# Late coronary artery injury following chemoradiotherapy for thymic carcinoma: a case report

**Authors:** Sigan Hu, Jun Wang, Zhen Cui, Yongchun Zhou, Dasheng Gao

PMC · DOI: 10.1186/s12872-024-03948-2 · 2024-05-22

## TL;DR

A patient with thymic carcinoma developed late coronary artery injury after chemoradiotherapy, highlighting a rare but serious long-term side effect.

## Contribution

This case report provides new insights into the characteristics of coronary artery injury following chemoradiotherapy for thymic carcinoma.

## Key findings

- The patient developed acute myocardial infarction seven years after chemoradiotherapy for thymic carcinoma.
- Intravascular ultrasound showed significant negative remodeling of the coronary artery with minimal atherosclerotic plaque.
- Chemoradiotherapy-induced endothelial damage and inflammation may lead to vascular remodeling rather than plaque buildup.

## Abstract

Surgery remains the primary treatment modality for thymic carcinoma, with adjuvant radiotherapy being recommended to effectively mitigate local recurrence and metastasis rates subsequent to incomplete or complete resection. Chemoradiotherapy has the potential to induce coronary artery occlusion, thereby potentially impacting patients’ long-term survival rates. The existing literature currently lacks comprehensive research on the lesion characteristics of coronary artery injury resulting from chemoradiotherapy.

The male patient, aged 55, was admitted to the hospital due to recurrent chest tightness and pain persisting for one week. Notably, the patient had previously undergone curative resection surgery for thymic carcinoma seven years ago. After the surgical procedure, the patient underwent a course of adjuvant chemotherapy comprising docetaxel and platinum. 11 months later, imaging examination diagnosed tumor recurrence, and concurrent chemoradiotherapy was administered at a total dose of 62 Gy/31F for planning gross target volume (PGTV) and 54 Gy/31F for planning target volume (PTV) with 2 cycles of paclitaxel and cisplatin. Re-admission of the patient occurred after a 7-year interval subsequent to the completion of concurrent chemoradiotherapy, leading to a subsequent diagnosis of acute non-ST segment elevation myocardial infarction. Following administration of antiplatelet, anticoagulant, and anti-myocardial ischemia therapy, coronary angiography revealed the presence of a bifurcation lesion at the distal end of the left main trunk. Intravascular ultrasound (IVUS) examination demonstrated significant negative remodeling of both the main trunk and its branches at the bifurcation site, characterized by minimal atherosclerotic plaque components.

Chemoradiotherapy may induce damage to endothelial cells, resulting in an inflammatory response. Negative remodeling of blood vessels is likely to occur, primarily characterized by vasoconstriction but with less atherosclerotic plaque burden. Routine stent implantation in negatively remodeled areas may lead to vascular rupture, necessitating intravascular imaging examination.

The online version contains supplementary material available at 10.1186/s12872-024-03948-2.

## Linked entities

- **Chemicals:** docetaxel (PubChem CID 148124), platinum (PubChem CID 23939), paclitaxel (PubChem CID 36314), cisplatin (PubChem CID 5460033)
- **Diseases:** thymic carcinoma (MONDO:0006451)

## Full-text entities

- **Diseases:** coronary artery injury (MESH:D003324), inflammatory (MESH:D007249), vascular rupture (MESH:D012421), thymic carcinoma (MESH:D013945), pain (MESH:D010146), myocardial ischemia (MESH:D017202), metastasis (MESH:D009362), tumor (MESH:D009369), ST segment elevation (MESH:D000072657), chest tightness (MESH:D002637), atherosclerotic plaque (MESH:D058226), myocardial infarction (MESH:D009203), coronary artery occlusion (MESH:D054059)
- **Chemicals:** platinum (MESH:D010984), docetaxel (MESH:D000077143), paclitaxel (MESH:D017239), cisplatin (MESH:D002945)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11110269/full.md

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Source: https://tomesphere.com/paper/PMC11110269