summarize this "One downside of my profession is that too much knowledge can
become its own kind of curse. As I delved back into the practice of medicine,
after my hiatus in the business world, it dawned on me that I already know
how I am likely to die: I seem destined to die from heart disease.
I wonder what took me so long to get the hint. When I was five, my
father’s older brother Francis—his favorite of eight siblings—died of a
sudden heart attack at forty-six. When my own brother Paul was born two
days later, my grief-stricken father chose Francis as his middle name. Just as
certain names run in families, a propensity for early cardiovascular disease
seems to run in mine. Another uncle suffered a fatal heart attack at forty-two,
while a third made it to age sixty-nine before his heart killed him, which is
perhaps more typical but still way too young.
My dad is lucky, because he has lived to the ripe old age of eighty-five (so
far). But even he has a stent in one of his coronary arteries, a souvenir of his
own minor event in his midsixties. He felt chest pain one day at the limestone
quarry where he worked, and ended up in the ER, where it was determined
that he had had a recent infarction. The stent, a little sleeve of metal wire, was
put in a year or so later. I’m not actually convinced that the stent did anything
—he was not experiencing symptoms at the time it was placed—but perhaps
it scared him enough to be more diligent with his medications and his diet.
So even though my cholesterol profile is excellent, and I eat sensibly,
never smoke, have normal blood pressure, and rarely drink alcohol, I’m still at
risk. I feel like I’m trapped in that Charlie Munger anecdote, about the guy
who just wants to know where he’s going to die, so he’ll make sure never to
go there. Unfortunately, too often heart disease finds you.
When I was in medical school, my first-year pathology professor liked to
ask a trick question: What is the most common “presentation” (or symptom)
of heart disease? It wasn’t chest pain, left arm pain, or shortness of breath, the
most common answers; it was sudden death. You know the patient has heart
disease because he or she has just died from it. This is why, he claimed, the
only doctors who truly understand cardiovascular disease are pathologists. His
point: by the time a pathologist sees your arterial tissue, you are dead.
While mortality rates from those first, surprise heart attacks have dropped
significantly, thanks to improvements in basic cardiac life support and timesensitive interventions such as cardiac catheterization and clot-obliterating
drugs that can halt a heart attack almost in its tracks, they are still fatal
roughly one-third of the time, according to Ron Krauss, senior scientist and
director of atherosclerosis research at Children’s Hospital Oakland Research
Institute.
Globally, heart disease and stroke (or cerebrovascular disease), which I
lump together under the single heading of atherosclerotic cardiovascular
disease, or ASCVD, represent the leading cause of death, killing an estimated
2,300 people every day in the United States, according to the CDC—more
than any other cause, including cancer. It’s not just men who are at risk:
American women are up to ten times more likely to die from atherosclerotic
disease than from breast cancer (not a typo: one in three versus one in thirty).
But pink ribbons for breast cancer far outnumber the American Heart
Association’s red ribbons for awareness of heart disease among women.
My uncles’ deaths remain a mystery to me. They lived in Egypt, and I
have no idea what their blood work looked like or, more importantly, what
kind of shape their coronary arteries were in. I’m pretty sure they smoked, but
perhaps if they had had access to better medical care they too might have
survived their heart attacks, as my father did. Or perhaps their fates were
inescapable, tied to their genes. All I know is that forty-two seems really
young to keel over from a heart attack.
I’d known about my uncles all my life, but the implication of their stories
only really hit me in my midthirties, when I became a father for the first time.
All of a sudden, the awareness of my own mortality crashed over my head
like a rogue wave, coming out of nowhere on one of my long swims. This
book probably wouldn’t have been written if not for that family history.
Like most thirty-six-year-olds, Not-Thin Peter scarcely gave a thought to
heart disease. Why should I have? My heart was strong enough to have
propelled me across the twenty-one-mile-wide Catalina Channel, working
steadily for more than fourteen hours, like a Mercedes diesel engine purring
along smoothly inside my chest. I was in great shape, I thought. But I was
nevertheless worried, on account of my family history. So I insisted that my
doctor order a CT scan of my heart, and it wound up changing my whole
outlook on life.
The scan was calibrated to detect calcification in my coronary arteries, a
sign of advanced atherosclerosis. The results showed that I had a calcium
“score” of 6. That sounds low, and in absolute terms it was; someone with
severe disease could return a score well over 1,000. But for someone age
thirty-six, it should have been zero. My score of 6 meant that I had more
calcium in my coronary arteries than 75 to 90 percent of people my age. As I
dug deeper into the pathology of this disease, I was dismayed to learn that it
was already fairly late in the game. A calcium score is treated as a predictor
of future risk, which it is, but it is also a measure of historical and existing
damage. And I was already off the charts. I was only in my midthirties, but I
had the arteries of a fifty-five-year-old.
I was upset by this revelation, although knowing what I know now, it’s not
at all surprising. At the time, I was overweight and borderline insulin resistant,
two huge risk factors that by themselves help create an environment that
fosters and accelerates the development of atherosclerotic lesions. Yet
because my calcium score was “only” 6, and my all-important LDL (“bad”)
cholesterol was “normal,” the medical advice I received was—wait for it—to
do nothing. Sound familiar?
Doing nothing is not my style, as you may have gathered by now. I sensed
that I was not on a good trajectory, and I needed to figure out how to change
it. My curiosity launched me on a years-long quest to truly understand
atherosclerosis. The story I uncovered, with the generous help of my mentors
Tom Dayspring, Allan Sniderman, and Ron Krauss (among others), all of
whom are world-renowned experts in cardiac pathology and/or the study of
lipids, was flabbergasting.
While heart disease is the most prevalent age-related condition, it is also
more easily prevented than either cancer or Alzheimer’s disease. We know a
lot about how and why it begins and the manner in which it progresses. While
it can’t exactly be cured or reversed the way type 2 diabetes (sometimes) can,
it is relatively easy to delay if you’re smart and you get on the case early. It’s
also the rare example of a chronic disease where Medicine 2.0 already does
focus on prevention, to some extent. We have a cabinet full of blood
pressure–and cholesterol–lowering medications that really do reduce the risk
of death for many patients, and we have blood tests and imaging tests (like
my calcium scan) that can at least give us a snapshot, however blurry, of
someone’s cardiovascular health. It’s a start.
In spite of how well we understand atherosclerotic disease and its
progression, and how many tools we have to prevent it, it still kills more
people than cancer in the United States each year, many of them completely
out of the blue. We’re losing the war. I don’t claim to have all the answers, but
I think this is at least partly due to the fact that we still have some major blind
spots in our understanding of what truly drives our risk for the disease, how it
develops, and most of all when we need to act to counter its momentum.
The fundamental problem, I believe, is classic Medicine 2.0: guidelines
for managing cardiovascular risk are based on an overly short time horizon,
compared to the time line of the disease. We need to begin treating it, and
preventing it, much earlier. If we could get it right, the potential payoff would
be huge: the high prevalence of male centenarians on the island of Sardinia,
for example, has largely been attributed to their ability to avoid or delay
circulatory disease. Fewer Sardinian men die from heart disease between the
ages of eighty and one hundred than anywhere else in Italy.
But we’re nowhere near that. Heart disease remains our deadliest killer,
the worst of the Horsemen. In the next few pages, I hope to convince you that
it need not be—that with the right strategy, and attention to the correct risk
factors at the correct time, it should be possible to eliminate much of the
morbidity and mortality that is still associated with atherosclerotic
cardiovascular and cerebrovascular disease.
Bluntly put: this should be the tenth leading cause of death, not the first."