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Objectives: To identify risk factors associated with cardiac valve calcification that is easily detectable through routine blood tests in patients who received valve replacement therapy. Methods: Four hundred patients with valvular heart disease who underwent valve replacement surgery between December 2009 and January 2013 were enrolled in this study. Of these, 77 had valve calcification; the other 323 did not. Multivariate logistic regression analysis was used to assess for risk factors associated with valve calcification. Results: In our study population, rheumatic valve lesions were the most common reason for valve replacement. Degenerative nonstenotic valve lesion was a protective factor and degenerative stenotic valve lesion was a strong risk factor for valve calcification. Serum levels of gamma-glutamyl transferase (GGT) of between 30 and 46 IU/l and >90 IU/l and total bilirubin (TBIL) of between 15 and 20 µmol/l were positively correlated with valve calcification. Meanwhile, serum calcium (Ca2+) levels of between 2.3 and 2.4 mmol/l were negatively correlated with rheumatic valve calcification. Conclusions: Degenerative stenotic lesion is a risk factor and degenerative nonstenotic lesion a protective factor for cardiac valve calcification. Serum GGT and TBIL levels are positively correlated and serum Ca2+ levels negatively correlated with rheumatic cardiac valve calcification. [ABSTRACT FROM AUTHOR]

Aging has a remarkable impact on the function of the heart, and is independently associated with increased risk for cardiovascular diseases. Cardiac aging is an intrinsic physiological process that results in impaired cardiac function, along with lots of cellular and molecular changes. Non-coding RNAs include small transcripts, such as microRNAs and a wide range of long non-coding RNAs (lncRNAs). Emerging evidence has revealed that non-coding RNAs acted as powerful and dynamic modifiers of cardiac aging. This review aims to provide a general overview of non-coding RNAs implicated in cardiac aging, and the underlying mechanisms involved in maintaining homeo-stasis and retarding aging. [ABSTRACT FROM AUTHOR]

Background/Aims: Diabetic cardiomyopathy (DCM) represents the major cause of morbidity and mortality among diabetics. Exercise has been reported to be effective to protect the heart from cardiac injury during the development of DCM. However, the potential cardioprotective effect of exercise in advanced DCM remains unclear. Methods: Seven-week old male C57BL/6 wild-type or db/db mice were either subjected to a running exercise program for 15 weeks or kept sedentary. Cardiac function, myocardial apoptosis and fibrosis, and mitochondrial biogenesis were examined for evaluation of cardiac injury. Results: A reduction in ejection fraction and fractional shortening in db/db mice was significantly reversed by exercise training. DCM induced remarkable cardiomyocyte apoptosis and increased ratio of Bax/Bcl-2 at the protein level. Meanwhile, DCM caused slightly myocardial fibrosis with elevated mRNA levels of collagen I and collagen III. Also, DCM resulted in a reduction of mitochondrial DNA (mtDNA) replication and transcription, together with reduced mtDNA content and impaired mitochondrial ultrastructure. All of these changes could be abolished by exercise training. Furthermore, DCM-associated inhibition of PGC-1α and Akt signaling was significantly activated by exercise, indicating that exercise-induced activation of PGC-1α and Akt signaling might be responsible for mediating cardioprotective effect of exercise in DCM. Conclusion: Exercise preserves cardiac function, prevents myocardial apoptosis and fbrosis, and improves mitochondrial biogenesis in the late stage of DCM. Exercise-induced activation of PGC-1α and Akt signaling might be promising therapeutic targets for advanced DCM. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background/Aims: PID1 was originally described as an insulin sensitivity relevance protein, which is also highly expressed in heart tissue. However, its function in the heart is still to be elucidated. Thus this study aimed to investigate the role of PID1 in the heart in response to hypertrophic stimuli. Methods: Samples of human failing hearts from the left ventricles of dilated cardiomyopathy (DCM) patients undergoing heart transplants were collected. Transgenic mice with cardiomyocyte-specific overexpression of PID1 were generated, and cardiac hypertrophy was induced by transverse aortic constriction (TAC). The extent of cardiac hypertrophy was evaluated by echocardiography as well as pathological and molecular analyses of heart samples. Results: A significant increase in PID1 expression was observed in failing human hearts and TAC-treated wild-type mouse hearts. When compared with TAC-treated wild-type mouse hearts, PID1-TG mouse showed a significant exacerbation of cardiac hypertrophy, fibrosis, and dysfunction. Further analysis of the signaling pathway in vivo suggested that these adverse effects of PID1 were associated with the inhibition of AKT, and activation of MAPK pathway. Conclusion: Under pathological conditions, over-expression of PID1 promotes cardiac hypertrophy by regulating the Akt and MAPK pathway. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aims: The aims of this study were to investigate the efficacy and identify the prognostic factors of continuous hemofiltration in patients with cardiorenal syndrome (CRS) and, finally, to optimally select patients who could benefit more from this therapy. Methods: A total of 59 patients with CRS type 1 or type 2 treated with continuous hemofiltration were enrolled. We collected their clinical data and divided them into 2 groups according to their survival or death during hospitalization to conduct a retrospective analysis on factors affecting mortality. Results: The following items were significantly different between the survival (n = 30) and death (n = 29) groups: serum creatinine, serum total bilirubin, direct bilirubin, white blood cells, hemoglobin, hematocrit, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, systolic blood pressure and mean arterial pressure before hemofiltration, and average dehydration volume during the hemofiltration process. Leukocytosis was a risk factor for death (OR 1.242, 95% CI 1.242-1.480), and elevated sCr was not a key negative factor in the prognosis of CRS (OR 0.994, 95% CI 0.989-1.000). Conclusions: Cardiac function before hemofiltration and the amount of dehydration during the hemofiltration process both affected the prognosis. Infection and fluid overload condition at the beginning of hemofiltration were independently associated with mortality during hospitalization. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]