coronary artery disease

Too Much Exercise, Revisited

May 21, 2014 By Larry Creswell, MD 2 Comments

The issue of “too much exercise” is in the news again this week. In last week’s edition of the medical journal, Heart, a group of German investigators headed by Dr. Ute Mons from the Division of Clinical Epidemiology and Aging Research at the German Cancer Research Center in Heidelberg reported on “A reverse J-shaped association of leisure time physical activity with prognosis in patients with stable coronary heart disease: evidence from a large cohort with repeated measurements.” This study extends our understanding of the importance of exercise in patients with known heart disease and the findings are very much worth noting.

In the popular press, this study received considerable attention in the past few days. In Forbes, we had a short article by Larry Husten, entitled “Exercise: Can There Be Too Much of a Good Thing?” In the Wall Street Journal, we had a short article by Kevin Helliker, entitled “Too Much Exercise May be Harmful to Your Health.” There were many other articles; these are representative. The headlines were all similar.

There was also interest in social media and the blogosphere. The research was shared along with admonitions about exercising too much, all in rather broad strokes.

Let’s take a look at the study….

The Study

Back in 1999-2000, just more than 1100 German individuals were enrolled in a longitudinal study. These were individuals who were undergoing inpatient cardiac rehabilitation (a monitored exercise program) after some sort of aucte heart problem–acute coronary syndrome, heart attack or myocardial infarction (MI), or coronary revascularization (with a stent or bypass surgery). As such, they were all known to have significant coronary artery disease (CAD). At the time of enrollment, they ranged in age from 30 to 70 years.

Over the following 10 years, these individuals answered questionnaires about their health at 1, 3, 4.5, 6, 8, and 10 years. At the time of the 1-year questionnaire, the median age of respondents was 61 years. The typical participant was male, overweight, a current or former smoker, with a history of heart attack, and high blood pressure. On each of the questionnaires, there was a question about physical activity:

“On average, how often have you engaged in physically strenuous and sweat-inducing activity in your leisure time in the past 12 months (ie, cycling, speedy hiking, gardening, sport)?”

And the possible answers included:

Daily
5-6 times per week
2-4 times per week
1-4 times per month
Rarely or never.

The respondents were also asked to estimate the number of hours per week, on average, they spent doing strenuous physical activity.

In addition to physical activity, the investigators collected information about the important outcome measures: major cardiovascular events (MI and stroke); cardiovascular mortality (death due to a heart-related cause); non-fatal cardiovascular events; and all-cause mortality.

The Results

At the time of the 1-year questionnaire, most individuals were physically active, with just 9.1% reporting “rarely or never” exercising. Most (41.3%) were in the “2-4 times per week” category. The “5-6 times per week” group accounted for 15.8% and the “daily” group accounted for 15.3%. For context, the current American Heart Association (AHA) guidelines on physical activity (generally, and not specific to patients with known CAD) call for 3 to 5 days of exercise per week, depending upon the intensity of the exercise. In terms of time, those guidelines suggest 150 minutes (2 1/2 hours) of moderate-intensity exercise OR 75 minutes of vigorous exercise per week.

Perhaps not surprisingly, as the individuals aged over the 10-year period of the study, their activity levels decreased. Perhaps their interest in well-being or focus on their heart condition waned as well. There was a relatively constant percentage of enrollees in the “2-4 times per week” category, but there was a decrease in those exercising more….and an increase in those exercising less.

Statistical analysis was used to try to isolate the influence of physical activity as a variable….and eliminate the influence of other confounding variables (employment status, smoking, obesity, self-reported “poor health,” history of MI, diabetes, high blood pressure, poor heart function, and number of coronary arteries that were diseased) as well as the influence of changes in the amount of exercise over time. Many of these confounding variables would otherwise have influenced the outcome measures.

The primary finding was that individuals who exercised the least (either “rarely or never” or “1-4 times per month) were at greatest risk for all 4 of the outcome measures. This isn’t surprising. This study confirms the findings of many previous studies.

The investigators also found that there was a sweet spot in terms of the frequency of exercise, where there was the greatest benefit, and lowest risk for the outcome measures. For all-cause mortality, cardiovascular mortality, and major cardiovascular events, the sweet spot was “2-4 times per week” of exercise. Either more or less exercise was associated with greater risk. For the outcome measure of non-fatal cardiovascular events, though, there was little association with the frequency of exercise. These results are the ones that received attention in the press this week.

