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............................................................................................................................................................................. administration of other cardiotoxic drugs, and patient factors (which include, amongst other factors, younger age, traditional risk factors, and history of heart disease).226,227 Furthermore, radio- and chemotherapy may exert direct vascular effects and increase atherosclerosis-related CVD outcomes.227,228

3.4.4.1 Diagnosis and screening Signs or symptoms of cardiac dysfunction should be monitored before and periodically during and after cancer treatment for early detection of abnormalities in patients receiving potentially cardiotoxic chemotherapy. Detection of subclinical abnormalities using imaging and measurement of circulating biomarkers (such as cardiac troponins and natriuretic peptides) is currently recommended.173,229 Measures of myocardial strain, particularly systolic global longitudinal strain, may precede a significant decline in LVEF.230233

3.4.4.2 Prevention of cardiotoxicity and cardiovascular risk factors RCTs of preventive therapy with renin-angiotensin-aldosterone system (RAAS) inhibitors and/or beta-blockers after trastuzumab or anthracyclines have reported contradictory results.230,234,235 The main benefits are less marked LV remodelling or a reduced decline in LVEF observed with cardiac magnetic resonance, but translation into better outcomes remains speculative. Exercise should be strongly advised. In particular, aerobic exercise is considered a promising non-pharmacological strategy to prevent and/ or treat chemotherapy toxicity.236 A study showed a significantly higher risk of CVD in survivors of childhood cancer than in non-cancer adult controls, and particularly in survivors of adult-onset cancer with underlying ASCVD risk factors.237 Therefore, aggressive management of ASCVD risk factors in this population is recommended.

3.4.5. Chronic obstructive pulmonary disease Chronic obstructive pulmonary disease (COPD) is a complex, progressive respiratory disorder and currently the fourth leading cause of death worldwide. It is characterized by chronic airflow limitation with respiratory symptoms and is associated with an increased inflammatory response and abnormalities of the airways caused by significant exposure to noxious particles or gases (mainly smoking). Although COPD is recognized and thoroughly investigated as a CVD comorbidity, its role as an ASCVD risk factor is not well established. Nevertheless, COPD patients have a two- to three- fold increased risk of CVD compared with age-matched controls when adjusted for tobacco smoking. Patients with mild-to-moderate COPD are 810 times more likely to die from ASCVD than respiratory failure, having higher rates of hospitalization and death due to CVD, stroke, and HF.238,239 CVD also runs undiagnosed; less than one-third of COPD patients with electrocardiographic (ECG) evidence of myocardial infarction are diagnosed with CVD.240 CVD mortality increases by 28%, and the frequency of non-fatal coronary events by 20%, for every 10% decrease in the forced expiratory volume in 1 second (FEV1).241 Acute COPD exacerbations, mainly due to infections, are frequent and are responsible for a four-fold increase of CVD events.242 The risk of both myocardial infarction and ischaemic stroke is increased during the 3 months after an acute exacerbation.243 The high prevalence of CVD in COPD patients may be explained by the fact that both diseases share common risk factors, such as smoking, ageing, hypertension, and dyslipidaemia.244 Metabolic syndrome and reduced PA is present in 34% of COPD patients, with its most prevalent components being hypertension (56%), abdominal obesity (39%), and hyperglycaemia (44%).245 CVD may be caused by hypoxia during exercise due to lung hyperinflation, high resting heart rates, impaired vasodilatory capacity, and peripheral, cardiac, and neurohumoral sympathetic stress. Atherosclerosis and coronary artery calcification may be the result of oxidative stress, and reductions in antiaging molecules causing both lung and vascular ageing.246

Systemic inflammation is prominent in COPD, with circulating biomarkers in high concentrations and associated with increased mortality.247 Troponin is elevated during an acute exacerbation of COPD, and 10% of hospitalized patients meet the definition of acute myocardial infarction (AMI).248 B-natriuretic peptide level, if elevated, increases the mortality risk.249 Systemic inflammation and oxidative stress caused by COPD promote vascular remodelling, stiffness, and atherosclerosis, and induce a ‘procoagulant’ state that affects all vasculature types.250 Cognitive impairment and dementia due to cerebral microvascular damage is correlated with COPD severity; patients have a 20% increased risk for both ischaemic and haemorrhagic stroke, which may be up to seven-fold higher following an acute exacerbation.251 PAD is present in about 9% of COPD patients,252 who have an almost doubled risk of developing PAD,253 as well as an increased prevalence of carotid plaques related to the disease severity.254 Finally, COPD is positively associated with abdominal aortic aneurysm, regardless of smoking status.255 Cardiac arrhythmias are common and may be due to the haemodynamic effects (pulmonary hypertension, diastolic dysfunction, atrial structural, and electrical remodelling) caused by the disease in combination with autonomic imbalance and abnormal ventricular repolarization.256 AF is frequent, directly associated with FEV1, usually triggered by acute exacerbations of COPD, and an independent predictor of in-hospital COPD mortality.257,258 COPD is also a risk factor for ventricular tachycardia independent of LVEF,259 and for sudden cardiac death independent of CVD risk profile.260

Unrecognized ventricular dysfunction is common in COPD,261 although HF is 3.8 times more common in COPD patients than in controls.262 Patients with frequent acute exacerbations have a high frequency of diastolic dysfunction; HFpEF risk is higher because of a high prevalence of hypertension and DM.263 Considering these facts, it seems of upmost importance to screen COPD patients for ASCVD and ASCVD risk factors, bearing in mind that COPD affects the accuracy of CVD diagnostic tests. Achieving adequate exercise is difficult, vasodilators for myocardial perfusion scanning may be contraindicated because of the risk of bronchospasm, and stress or transthoracic echocardiography is often disturbed by poor ultrasound windows. Computed tomography coronary angiography or magnetic resonance imaging may be alternatives, but remain expensive, time consuming, and not always available. The use of COPD medications (i.e. long-acting muscarinic antagonists and long-acting beta agonists) is not associated with overall CV adverse events in patients with stable COPD. Olodaterol may reduce the risk of overall CV adverse events and formoterol may decrease the risk of cardiac ischaemia. Long-acting beta agonists may reduce the incidence of hypertension, but may also increase the risk of HF, so should be used with caution in HF patients.264 Downloaded from academic.oup.com/eurheartj/article/42/34/3227/6358713 by guest on 07 October 2026