Zoobiquity (19 page)

As you’ve probably felt yourself, our hearts react when something startles us, whether it’s an unexpected balloon pop or the ground rumbling to life beneath our feet. Our bodies sometimes respond before our brains can sort out the lethal threats from the harmless jolts. And armchair athletes, take note: you don’t need to be actually playing a game for your ventricles to act out the agony of defeat.

Take the 1998 soccer World Cup. England and Argentina had clawed their way up the ladder and were facing off for the chance to compete against the Netherlands in the quarterfinals. While international soccer rivalries are always fierce, this pairing had special resonance for the fans. Sixteen years earlier, the two countries had gone to war over the Falkland Islands. Although Britain officially won the skirmish, many Argentines refused to acknowledge defeat. Every time the two teams subsequently met on the soccer pitch, it turned into a grudge match. This game (which featured a young David Beckham, fouling out after kicking another player in full view of the ref) ended in a tie. The winner would be decided by a penalty kick shoot-out.

One by one, the players lined up in front of the goalie to take their shots. The score had reached Argentina 4, England 3 when the English
player David Batty jogged onto the field. He took a few short sharp strides toward the ball … made contact … and sent it soaring. But between Batty’s Puma cleats and the expanse of the goalposts, the ball met the gloved fingers of goalkeeper Carlos Roa—and the winner was Argentina.

The Argentine fans erupted in relieved, joyful mayhem. But English fans watching on TVs in pubs back home gaped in stunned horror.
And that day heart attacks across the United Kingdom
increased by more than 25 percent
.

Multiple European studies have corroborated this unusual link between spectator stress and heart health.
Interestingly, soccer matches that end in penalty kicks—and, worse, portentously named “sudden-death” shoot-outs—are the deadliest.
Richard Williams, a sportswriter for the
Guardian
newspaper in London, has called them sadistic, “the modern equivalent of a flogging in the market square.” In fact, penalty kick shoot-outs are so reliably anxiety-producing that soccer groups from the Fédération Internationale de Football Association (FIFA) to the American Youth Soccer Organization (AYSO) have considered banning this form of tie breaking.

Having stood tensely, hands clenched to my chest, blood pressure rising, at my own children’s championship bouts (fencing is their game), I appreciate how this proposed change might diminish dangerous heart rhythms in the nervous parents and grandparents squirming in nylon spectator chairs on the sidelines.

Until as recently as the mid-1990s, the relationship between the heart and the mind was only murkily understood. Among many physicians, the idea that emotions could cause actual physical effects within the architecture of the heart was viewed with nearly the same sideways glance as an interest in healing crystals or homeopathy. Real cardiologists concentrated on real problems you could see: arterial plaque, embolizing blood clots, and rupturing aortas. Sensitivity was for psychiatrists.

A shift came in the 1990s. A team of Japanese cardiologists noticed that the hearts of some patients who came to the emergency room with severe, crushing chest pain after moments of extreme emotional stress were not normal. Their EKGs indicated that they were having a heart attack. But when the doctors injected dye into the heart vessels,
they found perfectly healthy, “clean” coronary arteries—no signs of blockage. The only unusual finding was a strange lightbulb-shaped bulge at the bottom of the heart. The shape reminded these doctors of the rounded
takotsubo
pots Japanese fishermen use to catch octopuses. So that’s what they named it.
Takotsubo cardiomyopathy was a new description—direct, physical evidence that severe stress (fear, grief, agony) alone could alter the heart’s chemistry, shape, and even the way it pumps blood.
^†

The condition quickly acquired a nickname, “broken-heart syndrome.” When it was newly named and freshly in vogue, takotsubo cases cropped up in ERs all over the country. One young woman had watched her beloved dog run into traffic and she arrived at an ER covered in blood, clutching her limp pet
and
her chest. (Like most takotsubo patients, she was treated and survived, although some do die.) Another patient was thirty minutes into an intense 3-D blockbuster when extreme palpitations, shortness of breath, and repeated vomiting forced her to flee the theater. Her doctors diagnosed takotsubo.

To understand how any intense emotion can physically harm your heart, it helps to know some cardiology basics. Under normal circumstances, your heart is probably the most important thing you never pay attention to. Like the perfect valet, it’s toiling away in your chest right now, meticulous yet unseen, as it has since the twenty-third day after your father’s sperm met your mother’s receptive egg.
Every year your heart beats 37 million times, pumping 2.5 million liters of blood.

