Cardiovascular Assessment in the Older Athlete

The cause of exercise-related sudden cardiac death depends heavily on age. In young athletes it is usually an inherited or structural condition such as hypertrophic cardiomyopathy or a channelopathy. In older or masters athletes, conventionally those aged thirty-five and over, it is usually atherosclerotic coronary artery disease (CAD). Thirty-five is a conventional threshold rather than a biological boundary, and a practical point is that warning symptoms are often absent before a coronary event, so assessment cannot rely on symptoms alone.

The relationship between endurance exercise and the coronary arteries is nuanced. Some cohorts, particularly male lifelong endurance athletes, show more coronary calcification than sedentary peers. Coronary calcification remains evidence of coronary atherosclerosis and carries prognostic importance; while a more calcified plaque phenotype may be relatively stable, this is not used to reassure that a raised score is benign, and higher fitness attenuates but does not eliminate risk. A second age-related issue is rhythm: the risk of atrial fibrillation (AF) is increased, most evidently in men with long-term, high-volume endurance exposure, and the proposed mechanisms, including raised vagal tone, atrial stretch and fibrosis, remain hypotheses rather than settled explanations. New palpitations or an unexplained drop in performance are therefore taken seriously.

Assessment begins with the history and examination. Exertional chest pain, breathlessness out of keeping with fitness, palpitations, and syncope are red flags that prompt investigation. Traditional cardiovascular risk factors are reviewed, including age, sex, a family history of premature coronary disease, smoking, blood pressure, lipids and diabetes, and risk is estimated with a calculator; in the UK, QRISK3 is used and applies to primary prevention in adults aged twenty-five to eighty-four without established cardiovascular disease. A lipid-lowering statin such as atorvastatin twenty milligrams is offered after discussion when the ten-year cardiovascular risk is ten percent or more, and may also be considered below that threshold where clinical judgement supports it, so it is not an automatic consequence of crossing a line. A resting electrocardiogram (ECG) is used where symptoms, examination, sporting context or risk assessment indicate, rather than as a routine baseline for every asymptomatic athlete.

Further testing is selective and targeted. For suspected stable angina in someone without known coronary disease, an exercise electrocardiogram should not be used to diagnose or exclude angina; in current UK practice, computed tomography coronary angiography (CCTA), often called CT coronary angiography, is the first-line anatomical test. Exercise testing remains useful for assessing functional capacity, provoking exercise-induced arrhythmia and evaluating selected known disease. Coronary artery calcium (CAC) scoring is not routinely recommended for every asymptomatic low-risk athlete; it may refine risk in selected borderline or intermediate-risk cases but does not by itself determine statin treatment or exercise eligibility. Echocardiography is used where structural disease is suspected from symptoms, examination or the electrocardiogram, rather than as a general test of coronary risk.

Management centres on treating cardiovascular risk factors and on shared decision-making with the athlete. Blood pressure, lipids (with a statin where indicated), smoking, diabetes and weight are all addressed, and the conversation is a genuine dialogue, since athletes may be reluctant to start medication and bring their own data from wearable devices. Continued exercise is generally encouraged, but the exercise prescription is not a blanket reassurance: it depends on symptoms, the presence of obstructive coronary disease, left ventricular function, inducible ischaemia, arrhythmias and treatment, and it is tailored accordingly.

Restriction or modification of exercise is reserved for specific situations, such as significant inducible ischaemia, unstable coronary disease or impaired ventricular function, and these athletes are referred to cardiology for individualised advice. Atrial fibrillation is managed on its merits, with attention to rate or rhythm control and to anticoagulation, which follows standard stroke-risk assessment with an athlete-specific discussion of trauma and bleeding exposure. Symptomatic athletes and those found to be at high risk are referred for cardiology assessment before or around their return to exercise. For the great majority, once symptoms and inducible ischaemia have been excluded, the outcome is continued, well-supported participation with sensible risk-factor management rather than withdrawal from sport.

• •In the older (masters) athlete, taken conventionally as 35 and over, sudden cardiac death is usually from atherosclerotic coronary artery disease; 35 is a conventional threshold, not a biological boundary, and warning symptoms are often absent.
• •Coronary calcification, seen more in male lifelong endurance athletes, is evidence of atherosclerosis with prognostic importance, so a raised score is not treated as benign; fitness attenuates but does not eliminate risk.
• •Atrial fibrillation risk is increased mainly in men with long-term high-volume endurance exposure; proposed mechanisms remain hypotheses.
• •Use symptoms, risk factors and QRISK3 (primary prevention, ages 25 to 84); a statin is offered after discussion at a 10-year risk of 10 percent or more, and considered in some below that.
• •A resting electrocardiogram is selective; for suspected stable angina CT coronary angiography is first-line, and an exercise electrocardiogram is not used to diagnose or exclude angina without known disease; calcium scoring and echocardiography are selective.
• •Encourage continued exercise once symptoms and inducible ischaemia are excluded, but tailor the prescription to symptoms, obstructive disease, ventricular function, ischaemia and arrhythmias.