Cardiac Tumors: Clinical Perspective and Therapeutic Considerations.

BACKGROUND: Cardiac tumors rare cardiac disorders with an overall incidence rate < 0.33%. Cardiac tumors can be classified as primary or secondary depending on the origins of tumors. Primary cardiac tumors (5% incidence) are rare compared with the secondary (95%, metastases of the heart) cardiac tumors. OBJECTIVE: Given that cardiac tumors exhibit some nonspecific symptoms compared with other heart diseases, clinical diagnosis of cardiac tumors is rather challenging. Thus we will try to review the classification and pathogenesis of cardiac tumors. CONCLUSION: Current evidence revealed that 75% of cardiac tumors are considered benign (myxoma, fibromas, lipomas, rhabdomyomas, hemangiomas, teratomas, papillary fibroelastomas, pericardial cysts or cystic tumor of atrioventricular node). Clinical differential diagnosis of cardiac tumors is mainly based on imaging techniques including transthoracic and transesophageal echocardiograms, computed tomography (CT) scans and magnetic resonance imaging (MRIs). This mini-review tries to summarize recent understanding of the pathogenesis and therapeutics of cardiac tumors.

Alcohol Dehydrogenase Protects against Endoplasmic Reticulum Stress-Induced Myocardial Contractile Dysfunction via Attenuation of Oxidative Stress and Autophagy: Role of PTEN-Akt-mTOR Signaling.

BACKGROUND: The endoplasmic reticulum (ER) plays an essential role in ensuring proper folding of the newly synthesized proteins. Aberrant ER homeostasis triggers ER stress and development of cardiovascular diseases. ADH is involved in catalyzing ethanol to acetaldehyde although its role in cardiovascular diseases other than ethanol metabolism still remains elusive. This study was designed to examine the impact of ADH on ER stress-induced cardiac anomalies and underlying mechanisms involved using cardiac-specific overexpression of alcohol dehydrogenase (ADH). METHODS: ADH and wild-type FVB mice were subjected to the ER stress inducer tunicamycin (1 mg/kg, i.p., for 48 hrs). Myocardial mechanical and intracellular Ca(2+) properties, ER stress, autophagy and associated cell signaling molecules were evaluated. RESULTS: ER stress compromised cardiac contractile function (evidenced as reduced fractional shortening, peak shortening, maximal velocity of shortening/relengthening, prolonged relengthening duration and impaired intracellular Ca(2+) homeostasis), oxidative stress and upregulated autophagy (increased LC3B, Atg5, Atg7 and p62), along with dephosphorylation of PTEN, Akt and mTOR, all of which were attenuated by ADH. In vitro study revealed that ER stress-induced cardiomyocyte anomaly was abrogated by ADH overexpression or autophagy inhibition using 3-MA. Interestingly, the beneficial effect of ADH was obliterated by autophagy induction, inhibition of Akt and mTOR. ER stress also promoted phosphorylation of the stress signaling ERK and JNK, the effect of which was unaffected by ADH transgene. CONCLUSIONS: Taken together, these findings suggested that ADH protects against ER stress-induced cardiac anomalies possibly via attenuation of oxidative stress and PTEN/Akt/mTOR pathway-regulated autophagy.