Cardiovascular (CV) complications from cancer therapy have become a major concern in the management of patients with cancer [1]. Cancer therapy-related cardiovascular toxicity (CTR-CVT) has been observed with the use of various antineoplastic agents, including proteasome inhibitors used for multiple myeloma treatment. These adverse events can lead to increased morbidity and mortality, affecting both the quality of life and the continuation of cancer treatment. Identifying widely accessible and noninvasive biomarkers for CV risk assessment is crucial for optimizing the management of patients undergoing antineoplastic treatments.

Blood pressure variability (BPV), which reflects fluctuations in blood pressure (BP) over time, is recognized as an independent predictor of CV events and overall mortality in patients with hypertension [2]. Furthermore, BPV has been associated with endothelial dysfunction [3] and atherosclerosis [4], both of which are associated with adverse CV outcomes. Despite its established prognostic value in the hypertensive and general CV disease populations, the potential role of BPV in predicting CTR-CVT remains largely unexplored.

In this issue of Hypertens Res, Fanelli et al. [5] investigated the significance of short-term BPV in patients with multiple myeloma undergoing proteasome inhibitor therapy. They estimated BPV using data from ambulatory blood pressure monitoring (ABPM) and found that individuals who developed CTR-CVT had a higher baseline BPV. Moreover, nighttime BPV was associated with CTR-CVT, independent of age, smoking, BP, diabetes, dyslipidemia, and kidney function. Clustering analysis revealed that subgroups characterized by the highest BPV had a greater prevalence of events despite no differences in other CV risk determinants. These findings suggest that nighttime BPV is a strong and independent predictor of CTR-CVT, even after controlling for traditional CV risk factors. This discovery has significant implications for the clinical management of cancer patients at risk of cardiotoxicity.

The inclusion of BPV in CTR-CVT risk assessment could lead to improved monitoring strategies for oncology patients receiving proteasome inhibitors. ABPM is a widely accessible and cost-effective tool that allows for a more nuanced evaluation of BP beyond office measurements. Identifying high-risk patients based on BPV could prompt earlier intervention, such as intensified BP management or closer cardiology follow-up, ultimately mitigating the CTR-CVT risk.

This study demonstrated an association between nighttime BPV and CTR-CVTs. However, this study did not clarify whether BPV directly contributes to CV events or merely reflects an underlying predisposition to CV complications. Determining whether modifying BPV can reduce the risk of CTR-CVT requires prospective interventional studies.

This study highlights the potential utility of BPV monitoring, particularly in patients with multiple myeloma undergoing proteasome inhibitor treatment, in whom autonomic dysfunction, endothelial dysfunction, and increased arterial stiffness are implicated [6, 7] (Fig. 1). Future studies are required to investigate the predictive value of BPV in diverse cancer populations receiving various cardiotoxic therapies.

Fig. 1
Fig. 1The alternative text for this image may have been generated using AI.
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Proposed mechanisms linking proteasome inhibitor treatment in multiple myeloma patients to increased blood pressure variability. Proteasome inhibitors may induce endothelial dysfunction, leading to increased arterial stiffness and alterations in the autonomic nervous system. In addition, multiple myeloma is also associated with autonomic dysfunction. These factors may contribute to the increased BPV. BPV, blood pressure variability

Furthermore, this study provides compelling evidence supporting BPV’s role as a novel predictor of CTR-CVT in patients with multiple myeloma undergoing proteasome inhibitor therapy. Given the widespread availability of ABPM, incorporating BPV into routine CV risk assessment could enhance the precision of CTR-CVT predictions and facilitate personalized monitoring strategies. Future studies should focus on validating these findings in larger, more diverse cohorts and exploring whether BPV-targeted interventions can mitigate the CTR-CVT risk. If validated, BPV monitoring could represent an important advancement in cardio-oncology by bridging the gap between BP regulation and CTR-CV. Integrating BPV assessments into routine oncology care may improve patient outcomes and reduce the burden of CTR-CVTs.