Background: Although several studies suggest that heparins prevent arrhythmias caused by acute myocardial infarction (AMI), the molecular mechanisms involved remain unclear. To investigate the involvement of pharmacological modulation of adenosine (ADO) signaling in cardiac cells by a low-molecular weight heparin (enoxaparin; ENOX) used in AMI therapy, the effects of ENOX on the incidences of ventricular arrhythmias (VA), atrioventricular block (AVB), and lethality (LET) induced by cardiac ischemia and reperfusion (CIR) were evaluated, with or without ADO signaling blockers. Methods: To induce CIR, adult male Wistar rats were anesthetized and subjected to CIR. Electrocardiogram (ECG) analysis was used to evaluate CIR-induced VA, AVB, and LET incidence, after treatment with ENOX. ENOX effects were evaluated in the absence or presence of an ADO A1-receptor antagonist (DPCPX) and/or an inhibitor of ABC transporter-mediated cAMP efflux (probenecid, PROB). Results: VA incidence was similar between ENOX-treated (66%) and control rats (83%), but AVB (from 83% to 33%) and LET (from 75% to 25%) incidences were significantly lower in rats treated with ENOX. These cardioprotective effects were blocked by either PROB or DPCPX. Conclusion: These results indicate that ENOX was effective in preventing severe and lethal arrhythmias induced by CIR due to pharmacological modulation of ADO signaling in cardiac cells, suggesting that this cardioprotective strategy could be promising in AMI therapy.
To evaluate, describe and compare the pharmacological treatments available for heart failure (HF). This is a literature review about the pharmacological treatment of HF based on articles selected from the PubMed database, as well as relevant guidelines, using pertinent keywords and application of inclusion and exclusion criteria. Chronic heart failure is a common condition that, if untreated, harms quality of life and is associated with a high risk of mortality, morbidity, and recurrent hospitalization. However, the prognosis of patients with this condition has been improved with knowledge of the pathophysiology of HF and, therefore, assertive application of both non-pharmacological and pharmacological treatment recommendations. Pharmacotherapy is based on neurohormoral inhibition of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system to improve the health status and survival of these patients. Currently, the recommendation for the treatment of HF with reduced ejection fraction (HFrEF) includes 4 drug classes: an angiotensin/neprilysin receptor inhibitor (ANRi), beta-blockers, mineralocorticoid receptor antagonists (MRA) and SGLT2 inhibitors (SGLT2ii). Mortality-reducing pharmacotherapy in HF currently includes ANRi, beta-blockers, MRA and SGLT2. Therefore, the challenge is to transform the results achieved in clinical studies into reality for the majority of patients with HF. This path must be promoted through multidisciplinary care with improved access to recommended drugs, close monitoring of patients, healthy habits, control of comorbidities and therapeutic adherence.
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