Type 2 diabetes mellitus (T2DM), a prevalent chronic disease affecting over 400 million people globally, is driven by genetic and environmental factors. The pathogenesis involves insulin resistance and β-cell dysfunction, mediated by mechanisms such as the dedifferentiation of β-cells, mitochondrial dysfunction, and oxidative stress. Treatment should be based on non-pharmacological therapy. Strategies such as increased physical activity, dietary modifications, cognitive-behavioral therapy are important in maintaining normal glycemia. Advanced therapies, including SGLT2 inhibitors and GLP-1 receptor agonists, complement these treatments and offer solid glycemic control, weight control, and reduced cardiovascular risk. Complications of T2DM, such as diabetic kidney disease, retinopathy, and neuropathy, underscore the need for early diagnosis and comprehensive management to improve patient outcomes and quality of life.

Hypertension is a leading global cause of cardiovascular disease and mortality, with resistant hypertension (RH) posing treatment challenges. Aldosterone synthase inhibitors (ASIs) are a novel drug class that reduce blood pressure by lowering aldosterone levels. Baxdrostat is a selective ASI that inhibits the CYP11B2 enzyme, responsible for aldosterone synthesis, without affecting cortisol production. This selectivity minimizes hormonal side effects. Clinical trials have shown that baxdrostat reduces plasma aldosterone in a dose-dependent manner while preserving cortisol levels. In the Phase 2 BrigHTN trial, baxdrostat significantly lowered systolic and diastolic blood pressure in patients with RH, with the 2 mg dose showing the most consistent efficacy. However, in the HALO trial, similar blood pressure reductions were observed in the placebo group, possibly due to improved adherence to background antihypertensive therapy. Baxdrostat has demonstrated a favorable safety profile, with mostly mild adverse effects and no significant impact on kidney function. It is considered safe for use with other medications, including metformin. Ongoing trials are investigating its potential in patients with chronic kidney disease (CKD) and primary hyperaldosteronism (PA). Baxdrostat represents a promising therapeutic option for aldosterone-driven hypertension, especially in patients unresponsive to standard treatments.

Background: Acute coronary syndrome (ACS) remains the primary cause of mortality worldwide. Performing complex coronary intervention in patients with ACS is considered a significant factor for worsening prognosis. This study aimed to evaluate the prognosis of patients with ACS treated with complex procedures compared to patients with chronic coronary syndrome (CCS). Methods: Among 980 patients from the Polish Complex Registry, we enrolled 829 consecutive patients who underwent complex percutaneous coronary intervention (PCI) for acute or chronic coronary syndrome with a completed one-year follow-up. The primary endpoint is defined as the major adverse cardiac event (MACE) at 12 months, a composite endpoint including all-cause death, target lesion revascularization, target vessel revascularization, and non-fatal myocardial infarction. Results: The incidence of the composite endpoint of MACE at one-year follow-up was comparable between the patients with acute and chronic coronary syndrome who underwent complex PCI (12.4% vs. 7.6%, LogRank p = 0.035). Cox multivariate analysis indicated that ACS is an independent risk factor for death at one-year follow-up. Additionally, age and comorbidities, such as heart failure and chronic kidney disease, along with procedural factors, including lesion length and pre-procedural diameter stenosis, are independent predictors of death in patients with complex lesions. Independent risk factors for MACE at one-year follow-up include age, heart failure, previous PCI, in-stent restenosis, and pre-procedural diameter stenosis. Conclusions: The prognosis of patients with acute and chronic coronary syndrome in the annual follow-up is comparable in the context of cardiovascular events. The clinical presentation of ACS is an independent risk factor for all-cause death.

Hypertrophic cardiomyopathy (HCM) is a heterogeneous group of heart muscle disorders that affects millions, with an incidence from 1 in 500 to 1 in 200. Factors such as genetics, age, gender, comorbidities, and environmental factors may contribute to the course of this disease. Diagnosis of HCM has improved significantly in the past few decades from simple echocardiographic evaluations to a more complex, multimodal approach embracing advanced imaging, genetic, and biomarker studies. This review focuses on Mavacamten, a selective allosteric inhibitor of cardiac myosin, as a pharmacological treatment for HCM. Patients with HCM experience pathological actomyosin interactions, leading to impaired relaxation and increased energy expenditure. Mavacamten decreases available myosin heads, reducing actomyosin cross-bridges during systole and diastole. By reducing the number of bridges left ventricular outflow tract pressure is normalized and cardiac cavities are filled. This mechanism enhances patient performance and alleviates symptoms such as chest pain and dyspnea. The results suggest the potential for Mavacamten to transform the treatment of obstructive hypertrophic cardiomyopathy. Studies to date have shown significant improvement in exercise capacity, symptom relief, and a reduction in the need for invasive procedures such as septal myectomy. Further studies are needed to confirm the clinical results.

Background: Coronary artery aneurysm and ectasia (CAAE) represent uncommon forms of coronary artery disease characterized by abnormal arterial dilatation and complex remodeling. The mechanisms underlying their development remain poorly defined. Optical coherence tomography (OCT) provides high-resolution evaluation of plaque morphology and vessel wall structure, offering insights into the pathophysiology of CAAE. Methods: We analyzed 21 patients with angiographically confirmed CAAE who underwent intracoronary OCT. Dilated segments were compared with adjacent non-dilated reference segments. Quantitative measurements included the maximal dilated segment’s diameter, reference diameter, and intima–media thickness. Qualitative assessment focused on plaque composition, calcification, neovascularization, fibrous cap characteristics, and thrombus. Results: Aneurysmal segments displayed larger lumen dimensions but no proportional increase in plaque burden, consistent with exaggerated positive remodeling. Compared with non-aneurysmal regions, CAAE segments exhibited significantly smaller calcification arcs and a lower prevalence of lipid plaques and neovascularization, suggesting a heterogeneous and potentially more fibrotic remodeling pattern. Classical features of plaque vulnerability were not consistently present in dilated segments, suggesting that hemodynamic factors, such as disturbed flow and stenosis, may contribute substantially to the thrombotic risk. Conclusions: OCT reveals distinct structural and compositional characteristics in CAAE, supporting the concept of maladaptive remodeling rather than uniformly unstable plaque. High-resolution intracoronary imaging enhances understanding of CAAE pathophysiology and may facilitate individualized clinical assessment and management.