On the face of it, though, these findings about frequency of exercise might be deceiving.

The investigators also reported on the amount of exercise–the number of hours spent per week in physical activity. Again, there appeared to be a sweet spot where the risk of the outcome measures was least: 10-11 hours per week, for all-cause mortality and cardiovascular mortality and ~9 hours per week for major cardiovascular events. In each of these cases, a broad range in the amount of exercise, perhaps 5 to 16 hours per week, conveyed a benefit over no exercise at all. And similar to their findings for the frequency of exercise, the investigators found very little relationship between the amount of exercise and the outcome measure of non-fatal cardiovascular events. I don’t recall seeing these results reported in the media.

Take Home Messages

There’s always more to the story than the headlines suggest.
This study is a longitudinal, observational study. It is not a prospective trial, or experiment. Because of the study design, some will be critical about the results and conclusions. But realize that, for a variety of reasons, there will never be a 10-year trial where one group is told to exercise and another group is told not to exercise. As a result, the current study is the type of investigation that will continue to inform us about the issue of “too much exercise.” We should pay attention to the results.
This study involves individuals with known CAD. And recall that the typical enrollee was male, age 61, overweight, current/former smoker, with a history of MI and high blood pressure. Remember to keep in mind, then, that the results and conclusions apply to THIS group of individuals. This study does NOT speak to the issue of “too much exercise” for healthy individuals.
The greatest risk for the outcome measures was identified for those individuals who exercised the least. This is the most important finding of the study. This finding is consistent with my personal experience caring for such patients. In this group of patients, like elsewhere in our society, we have a problem of too little exercise, not too much. Don’t lose sight of this message.
CAD is common. For the very large group of patients with CAD, there is a real and practical issue of how much exercise to recommend, or to “prescribe.” We want patients to derive the most benefit possible. And we want them to avoid unnecessary risk. This study suggests that “2-4 times per week” is the sweet spot for frequency of exercise but that a rather generous ~9-10 hours per week is the sweet spot for the amount of exercise. We should pay attention to these findings when we make recommendations to patients with CAD.
For patients with CAD who choose to exercise beyond these sweet spots, I’d advise caution. Obviously, “2-4 times per week” and ~9-10 hours is quite a bit of exercise, and possibly far in excess of what is recommended by the AHA guidelines. So there’s obviously room for considerable activity and sports participation up to these sweet spots. For any level of planned exercise, individuals with known CAD ought to work with their doctor(s) to settle on what is safe and appropriate given their particular circumstances, realizing that the benefits and risks will not be the same for every individual. Beyond these sweet spots, though, the motivation for additional exercise is probably something other than one’s health. In that situation, judgements need to be made about the trade-off between additional exercise and additional risk.

Related Posts:

1. Don’t Stop Running Yet!

2. Interesting Research from the ACC Meeting 2014

3. Do Elite Athletes Live Longer?

In the News: Marathoners and Coronary Plaque

April 3, 2014 By Larry Creswell, MD 18 Comments

Every so often, a scientific report about runners and heart disease really captures the attention of the media. About a week ago, a report in the March/April edition of Missouri Medicine entitled “Increased Coronary Artery Plaque Volume Among Male Marathon Runners” generated quite a bit of interest and discussion. I’ve written previously here at the blog about the general issue of the “heart healthiness” of long-distance running in a post entitled “Don’t Stop Running Yet!” I still feel that way. But let’s take a look, though, at this new article about marathoners and coronary plaque.

The report is written by a large group of very credible investigators from the Minneapolis Heart Institute, Integra Group, University of Colorado, Medtronic Inc., University of Minnesota, and the Mid America Heart Institute. Included in the group of authors is Kevin Harris, MD, who authored an important 2010 report on triathlon-related fatalities, William Roberts, the Runners World “Sports Doc” and medical director of the Twin Cities Marathon, and James O’Keefe, MD, a one-time triathlete who has been an outspoken critic in recent years of excess exercise.

