Anti-inflammatory Therapy Progress in Major Adverse Cardiac Events after PCI: Chinese and Western Medicine.

Acute coronary syndrome (ACS) is one of the leading causes of death in cardiovascular disease. Percutaneous coronary intervention (PCI) is an important method for the treatment of coronary heart disease (CHD), and it has greatly reduced the mortality of ACS patients since its application. However, a series of new problems may occur after PCI, such as in-stent restenosis, no-reflow phenomenon, in-stent neoatherosclerosis, late stent thrombosis, myocardial ischemia-reperfusion injury, and malignant ventricular arrhythmias, which result in the occurrence of major adverse cardiac events (MACE) that seriously reduce the postoperative benefit for patients. The inflammatory response is a key mechanism of MACE after PCI. Therefore, examining effective anti-inflammatory therapies after PCI in patients with ACS is a current research focus to reduce the incidence of MACE. The pharmacological mechanism and clinical efficacy of routine Western medicine treatment for the anti-inflammatory treatment of CHD have been verified. Many Chinese medicine (CM) preparations have been widely used in the treatment of CHD. Basic and clinical studies showed that effectiveness of the combination of CM and Western medicine treatments in reducing incidence of MACE after PCI was better than Western medicine treatment alone. The current paper reviewed the potential mechanism of the inflammatory response and occurrence of MACE after PCI in patients with ACS and the research progress of combined Chinese and Western medicine treatments in reducing incidence of MACE. The results provide a theoretical basis for further research and clinical treatment.

S100A4+ macrophages facilitate zika virus invasion and persistence in the seminiferous tubules via interferon-gamma mediation.

Testicular invasion and persistence are features of Zika virus (ZIKV), but their mechanisms are still unknown. Here, we showed that S100A4+ macrophages, a myeloid macrophage subpopulation with susceptibility to ZIKV infection, facilitated ZIKV invasion and persistence in the seminiferous tubules. In ZIKV-infected mice, S100A4+ macrophages were specifically recruited into the interstitial space of testes and differentiated into interferon-γ-expressing M1 macrophages. With interferon-γ mediation, S100A4+ macrophages down-regulated Claudin-1 expression and induced its redistribution from the cytosol to nucleus, thus increasing the permeability of the blood-testis barrier which facilitated S100A4+ macrophages invasion into the seminiferous tubules. Intraluminal S100A4+ macrophages were segregated from CD8+ T cells and consequently helped ZIKV evade cellular immunity. As a result, ZIKV continued to replicate in intraluminal S100A4+ macrophages even when the spermatogenic cells disappeared. Deficiencies in S100A4 or interferon-γ signaling both reduced ZIKV infection in the seminiferous tubules. These results demonstrated crucial roles of S100A4+ macrophages in ZIKV infection in testes.

Diagnosis of myocardial infarction with nonobstructive coronary arteries in a young man in the setting of acute myocardial infarction after endoscopic retrograde cholangiopancreatography: A case report.

BACKGROUND: Acute myocardial infarction (AMI) is characterized by chest pain as well as cardiac troponin I (cTnI) and electrocardiography (ECG) changes. Recently, clinical researchers have used the term "MINOCA" to indicate myocardial infarction with nonobstructive coronary arteries. To the best of our knowledge, no report has documented MINOCA in a young patient after choledocholithiasis by endoscopic retrograde cholangiopancreatography (ERCP). CASE SUMMARY: An 18-year-old Chinese man presented to the cardiac intensive care unit with chest pain radiating to the left shoulder for 1 h after choledocholithiasis by ERCP and the following treatment. ECG showed a sinus rhythm with ST-segment elevation in the II, III, and aVF leads compared with the baseline. Laboratory data revealed cTnI levels of 67.55 ng/mL and 80 ng/mL at the peak (relative index below 0.034 ng/mL) and creatine kinase-MB levels of 56 U/L and 543 U/L at the peak (relative index below 24 U/L). AMI was suspected, and coronary angiography was performed the second day. The results revealed a smooth angiographic appearance of all arteries. The patient had been diagnosed with gallstones and cholecystitis for four years but had not accepted treatment. He had abdominal pain and bloating a week previously and underwent ERCP and subsequent treatments on the second day of admission; 1.4 cm × 1.6 cm of stones were removed from his common bile duct during surgery. The results of his laboratory tests at admission revealed abnormal alanine aminotransferase, aspartate aminotransferase, glutamyl transpeptidase, total bile acid, total bilirubin, direct bilirubin, and indirect bilirubin levels. His temperature, heart rate, blood pressure, and body mass index were normal. His echocardiographic examination revealed no obvious abnormalities in the structure and movement of the ventricular wall and an estimated left ventricular ejection fraction of 57% after the heart attack. His cholesterol and triglycerides were within normal ranges, and his low-density lipoprotein cholesterol was 2.23 mmol/L (normal range 2.03-3.34 mmol). Further testing after AMI revealed nothing remarkable in his erythrocyte sedimentation rate, thyroid function, and tumour markers. CONCLUSION: We ultimately made a diagnosis of MINOCA caused by coronary artery spasm, which seemed to be the most suitable diagnosis of this young patient. We are concerned that the heart attack may have been induced by the ERCP rather than occurred coincidentally afterward, so we should investigate the timing of the event further. Additional studies are needed to unravel the underlying pathophysiology.