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Sökning: WFRF:(Galanti Kristian)

  • Resultat 1-6 av 6
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1.
  • Bisaccia, Giandomenico, et al. (författare)
  • Cardiovascular Morbidity and Mortality Related to Non-Alcoholic Fatty Liver Disease : a Systematic Review and Meta-Analysis
  • 2023
  • Ingår i: Current Problems in Cardiology. - : Elsevier BV. - 0146-2806 .- 1535-6280. ; 48:6
  • Forskningsöversikt (refereegranskat)abstract
    • BACKGROUND AND AIMS: Whether non-alcoholic fatty liver disease (NAFLD) is a cardiovascular (CV) risk factor is debated. We performed a systematic review and meta-analysis to assess the CV morbidity and mortality related to NAFLD in the general population, and to determine whether CV risk is comparable between lean and non-lean NAFLD phenotypes.METHODS AND RESULTS: We searched multiple databases, including PubMed, Embase, and the Cochrane Library, for observational studies published through 2022 that reported the risk of CV events and mortality. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for all-cause mortality, CV mortality, myocardial infarction (MI), stroke, atrial fibrillation (AF), and major adverse cardiovascular and cerebrovascular events (MACCE) were assessed through random-effect meta-analysis. We identified 33 studies and a total study population of 10,592,851 individuals (mean age 53±8; male sex 50%; NAFLD 2,9%). Mean follow-up was 10±6 years. Pooled ORs for all-cause and CV mortality were respectively 1.14 (95%CI 0.78-1.67) and 1.13 (95%CI 0.57-2.23), indicating no significant association between NAFLD and mortality. NAFLD was associated with increased risk of MI (OR 1.6; 95%CI 1.5-1.7), stroke (OR 1.6; 95%CI 1.2-2.1), atrial fibrillation (OR 1.7; 95%CI 1.2-2.3) and MACCE (OR 2.3; 95%CI 1.3-4.2). Compared with non-lean NAFLD, lean NAFLD was associated with increased CV mortality (OR 1.50; 95%CI 1.1-2.0), but similar all-cause mortality and risk of MACCE.CONCLUSIONS: While NAFLD may not be a risk factor for total and CV mortality, it is associated with excess risk of non-fatal CV events. Lean and non-lean NAFLD phenotypes exhibit distinct prognostic profiles and should receive equitable clinical care.
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2.
  • Clark, Joseph, et al. (författare)
  • Interchangeability in Left Ventricular Ejection Fraction Measured by Echocardiography and cardiovascular Magnetic Resonance : Not a Perfect Match in the Real World
  • 2023
  • Ingår i: Current Problems in Cardiology. - : Elsevier BV. - 0146-2806. ; 48:8
  • Forskningsöversikt (refereegranskat)abstract
    • Comparisons of transthoracic echocardiography (TTE) and cardiovascular magnetic resonance (CMR) derived left ventricular ejection fraction (LVEF) have been reported in core-lab settings but are limited in the real-world setting. We retrospectively identified outpatients from 4 hospital sites who had clinically indicated quantitative assessment of LVEFTTE and LVEFCMR and evaluated their concordance. In 767 patients (mean age 47.6 years; 67.9% males) the median inter-modality interval was 35 days. There was significant positive correlation between the 2 modalities (r = 0.75; P < 0.001). Median LVEF was 54% (IQR 47%, 60%) for TTE and 59% (IQR 51%, 64%) for CMR, (P < 0.001). Normal LVEFTTE was confirmed by CMR in 90.6% of cases. Of patients with severely impaired LVEFTTE, 42.3% were upwardly reclassified by CMR as less severely impaired. The overall proportion of patients that had their LVEF category confirmed by both imaging modalities was 64.4%; Cohen's Kappa 0.41, indicating fair-to-moderate agreement. Overall, CMR upwardly reclassified 28% of patients using the British Society of Echocardiography LVEF grading, 18.6% using the European Society of Cardiology heart failure classification, and 29.6% using specific reference ranges for each modality. In a multi-site “real-worldˮ clinical setting, there was significant discrepancy between LVEFTTE and LVEFCMR measurement. Only 64.4% had their LVEF category confirmed by both imaging modalities. LVEFTTE was generally lower than LVEFCMR. LVEFCMR upwardly reclassified almost half of patients with severe LV dysfunction by LVEFTTE. Clinicians should consider the inter-modality variation before making therapeutic recommendations, particularly as clinical trial LVEF thresholds have historically been guided by echocardiography.
