Background and Objectives: Cardiovascular disease is a leading cause of global death with a rising prevalence and a heavy economic burden. Periodontal disease has been associated with cardiovascular diseases—including incident coronary heart disease, peripheral artery disease and ischemic stroke. The study evaluates the quality of life of patients with cardiovascular and periodontal disease from the point of view of oral health by using the short version of the Oral Health Impact Profile (OHIP-14) questionnaire. Materials and Methods: This study included a total of 221 patients (61.86 ± 15.03 years old) selected from the Emergency Hospital of Sibiu, Romania. The participants self-completed the OHIP-14 questionnaire and they benefited from an oral health examination conducted to assess the presence and the severity of periodontal disease. Results: Out of the 147 patients with cardiovascular disease, 77.5% had periodontal disease (32.6% stage I, 29.2% stage II, and 15.6% stage III and IV). The presence of periodontal disease was associated with a lower oral-health-related quality of life (p < 0.001, ANOVA) and with a higher OHIP-14 score in patients with cardiovascular disease (18.67 ± 8.17, p < 0.001 ANOVA). No significant difference was observed concerning patient sex and background; however, age, body mass index and the lack of an appropriate oral hygiene routine had a strong association with the individual quality of life. The general OHIP-14 score was higher in patients with periodontal disease and associated cardiovascular disease, the presence of both cardiovascular and periodontal disease being associated with a lower quality of life. Conclusions: By increasing the patients’ awareness to oral healthcare measures, better outcomes and improved oral-health-related quality of life could be observed.

Polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) are classical myeloproliferative neoplasms (MPN), characterized by specific somatic mutations in JAK2, CALR or MPL genes. JAK2 46/1 and TERT rs2736100 polymorphisms are known to significantly predispose to MPN. This study aimed to establish the additional contribution of the recently described MECOM rs2201862, HBS1L‐MYB rs9376092 and THRB‐RARB rs4858647 polymorphisms to the occurrence of MPN. These three polymorphisms, along with JAK2 46/1 and TERT rs2736100 were genotyped in 939 MPN patients (454 with ET, 337 with PV and 148 with PMF) and 483 controls. MECOM rs2201862 associated significantly with each MPN entity, except for ET, and with all major molecular sub‐types, especially those CALR‐mutated (OR = 1.4; 95% CI = 1.1‐1.8; P‐value = .005). HBS1L‐MYB rs9376092 associated only with JAK2 V617F‐mutated ET (OR = 1.4; 95% CI = 1.1‐1.7; P‐value = .003). THRB‐RARB rs4858647 had a weak association with PMF only (OR = 1.5; 95% CI = 1‐2.1; P‐value = .04). Surprisingly, JAK2 46/1 haplotype was associated significantly not only with JAK2 V617F‐mutated MPN, but also with CALR‐mutated MPN (OR = 1.4; 95% CI = 1.1‐1.8; P‐value = .01). TERT rs2736100 was associated equally strong with all MPN, regardless of phenotype or molecular sub‐type. In conclusion, JAK2 46/1, TERT rs2736100 and MECOM rs2201862 are the chief predisposing polymorphisms to MPN.

Metabolic-associated steatotic liver disease (MASLD), previously termed non-alcoholic fatty liver disease (NAFLD), has emerged as a prominent global cause of chronic liver disease and is increasingly recognized as associated with atherosclerotic vascular illness, consolidating its position along traditional cardiovascular risk factors. Individuals with MASLD exhibit a combination of metabolic syndrome risk factors, carotid atherosclerosis, and increased arterial stiffness, hinting at shared pathogenesis. In this study, we aim to explore liver involvement and arterial stiffness within metabolic syndrome. We enrolled 75 patients (30 male and 45 female) with either liver steatosis on conventional ultrasound, altered liver function tests, or the presence of cardiometabolic risk factors after excluding liver pathology other than MASLD. Clinical evaluation, laboratory measurements, abdominal and carotid ultrasounds, vibration-controlled transient elastography (VCTE, Fibroscan), and assessment with the Arteriograph (Tensiomed) were performed. The 26 patients diagnosed with MetS had significantly higher liver involvement as quantified via the hepatic steatosis index (HSI), Fibrosis-4 (FIB4), aspartate aminotransferase to platelet ratio index (APRI) category, and VCTE measurements, as well as Agile 3+ and Agile 4 scores which use a combination of clinical and laboratory parameters together with results obtained from VCTE to reflect the probability of advanced liver fibrosis or cirrhosis. Patients with MetS also exhibited more pronounced vascular involvement as quantified via arterial stiffness measurements and CIMT (carotid intima–media thickness). We applied a two-step clustering algorithm to enhance our analysis, which gave us pertinent insight into the interplay between metabolic syndrome elements and typologies of hepatic steatosis and arterial stiffness degrees. Notably, of the three obtained clusters, the cluster showing increased levels of hepatic steatosis and arterial stiffness also exhibited the highest prevalence of metabolic syndrome and its constituting components. The results have significant clinical implications, advocating for a comprehensive diagnostic approach when MetS or MASLD is suspected.

Myeloproliferative neoplasms (MPNs), encompassing disorders like polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), are characterized by clonal hematopoiesis without the Philadelphia chromosome. The JAK2 V617F mutation is prevalent in PV, ET, and PMF, while mutations in MPL and CALR also play significant roles. These conditions predispose patients to thrombotic events, with PMF exhibiting the lowest survival among MPNs. Chronic inflammation, driven by cytokine release from aberrant leukocytes and platelets, amplifies cardiovascular risk through various mechanisms, including atherosclerosis and vascular remodeling. Additionally, MPN-related complications like pulmonary hypertension and cardiac fibrosis contribute to cardiovascular morbidity and mortality. This review consolidates recent research on MPNs’ cardiovascular implications, emphasizing thrombotic risk, chronic inflammation, and vascular stiffness. Understanding these associations is crucial for developing targeted therapies and improving outcomes in MPN patients.

Background: Dyslipidemia is the main factor involved in the occurrence and progression of coronary artery disease. Objective: The research strategy is aimed at analyzing new data on the pathophysiology of dyslipidemia involvement in coronary artery disease, the modalities of atherogenic risk estimation and therapeutic advances. Method: Scientific articles published in PubMed from January 2017 to February 2018 were searched using the terms "dyslipidemia" and "ischemic heart disease". Results: PCSK9 contributes to the increase in serum levels of low-density lipoprotein-cholesterol and lipoprotein (a). The inflammation is involved in the progression of hyperlipidemia and atherosclerosis. Hypercholesterolemia changes the global cardiac gene expression profile and is thus involved in the increase of oxidative stress, mitochondrial dysfunction, and apoptosis initiated by inflammation. Coronary artery calcifications may estimate the risk of coronary events. The cardioankle vascular index evaluates the arterial stiffness and correlates with subclinical coronary atherosclerosis. The carotid plaque score is superior to carotid intima-media thickness for risk stratification in patients with familial hypercholesterolemia and both can independently predict coronary artery disease. The lipoprotein (a) and familial hypercholesterolemia have a synergistic role in predicting the risk of early onset and severity of coronary atherosclerosis. A decrease in atherosclerotic coronary plaque progression can be achieved in patients with plasma LDL-cholesterol levels below 70 mg/dL. A highly durable RNA interference therapeutic inhibitor of PCSK9 synthesis could be a future solution. Conclusion: The prophylaxis and treatment of coronary artery disease in a dyslipidemic patient should be based on a careful assessment of cardio-vascular risk factors and individual metabolic particularities, so it may be personalized.