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Cancer and cardiovascular (CV) disease are the most prevalent diseases in the developed world. Evidence increasingly shows that these conditions are interlinked through common risk factors, coincident in an ageing population, and are connected biologically through some deleterious effects of anticancer treatment on CV health. Anticancer therapies can cause a wide spectrum of short- and long-term cardiotoxic effects. An explosion of novel cancer therapies has revolutionised this field and dramatically altered cancer prognosis. Nevertheless, these new therapies have introduced unexpected CV complications beyond heart failure. Common CV toxicities related to cancer therapy are defined, along with suggested strategies for prevention, detection and treatment. This ESMO consensus article proposes to define CV toxicities related to cancer or its therapies and provide guidance regarding prevention, screening, monitoring and treatment of CV toxicity. The majority of anticancer therapies are associated with some CV toxicity, ranging from asymptomatic and transient to more clinically significant and long-lasting cardiac events. It is critical however, that concerns about potential CV damage resulting from anticancer therapies should be weighed against the potential benefits of cancer therapy, including benefits in overall survival. CV disease in patients with cancer is complex and treatment needs to be individualised. The scope of cardio-oncology is wide and includes prevention, detection, monitoring and treatment of CV toxicity related to cancer therapy, and also ensuring the safe development of future novel cancer treatments that minimise the impact on CV health. It is anticipated that the management strategies discussed herein will be suitable for the majority of patients. Nonetheless, the clinical judgment of physicians remains extremely important; hence, when using these best clinical practices to inform treatment options and decisions, practitioners should also consider the individual circumstances of their patients on a case-by-case basis.

Objective: To review the literature on early management of myocardial infarction.Data Sources: Papers published or referenced in major English-language cardiology journals for the last 15 years.Study Selection: Large recent multicenter studies and the guidelines for early management of patients with acute myocardial infarction (American College of Cardiology/American Heart Association Task Force) were emphasized.Data Synthesis: A strategy for risk stratification was developed from information available in the emergency department, from the first days of the hospitalization, and before discharge to identify patients in whom intervention might improve prognosis.Conclusions: Treatment of myocardial infarction requires establishing patency of the infarct-related artery, usually with thrombolysis. Risk stratification begins in the emergency department (phase 1) using clinical (primarily the electrocardiogram) and historical data to identify patients at risk for massive infarction. For patients at highest risk, the efficacy of thrombolytic therapy must be assured and, if not effective, emergency angiography and mechanical reperfusion should be considered. During days 2 to 5, (phase 2), patients with large amounts of ischemic myocardium, postinfarction angina, "flash" pulmonary edema, or anterior non-Q infarctions are identified and studied. Predischarge (phase 3) stratification identifies those patients at risk for early death. A previous infarction, an ejection fraction less than 0.40, pulmonary congestion during the hospitalization, delayed afterpotentials on signal-averaged electrocardiography, symptomatic ventricular ectopic beats, decreased heart rate variability, limited exercise tolerance, or ischemia on exercise testing identifies patients at high risk. Patients with jeopardized myocardium must be identified for revascularization to try to improve survival. More data are needed to determine whether angioplasty or bypass surgery will improve prognosis in these patients. [ABSTRACT FROM AUTHOR]

Objective: To determine the clinical significance of silent and symptomatic myocardial ischemia detected by noninvasive testing in stable postcoronary patients.Design: Cohort study with a mean 23-month follow-up.Setting: Ambulatory outpatients after recent hospitalization for an acute coronary event.Patients: Nine hundred thirty-six patients (76% male; mean age, 58 years) who were clinically stable 1 to 6 months after hospitalization for acute myocardial infarction or unstable angina.Interventions: Noninvasive testing involved rest, ambulatory, and exercise electrocardiograms and stress thallium-201 scintigraphy.Main Outcome Measures: Cox regression analysis was used to evaluate the risk (hazard ratio) of first recurrent primary events (cardiac death, nonfatal infarction, or unstable angina) or restricted events (cardiac death or nonfatal infarction) associated with ischemic noninvasive test results.Results: ST segment depression on the rest electrocardiogram was the only noninvasive test variable that identified a significantly increased risk (P = .05) for first recurrent primary events (hazard ratio; 95% confidence limits): rest electrocardiogram ST depression (1.5; 1.00, 2.25); ambulatory electrocardiogram ST depression (0.86; 0.49, 1.51); exercise electrocardiogram ST depression (1.13; 0.82, 1.56); and stress thallium-201 reversible defects (1.3; 0.96, 1.74). Test results were similar for first recurrent restricted events, and in patients with and without angina. Significantly increased risk (P < .05) was noted when exercise-induced ST depression occurred in patients who also had reduced exercise duration (hazard ratio, 3.4) or when reversible thallium-201 defects occurred in patients who also had increased lung uptake (hazard ratio, 2.8). Each high-risk subset made up less than 3% of the population and contained less than 6% of patients with first primary events.Conclusion: Detection of silent or symptomatic myocardial ischemia by non-invasive testing in stable patients 1 to 6 months after an acute coronary event is not useful in identifying patients at increased risk for subsequent coronary events. [ABSTRACT FROM AUTHOR]