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Cardiotoxicity is a relatively frequent and potentially serious side effect of anticancer treatments, particularly anthracyclines and trastuzumab, widely used in the treatment of breast cancer. The increase in cancer survivors has generated a growing interest in the prevention of cardiotoxicity. Although early studies suggested an overall benefit on cardiac function with the use of ACE inhibitors (ACEIs) and beta blockers (BBs), more recent randomized trials have demonstrated little or no effect of pharmacological interventions. Even the various meta-analyses conducted in this area have provided weak results in favour of cardioprotective therapies for which the benefit would not always justify the risk of developing side effects. Given the incompleteness of the evidence, there is no clear consensus on which patients should initiate cardioprotective therapy. As recommended in the new guidelines of the European Society of Cardiology, risk stratification before treatment is crucial to identify high-risk patients who would benefit most from the use of cardioprotective therapy. Randomized trials are currently underway to evaluate other therapeutic strategies such as sacubitril/valsartan, and the possibility of using gliflozins in the future cannot be excluded. However, rigorous control and treatment of risk factors remain the primary focus in the management of these patients., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Prevention of left ventricular dysfunction predominantly induced by anthracyclines and/or trastuzumab still represents a challenge for cardio-oncology today. Indeed, this complication threatens to limit the significant gain in cancer survival achieved to date. Oncology strategies with cumulative dose limitation, continuous infusion, dexrazoxane, and liposomal formulations have been shown to decrease the risk of anthracycline cardiotoxicity. The preventive use of ace inhibitors, sartans, and/or beta-blockers has not yet provided convincing evidence and the positive effect on left ventricular ejection fraction decline appears poor without a clear clinical relevance. Assessment of the cardiovascular risk profile is a key aspect of the baseline evaluation of any patient scheduled for cancer therapy. Control and/or correction of modifiable cardiovascular risk factors is the first form of primary prevention of cardiotoxicity. It will be necessary to select populations at higher risk of developing cardiac dysfunction, identify patients genetically predisposed to develop cardiotoxicity in order to build the most appropriate strategies to correctly and timely target cardioprotective therapies., (Published on behalf of the European Society of Cardiology. © The Author(s) 2021.)

Cardiac oncology is a subspecialty of cardiology engaging cardiologists and oncologists alike, in order to provide the best possible oncologic treatment for patients at high cardiovascular risk or developing cardio-toxicity during the course of their treatment, thus avoiding discontinuing it, and aiming at improving survival and quality of life. Early diagnosis and the effectiveness of the newer cancer treatments delivered an increasing number of long-term survivors (presently almost 30 million worldwide), at high risk of developing cardiovascular diseases. This predisposition has been correlated not only to the toxic side effects of the oncologic treatment but also to a real vulnerability to the risk factors in this patients population. For decades, the concept of cardio-toxicity in cardiac oncology has been restricted to ventricular dysfunction, but during the last few years the Food and Drug Administration has approved hundreds of new molecules and cardiac oncology has escalated its complexity. The introduction of new target therapy, proteasome inhibitors, immuno-modulators, and inhibitors of the immunitary checkpoint, magnified the concept of cardio-toxicity to a wider definition of 'cardiovascular toxicity' incorporating arterial hypertension, ischaemia, cardiomyopathy, myocarditis, arrhythmic complications, long QT, and arterial and venous thrombosis. We are still lacking guidelines on the new and varied forms of toxicity, as well as monitoring strategies in the short- and long-term follow-up., (Published on behalf of the European Society of Cardiology. © The Author(s) 2020.)

Previous clinical studies suggest that intravenous (IV) recombinant tissue plasminogen activator (rt-PA) benefits stroke patients regardless of the underlying etiology. In this study, we assessed the possible differences in response to IV rt-PA between cardioembolic stroke and other stroke subtypes. A total of 303 consecutive stroke ischemic patients (from January 2005 to April 2014) admitted to our Stroke Unit and treated with IV rt-PA were retrospectively reviewed. All patients were classified in two groups: Cardioembolic (CE) and Non-Cardioembolic (NCE). We analyzed a total of 303 patients. Thirty patients died in the first hours after fibrinolysis and no statistically significant differences were found in two groups (14 CE vs 18 N-CE). We observed a significant differences in clinical outcome in terms of symptoms "improvement" (p< 0.01 .2) and symptoms" regression" (p<0.057 .2) even if this last result did not reach statistical significance in CE patients respect to N-CE patients. In conclusion, the intravenous fibrinolysis is more effective in CE group than in N-CE regarding symptoms "improvement" and the PFO-Stroke patients treated with fibrinolysis have better outcome than other patients and they have high rate of symptoms" regression". Moreover the main predictor of good outcomes were younger age and milder stroke severity on hospital admission.