Background: The COVID-19 pandemic has caused severe health issues worldwide and contributed to huge financial losses. Key comorbidities linked to an increased risk of severe COVID-19 and higher mortality rates include cardio-metabolic disorders such as type 1 and type 2 diabetes mellitus (T1DM and T2DM), atherosclerotic cardiovascular disease, chronic kidney disease, hypertension, heart failure, and obesity. The persistence of symptoms even after the acute phase is over is termed long COVID-19 syndrome. This study aimed to evaluate the relationship between long COVID-19 syndrome and the development of insulin resistance in previously non-diabetic patients. Methods: A prospective observational study was performed on 143 non-diabetic patients who had tested positive for SARS-CoV-2 infection by a PCR test and were hospitalized in our hospital between January 2020 and December 2022. The clinical and para-clinical data at 0, 4, and 12 months of hospital admission for post-COVID-19 infection follow-up was collected and labeled as t0, t4, and t12. Blood glucose, insulin, and C-peptide levels were measured at the beginning and further at 2, 5, 10, and 30 min after the intravenous arginine stimulation test. Similarly, BMI was calculated, and hs-CRP and ESR levels were noted. The results obtained were statistically analyzed. Results: More than one-third (30.7%) of the included patients developed long COVID-19 syndrome. It was found that 75% of patients with long COVID-19 hospitalized in our clinic developed diabetes within a year of acute infection with COVID-19; therefore, it can be said that the presence of long COVID-19 is a major risk for an altered metabolic status, which can cause diabetes. When comparing the glycemia levels (106 mg/dL) with the BMI at t0, t4, and t12 time intervals, the p-values were found to be 0.214, 0.042, and 0.058, respectively. Almost 62% of the patients having BMI > 30 kg/m² were found to have an increase in blood glucose levels at 1 year. Similarly, insulin resistance was noted during this interval. A negative correlation of 0.40 for hsCRP and 0.38 for ESR was noted when compared with acute infection with COVID-19. Conclusions: The association between long COVID-19 and insulin resistance highlights the varied and widespread impacts of SARS-CoV-2 infection. Addressing the complexities of long COVID-19 requires a holistic strategy that encompasses both respiratory and metabolic considerations, which is crucial for enhancing the well-being of those enduring this persistent condition.

Hypercholesterolemia is a major modifiable risk factor for atherosclerotic cardiovascular disease (ASCVD), affecting a significant proportion of the adult population worldwide. This narrative review provides a comprehensive and up-to-date overview of hyperlipidemia management, spanning from epidemiological trends and underlying pathophysiological mechanisms to the limitations of conventional therapies such as statins and ezetimibe. Particular emphasis is placed on cardiovascular risk assessment, current stratification tools, and international guideline-based interventions. The present paper, focusing primarily on the biological mechanisms of dyslipidemia and the clinical use of traditional lipid-lowering agents, serves as the first part of a two-part series, preceding a forthcoming review of novel pharmacological approaches. Our data synthesis is based on a structured literature search conducted across Google Scholar, PubMed, and Scopus, including studies published up to June 2025. The review also includes aspects related to non-pharmacological strategies, pharmacoeconomic considerations, and pharmacogenetic influences on treatment response. Ultimately, this work aims to equip clinicians with evidence-based, nuanced insights essential for optimizing lipid management and reducing cardiovascular risk, while setting the foundation for understanding how emerging therapies may overcome current therapeutic limitations.

Since the prevalence of heart failure (HF) increases with age, HF is now one of the most common reasons for the hospitalization of elderly people. Although the treatment strategies and overall outcomes of HF patients have improved over time, hospitalization and mortality rates remain elevated, especially in developed countries where populations are aging. Therefore, this paper is intended to be a valuable multidisciplinary source of information for both doctors (cardiologists and general physicians) and pharmacists in order to decrease the morbidity and mortality of heart failure patients. We address several aspects regarding pharmacological treatment (including new approaches in HF treatment strategies [sacubitril/valsartan combination and sodium glucose co-transporter-2 inhibitors]), as well as the particularities of patients (age-induced changes and sex differences) and treatment (pharmacokinetic and pharmacodynamic changes in drugs; cardiorenal syndrome). The article also highlights several drugs and food supplements that may worsen the prognosis of HF patients and discusses some potential drug–drug interactions, their consequences and recommendations for health care providers, as well as the risks of adverse drug reactions and treatment discontinuation, as an interdisciplinary approach to treatment is essential for HF patients.

