Myocardial ischemia represents a state of reduced coronary perfusion with oxygenated blood, insufficient to meet the metabolic demands of the myocardium. Both acute and chronic ischemia trigger a cascade of cellular events that lead to disturbances in ionic balance, mitochondrial function and energy metabolism. During ischemia, cardiomyocytes (CMs) shift from aerobic to anaerobic metabolism, resulting in adenosine triphosphate (ATP) depletion, loss of ionic homeostasis and calcium (Ca²⁺) overload that activate proteases, phospholipases and membrane damage. Reperfusion restores oxygen supply and prevents irreversible necrosis but paradoxically initiates additional injury in marginally viable myocardium. The reoxygenation phase induces excessive production of reactive oxygen species (ROS), endothelial dysfunction and a strong inflammatory response mediated by neutrophils, platelets and cytokines. Mitochondrial dysfunction and opening of the mitochondrial permeability transition pore (mPTP) further amplify oxidative stress and inflammation and trigger apoptosis and necroptosis. Understanding these intertwined cellular and molecular mechanisms remains essential for identifying novel therapeutic targets aimed at reducing reperfusion injury and improving myocardial recovery after ischemic events.

Coronary artery bypass grafting (CABG) remains the gold standard for patients with advanced multivessel coronary artery disease. Optimal myocardial protection versus ischemia during reversible and controlled cardiac arrest is a cornerstone of successful outcomes. Myocardial ischemia represents a state of reduced coronary perfusion with oxygenated blood, insufficient to meet the metabolic demands of the myocardium. Conventional cardioplegic solutions offer controlled and reversible cardiac arrest while actively modulating the molecular and cellular mechanisms that mediate ischemia–reperfusion injury. Cardioplegia dramatically elongates the reversible period of ischemic injury and restricts cardiomyocyte death by shutting down electromechanical activity, lowering metabolic demand, stabilizing ionic homeostasis, protecting mitochondrial integrity, and slowing oxidative stress and inflammatory signaling. During ischemia, cardiomyocytes shift from aerobic to anaerobic metabolism, resulting in adenosine triphosphate (ATP) depletion, loss of ionic homeostasis and calcium overload that activate proteases, phospholipases and membrane damage. Reperfusion restores oxygen supply and prevents irreversible necrosis but paradoxically initiates additional injury in marginally viable myocardium. The reoxygenation phase induces excessive production of reactive oxygen species (ROS), endothelial dysfunction and a strong inflammatory response mediated by neutrophils, platelets and cytokines. Mitochondrial dysfunction and opening of the mitochondrial permeability transition pore (mPTP) further amplify oxidative stress and inflammation, and trigger apoptosis and necroptosis. Understanding these intertwined cellular and molecular mechanisms remains essential for identifying novel therapeutic targets aimed at reducing reperfusion injury and improving myocardial recovery after ischemic events, particularly in coronary surgery.

The aim of this study was to examine the incidence and significance of right heart failure (RHF) in the early and late phase of left ventricular assist device (LVAD) implantation with the identification of predictive factors for the development of RHF. This was a prospective observational analytical cohort study. The study included 92 patients who underwent LVAD implantation and for whom all necessary clinical data from the follow-up period were available, as well as unambiguous conclusions by the heart team regarding pathologies, adverse events, and complications. Of the total number of patients, 43.5% died. The median overall survival of patients after LVAD implantation was 22 months. In the entire study population, survival rates were 88.04% at one month, 80.43% at six months, 70.65% at one year, and 61.96% at two years. Preoperative RHF was present in 24 patients, 12 of whom died and 12 survived LVAD implantation. Only two survivors developed early RHF (ERHF) and two late RHF (LRHF). The most significant predictors of ERHF development are brain natriuretic peptide (BNP), pre-surgery RHF, FAC < 20%, prior renal insufficiency, and total duration of ICU stay (HR: 1.002, 0.901, 0.858, 23.554, and 1.005, respectively). RHF following LVAD implantation is an unwanted complication with a negative impact on treatment outcome. The increased risk of fatal outcome in patients with ERHF and LRHF after LVAD implantation results in a need to identify patients at risk of RHF, in order to administer the available preventive and therapeutic methods.

