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Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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Dr. Christian Seiler
This session entitled “collateral damage to the heart” focused on cardiovascular side effects of novel molecular therapies in oncology and ophthalmology. The first speaker, Dr. Albini, covered two speeches about cardiac side effects of conventional as well as targeted chemotherapy. She reviewed the targets of oncological therapy, i.e., cell growth, motility, survival, proliferation and angiogenesis and listed the therapeutics aiming at them: anthracyclines, cytarabine, 5-FU, paclitaxel, cyclophosphamide and the targeted chemotherapy by tyrosinkinase inhibitors. Also, she updated the audience on the definition of cardiotoxicity, namely a reduced left ventricular ejection fraction, a manifestation of heart failure symptoms and signs or the evolution of vascular effects such as thromboembolism, hypertension, heart rhythm and conduction disturbances. The occurrence of such cardiac events in the case of targeted chemotherapy using trastuzumab in addition to anthracyclines is actually quite low, at a rate of 0.7-4.3%. Conversely, the benefit from this treatment with regard to disease-free or overall survival in about 14,000 patients with breast cancer is clearly present. In his talk, Dr. Leveziel gave an overview about the cardiovascular side effects of anti-angiogenic therapy applied locally for macular degeneration. The serum levels of the anti-VEGF substance used are, naturally much lower than in systemic application, but they are still in a higher-than-normal range. Thus, it is not surprising that arterial hypertension occurs as a side effect. Finally, Dr. Virmani talked about inhibition of tumour angiogenesis in particular and the related side effects. She reviewed how anti-VEGF drugs induce arterial hypertension by endothelial injury and reduced nitric oxide production with subsequent vasoconstriction and increase of microvascular resistance. As a pathologist, she also presented some nice microscopic images illustrating the reduced density of microvessels in the myocardium of animals treated with anti-angiogenic substances. This evidence of damage to the heart muscle by molecular therapies in oncology can be viewed in the actual sense of the session’s title, collateral damage. However, all of the speakers obviously interpreted it only in the metaphoric sense, because none directly talked about the potential or overt damage of anti-angiogenic drugs to an in-built salvaging mechanism of the heart in case of an ischemic insult: the coronary collateral circulation. In that sense and as a “collaterologist”, this reporter did not gather much new information on the topic.
Collateral damage to the heart: effects of novel molecular therapies in oncology and ophtalmology
Our mission: To reduce the burden of cardiovascular disease
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