Discussion
This is the first study to ascertain the cardiovascular risk in masters athletes in Canada. CVD and high cardiovascular risk profiles (FRS ≥20%) were found in 11.4% and 8.5% of athletes, respectively. Most participants (73.0%) diagnosed with CAD were asymptomatic and were unaware of their elevated cardiovascular risk. Compared with the Canadian general population, participants had a lower prevalence of risk factors (figure 3).
Figure 3Prevalence of cardiovascular risk factors compared with the Canadian population. Data from the Canadian Health Measures Survey (CHMS) and Canadian Community Health Survey (CCHS) from a nationally representative sample of Canadians compared with the current population, aged >35. Data for those aged >35 were not available for all risk factors. The age and source for each risk factor were reported as follows: dyslipidaemia: aged 18–79, source: CHMS, 2012–2014; hypertension: aged 20–79, source: CHMS, 2012–2014; smoking (self-reported): aged 12–49, source: CHMS, 2012 and 2013; diabetes (diagnosed by a health professional): aged 12 and over, source: CCHS, 2015; inactivity: aged 12 and older, source: CCHS, 2014; obesity (directly measured): aged 18–79, source: CHMS, 2010; depression (major depressive episode in the last 12 months): aged 15 and older, source: CCHS, 2012; heavy drinking: aged 12 or older, source: CCHS, 2014. Dyslipidaemia was defined as having a low-density lipoprotein >3.5, or total cholesterol to high-density lipoprotein cholesterol ratio >5.0, or self-reported use of a lipid-modifying medication. Hypertension was defined as >140 mm Hg systolic or >90 mm Hg diastolic, or self-reported use of antihypertensive medication. Hyperglycaemia was defined as having a fasting glucose >5.5 mmol/L. Heavy drinker was defined as >5 drinks on one occasion, at least once a month. Obesity was defined as body mass index >30 (http://www.statcan.gc.ca).
The prevalence of CVD was higher in our study compared with previous prospective studies. Menafoglio et al
10 studied 785 highly active individuals (>6 hours of physical activity per week) using the EACPR protocol and detected 22 individuals (2.8%) with significant CVD. One (0.1%) individual had CAD compared with 63 (7.9%) present in this study and 9 (1.1%) had valvular disease, similar to this study (n=15, 1.9%). Using the EACPR guidelines and an echocardiogram, Aagaard et al
7 reported significant CVD (ie, long QT syndrome, AF, third-degree AV block) in 5.9% of participants, and none had CAD or valvular disease. The greater prevalence of CVD in our population compared with Menafoglio et al and Aagaard et al’s studies may be attributed to (1) higher mean age (54.6±9. vs 46.8±7.3 vs 51.5±5 years, respectively); (2) long-term activity habits (35.1±14.8 years vs 20.0±14.5 years, and novice runners, respectively); (3) more participants undergoing EST due to an intermediate FRS (24.6% vs 0% vs 0%, respectively); and/or (4) a greater number of secondary investigations. Over half of our population (63.3%) underwent EST compared with the 14.3% and 9.0% reported by Menafoglio et al and Aagaard et al, respectively. Aagaard et al included a more comprehensive onsite assessment by physicians (echocardiogram in all participants), which likely resulted in fewer participants proceeding to subsequent testing (ie, EST).
