Challenges and Management of Acute Coronary Syndrome in Cancer Patients

BackgroundClinical characteristics and long-term outcomes of patients with myocardial infarction with non-obstructive coronary arteries (MINOCA) and cancer are insufficiently elucidated.ObjectivesWe sought to characterize these patients hospitalized in a tertiary cardio-oncology center and to find the potential determinants affecting their long-term mortality.MethodsMINOCA was diagnosed in 72 of the 1,011 patients with consecutive myocardial infarction who underwent coronary angiography. Mortality rates and their determinants were analyzed within a median follow-up of 69.2 (37.8–79.9) months.ResultsActive cancer was identified in 21 (29.2%) of patients with MINOCA and in 113 (12.0%) patients with myocardial infarction and obstructive coronary artery disease (MI-CAD) (p < 0.001). MINOCA patients with cancer were characterized by a higher incidence of anemia (47.6 vs. 21.6%, p = 0.03) and more frequently Takotsubo syndrome (19.1 vs. 2.0%, p = 0.01) than in non-cancer MINOCA. The troponin T/hemoglobin ratio was higher in both cancer MINOCA and MI-CAD groups when compared with their respective non-cancer patients (both p < 0.05). The age and sex-standardized mortality rates were significantly higher in cancer MINOCA (26.7%/year) when compared with non-cancer MINOCA (2.3%/year, p = 0.002) and in cancer MI-CAD (25.0%/year) vs. non-cancer MI-CAD (3.7%/year, p < 0.001). Active cancer (HR 3.12, 95% CI 2.41–4.04) was independently associated with higher long-term mortality, while higher hemoglobin levels (HR 0.93, 95% CI 0.88–0.99, per g/dl) and a MINOCA diagnosis (HR 0.69, 95% CI 0.47–0.97) improved long-term survival.ConclusionPatients with MINOCA were comorbid with cancer more frequently than MI-CAD. In turn, an active malignancy was associated with an unfavorable long-term survival both in MI-CAD population and in patients with MINOCA.

Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Clinical Characteristics and Long-Term Outcomes of MINOCA Accompanied by Active Cancer: A Retrospective Insight Into a Cardio-Oncology Center Registry

Stępień

Nowak

Szlósarczyk

et al. 2022

“…The prothrombogenic state and hyper viscosity of blood in patients with cancer can lead to the formation of arterial thrombosis, while the use of drugs as part of chemotherapy can lead to endothelial cell damage predisposing to erosion and rupture of the atherosclerotic plaque and thus lead to AMI type I. On the other hand, AMI Type II can be provoked by tachycardia, hypotension, hypoxia or anemia, as well as vasospasm due to the use of chemotherapy drugs ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

Case report: Acute toxic myocardial damage caused by 5-fluorouracil—from enigma to success

Lasica

Spasić

Djukanovic

et al. 2022

Considering the pandemic of both cardiovascular diseases and oncological diseases, there is an increasing need for the use of chemotherapy, which through various pathophysiological mechanisms leads to damage to heart function. Cardio toxicity of chemotherapy drugs can manifest itself in a variety of clinical manifestations, which is why establishing a valid diagnosis is a real mystery for clinicians. Acute systolic heart failure (AHF) due to the use of 5-fluorouracil (5-FU) is a rare occurrence if it is not associated with myocardial infarction, myocarditis or Takotsubo cardiomyopathy. Therefore, we decided to present a case of an 52-year-old male who was diagnosed with stage IV RAS wild-type adenocarcinoma of the rectum and in whom the direct toxic effect 5-FU is the main reason for the appearance of toxic cardiomyopathy.

“…Coronary vasospasm is one of the most described mechanisms and is typically caused by 5-fluoro-uracil (5-FU) or its prodrug capecitabine ( 19 ). Other mechanisms may include plaque rupture resulting from cisplatin and vinca alkaloids ( 20 ), or coronary thrombosis due to pro-inflammatory and prothrombotic conditions associated with increased platelet aggregability induced by specific cancer therapies (e.g., cisplatin, vascular endothelial growth factor (VEGF) signaling pathway inhibitors and cyclophosphamide) ( 21 ). Direct endothelial injury associated with accelerated coronary artery disease induced by radiotherapy ( 22 ) can cause ACS typically within 10 to 30 years following treatment but rarely during treatment ( 23 ).…”

Section: Epidemiologymentioning

confidence: 99%

Cardiogenic shock among cancer patients

Curtiaud

Delmas

Gantzer

et al. 2022

Sophisticated cancer treatments, cardiovascular risk factors, and aging trigger acute cardiovascular diseases in an increasing number of cancer patients. Among acute cardiovascular diseases, cancer treatment, as well as the cancer disease itself, may induce a cardiogenic shock. Although increasing, these cardiogenic shocks are still relatively limited, and their management is a matter of debate in cancer patients. Etiologies that cause cardiogenic shock are slightly different from those of non-cancer patients, and management has some specific features always requiring a multidisciplinary approach. Recent guidelines and extensive data from the scientific literature can provide useful guidance for the management of these critical patients. Even if no etiologic therapy is available, maximal intensive supportive measures can often be justified, as most of these cardiogenic shocks are potentially reversible. In this review, we address the major etiologies that can lead to cardiogenic shock in cancer patients and discuss issues related to its management.