Search

The hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is about 6% and has not decreased in recent years. The leading cause of death of these patients is ischemia/reperfusion (I/R) cardiac injury. It is quite obvious that there is an urgent need to create new drugs for the treatment of STEMI based on knowledge about the pathogenesis of I/R cardiac injury, in particular, based on knowledge about the molecular mechanism of ferroptosis. In this study, it was demonstrated that ferroptosis is involved in the development of I/R cardiac injury, antitumor drug-induced cardiomyopathy, diabetic cardiomyopathy, septic cardiomyopathy, and inflammation. There is indirect evidence that ferroptosis participates in stress-induced cardiac injury. The activation of AMPK, PKC, ERK1/2, PI3K, and Akt prevents myocardial ferroptosis. The inhibition of HO-1 alleviates myocardial ferroptosis. The roles of GSK-3β and NOS in the regulation of ferroptosis require further study. The stimulation of Nrf2, STAT3 prevents ferroptosis. The activation of TLR4 and NF-κB promotes ferroptosis of cardiomyocytes. MiR-450b-5p and miR-210-3p can increase the tolerance of cardiomyocytes to hypoxia/reoxygenation through the inhibition of ferroptosis. Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-208a/b, miR-375-3p, miR-26b-5p and miR-15a-5p can aggravate myocardial ferroptosis.

Aim: Some truncal blocks could provide adequate surgical anesthesia and postoperative analgesia in cardiac implantable electronic devices (CIED) insertion. The aim of this study was to evaluate the feasibility of the pectoral nerves (PECS) II block for CIED insertion., Methods: PECS II blocks were performed on the left side using the ultrasound-guided single injection technique in all patients. The primary outcome for feasibility was the percentage of the cases completed without intraoperative additional local anesthesia. Secondary outcomes were the amount of intraoperative additional local anesthetic, intraoperative opioid requirement, postoperative pain scores, first requirement for postoperative analgesia, postoperative analgesic consumption, patient satisfaction, and block-related complications., Results: Of the total 30 patients, 19 (63.3%) required intraoperative additional local anesthetic. The median (IQR [range]) volume of the additional local anesthetic used was 7 (4-10 [2.5-12]) mL. Two patients needed additional IV analgesics in the first 24 h postoperatively. No statistically significant differences were determined between the patients requiring and not requiring intraoperative additional local anesthetic in respect of age, gender, duration of surgery, block performance time, and hospital stay. A total of 26 (86.6%) patients reported a high level of satisfaction with the procedure., Conclusions: PECS II block for cardiac electronic implantable device insertion provides effective postoperative analgesia for at least 24 h. Although PECS II block alone could not provide complete surgical anesthesia in the majority of the patients, when combined with supplementary local anesthetic, contributes to a smooth intraoperative course for patients., (© 2023 Wiley Periodicals LLC.)

An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ 2 -opioid receptor (δ 2 -OR) increases the cardiac tolerance to reperfusion. It has been found that this δ 2 -OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion. The infarct-limiting effect of the δ 2 -OR agonist deltorphin II depends on the activation of several protein kinases, including PKCδ, ERK1/2, PI3K, and PKG. Hypothetical end-effectors of the cardioprotective effect of deltorphin II are the sarcolemmal K ATP channels and the MPT pore.

In-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is 5-6%. Consequently, it is necessary to develop fundamentally novel drugs capable of reducing mortality in patients with acute myocardial infarction. Apelins could be the prototype for such drugs. Chronic administration of apelins mitigates adverse myocardial remodeling in animals with myocardial infarction or pressure overload. The cardioprotective effect of apelins is accompanied by blockage of the MPT pore, GSK-3β, and the activation of PI3-kinase, Akt, ERK1/2, NO-synthase, superoxide dismutase, glutathione peroxidase, matrix metalloproteinase, the epidermal growth factor receptor, Src kinase, the mitoK ATP channel, guanylyl cyclase, phospholipase C, protein kinase C, the Na + /H + exchanger, and the Na + /Ca 2+ exchanger. The cardioprotective effect of apelins is associated with the inhibition of apoptosis and ferroptosis. Apelins stimulate the autophagy of cardiomyocytes. Synthetic apelin analogues are prospective compounds for the development of novel cardioprotective drugs.