Cardiac hepatopathy has generally been used to describe any liver damage caused by cardiac disorders in the absence of other possible causes of liver damage. Although there is no consensus on the terminology used, cardiac hepatopathy can be examined as congestive hepatopathy (CH) and acute cardiogenic liver injury (ACLI). CH is caused by passive venous congestion of the liver that generally occurs in the setting of chronic cardiac conditions such as chronic HF, constrictive pericarditis, tricuspid regurgitation, or right-sided heart failure (HF) of any cause, and ACLI is most commonly associated with acute cardiocirculatory failure resulting from acute myocardial infarction, acute decompensated HF, or myocarditis. Histologically, CH is characterized by sinusoidal dilation, replacement of hepatocytes with red blood cells extravasating from the sinusoids, and necrosis/apoptosis of zone 3 of the Rappaport acinus, and it could progress to cirrhosis in advanced cases. In ACLI, however, massive necrosis of zone 3 is the main histological finding. Primary laboratory findings of CH are elevated serum cholestasis markers including bilirubin, alkaline phosphatase, and γ-glutamyl-transpeptidase levels, whereas those of ACLI are a striking elevation in transaminase and lactate dehydrogenase levels. Both CH and ACLI have a prognostic value for identifying cardiovascular events and mortality and have some special implications in the management of patients undergoing ventricular assist device implantation or cardiac transplantation. There is no specific treatment for CH or ACLI other than treatment of the underlying cardiac disorder.

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Mean platelet volume (MPV) is an indicator of platelet activation, a central process in the pathophysiology of coronary heart disease (CAD). The importance of slow coronary flow (SCF) phenomenon results from its association with angina pectoris, acute myocardial infarction, hypertension and sudden cardiac death. The aim of this study is to evaluate the values of MPV in patients with SCF. MPV was measured in 84 consecutive patients with SCF and 88 patients with CAD and 84 control subjects. The association between thrombolysis in myocardial infarction (TIMI) frame count (TFC) and MPV level and other clinical and laboratory parameters were evaluated. There were no statistically significant differences in MPV between SCF group and CAD group. MPV was significantly higher in patients in the both SCF and CAD groups, compared with control group. The TFC for all the epicardial coronary arteries and the mean TFC were significantly higher in the SCF group than the both CAD group and control group. The mean TFC was positively and moderately correlated with MPV in the whole study population. To determine the independent predictors of mean TFC, a stepwise linear regression analysis was performed by including the parameters that were correlated with the mean TFC in the bivariate analysis. MPV level was the only independent predictor of the mean TFC (b = 0.312, p < 0.001). These findings have shown that MPV level is significantly associated with coronary blood flow and that elevated MPV level might be an independent predictor for the presence of SCF. We believe that further studies are needed to clarify the role of MPV in SCF complicated CAD, especially in relation to angiographic and clinical parameters, before we conclude that MPV to be used as a follow-up marker during the management of relevant patients.

In patients with newly diagnosed and untreated essential HT, increased EFT thickness and hs-CRP level are significantly related to impaired LV diastolic function independent from other factors, including age, waist circumference, and 24-h systolic blood pressure.