The investigators report on a group of 50 male participants in the Twin Cities Marathon who had run at least 1 marathon per year for 25 years in a row. The average age was 59 years. None of these subjects had any history of heart disease or any current symptoms suggestive of heart disease. The runners underwent testing that included measurement of the height and weight, blood pressure, and resting heart rate; a 12-lead EKG; and blood tests for serum lipids and creatinine. The subjects also completed a questionnaire about historical lifestyle and risk factors. Each of the athletes underwent a high-resolution coronary computed tomographic angiography (CCTA) study. A control group of 23 sedentary men were identified from a contemporaneous group who were undergoing a CCTA study for some clinically-necessary reason and also underwent the other tests just like the runners did. The subjects and controls were similar in terms of: age, resting blood pressure, height, smoking history, serum creatinine, total cholesterol, and low density lipoprotein (LDL) levels.

Coronary artery plaque “lesions” were identified in both the runners and the controls: 95 lesions in 30 of the 50 runners, and 46 lesions in 12 of the 23 controls. The total volume of plaque was greater among the runners and this was also true for the amount of calcified or non-calcified plaque, as well. There was no difference in the lesion area, lesion diameter, or lesion length between the runners and controls.

Why is this all important? Because coronary plaque is generally associated with problems like heart attack. In clinical practice, we ordinarily discover coronary plaque when we search for a cause of a patient’s heart attack. Or, in recent years, we discover the plaque when an individual undergoes a screening test like a coronary calcium scoring CT scan. And we know from studies of individuals (not necessarily runners) who’ve undergone coronary calcium scoring CT scans that those with high calcium scores, indicating plaques, there is a greater risk of future heart attack. So it’s somewhat surprising that seemingly healthy long-time runners would have more coronary plaque than the sedentary controls.

On the bright side, despite being nearly 5 years older on average than the controls, the runners had significantly lower resting heart rate, weight, and body-mass index (BMI), less hypertension (high blood pressure), less diabetes, and an increased level of high density lipoprotein (HDL), the “good” cholesterol.

All of this news isn’t really new, though. These investigators first reported their findings at the 2011 meeting of the American Heart Association. It’s just now making its way into print, and into a rather unlikely and somewhat obscure medical journal for some reason. Missouri Medicine, the journal of the Missouri State Medical Association, even sent out a press release with advance copies of the article and accompanying editorials to a wide distribution list, all to take advantage of the lead-up to this year’s Boston Marathon. All pretty sensational, really. I can’t recall anything quite like this for research that was already more than 2 years old.

Given their findings, the authors conclude that “chronic excessive high intensity exercise” is the cause for the plaque build-up in the runners. They hypothesize that the mechanism is related to metabolic or mechanical stresses placed on the heart and coronary arteries during running that may be mediated by inflammation. The authors suggest, then, that “some runners” ought to “choose shorter, less exhausting challenges” in order to avoid this problem. On the face of it, this is a neat narrative, but….

1. Although the plaque volume (the total amount of plaque) was greater in the runners than the controls, the percentage of affected individuals in the running and control groups was not significantly different. Remember that 30 out of 50 (60%) runners had plaque identified and so did 12 out of 23 (52.2%) controls. In the statistical sense, those percentages are not significantly different. In terms of the most obvious, and perhaps most important, endpoint–the number of affected individuals with coronary plaque, the prevalence of coronary plaque–the study is essentially a negative study. Negative studies are hard to get published and I suspect this is why this report was published 2+ years after the study was completed.

2. If running was the cause of the plaque build-up, then why did only 60% of the long-time runners have this problem? And why did 52.2% of the controls have this problem, assuming that they were truly sedentary? Obviously the “cause” of plaque build-up in the coronary arteries is multifactorial. The authors can’t have it both ways: running cannot be responsible in the runners yet not responsible in the controls. For the runners, the real question is: what unmeasured variables might account for the finding of coronary plaque. We simply don’t know.

3. What is the consequence of having asymptomatic coronary plaque in a long-time runner? We don’t know. The current study doesn’t address this issue and to my knowledge, no study has. I’ve certainly heard from long-time endurance athletes who’ve been found to have coronary plaque, or elevated score on a coronary calcium scoring CT scan, who ask about the significance of the finding. We obviously need studies to find out what happens to such athletes.

4. What about….other endurance sports? And women? And younger athletes? There are just many, many questions left to be answered.

So, what’s the runner to do? I would still suggest that you not stop running. There’s every reason to believe that exercise is a healthy pursuit and there’s every reason to believe that exercise leads to better longevity, even for long-time endurance athletes. But stay informed. The general issue about the possibility of too much exercise is receiving a lot of attention. More studies are sure to come. And little by little, we’ll piece together the information that will help us determine if there is some sort of “sweet spot” in terms of the amount of exercise that is most heart-healthy.

