# Malnutrition, cachexia and sarcopenia as susceptibility factors for cardiovascular complications in patients with cancer

**Authors:** Ionas Papasotiriou, Anastasios Tentolouris, Ioannis Ntanasis-Stathopoulos, Michalis Liontos

PMC · DOI: 10.3389/fphar.2026.1762196 · Frontiers in Pharmacology · 2026-02-13

## TL;DR

This paper reviews how poor nutrition and muscle loss in cancer patients increase their risk of heart problems and suggests possible interventions.

## Contribution

The paper highlights malnutrition, sarcopenia, and cachexia as susceptibility factors for cardiovascular complications in cancer patients.

## Key findings

- Poor nutritional status is linked to cardiovascular burden in cancer patients.
- Sarcopenia and cachexia are associated with higher risk of cardiotoxicity from cancer treatment.
- Nutritional interventions and drugs preventing muscle wasting may reduce cardiovascular complications.

## Abstract

Cancer remains a leading cause of morbidity and mortality, although cancer survivorship has increased impressively in the past decades. Patients with cancer often face cardiovascular complications, either due to cancer itself or due to anti-cancer therapy, that may affect their quality of life and survival. Several studies have examined possible risk factors for cardiovascular susceptibility and/or cancer treatment-related cardiotoxicity, and some of them found a link between nutritional status and cardiovascular complications. In this review, we discuss the role of malnutrition, sarcopenia and cachexia, as susceptibility factors for cardiovascular complications and cardiotoxicity in cancer. The limited evidence shows that poor nutritional status and sarcopenia or cachexia is related to a cardiovascular burden in this population, and with a higher risk for cancer treatment-related cardiotoxicity. This relation may be mediated through several mechanisms and pathways, including cardiac wasting. Nutritional interventions should be examined for their effectiveness in reducing cardiovascular complications in patients with cancer, alongside with novel drugs that can prevent both skeletal and cardiac muscle wasting.

## Linked entities

- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891] {aka LEM6, PGC-1(alpha), PGC-1alpha, PGC-1v, PGC1, PGC1A}, ERBB2 (erb-b2 receptor tyrosine kinase 2) [NCBI Gene 2064] {aka CD340, HER-2, HER-2/neu, HER2, MLN 19, MLN-19}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** loss of muscle strength (MESH:D009135), cardiac remodeling (MESH:D020257), thromboembolic (MESH:D013923), Hematologic, lung, kidney, and ovarian cancers (MESH:D010051), loss of appetite (MESH:D001068), Cardiac wasting (MESH:D006331), coronary artery disease (MESH:D003324), embolism (MESH:D004617), breast cancer (MESH:D001943), heart failure (MESH:D006333), venous thromboembolism (MESH:D054556), skeletal and cardiac muscle wasting (OMIM:615441), Malnutrition (MESH:D044342), premature death (MESH:D003643), hypertension (MESH:D006973), malabsorption (MESH:D008286), Atherosclerosis (MESH:D050197), pericarditis (MESH:D010493), thrombosis (MESH:D013927), weight (MESH:D015431), toxicities (MESH:D064420), vascular dysfunction (MESH:D002561), idiopathic pulmonary hypertension (MESH:D065627), pericardial disease (MESH:D008476), cardiovascular complication (MESH:D002318), immunological disturbances (MESH:D007154), functional loss (MESH:D006315), wasting (MESH:D019282), cardiomyopathy (MESH:D009202), Cachexia (MESH:D002100), stroke (MESH:D020521), diarrhea (MESH:D003967), myocarditis (MESH:D009205), obesity (MESH:D009765), gastric cancer (MESH:D013274), arrhythmias (MESH:D001145), low muscle mass (MESH:C536030), paraneoplastic syndromes (MESH:D010257), vomiting (MESH:D014839), cardiotoxic (MESH:D066126), pulmonary embolism (MESH:D011655), genitourinary, gastrointestinal, thoracic, nervous system, and hematologic malignancies (MESH:D019337), Inflammatory (MESH:D007249), muscle and cardiac muscle wasting (MESH:D009133), sarcopenia (MESH:D055948), cardiomyocyte injury (MESH:D014947), metabolic disturbances (MESH:D024821), esophageal, urothelial, prostate and other cancers (MESH:D011471), atrophy (MESH:D001284), atrophic (MESH:D020966), anorexia (MESH:D000855), Anti-cancer (MESH:D009369), endothelial dysfunction (MESH:D014652), valvular dysfunction (MESH:D006349), diabetes (MESH:D003920)
- **Chemicals:** vericiguat (MESH:C000603960), ROS (MESH:D017382), doxorubicin (MESH:D004317), tyrosine (MESH:D014443), daunorubicin (MESH:D003630), cyclophosphamide (MESH:D003520), carfilzomib (MESH:C524865), Anthracyclines (MESH:D018943), trastuzumab (MESH:D000068878)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

62 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945785/full.md

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Source: https://tomesphere.com/paper/PMC12945785