title: [Cardiovascular complications of cancers and anti-cancer therapy].
abstract: In our aging population the incidence of cancer is increasing in the elderly. We are thus facing a new challenge especially considering incidence of cardiovascular diseases (CVD) in this patients population. Overall survival of cancer patients has significantly improved therefore cancer has become in many cases a chronic disease. We are about to be treating patients who either may develop a new CVD or their current CVD may deteriorate. Cancer can cause various cardiovascular conditions locally (pressure in mediastinum, effusions) or systemically (increased risk of pulmonary embolism, arrhythmias, carcinoid heart disease). Medical cancer therapy can lead to congestive heart failure (CHF) per se, by anthracycline or antiHER2 therapy direct cardiac toxicity or by number of other cardiac conditions medical treatment can cause, such as accelerated arterial hypertension due to anti-angiogenic therapy (tyrosine-kinase inhibitors, bevacizumab) or even standard chemotherapy (alkylating agents, cisplatin) or overusing steroids in cancer patients. Atrial fibrillation (AFib) also contributes to CHF development. AFib in cancer patients may develop secondary to ischaemia in anaemic patients, metabolic disorders caused by cancer or treatment, pulmonary embolism, sepsis or even as a result of direct impact of cytotoxic treatment (cisplatin, ifosfamide, gemcitabine, 5-fluorouracil, etoposide). One of major risk factors for CHF is coronary artery disease (CAD), which is a very serious late sequel of cancer therapy mainly in long time cancer survivors (testicular cancer, childhood cancer, hematologic malignancies, breast cancer). CAD may develop secondary to thoracic irradiation, dyslipidemia caused by hormonal treatment or simply as results of endothelial dysfunction caused by alkylating agents. In summary, long time cancer survivors represent a subgroup of patients at great risk of developing CVD in any form. It is crucial to mention that these patients can develop typical CVD much earlier compared to standard population and therefore require special follow-up with active surveillance.Key words: anthracycline - atrial fibrillation - cardiac toxicity - heart failure - pulmonary embolism.
authors.forename: Jiří
authors.initials: J
authors.lastname: Vyskočil
authors.forename: Katarína
authors.initials: K
authors.lastname: Petráková
authors.forename: Petr
authors.initials: P
authors.lastname: Jelínek
authors.forename: Michal
authors.initials: M
authors.lastname: Furdek
mesh_terms: D018943:Anthracyclines / Q000009:adverse effects; D000970:Antineoplastic Agents / Q000009:adverse effects*; D001281:Atrial Fibrillation / Q000209:etiology; D002275:Carcinoid Heart Disease / Q000209:etiology; D066126:Cardiotoxicity; D002318:Cardiovascular Diseases / Q000209:etiology*; D003324:Coronary Artery Disease / Q000209:etiology; D006331:Heart Diseases / Q000209:etiology; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D009369:Neoplasms / Q000150:complications / Q000628:therapy*; D011878:Radiotherapy / Q000009:adverse effects*; D012307:Risk Factors; D017741:Survivors; D000068878:Trastuzumab / Q000009:adverse effects
chemical_list: D018943:Anthracyclines; D000970:Antineoplastic Agents; D000068878:Trastuzumab