An unusual case of chronic coronary artery dissection: Did cisplatin play a role?

Ghosh, Nina; Chow, Chi-Ming; Korley, Victoria; Chisholm, Robert J.

doi:10.1016/s0828-282x(08)70688-3

Cited by 11 publications

(6 citation statements)

References 12 publications

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“…Patients with existing cardiovascular pathology have a high risk of this disease [10]. Some cases of myocardial infarction, sudden death and cardiac arrest associated with the capecitabine intake have been described [11,12].…”

Section: Discussionmentioning

confidence: 99%

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy

Somov

Марчак

Матусов

et al. 2019

Annals of Medicine and Surgery

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Introduction Spontaneous coronary artery dissection is a rare cardiovascular disease that can cause acute myocardial infarction and sudden cardiac death. The mechanism of this pathology and the optimal treatment are not fully understood. Presentation of case An acute myocardial infarction developed while a fifty five years old woman with a rectal adenocarcinoma was receiving a cisplatin and capecitabine therapy. Coronary angiography demonstrated a multivessel occlusion of coronary arteries. Discussion The authors discuss several factors that may lead to the spontaneous coronary artery dissection including chemotherapy-induced vasospasm. Chemotherapy based on the cisplatin and capecitabine intake can cause a cardiotoxic effect. Conclusion Thus, spontaneous coronary artery dissection is a disease with an extremely complex etiololy, which does not have a special treatment guide. Management should be considered individually for each case.

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Section: Discussionmentioning

confidence: 99%

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy

Somov

Марчак

Матусов

et al. 2019

Annals of Medicine and Surgery

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“…Spontaneous coronary artery dissection has been reported with multiple factors including the peripartum period [ 4 - 5 ], postpartum period [ 6 - 7 ], oral contraceptives use [ 8 ], and connective tissue disorders including Ehlers-Danlos syndrome [ 9 ], systemic lupus erythematosus [ 10 ], neurofibromatosis [ 11 ], sexual intercourse [ 12 ], and bleomycin-etoposide-cisplatin therapy for testicular cancer [ 13 ]. It occurs most commonly in females and the LAD is the vessel affected most often [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

Spontaneous Left Anterior Descending Artery Dissection in a Middle-Aged Woman with Vitamin B12 Deficiency Treated with Coronary Artery Bypass Grafting

Masood¹,

Asad²,

Tariq³

et al. 2018

Cureus

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Spontaneous coronary artery dissection (SCAD) is one of the rarest causes of acute coronary syndromes, which include myocardial infarction (MI), stable and unstable angina, cardiogenic shock, and sudden death. The course of the disease, its etiology, prevalence, prognosis, and treatment remain ill-defined. Adding to the complexity is the fact that patients may lack typical risk factors for coronary heart disease. Herein, we report a case of a 42-year-old woman with vitamin B12 deficiency, who presented with chest pain; electrocardiography (ECG) findings were consistent with the acute anterior wall MI. Cardiac catheterization was done, which showed a very large left anterior descending (LAD) artery dissection.

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“…Cisplatin was reported to lead to aortic occlusion in some cases and this impairment was usually irreversible (28,29). In one case, a 36-year-old man who was treated with bleomycin-etoposide-cisplatin therapy for testicular cancer received chronic coronary artery dissection (30). A long-term follow-up in a large cohort of testicular cancer survivors showed that compared with healthy controls, cisplatin-treated patients had, at follow-up, increased systolic blood pressure, increased diastolic blood pressure and a higher prevalence of hypertension (18).…”

Section: Discussionmentioning

confidence: 99%

Effects of cisplatin on the contractile function of thoracic aorta of Sprague-Dawley rats

et al. 2014

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Abstract. DNA-damaging agents have been reported to be associated with cardiovascular complications, however, the underlying mechanisms remain to be clarified. In the present study, the possible vascular effects of cisplatin was assessed by measuring its effects on the contractile function of thoracic aortic rings dissected from Sprague-Dawley (SD) rats. Contraction of the aortic ring was induced by 60 mM KCl or 10 -6 M phenylephrine (PE) in an ex vivo perfusion system. Cisplatin (200 µM) counteracted KCl-and PE-induced contraction by 57.6 and 91.8%, respectively, in endothelium-intact aortic rings. Similar results were obtained in endothelium-denuded aortas. Electromicroscopy analysis revealed severe damage to blood vessel walls in vivo by cisplatin. In addition, cisplatin significantly inhibited adenosine triphosphate (ATP)-induced intracellular Ca 2+ concentration ([Ca 2+ ] i ) increases in human umbilical vein endothelial cells (HUVECs). These results suggested that the DNA-damaging agent cisplatin can affect the contractile function of thoracic aortas. In addition, in accordance with its DNA-damaging properties, the cardiovascular toxicity of cisplatin may be the result of its direct cytotoxicity. IntroductionDNA-damaging agents, or genotoxic agents, are those chemicals that can produce alterations in the genetic material of the host. Such agents can be further subdivided into direct-and indirect-acting agents. Direct-acting agents are intrinsically reactive and do not require metabolic activation by cellular enzymes to interact with DNA. By contrast, indirect-acting agents require metabolic activation by cellular enzymes to form the DNA-reactive metabolite. DNA-damaging agents exist widely in our natural and social environment, with examples including some of the chemotherapeutic agents and environmental pollutants (1).Cisplatin, a direct-acting agent, is one of the most widely used chemotherapeutic agents in the treatment of a wide variety of malignancies (2). Although its biochemical mechanism of action has yet to be elucidated, cisplastin is believed to exert cytotoxic effects through the interaction and formation of adducts with DNA, which then leads to apoptosis and necrosis (3,4). Despite its clinical efficacy in treating malignancies, cisplatin-based chemotherapy regimens have been reported to be associated with vascular toxicity and serious vascular complications (e.g., myocardial infarction and stroke) (5-7). Such vascular toxicity has been manifested by increased von Willebrand factor plasma levels as well as an enhanced intima-media thickness of the carotid artery (8). In addition, cisplatin has the potential to induce ototoxicity and toxicity towards renal, peripheral sensory and autonomic nervous systems, potentially attributed to cisplatin-caused microvascular damage (9-11). Ca 2+ plays an important role in the regulation of vascular tone, which is generally relatively constant. Initiation of contraction in vascular smooth muscle is due to an increase in the free cytosolic Ca 2+ concentr...

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An unusual case of chronic coronary artery dissection: Did cisplatin play a role?

Cited by 11 publications

References 12 publications

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy

Spontaneous Left Anterior Descending Artery Dissection in a Middle-Aged Woman with Vitamin B12 Deficiency Treated with Coronary Artery Bypass Grafting

Effects of cisplatin on the contractile function of thoracic aorta of Sprague-Dawley rats

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