Two articles on this topic caught my eye this week. Both are good reading. Amby Burfoot, the long-time editor at Running World and winner of the 1968 Boston Marathon, wrote an online piece for his magazine entitled “Heart Risk? Marathoners Have Increased Artery Plaque.” Interestingly, Amby learned last spring that he falls into the category of long-time runners with an (asymptomatic) high coronary calcium score. The second article was by Kevin Helliker in the Wall Street Journal, entitled “Why Runners Can’t Eat Whatever They Want.”

Related Posts:

1. Don’t Stop Running Yet!

2. More on Long-term Cardiac Risk and Endurance Sport

Sergei M. Grinkov, Figure Skater, 1967 – 1995

September 29, 2013 By Larry Creswell, MD 1 Comment

At the time of his death at age 28 in 1995, Russian Sergei Grinkov was at the top of his career in figure skating. He and his wife, Ekaterina Gordeeva, had won four world doubles figure skating championships and were the Olympic champions in 1988 and 1994.

While skating during a practice session in Lake Placid on November 20, 1995, Grinkov became light-headed, slumped to the ice, and then lost consciousness. His coach recognized the urgency of the situation and provided CPR almost immediately. EMS personnel arrived within minutes and inserted a breathing tube. But despite their efforts for more than an hour, Grinkov never regained a heartbeat and died later at the Adirondack Medical Center.

An autopsy showed extensive coronary artery disease (CAD), with nearly occlusive blockages affecting two of the three main coronary arteries. Moreover, there was significant enlargement of the heart. The pathologist concluded that Grinkov had suffered from an acute myocardial infarction, seemingly unrecognized, sometime during the 24 hours preceding his death and then suffered a fatal arrhythmia at the ice rink.

Grinkov’s death was obviously unexpected. In retrospect, it was learned that Grinkov had long-standing, untreated high blood pressure, with typical diastolic blood pressure measurements of more than 110 mm Hg. This was thought to contribute to the marked enlargement of his heart. According to reports, though, the high blood pressure measurements had often been attributed simply to “nerves.”

It also turns out that Grinkov’s father, Mikhail Grinkov, died at age 52 after his fourth heart attack. But like Sergei, his father had none of the typical risk factors for CAD. These unusual facts caught the attention of Johns Hopkins cardiologist, Pascal Goldschmidt, MD, who was able to study a sample of Grinkov’s blood and find through DNA analysis that he carried a variant of a platelet antigen gene that we now know as PLA-2 or the Grinkov factor. That variant, present in about 20% of the general population, is now known to be associated with both heart attack and stroke at an earlier age than the general population.

George W. Bush Gets a Stent

August 21, 2013 By Larry Creswell, MD 1 Comment

We learned from news reports earlier this month that former President George W. Bush was treated with a coronary stent for a blockage in a coronary artery that was discovered during his annual medical check-up. Of course, a great many Americans are treated each day for coronary artery disease (CAD), but Bush’s case draws my attention not only because he’s the former President but also because he’s known to be physically active, especially with cycling.

Bush’s Medical History

The fine details of Bush’s most recent health matters haven’t been made public, and might never be. But we know that while President from 2001 to 2009 he enjoyed comprehensive medical check-ups performed at the Bethesda Naval Medical Center. Each year, short statements were issued by the White House that summarized the President’s health. We can take a look back at some of that reporting.

Before taking office, the President received annual medical check-ups from Dr. Kenneth Cooper at the Cooper Clinic in Dallas, Texas. We know that, at the time he took office in 2009, he had no heart problems and no significant family history of heart disease. He occasionally smoked a cigar, did not drink alcohol, and had typical caffeine intake in the form of diet soft drinks and coffee.

From his examination at age 58 in 2004, we know that: he was 6 feet tall, weighing 200 pounds; his body fat was 18.25%; his resting heart rate was 52 and the blood pressure was 110/60; and the total serum cholesterol level was 170 mg/dL, with a decrease in the LDL (bad cholesterol) and increase in the HDL (good cholesterol) from one year previously. He was noted to have mild calcification of the coronary arteries (presumably based on a screening cardiac CT scan) and both aspirin and a cholesterol-lowering agent were prescribed. At the time, he was running 7 1/2 minute miles on the treadmill and was cycling several times per week.

