fatty Liver/epidemiology , Humans , Lipid Metabolism/physiology , Lipodystrophy/metabolism , Liver/blood supply , Microcirculation , Prevalence
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