Objection: Cumulative studies have identified the effectiveness of cardiac shock wave therapy (CSWT) in treating heart failure after acute myocardial infarction (AMI), but little have been discussed with regard to the beneficial effects of CSWT on anti-fibrosis along with the underlying mechanism. In this study, we investigated whether CSWT could reduce post-AMI fibrosis and further explored the molecular mechanism.Methods: Rat heart failure (HF) models induced by ligating the left anterior descending coronary artery were established and validated by echocardiography. Eligible animals were randomly categorized into five groups: the sham group, the HF group, the HF + CSWT group, the HF + LY294002 group, and the HF + CSWT + LY294002 group. The cardiac weight, serum level of BNP, NT-pro BNP and echocardiography parameters were measured to assess cardiac function in different groups. Masson's trichrome staining was used to assess the proportions of the fibrotic area. The expression level of CD34, αSMA was measured by RT-PCR, Immunohistochemistry and Immunofluorescent analyses and the level of PI3K/Akt was quantified by Immunohistochemistry and Western blotting.Results: The application of CSWT significantly improved cardiac function and reduced myocardial fibrosis and level of CD34 and αSMA, compared to the HF group. CSWT led to significant elevations of p-PI3K and p-Akt expression levels compared to that of the HF group and the inhibition of the PI3K/Akt pathway abolished the observed beneficial effects of CSWT.Conclusion: CSWT can facilitate the alleviation of cardiac fibrosis induced by AMI through the activation of PI3K/Akt signaling pathway.

The results suggested that these disease-causing genes, which were previously discovered in familial cases, might not be the major genetic factors causing the development of ns-CHD in Chinese.

Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a potentially multipathogenic syndrome that affects a subgroup of patients who present with acute myocardial infarction yet have no significant coronary artery disease on angiography. We herein describe a 71-year-old man with typical angina who showed inferior ST-segment elevation on electrocardiography and an increased troponin-I level. Emergency coronary angiography showed no angiographic stenosis. Cardiac magnetic resonance imaging (CMR) and myocardial contrast echocardiography (MCE) with two-dimensional speckle tracking imaging (2D-STI) were performed after coronary angiography. Good consistency was observed between the CMR findings and MCE with 2D-STI findings in identifying the potential causes of MINOCA. We explored an imaging method that is potentially more effective and accurate than CMR, namely MCE combined with 2D-STI, to identify myocardial abnormalities when angiography reveals no obstruction. This application of MCE with 2D-STI may optimize timely treatment. MINOCA has various causes, and the patient in this case was discharged with aspirin, verapamil, and atorvastatin on the presumption that the infarct had arisen from either plaque disruption or coronary spasm. In this study, we analyzed the etiology, clinical diagnosis, and treatment of MINOCA with reference to the relevant literature.

We reported a very rare case, a 59-year-old female whose heart myxoma was present in both atrium, the mass in biatrial was connected to each other at the oval foramen, resembling "dumbbell-like." By means of multimodality echocardiography techniques such as transthoracic echocardiography (TTE), contrast enhanced ultrasound (CEUS), and Real-time three-dimensional transesophageal echocardiography (RT-3D TEE), we have clarified the diagnosis. The patient underwent open-heart surgery to remove the biatrial myxoma which adhered to the oval fossa, with a slightly wider base and smooth lobulated surface. This case demonstrates the importance of multimodality echocardiography in the diagnosis of atypical myxomas.