Sarcopenia in Patients with Cardiovascular Disease Can Also Be Triggered by Other Risk Factors

Abstract

We read with great interest the review article by Rivera et al. on the influence of cardiovascular disease on the development of sarcopenia.¹ The review aimed to explore the pathophysiological mechanisms underlying the relationship between sarcopenia and cardiovascular disease, as well as its clinical assessment and management.¹ The authors highlighted inflammation, oxidative stress, endothelial dysfunction, neuronal and hormonal changes, and other metabolic disturbances as key contributors to sarcopenia in patients with cardiovascular disease.¹ While the overview is comprehensive, we believe several important aspects warrant further discussion, as certain causes of sarcopenia associated with cardiovascular disease were not addressed.

First, there is evidence that sarcopenia is associated with low hemoglobin levels. Patients with sarcopenia should therefore also be screened for anemia.² Several studies have demonstrated a strong association between anemia and sarcopenia, suggesting that management should include dietary modifications—such as increased intake of antioxidants, high-quality proteins, and micronutrients—along with moderate physical activity and healthy weight maintenance.³ Furthermore, sarcopenia has been observed in survivors of severe aplastic anemia treated with allogeneic hematopoietic stem cell transplantation.⁴ The deleterious effects of anemia on skeletal muscle may be further aggravated by concomitant heart failure.

Second, arterial hypotension and blood pressure reduction from beta-blocker therapy were not mentioned in the review as potential contributors to sarcopenia.⁵ Chronic hypotension can compromise skeletal muscle perfusion, thereby reducing muscle mass and accelerating sarcopenia. Adequate blood flow is essential for maintaining skeletal muscle, and reduced capillarization may impair the diffusion of oxygen, substrates, hormones, and nutrients, further exacerbating muscle loss.⁶

Third, long-term medication use was insufficiently discussed as a potential cause of sarcopenia. Statins, for example, can induce myopathy in approximately 1% of cases, and sulfonylureas and glinides have also been implicated.⁷ Additional drug classes associated with sarcopenia include GLP-1 receptor agonists, SGLT2 inhibitors, glucocorticoids, antineoplastics, immune checkpoint inhibitors, antiandrogens, chloroquine/hydroxychloroquine, colchicine, nucleoside analogs, loop diuretics, and D-penicillamine.⁸

Fourth, hemodialysis—commonly performed in patients with cardiovascular disease—was not considered in the review, despite being a recognized cause of sarcopenia.⁹ In patients with end-stage renal disease on maintenance hemodialysis, sarcopenia can result from accelerated protein depletion, nutrient deficiencies, and multiple metabolic disturbances.¹⁰

Finally, we respectfully disagree with the review’s suggestion that beta-blockers exert a beneficial effect on sarcopenia.¹ On the contrary, several studies have reported an increased risk of sarcopenia in patients receiving beta-blockers.⁵ Moreover, evidence that beta-agonists can increase muscle mass and strength further supports the sarcopenic effect of beta-blockers.

In summary, although Rivera et al. provide a valuable overview, the review has limitations that may affect the strength and interpretation of its conclusions. Sarcopenia in cardiovascular disease is multifactorial and may be exacerbated or caused by genetic predisposition, immobility, hematologic disorders, medications, dialysis, endocrine factors, inflammation, and nutritional deficiencies. Recognizing these additional contributors would enhance the comprehensiveness and validity of the review.