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  • Ottaviani, Andrea, et al. (författare)
  • Revisiting Diagnosis and Treatment of Hypertrophic Cardiomyopathy : Current Practice and Novel Perspectives
  • 2023
  • Ingår i: Journal of Clinical Medicine. - 2077-0383. ; 12:17
  • Forskningsöversikt (refereegranskat)abstract
    • Sarcomeric hypertrophic cardiomyopathy (HCM) is a prevalent genetic disorder characterised by left ventricular hypertrophy, myocardial disarray, and an increased risk of heart failure and sudden cardiac death. Despite advances in understanding its pathophysiology, treatment options for HCM remain limited. This narrative review aims to provide a comprehensive overview of current clinical practice and explore emerging therapeutic strategies for sarcomeric HCM, with a focus on cardiac myosin inhibitors. We first discuss the conventional management of HCM, including lifestyle modifications, pharmacological therapies, and invasive interventions, emphasizing their limitations and challenges. Next, we highlight recent advances in molecular genetics and their potential applications in refining HCM diagnosis, risk stratification, and treatment. We delve into emerging therapies, such as gene editing, RNA-based therapies, targeted small molecules, and cardiac myosin modulators like mavacamten and aficamten, which hold promise in modulating the underlying molecular mechanisms of HCM. Mavacamten and aficamten, selective modulators of cardiac myosin, have demonstrated encouraging results in clinical trials by reducing left ventricular outflow tract obstruction and improving symptoms in patients with obstructive HCM. We discuss their mechanisms of action, clinical trial outcomes, and potential implications for the future of HCM management. Furthermore, we examine the role of precision medicine in HCM management, exploring how individualised treatment strategies, including exercise prescription as part of the management plan, may optimise patient outcomes. Finally, we underscore the importance of multidisciplinary care and patient-centred approaches to address the complex needs of HCM patients. This review also aims to encourage further research and collaboration in the field of HCM, promoting the development of novel and more effective therapeutic strategies, such as cardiac myosin modulators, to hopefully improve the quality of life and outcome of patients with sarcomeric HCM.
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  • Ricci, Fabrizio, et al. (författare)
  • Orthostatic hypotension is associated with higher levels of circulating endostatin
  • 2024
  • Ingår i: European Heart Journal Open. - 2752-4191.
  • Tidskriftsartikel (refereegranskat)abstract
    • AimsThe pathophysiology of orthostatic hypotension (OH), a common clinical condition, associated with adverse outcomes, is incompletely understood. We examined the relationship between OH and circulating endostatin, an endogenous angiogenesis inhibitor with antitumor effects proposed to be involved in blood pressure (BP) regulation.MethodsWe compared endostatin levels in 146 patients with OH and 150 controls. A commercial chemiluminescence sandwich immunoassay was used to measure circulating levels of endostatin. Linear and multivariate logistic regressions were conducted to test the association between endostatin and OH.ResultsEndostatin levels were significantly higher in OH patients (59,024 ± 2513 pg/mL) versus controls (44,090 ± 1978 pg/mL, p<0.001). A positive linear correlation existed between endostatin and the magnitude of systolic BP decline upon standing (p<0.001). Using multivariate analysis, endostatin was associated with OH (adjusted odds ratio per 10% increase of endostatin in the whole study population = 1.264, 95%CI 1.141-1.402), regardless of age, sex, prevalent cancer, and cardiovascular disease, as well as traditional cardiovascular risk factors.ConclusionCirculating endostatin is elevated in patients with orthostatic hypotension and may serve as a potential clinical marker of increased cardiovascular risk in patients with orthostatic hypotension. Our findings call for external validation. Further research is warranted to clarify the underlying pathophysiological mechanisms.
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  • Resultat 1-6 av 6

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