In 2005 we learned that the President’s weight had decreased by a few pounds and the blood pressure and resting heart rate remained low. He underwent an exercise treadmill test that was normal and his doctors concluded that he was at “very low risk of coronary artery disease.” By 2005 Bush had given up running because of difficulties with knee pain, but continued to be active with cycling and weightlifting.

In 2006 at age 60 he was noted to have an EKG without worrisome abnormalities and a normal stress echocardiogram. Doppler ultrasound studies of the arterial blood supply to the legs was normal and a screening ultrasound of the abdomen showed no evidence of abdominal aortic aneurysm. Laboratory values included: total cholesterol 174 mg/dL, HDL 60 mg/dL, LDL 101 mg/dL, triglycerides 61 mg/dL, and normal values for C-reactive protein (CRP) and homocysteine. Interestingly, it was reported that he was taking no prescription medications despite the 2004 statement about the recommendation for a cholesterol-lowering agent. On the basis of the available information, the President was thought to have “low” to “very low” coronary artery disease risk.

The Coronary Stent

As we all know, Bush left office in 2009. Since then, his medical affairs have been private. So, fast forward to 2013….

We know that Bush went recently for his annual medical check-up at the Cooper Clinic and the following day at Texas Health Presbyterian Hospital was treated with a coronary stent for a blockage in a coronary artery that had been discovered duringn his evaluation. The details have not been made public, but it’s probably fair to assume that he underwent a stress test that was abnormal and that coronary arteriography was organized for the following day, with implantation of the coronary stent at the same setting.

The fact that Bush was treated with a stent for the coronary artery blockage has created a bit of a stir in the medical community. For those who are interested you can read more at:

“Did George W. Bush really need a stent?,” an article by Larry Huston in Forbes.

“The George W. Bush stent case: An incredible teaching opportunity on the basics of heart disease,” a blog piece by Dr. John Mandrola.

“Heart stents still overused, experts say,” an article by Anahad O’Connor at NY Times Well.

Basically, the controversy revolves around the appropriate treatment for asymptomatic patients–those without chest pain, heart attack, etc.–or those with so-called “stable” symptoms–for instance, chest pain with exertion–who are found to have blockage(s) in the coronary arteries. In truth, there has been no public reporting on whether or not Bush had any such symptoms, either with exertion or at rest. And there has been no updated reporting on Bush’s physical activity level or other relevant risk factors for CAD. But information from the best scientific studies suggests that asymptomatic patients and those with “stable” CAD fare no better, with respect to heart attack, stroke, or death, with a stent than without, so long as the best possible medical therapy is provided.

At any rate, this controversy will be one for our community of heart professionals to discuss and sort out.

What Can We Learn?

From the athlete’s perspective, though, Bush’s story reminds us of the importance of coronary artery disease as we age, even if we remain physically active. A few thoughts….

1. The discovery of CAD is almost always a surprise….particularly for an athlete. Nobody is immune from this disease, even if remaining physically active helps guard against it.

2. There is a set of well-established risk factors for CAD. I’ve talked about this issue previously here at the blog. Let’s remember that there are some risk factors that, unfortunately, can’t be modified: increasing age, being male, and having a family history of early CAD. Other risk factors are under our control: obesity, high blood pressure, smoking, abnormal serum cholesterol and lipid levels, diabetes, and physical inactivity. Adult athletes should know where they stand with respect to these risk factors and work to improve any that can be modified favorably. An ongoing relationship with a healthcare provider will offer the necessary framework for this. Periodic measurement of the blood pressure and testing of the serum cholesterol/lipid levels every 5 years are recommended.

3. Our personal situation with CAD will likely change over time. The process in which plaque builds up in the coronary arteries can begin early in our lives. But this process is often progressive as we age. That’s why we say that increasing age is a risk factor. Bush’s story illustrates just how this can happen. In 2004-2006 he had very favorable clinical and laboratory data regarding his risk of CAD, including a normal stress echocardiogram in 2006. Yet today we know that an important blockage had formed, or more likely progressed, in the interim. It’s important, then, to periodically re-visit our circumstance with CAD.

