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Multiple myeloma (MM) is an incurable malignancy of clonal plasma cells. Various diagnostic methods are used in parallel to accurately determine stage and severity of the disease. Identifying a biomarker or a panel of biomarkers could enhance the quality of medical care that patients receive by adopting a more personalized approach. Metabolomics utilizes high-throughput analytical platforms to examine the levels and quantities of biochemical compounds in biosamples. The aim of this review was to conduct a systematic literature search for potential metabolic biomarkers that may aid in the diagnosis and prognosis of MM. The review was conducted in accordance with PRISMA recommendations and was registered in PROSPERO. The systematic search was performed in PubMed, CINAHL, SciFinder, Scopus, The Cochrane Library and Google Scholar. Studies were limited to those involving people with clinically diagnosed MM and healthy controls as comparators. Articles had to be published in English and had no restrictions on publication date or sample type. The quality of articles was assessed according to QUADOMICS criteria. A total of 709 articles were collected during the literature search. Of these, 436 were excluded based on their abstract, with 26 more removed after a thorough review of the full text. Finally, 16 articles were deemed relevant and were subjected to further analysis of their data. A number of promising candidate biomarkers was discovered. Follow-up studies with large sample sizes are needed to determine their suitability for clinical applications., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The development of cardiovascular diseases (CVDs) is often asymptomatic. Identification of initial indicators of cardiometabolic disruption may assist in its early detection. The objective was to determine the relationships between plasma acylcarnitines (ACs) and cardiometabolic risk factors in adults with and without CVDs. The AC profile in human plasma of healthy controls [non-CVD group, n = 13)] and individuals diagnosed with CVDs (CVD group, n = 34) were compared. A targeted analysis of 29 ACs was performed using flow injection analysis-tandem mass spectrometry. There were significant direct correlations (p < 0.05) between ACs and cardiometabolic risk factors. Comparing the groups after adjustment for covariates, showed that the ACs that were best differentiated (p < 0.05) between the two groups and that presented "good" diagnostic accuracy were carnitine [30.7 (25.5-37.7) vs. 37.7 (32.3-45.0) µM], the short-chain ACs: acetylcarnitine [8.9 (7.4-10.2) vs. 11.9 (9.2-14.4) µM] and isovalerylcarnitine [0.10 (0.06-0.13) vs. 0.13 (0.10-0.16) µM], and the medium-chain ACs: hexanoylcarnitine [0.04 (0.03-0.05) vs. 0.06 (0.05-0.07) µM] and decenoylcarnitine [0.18 (0.12-0.22) vs. 0.22 (0.17-0.32) µM]. This assessment contributes to the identification of the unique metabolic features exhibited in association with cardiometabolic risk in adults diagnosed with CVD. The altered metabolites have the potential to be used as biomarkers for early detection of CVD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

This study sought to determine the relationship between myocardial dysfunction and peripheral haemodynamic disorders to exercise intolerance in patients with chronic heart failure (CHF). Seventeen patients with mild to moderate CHF (peak oxygen consumption (VO2) >16 ml/min/kg) and 13 with severe CHF (peak VO2 <16 ml/min/kg) underwent invasive (Swan-Ganz) cardiopulmonary exercise testing and forearm venous occlusion plethysmography at rest and during maximal dilatation in reactive hyperaemia. There was a shift from central to peripheral haemodynamic factors limiting exercise, suggesting an increasing importance of peripheral factors in parallel to the progression of CHF. In mild to moderate CHF peak VO2 was closely related to central haemodynamics (r = 0.57 for cardiac index at rest; r = 0.76 for cardiac index at maximal workload; r = -0.54 for right arterial pressure at maximal workload; all p<0.05) and poorly correlated with peripheral haemodynamics (blood flow, vascular resistance and venous tone). In contrast, in severe CHF peak VO2 was closely related to peripheral haemodynamic factors (r = 0.79 for forearm blood flow; r = -0.82 for vascular resistance; r = -0.77 for venous tone; all p<0.05) and less to central ones. Thus, exercise tolerance of patients with mild to moderate CHF is predominantly determined by central haemodynamic factors, notably by the cardiac index. In severe CHF peripheral factors assume ever greater importance in the determining of exercise capacity.

Currently the problem of left ventricular remodelling in the early and late stages after myocardial infarction are under intense study. Studies of the role of remodelling of the left ventricle in patients with long-term arterial hypertension have been recently initiated. The purpose of this investigation was to study whether left ventricular remodelling is common for different primary myocardial disorders. The study population consisted of 212 patients with primary myocardial lesions (121 with dilated cardiomyopathy, 45 with chronic myocarditis and 46 with prolonged damage of the myocardium with alcohol; 196 male and 16 female, mean age 42.6+/-11.3 years) and 32 age matched normal subjects (24 male and eight female). Cardiac catheterization for ventriculography and coronary angiography was performed in all subjects for detection of left ventricular haemodynamics, including chamber volume and shape at end-systole and end-diastole. Worsening of heart failure was associated with a progressive enlargement of the left ventricle, with increases in end-systolic left ventricular wall stress, that lead to increases in left ventricular muscle mass, alteration of left ventricular geometry from a more ellipsoid to a more spherical shape and a progressive decrease of relative wall thickness index that reflects inadequate enlargement of the ventricular chamber in comparison with the increase in muscle mass. This process of left ventricular remodelling was common to all the primary myocardial disorders studied. Thus, regardless of the different etiological nature, most primary myocardial disorders show a similar left ventricular remodelling process suggesting common mechanisms for the development of chronic heart failure.