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. 2024 Sep 4;16(17):3081.
doi: 10.3390/cancers16173081.

Haemodynamic Forces: Emerging Markers of Ventricular Remodelling in Multiple Myeloma Cardiovascular Baseline Risk Assessment

Affiliations

Haemodynamic Forces: Emerging Markers of Ventricular Remodelling in Multiple Myeloma Cardiovascular Baseline Risk Assessment

Anna Colomba et al. Cancers (Basel). .

Erratum in

Abstract

Multiple myeloma (MM) affects a population with a high prevalence of cardiovascular (CV) disease. These patients benefit from an accurate CV risk evaluation in order to choose the safest drug regimen. Haemodynamic forces (HDFs) analysis allows for the earlier detection of myocardial damage compared with standard markers; the role played by MM in HDFs alteration, with or without the influence of hypertension, is yet to be studied. Therefore, we aimed to identify differences in HDFs analysis in patients with MM, hypertension or both versus normotensive non-oncologic subjects. A total of 173 patients (MM hypertensive patients, MMHT; MM normotensive patients, MMNT; non-oncologic hypertensive patients, CoHT; and non-oncologic normotensive patients, CoNT) underwent transthoracic echocardiography for HDFs analysis and pulse wave velocity (PWV) assessment. Hypertensive patients (MMHT, CoHT) showed decreased ejection fraction (EF), global longitudinal strain (GLS) and HDFs values compared with CoNT, whereas ventricular mass (LVMi) and PWV increased. MMNT displayed a significant reduction in systolic HDFs (p < 0.006) and systolic ejection HDFs (p < 0.008) compared with CoNT, without significant change in EF, GLS, LVMi or PWV. In conclusion, MM leads to ventricular remodelling regardless of hypertension; HDFs application for MM patients could help detect early myocardial damage, especially in patients receiving cardiotoxic drugs.

Keywords: arterial hypertension; cardiovascular risk; echocardiography; haemodynamic forces; multiple myeloma.

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Conflict of interest statement

A.M. received honoraria for advisory board work for educational purposes from Amgen and Janssen. S.B. has participated in speakers’ bureaus in Amgen, Bristol Myers Squibb, GlaxoSmithKline, Janssen, Sanofi and AbbVie; has served on the board of directors or advisory committees for Bristol Myers Squibb, Janssen, Takeda, Pfizer, Stemline Therapeutics and Oncopeptides; and has received consultancy fees from Sanofi. F.G. has received honoraria from Amgen, Celgene, Janssen, Takeda, Bristol Myers Squibb, AbbVie and GlaxoSmithKline; has served on the advisory boards and received honoraria from Sanofi and Pfizer; and has served on the advisory boards for Amgen, Celgene, Janssen, Takeda, Bristol Myers Squibb, AbbVie, GlaxoSmithKline, Roche, Oncopeptides and Pfizer. G.P. received scientific consultancy fee from Medis Medical Imaging. The other authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Haemodynamic apical–basal forces pattern. Sy_ab: HDFs during entire systole; Di_ab: HDFs during entire diastole; SyAcc_ab: HDFs during systolic acceleration phase; SyEj_ab: HDFs during systolic ejection phase; SyDec_ab: HDFs during systolic deceleration phase; DiRelax_ab: HDFs during diastolic relaxation phase; DiDec_ab: HDFs during diastolic deceleration phase.
Figure 2
Figure 2
Comparison between groups: systolic ejection subphase. MMHT: multiple myeloma hypertensive group, MMNT: multiple myeloma normotensive group, CoHT: non-oncologic hypertensive group, CoNT: non-oncologic normotensive group, SyEj_ab: HDFs during the systolic ejection phase.

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