Cardiac surgery (CS) with extracorporeal circulation (ECC), induces intense oxidative stress (OS) and systemic inflammatory response (SIR), which may seriously affect postoperative lung function. We aimed to test if high parenteral (200 mg/kg/24 h) daily doses of Vitamin C (VitC), given within 48 h after the beginning of the operation, may reduce the incidence and severity of postoperative pulmonary complications (PPCs) in CS patients. This single-center, prospective, randomized, single-blinded, interventional trial included 150 patients, assigned to control Group A (n = 75) and interventional Group B (n = 75). Group B intraoperatively received one-fourth (i.e., 50 mg/kg) of the planned daily Vit C dose, divided into three equal parts and diluted in 10 mL of normal saline, while Group A received an equal volume of normal saline at the same time frames (i.e., the induction of anesthesia, aortic cross-clamp release, and sternal closure). After 6 h from the first intraoperative dose, the following regimen was applied: Group B: 50 mg/kg, 30 min i.v. infusion of VitC in 50 mL of normal saline, every 6 h, for the next 48 h, and Group A: 30 min i.v. infusion of an equal volume of normal saline every 6 h, for the next 48 h. Modified Kroenke’s score was used to determine the incidence and severity of PPCs. The overall incidence of PPCs was 36.7% and was significantly lower in Group B (13.3% vs. 60.0%, p < 0.001). The PPCs severity score was also significantly lower in Group B (1 vs. 3, p < 0.001). In addition, patients from Group B had significantly less damaged lungs, better postoperative renal function, shorter ICU stays, fewer ICU re-admissions, and lower hospital mortality. No VitC-related adverse effects were recorded. High parenteral daily VitC doses given within 48 h after the beginning of CS are safe and effective in reducing the incidence and severity of PPCs. A multicenter RCT is needed to confirm these results.

Coronary artery vasospasm (CAV) is a transient, reversible constriction of the epicardial coronary arteries that reduces coronary blood flow and may cause myocardial ischemia. Despite its clinical significance, CAV remains underdiagnosed and can present as chest pain, acute coronary syndrome, malignant arrhythmias or sudden cardiac death. Vasospasm may occur in both angiographically normal coronary arteries and at sites of pre-existing atherosclerotic stenosis. The pathophysiology of CAV is multifactorial and involves vascular smooth muscle cells (VSMCs) hyperreactivity, endothelial dysfunction, chronic inflammation and autonomic dysregulation. VSMCs contraction is mediated by phosphorylation of the myosin light chain (MLC) through calcium (Ca²⁺)/calmodulin-dependent myosin light chain kinase (MLCK), while relaxation is regulated by myosin light chain phosphatase (MLCP). Increased intracellular Ca²⁺ levels and enhanced Ca²⁺ sensitivity contribute to excessive vasoconstriction. Rho-kinase (ROCK) plays a pivotal role in sustained vasospasm by inhibiting MLCP, thereby promoting prolonged smooth muscle contraction. Endothelial dysfunction contributes to CAV by disrupting normal vascular tone regulation, largely as a result of decreased nitric oxide (NO) mediated vasodilation. Chronic low-grade inflammation and oxidative stress exacerbate both endothelial dysfunction and VSMCs contraction. Understanding these molecular mechanisms is essential for identifying novel therapeutic targets. Emerging treatment strategies, including ROCK inhibitors, endothelin receptor antagonists and anti-inflammatory agents, may improve outcomes in patients with refractory CAV.

Objectives: This single-center retrospective comparative cohort study aimed to compare the outcomes of aortic valve replacement using a Perceval sutureless bioprosthesis versus a conventional stented bioprosthesis in patients with symptomatic severe aortic valve stenosis. Methods: A total of 233 consecutive elective patients undergoing aortic valve replacement (AVR) at the University Clinical Center of Serbia (July 2017–March 2021) were analyzed: 74 received a Perceval sutureless valve, and 159 received a conventional stented valve. Results: The baseline characteristics were similar between the groups, with most patients being male (54.1% vs. 56.6%), with a mean age of 72.6 years. Combined aortic valve replacement and coronary artery bypass grafting were performed in 19.3% of the patients. Mean aortic cross-clamp (ACC) time was significantly shorter in the Perceval group for combined procedures (104.5 ± 29.6 min, p < 0.05) but similar in isolated AVR, likely reflecting the early institutional learning curve. Thirty-day mortality was comparable (5.9% vs. 6.3%). Importantly, at 36 months, survival was higher in the Perceval group (88.3% vs. 76.8%, p = 0.048). Longer echocardiographic follow-up (up to 58 months) was available for the Perceval group. Conclusions: Perceval sutureless bioprostheses are a safe and effective option for elderly high-risk patients. The extended echocardiographic follow-up represents a novel contribution to the literature, although further data on long-term durability are needed.