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. 2025 Mar 18;14(6):2078.
doi: 10.3390/jcm14062078.

Deterioration of Myocardial Global Longitudinal Strain and Its Relationship with Arterial Stiffness in Patients with Cardiac Amyloidosis: A Six-Month Follow-Up

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Deterioration of Myocardial Global Longitudinal Strain and Its Relationship with Arterial Stiffness in Patients with Cardiac Amyloidosis: A Six-Month Follow-Up

Dafni Korela et al. J Clin Med. .

Abstract

Background: Cardiac amyloidosis (CA) is a progressive disorder characterized by amyloid fibril deposition in the heart, leading to heart failure and arrhythmias. Arterial stiffness, assessed by pulse wave velocity (PWV), is recognized as an adverse consequence of amyloidosis, yet its progression and relationship with myocardial dysfunction remain inadequately explored. This study examines the progression of PWV and its potential association with the deterioration of global longitudinal strain (GLS) in CA patients over a 6-month follow-up period. Methods: This prospective study enrolled 31 patients who were diagnosed with CA, including both the immunoglobulin light chain (AL) and transthyretin (ATTR) forms. All participants underwent a full echocardiographic study and PWV measurements (carotid-femoral [c-f] and carotid-radial [c-r] PWV) at baseline and 6-month follow-up. Age- and sex-matched individuals with similar cardiovascular risk factors were included as a control group. Results: In the CA group, the left ventricular mass index (LVMI) increased significantly from 119.4 ± 52.1 to 124 ± 53.2 g/m2 (p = 0.002). Both c-f and c-r PWV showed significant increases at the 6-month follow-up (p < 0.001 and p = 0.005, respectively). The GLS deteriorated significantly from -14 ± 4.4% to -12.8 ± 4.9% (p = 0.018). No significant changes were observed in the control group. A weak correlation (r = 0.3; p = 0.095) was found between increases in PWV and GLS deterioration. Conclusions: Both arterial stiffness and myocardial dysfunction worsen rapidly in CA patients. However, the weak correlation between PWV and GLS suggests that they may evolve through independent mechanisms, necessitating further research to understand their complex interplay in CA.

Keywords: amyloidosis; arterial stiffness; myocardial strain.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Progression of PWV in patients with cardiac amyloidosis compared to control group over a 6-month follow-up period. c-f PWV: Carotid–femoral pulse wave velocity; c-r PWV: Carotid–radial pulse wave velocity. Open circles denote outliers, i.e., observations that lie more than 1.5 × IQR away from the quartiles.
Figure 2
Figure 2
Deterioration of left ventricular GLS in patients with cardiac amyloidosis compared to control group over a 6-month follow-up period. GLS: global longitudinal strain. Open circles denote outliers, i.e., observations that lie more than 1.5 × IQR away from the quartiles. * denote extreme outliers, i.e., observations that lie more than 3 × IQR away from the quartiles. Circles represent the participants, *: <0.05.
Figure 3
Figure 3
Correlation between the changes in GLS and the changes in (A) c-f PWV and (B) c-r PWV in patients with cardiac amyloidosis. GLS: global longitudinal strain; c-f PWV: carotid–femoral pulse wave velocity; c-r PWV: carotid–radial pulse wave velocity (circles represent the participants, *: <0.05).

References

    1. Merlini G., Bellotti V. Molecular mechanisms of amyloidosis. N. Engl. J. Med. 2003;349:583–596. doi: 10.1056/NEJMra023144. - DOI - PubMed
    1. Pinney J.H., Hawkins P.N. Amyloidosis. Ann. Clin. Biochem. 2012;49:229–241. doi: 10.1258/acb.2011.011225. - DOI - PubMed
    1. Yamamoto H., Yokochi T. Transthyretin cardiac amyloidosis: An update on diagnosis and treatment. ESC Heart Fail. 2019;6:1128–1139. doi: 10.1002/ehf2.12518. - DOI - PMC - PubMed
    1. Wechalekar A.D., Gillmore J.D., Hawkins P.N. Systemic amyloidosis. Lancet. 2016;387:2641–2654. doi: 10.1016/S0140-6736(15)01274-X. - DOI - PubMed
    1. Falk R.H. Diagnosis and management of the cardiac amyloidoses. Circulation. 2005;112:2047–2060. doi: 10.1161/CIRCULATIONAHA.104.489187. - DOI - PubMed

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