The search for new drugs with the potential to ensure therapeutic success in the treatment of cardiovascular diseases has become an essential pathway to follow for health organizations and committees around the world. In June 2021, the World Health Organization listed cardiovascular diseases as one of the main causes of death worldwide, representing 32% of them. The most common is coronary artery disease, which causes the death of cardiomyocytes, the cells responsible for cardiac contractility, through ischemia and subsequent reperfusion, which leads to heart failure in the medium and short term. Metformin is one of the most-used drugs for the control of diabetes, which has shown effects beyond the control of hyperglycemia. Some of these effects are mediated by the regulation of cellular energy metabolism, inhibiting apoptosis, reduction of cell death through regulation of autophagy and reduction of mitochondrial dysfunction with further reduction of oxidative stress. This suggests that metformin may attenuate left ventricular dysfunction induced by myocardial ischemia; preclinical and clinical trials have shown promising results, particularly in the setting of acute myocardial infarction. This is a review of the molecular and pharmacological mechanisms of the cardioprotective effects of metformin during myocardial ischemia-reperfusion injury.

Currently, cardiovascular diseases are a major contributor to morbidity and mortality worldwide, having a significant negative impact on both the economy and public health. The renin–angiotensin system contributes to a high spectrum of cardiovascular disorders and is essential for maintaining normal cardiovascular homeostasis. Overactivation of the classical renin–angiotensin system is one of the most important pathophysiological mechanisms in the progression of cardiovascular diseases. The counter-regulatory renin–angiotensin system is an alternate pathway which favors the synthesis of different peptides, including Angiotensin-(1-7), Angiotensin-(1-9), and Alamandine. These peptides, via the angiotensin type 2 receptor (AT2R), MasR, and MrgD, initiate multiple downstream signaling pathways that culminate in the activation of various cardioprotective mechanisms, such as decreased cardiac fibrosis, decreased myocardial hypertrophy, vasodilation, decreased blood pressure, natriuresis, and nitric oxide synthesis. These cardioprotective effects position them as therapeutic alternatives for reducing the progression of cardiovascular diseases. This review aims to show the latest findings on the cardioprotective effects of the main peptides of the counter-regulatory renin–angiotensin system.

Cardiovascular diseases (CVD) are the leading cause of death worldwide, creating the need for new therapeutic strategies targeting the pathological processes involved. Mitochondria, which comprise one-third of cardiac cell volume, maybe a potential therapeutic target for CVD. Known primarily for energy production, mitochondria are also involved in other processes including intermediary metabolism, mitophagy, calcium homeostasis, and regulation of cell apoptosis. Mitochondrial function is closely linked to morphology, which is altered through mitochondrial dynamics, including processes such as fission and fusion, which ensure that the energy needs of the cell are met. Recent data indicate that mitochondrial dysfunction is involved in the pathophysiology of several CVDs, including cardiac hypertrophy, heart failure, ischemia/reperfusion injury, and cardiac fibrosis. Furthermore, mitochondrial dysfunction is associated with oxidative stress related to atherosclerosis, hypertension, and pulmonary hypertension. In this review, we first briefly present the physiological mechanisms of mitochondrial function in the heart and then summarize the current knowledge on the impact of mitochondrial dysfunction on CVD. And finally, we highlight the evidence from in vitro, in vivo, and clinical studies of the cardioprotective effects of drugs that preserve mitochondrial function in CVD. It is hoped that this review may provide new insights into the need to discover new pharmacological targets with direct actions on mitochondria that may provide combined therapeutic strategies to optimally treat these pathologies.

El síndrome de May-Thurner (SMT), también llamado síndrome de Cockett, es una condición anatomopatológica que conduce a obstrucción del flujo venoso debido a compresión externa en la zona venosa iliocava, por parte de la arteria ilíaca común derecha (AICD o RICA en inglés) y la columna lumbar inferior, generalmente a nivel de la quinta vértebra lumbar. Puede ser asintomática y desapercibida durante la vida, o causar morbilidad vascular, incluyendo trombosis venosa profunda (TVP), descrita sobre todo en mujeres en etapa fértil. Se reporta caso de una mujer añosa, con diagnóstico de TVP no provocado, hallazgo de Tromboembolismo Pulmonar (TEP) en estudios complementarios y de trombosis en vena iliaca y vena ileofemoral izquierda. Se sospechó SMT a través de una angiotomografía toracoabdominal, la cual se confirmó por estudio endovascular, seguido de tratamiento por misma vía y manejo médico. El reporte destaca una causa subdiagnosticada de TEV en un grupo etario inusual

Del Nido cardioplegia (DNC), a blood‐and‐crystalloid solution containing high and low concentrations of potassium and calcium, respectively, is used as a single‐dose antegrade infusion to induce immediate cardiac arrest in the surgery of patients with cardiovascular diseases requiring extracorporeal circulation. Adding cardioprotective molecules may further reduce the damage‐triggered ischemia/reperfusion (I/R) injury. Angiotensin‐(1–9) (Ang‐(1–9)) and angiotensin‐(1–7) (Ang‐(1–7)), members of the counter‐regulatory renin‐angiotensin system, have shown cardioprotective effects in cardiac hypertrophy and I/R models. This study aimed to evaluate the effects of Ang‐(1–9) and Ang‐(1–7), as adjuvants of the DNC, on cardioprotection and ventricular function in isolated rat hearts subjected to I/R and in cultured neonatal rat ventricular myocytes subjected to simulated I/R (sI/R). The addition of DNC and Ang‐(1–9) and Ang‐(1–7) decreased lactic dehydrogenase (LDH) release in cultured cardiomyocytes subjected to sI/R in comparison to those cardiomyocytes subjected to sI/R and incubated with DNC alone. Moreover, hearts treated with Ang‐(1–9) during reperfusion after DNC + I/R exhibited fewer arrhythmias and required less time to reach left ventricular developed pressure stability. Overall, reperfusion with DNC and Ang‐(1–9) improves the recovery of the left ventricular function of the heart.

Las sibilancias se definen como sonidos pulmonares adventicios, continuos y de tono alto. Predominantemente las sibilancias son de naturaleza espiratoria, pero también pueden ser inspiratorias o bifásicas. Su etiología es secundaria a la obstrucción de flujo en vía aérea superior extratorácica, vía área superior intratorácica o vía área inferior. Se cree que las sibilancias se deben a las vibraciones de las paredes de las vías respiratorias ocluidas, inducidas por una velocidad reducida del flujo de aire. Cuando se perciben sibilancias sin inducir exhalación forzada es necesario estudiar la causa, realizando una historia clínica dirigida a las diversas etiologías y un examen físico que incluya la exploración torácica completa: inspección, palpación, percusión y auscultación. Ayudas diagnósticas como la radiografía de tórax, la espirometría pre y posbroncodilatador, la tomografía computarizada de tórax y la broncoscopia pueden ser necesarias. El objetivo de este artículo es demostrar que las sibilancias representan un hallazgo semiológico retador para el clínico, que obliga no solo a pensar en asma o en enfermedad pulmonar obstructiva crónica (EPOC) como posible causa.