Case report: Primary pericardial angiosarcoma, a rare cause of cardiac tamponade.

Primary pericardial angiosarcoma is a rare malignancy of the pericardium with variable clinical features and imaging characteristics. Herein, we report a case of histopathologically confirmed pericardial angiosarcoma in a 66-year-old man. The patient developed cardiac tamponade in a short time period. The transthoracic echocardiography showed the presence of multiple irregular echodensities, heterogeneous in echogenicity, encasing the apex of both ventricles in the pericardial space, initially misinterpreted as pericardial effusion. The patient died of cardiogenic shock despite undergoing a surgical pericardiectomy. Pericardial angiosarcoma can manifest as a mass obliterating the pericardial sac, rather than the typical pericardial effusion observed on echocardiography. Multimodality imaging studies aid in diagnosing primary pericardial angiosarcoma, but the final diagnosis relies on tissue histopathology.

Renoprotective effect of Tanshinone IIA against kidney injury induced by ischemia-reperfusion in obese rats.

OBJECTIVE: Obesity enhances the frequency and severity of acute kidney injury (AKI) induced by renal ischemia-reperfusion (IR). Tanshinone IIA (TIIA) pre-treatment was used to alleviate renal injury induced by renal IR, and whether TIIA can attenuate renal cell apoptosis via modulating mitochondrial function through PI3K/Akt/Bad pathway in obese rats was examined. METHODS: Male rates were fed a high-fat diet for 8 weeks to generate obesity, followed by 30 min of kidney ischemia and 24 h reperfusion induced AKI. The male obese rates were given TIIA (5 mg/kg.d, 10 mg/kg.d, and 20 mg/kg.d) for 2 weeks before renal IR. RESULTS: TIIA alleviated the pathohistological injury and apoptosis induced by IR. In addition, TIIA improved renal function, inflammatory factor, and balance of oxidation and antioxidation in obese rats after renal IR. At the same time, TIIA can inhibit cell apoptosis by improving mitochondrial function through the PI3K/Akt/Bad pathway. Mitochondrial dysfunction was supported by decreasing intracellular ATP, respiration controlling rate (RCR), mitochondrial membrane potential (MMP), and mitochondrial respiratory chain complex enzymes, and by increasing ROS, the opening of mitochondrial permeability transition pore (mPTP), and the mtDNA damage. The injury to mitochondrial dynamic function was assessed by decreasing Drp1, and increasing Mfn1/2; and the injury of mitochondrial biogenesis was assessed by decreasing PGC-1, Nrf1, and TFam. CONCLUSIONS: Renal mitochondrial dysfunction occurs along with renal IR and can induce renal cell apoptosis. Obesity can aggravate apoptosis. TIIA can attenuate renal cell apoptosis via modulating mitochondrial function through PI3K/Akt/Bad pathway in obese rats.

A possible new activator of PI3K-Huayu Qutan Recipe alleviates mitochondrial apoptosis in obesity rats with acute myocardial infarction.

Obesity, which has unknown pathogenesis, can increase the frequency and seriousness of acute myocardial infarction (AMI). This study evaluated effect of Huayu Qutan Recipe (HQR) pretreatment on myocardial apoptosis induced by AMI by regulating mitochondrial function via PI3K/Akt/Bad pathway in rats with obesity. For in vivo experiments, 60 male rats were randomly divided into 6 groups: sham group, AMI group, AMI (obese) group, 4.5, 9.0 and 18.0 g/kg/d HQR groups. The models fed on HQR with different concentrations for 2 weeks before AMI. For in vitro experiments, the cardiomyocytes line (H9c2) was used. Cells were pretreated with palmitic acid (PA) for 24 h, then to build hypoxia model followed by HQR-containing serum for 24 h. Related indicators were also detected. In vivo, HQR can lessen pathohistological damage and apoptosis after AMI. In addition, HQR improves blood fat levels, cardiac function, inflammatory factor, the balance of oxidation and antioxidation, as well as lessen infarction in rats with obesity after AMI. Meanwhile, HQR can diminish myocardial cell death by improving mitochondrial function via PI3K/Akt/Bad pathway activation. In vitro, HQR inhibited H9c2 cells apoptosis, improved mitochondrial function and activated the PI3K/Akt/Bad pathway, but effects can be peripeteiad by LY294002. Myocardial mitochondrial dysfunction occurs following AMI and can lead to myocardial apoptosis, which can be aggravated by obesity. HQR can relieve myocardial apoptosis by improving mitochondrial function via the PI3K/Akt/Bad pathway in rats with obesity.

Case Report: Two Myxomas of Different Echodensities on Transthoracic Echocardiography in One Patient.

We report a rare case of coincidental left atrial and right ventricular myxomas manifesting as masses with different echodensities on transthoracic echocardiography. This patient had a history of left atrial myxoma, left intra-left internal carotid artery myxoma, and facial cutaneous myxoma 3 years prior to admission. A Carney complex was suspected, and the patient subsequently tested positive for PRKAR1A mutations. The patient was followed up regularly by a biannual echocardiography, which was free from abnormalities until the date of admission. A repeat transthoracic echocardiography revealed a massive left atrial mass of solid echodensity, and a minute hypoechoic entity in the right ventricular outflow tract. Both masses were confirmed for existence by an enhanced cardiac CT. Chest CT also revealed multiple pulmonary emboli. Successful surgical repair was performed revealing that both masses were hemorrhagic nipple-like lesions and that the pulmonary emboli were myxomatous in nature. Postoperative recovery was uneventful. Postoperative echocardiography showed a clear heart chamber, and the 1-year follow-up showed no abnormalities. Further research is needed to clarify the echocardiographic characteristics of multiple myxomas when they occurred simultaneously in different chambers.