Background: Thrombospondin-1 (TSP-1) is a matricellular functional protein of the extracellular matrix. As it is not constitutively present extracellularly, its secretion is enhanced in several situations, namely injury, chronic pathology, tissue remodeling, angiogenesis, and aging. Over the last decade, TSP-1 has been reported to be involved in complex and opposing biological effects on vasculature in the context of NO signaling. Several studies have reported high patient TSP-1 plasma levels, indicating that the protein can potentially serve as a prognostic marker for pulmonary arterial hypertension. Materials and methods: Here, we aimed to quantify TSP-1 serum levels in hypertensive patients with endothelial dysfunction before and after one year of treatment with Perindopril (an antihypertensive drug with vasoprotective properties). Results: After one year of treatment, TSP-1 levels increased in hypertensive patients compared to baseline (T0: 8061.9 ± 3684.80 vs T1: 15380±5887 ng/mL, p<0.001) and compared to non-hypertensive controls (9221.03 ± 6510.21 ng/mL). In contrast, pentraxin-3 plasma levels were decreased after one year of Perindopril treatment in both hypertensive (T0: 0.91 ± 0.51 vs T1: 0.50 ± 0.24 ng/mL, p<0.001) and control group (1.36 ±1.5 ng/mL) patients, although flow-mediated vasodilation and intima-media thickness assessment parameters were not significantly changed. Systolic and diastolic blood pressure values as well as levels of fibrinogen, high-sensitivity C-reactive protein, triglycerides, and alanine aminotransferase were found to be significantly lower after one year of treatment with Perindopril. High levels of TSP-1 strongly correlated with platelet count (positive), lymphocytes (positive), red cell distribution width-CV (positive), systolic blood pressure (negative), and mean corpuscular hemoglobin (negative) after one year of treatment. Blood urea nitrogen was found to be a protective factor for TSP-1, while glucose and heart rate were found to be risk factors prior to and after treatment.

Background: The clinical presentation of SARS-CoV-2 varies from patient to patient. The most common findings noted were respiratory tract infections, of different severity grades. In some cases, multi-organ damage was noted. Due to its high potential for causing severe systemic inflammation such as myositis and myocarditis, patients should be properly investigated, which carries high chances of SARS-CoV-2 being easily missed if not investigated on time and which can result in more fatal outcomes. Case report: We present a case of COVID-19 infection in a non-vaccinated male patient, who presented to our clinic with no symptoms of respiratory involvement but with severe muscle aches. Cardiac markers and procalcitonin levels were high, and concentric hypertrophy of the left ventricle, severe hypokinesia of the interventricular septum and of the antero-lateral wall, hypokinesia of the inferior and posterior wall and an ejection fraction of the left ventricle being around 34% was noted. Coronary angiography showed no lesions. Corticosteroids and antibiotics were instituted which showed improvement. A possible link to an autoimmune process was suspected, due to the presence of anti-PL-7 antibody, suggesting an antisynthetase syndrome. Conclusion: Each and every patient should be thoroughly investigated, and presently little is known in regards to this virus. Studies focusing on possible relationships between the COVID-19 and autoimmune disease can help to potentially generate better outcomes.

Background: Heart failure with preserved ejection fraction (HFpEF) represents a significant portion of heart failure cases, but diagnosis is challenging due to its diverse presentation and the limitations of traditional echocardiographic parameters. Left atrial (LA) strain provides valuable insights into LA function and is increasingly used to evaluate cardiac function, including left ventricular (LV) diastolic function. LA strain, particularly reservoir strain, is considered a reliable indicator of LV diastolic function and can be used to grade diastolic function and estimate LV filling pressure. Unlike traditional LA measurements, LA strain offers detailed insights into LA function, conduit, and booster-pump phases, making it crucial for evaluating both structural and functional cardiac performance, especially in HFpEF. HFpEF diagnosis currently relies on a combination of echocardiographic parameters, clinical symptoms, and natriuretic peptide levels, encompassing various pathophysiological entities and complicating standardized management. Precise characterization of cardiac pathologies in HFpEF patients is essential. This review assesses global longitudinal strain (GLS) and left atrial strain (LAS) as echocardiographic biomarkers for diagnosing and characterizing HFpEF. Strain imaging, particularly speckle tracking echocardiography, offers a refined assessment of myocardial deformation, providing detailed insights into left heart function beyond traditional measures. Normal ranges for GLS and LAS are discussed, acknowledging demographic and technical influences. Clinical studies confirm the prognostic value of GLS and LAS in HFpEF, especially for predicting cardiovascular outcomes and distinguishing HFpEF from other dyspnea causes. However, variability in strain measurements and false-negative risks necessitate cautious clinical interpretation. The HFA-PEFF scoring system includes these biomarkers but does not fully cover the HFpEF pathology spectrum. Combining GLS and LAS shows promise in defining HFpEF phenogroups, potentially guiding individualized treatments. Global longitudinal strain (GLS) and left atrial strain (LAS) are central to non-invasive HFpEF diagnosis and stratification, with potential for more tailored therapies. Integration of these biomarkers into standard diagnostic practice requires an organized approach, and future guidelines should recommend their combined use for comprehensive HFpEF assessment.