[Cardiotoxicity of cancer therapy]. / Kardiotoxicita onkologické lécby.

Due to advances in oncological care, the number of patients exposed to and surviving after anticancer chemotherapy is steadily increasing. Anticancer agents, however, are often associated with side-effects including cardiotoxicity which has been identified as one of the most serious and potentially life threatening complications. Cardiotoxicity manifestations range from asymptomatic alterations of heart and vasculature function to arterial hypertension, myocardial ischemia, arrhythmias (including QT-prolongation) and overt heart failure. Post-chemotherapy cardiovascular impairment has been associated with increased morbidity and may also contribute to increased mortality in these patients, both early and late after chemotherapy. This review article describes pathophysiology, clinical manifestation, diagnostic algorithms, monitoring and therapy of cardiotoxicity caused by anticancer agents. We also outline and discuss a variety of problems associated with patient management from the viewpoint of clinical cardiology according to latest published findings.

Arterial stiffening contributes to impairment of cerebrovascular reactivity in patients with coronary artery disease without carotid stenosis.

Impaired cerebrovascular reactivity (CVR), an important risk factor for future stroke, is affected by a presence carotid stenosis. However, in some cases CVR can be impaired in the absence of carotid stenosis due to several poorly characterized mechanisms. We hypothesized that arterial stiffening as observed in coronary heart disease (CHD) could be associated with alteration in CVR in CHD patients without carotid stenosis. The study population consisted of patients referred for coronary angiography without significant carotid stenosis (<50 %). CVR was evaluated by breath holding index (BHI) measured with transcranial color code duplex ultrasound. Arterial stiffness was assessed by pulse wave velocity (PWV) measured by the oscillometric method. The extent of coronary atherosclerosis was quantified by Gensini score (GS). Out of 186 subjects, sixty-two patients fulfilled the inclusion and exclusion criteria. BHI decreased with increasing PWV (r = -0.47, p<0.001). Decrease in BHI was significantly inversely associated with GS (r = -0.61, p<0.001). GS was associated with PWV (p<0.001). In conclusion, impaired CVR was associated with increased arterial stiffening in CHD patients in the absence of significant carotid stenosis. Thus, we speculate that increased arterial stiffness may at least partially contribute to the pathophysiology of CVR alteration in coronary artery disease.