Arrhythmias are a known complication after cardiac surgery and represent a major cause of morbidity, increased length of hospital stay, and economic costs. However, little is known about incidence, risk factors, and treatment of early postoperative arrhythmias. Both tachyarrhythmias and bradyarrhythmias can present in the postoperative period. In this setting, atrial fibrillation is the most common heart rhythm disorder. Postoperative atrial fibrillation is often self-limiting, but it may require anticoagulation therapy and either a rate or rhythm control strategy. However, ventricular arrhythmias and conduction disturbances can also occur. Sustained ventricular arrhythmias in the recovery period after cardiac surgery may warrant acute treatment and long-term preventive strategy in the absence of reversible causes. Transient bradyarrhythmias may be managed with temporary pacing wires placed at surgery, but significant and persistent atrioventricular block or sinus node dysfunction can occur with the need for permanent pacing. We provide a complete and updated review about mechanisms, risk factors, and treatment strategies for the main postoperative arrhythmias.

Hypertension exerts a profound impact on the microcirculation, causing both structural and functional alterations that contribute to systemic and organ-specific vascular damage. The microcirculation, comprising arterioles, capillaries, and venules with diameters smaller than 20 μm, plays a fundamental role in oxygen delivery, nutrient exchange, and maintaining tissue homeostasis. In the context of hypertension, microvascular remodeling and rarefaction result in reduced vessel density and elasticity, increasing vascular resistance and driving end-organ damage. The pathophysiological mechanisms underlying hypertensive microvascular dysfunction include endothelial dysfunction, oxidative stress, and excessive collagen deposition. These changes impair nitric oxide (NO) bioavailability, increase reactive oxygen species (ROS) production, and promote inflammation and fibrosis. These processes lead to progressive vascular stiffening and dysfunction, with significant implications for multiple organs, including the heart, kidneys, brain, and retina. This review underscores the pivotal role of microvascular dysfunction in hypertension-related complications and highlights the importance of early detection and therapeutic interventions. Strategies aimed at optimizing blood pressure control, improving endothelial function, and targeting oxidative stress and vascular remodeling are critical to mitigating the systemic consequences of hypertensive microvascular damage and reducing the burden of related cardiovascular and renal diseases.

The Increased Cardiovascular Risk in Patients Affected by Autoimmune Diseases: Review of the Various Manifestations

Renin-Angiotensin-Aldosterone (RAAS) is a hormone system which acts on multiple physiologic pathways primarily by regulating blood pressure and fluid balance, but also by local autocrine and paracrine actions. In pathophysiologic conditions RAAS also contributes to the development of atherosclerosis and its various manifestations, both directly and indirectly through the actions on other systems. RAAS mainly acts as a promoter of atherosclerosis by its action on vessels, and by promoting the developmentt of hypertension, insulin resistance and diabetes, obesity, vascular and systemic inflammation. As RAAS plays a key role in the pathogenesis of cardiovascular diseases, RAAS genes have been extensively studied as candidate genes for atherosclerosis and coronary artery disease. Several polymorphisms of its genes have been found to be in relationship with atherosclerosis and cardiovascular diseases. In this review we will discuss these issues and present the most recent advances about this topic.