Current screening tools (AHA 14-element recommendations, ECG interpretation criteria) are not specific for use in masters athletes and may need to be modified.19 20 For example, the presence of a 2/6 systolic murmur had low clinical significance (4.3% PPV) and should not warrant further testing. The presence of a mid-systolic click was associated with a slightly better PPV (18.2%) for detecting valvular disease. The ECG demonstrated a low PPV for detecting CAD (11.1%), although q-waves (33.3%) and PVCs (27.3%) increased the PPV for CAD. Left axis deviation elicited the greatest number of follow-ups (n=36), but had a low PPV (11.2%). As such, the presence of isolated left axis deviation may not warrant further testing. The ECG also has an ability to detect asymptomatic electrical disease (ie, AF, long QT syndrome and Wolff-Parkinson-White syndrome). In the current study, the ECG detected three (50.0%) individuals with AF. Positive responses to the symptoms and family history of unexplained SCD elicited the greatest number of follow-ups, yet had a low detection rate for CAD (PPV 11.6% and 6.3%, respectively). Increasing the sensitivity of the questionnaire (ie, differentiating cardiogenic symptoms from non-cardiogenic, and reviewing in conjunction with the ECG and family history) or a more comprehensive review by an onsite physician with appropriate training would reduce the number of participants having to undergo subsequent testing, and thereby reduce false-positives.
In the present study, a positive EST detected CAD in 63.5%. This is consistent with the findings by Sofi et al,26 whereby the majority of participants diagnosed with CVD demonstrated an abnormality on the EST. While previous reports suggest that ECG changes are masked in individuals at low risk of CAD (ie, active, physically fit population) and in those who can achieve >10 METs,27 28 our study did not show this (table 3). However, 81.0% of those diagnosed with CAD had an intermediate or high FRS, which is known to increase the likelihood of a positive EST in men.29 Although the FRS is widely used and is a good predictor of one’s 10-year CVD risk, it may underestimate cardiovascular risk in masters athletes.11 30 31 Masters athletes have been shown to have a higher prevalence of coronary plaques (44.3% vs 22.2%) when compared with sedentary men who were similar in age, sex and low FRS.11 However, a distinction between the detection of CAD is different from myocardial infarction and death.
Using coronary CT angiography improves detection rates as shown by Braber et al,30 who identified CAD in 60 of 318 (18.9%, 95% CI 14.9% to 23.5%) asymptomatic participants, of whom 300 had a low cardiovascular risk and a normal sports medical examination. Although the implications of increased coronary plaques in masters athletes are unknown, research suggests that individuals with elevated cholesterol levels benefit from statin therapy, even in the setting of high fitness. Kokkinos et al
32 reported a greater 10-year survival rate when high fitness was combined with statin therapy (fully adjusted HR 0.30; 0.21-0.41) versus no statin therapy (HR 0.53; 0.44–0.65) when compared with less fit individuals taking statins.
Limitations
A true prevalence of CVD cannot be reported because gold-standard cardiovascular examinations (ie, coronary artery calcium score, coronary CT angiography, echocardiogram) were not performed on all athletes. However, most athletes had an EST, which increased the likelihood of detecting those at risk by triggering subsequent examinations. In this study, the reference standard was the evaluation by cardiologists, who determined which cardiac evaluations were clinically indicated. Although gold-standard imaging tests that have sensitivities approaching 100% would be ideal to ascertain the prevalence of CVD, we did not perform these examinations on all participants because of the following reasons: (1) the current evidence for incorporating cardiac imaging into preparticipation screening is insufficient10; (2) cost; (3) time commitment; (4) potential radiation exposure; (5) testing a population of generally healthy asymptomatic low-risk patients is not clinically indicated; and (6) the potential psychological and insurance risks.
Additionally, since the reference standard was only available for those participants who went through all stages, the sample PPV for each individual screening method computed based on this set of biased samples might not estimate the population PPV, but rather the PPV of those that screened positive. However, we were able to assess the value of the screening test when it was reported positive, which may be of benefit in screening studies.
The reported cardiovascular risk may be overestimated due to selection bias. Participants with symptoms, previously known risk factors and/or known family history of CVD may have been more inclined to enrol in the study. Conversely, athletes who had a low FRS did not undergo further evaluations but may in fact have CVD as the FRS underestimates risk in masters athletes.
Our population was predominately Caucasian, limiting the generalisability of our results to other populations. Inclusion of a control group in a large, multisport, multiethnic, longitudinal study will be instrumental in determining whether preparticipation screening among masters athletes reduces morbidity, mortality and healthcare costs.