4. Warning signs are important. Important blockages in the coronary arteries often lead to symptoms of angina–chest pain/discomfort or perhaps difficulties with breathing. When angina occurs with exertion, we call it exertional or stable angina. When angina occurs at rest, we call it unstable or rest angina. Either form of angina should prompt timely evaluation. That evaluation may take the form of stress testing or coronary arteriography to look for blockages in the coronary arteries. Unfortunately, there are some patients whose first sign of trouble is a heart attack, or myocardial infarction. This can occur in athletes and non-athletes, alike.

Related Posts:
1. Coronary Artery Disease: The Essentials
2. Two Stories, Two Endings, a blog post about endurance athletes and CAD.
3. In the News: Coronary Plaque Build-up in Marathoners

Follow-up on Andrew Naylor, Victim at IMNY 2012

August 6, 2013 By Larry Creswell, MD 1 Comment

I can share some follow-up about Andrew Naylor, the triathlete who died during the swim portion of the Ironman New York triathlon on August 11, 2012.

Recall that Naylor, 43 years old, was rescued near the conclusion of the 2.4-mile swim in the Hudson River by watercraft EMS professionals, received CPR, was transferred to shore and then on to a New Jersey Hospital where he was pronounced dead.

This athlete’s death received considerable attention in both the American and worldwide press, due not only to the high-profile nature of the innagural Ironman event in New York but also the fact that the athlete was originally from the U.K. and had travelled from Hong Kong to participate in the event.

Although an autopsy was performed after the incident, the findings were not made public–or at least they hadn’t been reported in the American media–and there has been little follow-up reporting on this incident until last week. At an inquest held in the U.K., and reported in The Daily Mail and other outlets, it was disclosed that the autopsy showed severe blockage in one of the coronary arteries that was responsible for a “heart attack” during the swim. The coroner recorded the death as accidental. Experts testifying at the inquest suggested that Naylor was probably unaware of his heart condition and that he would probably not have died if he had not participated in the triathlon.

Let me start by saying that there are often details lost in translation in a case like this. The original autopsy report, in its entirety, would certainly be valuable and worth sharing.

Several features of this case are interesting, though. First, recent investigation into the causes of death during running events has shown that “heart attack”–or, acute myocardial infarction (MI), in medical terminology–is rarely responsible, even if athlete victims sometimes do have evidence of blockages in the coronary arteries, or coronary artery disease (CAD). For triathlon, specifically, less autopsy information has been made available, but I’m not aware of other cases of triathlon race-related acute MI. Instead, the race-related cardiac deaths are related to sudden arrhythmias–an electrical problem–rather than sudden, complete blockage of a coronary artery–a plumbing problem.

A second interesting feature of this athlete’s death relates to the swim itself. I’ve written previously here at the blog about the efforts this year by World Triathlon Corporation (WTC), the producers of the Ironman-branded triathlon events, to improve swim safety, particularly during the race start. Traditionally, the Ironman triathlon events have begun with a so-called mass start, in which the entire group of participants, sometimes numbering more than 2000, starts the race at the same time when the gun goes off. As you might imagine, it would be difficult to identify and rescue a lifeless swimmer at the beginning of a race that began with a mass start. In the case of last year’s Ironman New York triathlon, though, the participants began their race by jumping into the Hudson River from a barge, in somewhat of a rolling start. WTC is trialing a variety of swim start methods at their events this summer to determine what might be best from a safety and logistics standpoint. It’s worth mentioning that the small handful of athletes who have died over the years during an Ironman swim, much like Naylor, were rescued long after the start of the race.

The third interesting feature of this case is the fitness level of the victim. The myth is often perpetuated that the athletes who die at running or triathlon races are somehow not fit or unprepared for the race in some way. Naylor was an exceptional athlete, even if he wasn’t a long-time triathlete. He was a talented runner, with a personal-best time of 2:32 in the 2009 London Marathon that was good enough for 74th place.

A couple thoughts about prevention….and these thoughts come on a day where we’ve learned that former President George W. Bush had a coronary stent placed because of CAD discovered during an annual check-up yesterday. As we age, our risk of having unrecognized CAD increases. That likelihood is related to a set of risk factors such as sex, smoking history, blood pressure, blood cholesterol/lipid levels, etc. And it’s possible to have important CAD but have no typical symptoms such as exertional chest pain or discomfort. That’s the rationale for screening tests like a stress test or a calcium scoring cardiac CT scan. As one of the doctors who testified at Naylor’s inquest said, this particular athlete’s problem with CAD was very treatable had it been known.