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Background/Objectives: In patients with chronic primary mitral regurgitation (MR), postoperative persistent left ventricular (LV) dysfunction underlines the lack of a sensitive parameter that can identify subclinical LV dysfunction and optimize the timing of intervention. Left ventricular global longitudinal strain (LV-GLS) is a measure of the longitudinal left ventricular systolic function, with prognostic significance. Its role in the follow-up of asymptomatic patients with MR is, however, poorly defined. The aim of this study was to assess the relative changes in LV-GLS in a cohort of MR patients and to correlate these changes with the need for intervention during a follow-up period. Methods: We conducted a prospective study on a cohort of 218 patients, divided into three subgroups according to MR severity (mild, moderate, severe). LV-GLS was measured at baseline and every six months during a median follow-up period of 30 months. The composite endpoint was the occurrence of heart failure symptoms, hospitalization for heart failure, LVEF < 60%, LVEDD > 45 mm, new onset atrial fibrillation, or cardiovascular death. Results: Patients with moderate and severe MR had a significantly lower GLS at baseline than those with mild MR (19.5% and 19.1% versus 22.3%, p < 0.01) despite a normal LVEF in all subgroups. The relative decrease in LV-GLS occurred earlier (at 12 months vs. 24 months) and was more evident in patients with moderate and severe MR (13.6% and 14.5%, respectively) versus patients with mild MR (6.72%). The baseline LV-GLS being under 18% and a relative decrease of over 10% in GLS were independent predictors of a composite outcome (HR = 1.59, CI 95% 1.17-2.86; HR = 1.74, CI 95% 1.2-2.91, p < 0.01). Conclusions: LV-GLS is a valuable monitoring tool for asymptomatic MR patients, a relative decrease > 10% in GLS may be predictive for the need for valve intervention.
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BACKGROUND: Cardiac magnetic resonance (cMRI) is often used to diagnose acute myocarditis (AM). It is also performed after 6 months to monitor myocardial involvement. However, the clinical and predictive relevance of the 6-month cMRI is uncertain. OBJECTIVE: We used cMRI to assess the morphology and heart function of patients with AM, the correlation between left ventricular remodeling and biomarkers of heart dysfunction and myocardial fibrosis, and the involvement of myocardial fibrosis initially and 6 months after the acute episode. MATERIALS AND METHODS: We conducted a prospective study of 90 patients with the clinical suspicion of AM, where cMRI was performed within the first week after symptom onset and repeated after 6 months. RESULTS: Non-ischemic late gadolinium enhancement (LGE) was present in 88 (97.7%) patients and mainly involved the septum and inferior wall. cMRI at 6 months was associated with significantly reduced abnormalities of segmental kinetics (p < 0.001), myocardial edema (p < 0.001), presence of LGE (p < 0.05) and LGE mass (p < 0.01), native T1 mapping (p < 0.001), and presence of pericardial collection (p ≤ 0.001). At 6 months, signs of myocardial edema appeared in 34.4% of patients, and a complete cure (absence of edema and LGE) was found in 8.8% of patients. LGE disappeared in 15.2% of patients, and the mean number of myocardial segments involved decreased from 46% to 30%, remaining unchanged in 13% of patients. Patients with LGE without edema had a more severe prognostic condition than those with persistent edema. Patients with increased LGE extension on the control cMRI had a worse prognosis than those with modified or low LGE. The most significant independent predictive parameters for major cardiovascular events (MACEs) were LGE mass (adjusted OR = 1.27 [1.11-1.99], p < 0.001), myocardial edema (OR = 1.70 [1.14-209.3], p < 0.001), and prolonged native T1 (OR = 0.97 [0.88-3.06], p < 0.001). The mid-wall model of LGE and the presence of edema-free LGE were MACE-independent predictors. CONCLUSIONS: LGE, myocardial edema, and prolonged native T1 were predictors of MACEs. LGE does not necessarily mean constituted fibrosis in the presence of edema and may disappear over time. LGE without edema could represent fibrosis, whereas the persistence of edema represents active inflammation and could be associated with the residual chance of complete recovery. cMRI should be performed in all patients with AM at 6 months to evaluate progress and prognosis.
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This study investigates the distribution of hyperhomocysteinemia and cardiovascular metabolic syndrome (SM) among participants, shedding light on their prevalence and co-occurrence within the study cohort. Through an analysis of demographic characteristics and health parameters, including age, gender, and body mass index (BMI), alongside nutritional data, correlations between these factors and health risks are explored. Results reveal a notable prevalence of hyperhomocysteinemia, with 45.3% of participants exhibiting this condition. Furthermore, 31.4% of the cohort does not present hyperhomocysteinemia or SM, while 23.3% shows SM without hyperhomocysteinemia. The study underscores gender-specific dietary recommendations due to significant variations in nutrient intake patterns. Additionally, inverse correlations between health risks like obesity, hypertension, and hypercholesterolemia and nutrient requirements highlight the need for tailored dietary interventions. Age-related changes in nutrient needs and the positive correlation between physical activity levels and certain nutrient demands further emphasize the importance of personalized dietary strategies. Variations in nutrient intake by gender, inverse correlations with health risks, and age-related changes underscore the need for tailored dietary strategies. These findings provide valuable insights for healthcare professionals in developing targeted nutritional interventions to mitigate disease risk and promote overall health and well-being.
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Cardiac fibrosis, associated with right heart dysfunction, results in significant morbidity and mortality. Stimulated by various cellular and humoral stimuli, cardiac fibroblasts, macrophages, CD4+ and CD8+ T cells, mast and endothelial cells promote fibrogenesis directly and indirectly by synthesizing numerous profibrotic factors. Several systems, including the transforming growth factor-beta and the renin-angiotensin system, produce type I and III collagen, fibronectin and α-smooth muscle actin, thus modifying the extracellular matrix. Although magnetic resonance imaging with gadolinium enhancement remains the gold standard, the use of circulating biomarkers represents an inexpensive and attractive means to facilitate detection and monitor cardiovascular fibrosis. This review explores the use of protein and nucleic acid (miRNAs) markers to better understand underlying pathophysiology as well as their role in the development of therapeutics to inhibit and potentially reverse cardiac fibrosis.