Like a house, the heart contains both plumbing and electricity. Plumbing moves blood around your body’s pipes—its arteries and veins. Like the main lines carrying water into a house and the sewer lines carrying it out, these arteries and veins can get blocked, with devastating results. Sudden myocardial infarction, for example, the classic heart “attack,” is caused by a clog in the blood supply to the heart itself. Ruptures and
bursts in the plumbing can be devastating, too. When large arteries tear or rip open, the result is often fatal.

But a whole other category of cardiac woe comes from inborn or acquired damage to the electrical system. Its health can be discerned from an electrocardiogram (EKG)—the jagged, steep slopes that shoot up and down across graph paper or scroll along a computer monitor. You’ve seen these representations of the heart’s steady current countless times on medical dramas and in pharmaceutical ads. And you’ve heard audio translations of that electricity, too. When wired to an alarm signal, the clockwork electrical current creates that stable
beep … beep … beep
that indicates all is well. Nothing calms a nervous on-call doctor better than news that her patient’s heart is beating in that pattern. We call it normal sinus rhythm.

Tragically, however, this steadfast, pulsing electrical system fatally short-circuits in seven hundred human hearts every day in the United States
^‡
and in many thousands more worldwide. The dependable throb suddenly races out of control or becomes floppy and unpredictable. When you listen with a stethoscope, the
lub-dubs
take on an anxious, irregular, and muffled quality. When the beat speeds up—a condition we call ventricular tachycardia, or VT—it’s unmistakable on the EKG. The assembly-line predictable peaks and valleys of normal sinus rhythm loosen into rolling, closely spaced “hills.” The lopsided, irregular rhythm, on the other hand, is called ventricular fibrillation (VF). It’s equally easy to recognize. The jagged visual static lurches across the monitor or graph paper with a sickening randomness.

To those in the know, the sounds and sights of VT and VF instantly convey one thing: the urgent need for someone to place shock paddles on the sufferer’s naked chest; call “All clear!”; and send a few hundred joules coursing toward the malfunctioning heart. If this specialized electrical therapy doesn’t arrive immediately, the EKG landscape will devolve from the hilly and craggy warning shapes to the infamous horizontal configuration we refer to—with dreaded respect—as a flatline. The shift in rhythm from “life-sustaining” to “malignant” causes the heart’s pumping to decrease or stop. With more precision than poetry, doctors call
this electrical cardiac catastrophe sudden cardiac death (SCD or sudden death for short).
^§

Cardiac death can come rather predictably after years of plaque buildup in the brittle arteries of an overweight smoker. Or it can strike with a shock as happens when a high school athlete drops dead from a congenital defect he didn’t know he had. The “final common pathway” is the same. It’s an electrical malfunction, the shift from a life-sustaining, normal rhythm to the death-heralding arrhythmia of VF or VT.

But certain victims of sudden cardiac death have no previously identified heart problems. In these otherwise healthy patients, a massive emotional jolt alone converts the cardiac rhythm from safe and steady to malignant and deadly. Startled, terrified, horrified, or aggrieved, these patients spew stress hormones, including adrenaline, from their highly activated central nervous systems. These catecholamines gush into the bloodstream. Like a chemical cavalry they appear on the scene, ready to boost strength and stamina to aid an escape. But instead of rescuing the patient, this neuroendocrine burst may rupture plaque deposits, lodge a blocking clot in an artery, and cause a fatal heart attack. It might trigger an extra beat at just the wrong moment and send the heart into VT. And in huge amounts and all at once, the chemicals themselves can be enough to poison muscles, including some of the two billion heart muscle cells in a human ventricle. In these patients, the weapon is essentially the reactive nervous system itself, fully loaded with dangerous catecholamines, waiting for terror to pull the trigger.

That’s what happens with takotsubo. Whether activated by lost love or war, geological heaving or a ball game, the catecholamine torrent damages heart muscles, creates the octopus pot–shaped bulges, and sometimes causing dangerous arrhythmias.

But takotsubo is only a small part of the story, as I figured out when I started comparing notes with veterinarians.

• • •

Dan Mulcahy is the kind of guy you’d want along if you ever found yourself stranded in a Category 5 blizzard with the gas gauge on your Arctic Cat F1000 Sno Pro on empty. Part MacGyver, part Davy Crockett, with a full mustache, wire-rimmed glasses, and a basso profundo rumble, Mulcahy occupies that rare and desirable zone on the Venn diagram where superhero and supernerd overlap.
At forty-one, after two decades as a microbiologist studying fish diseases, he switched careers and became a wildlife veterinarian. When I met him, he was working in Alaska, tracking and treating walruses, tundra swans, caribou, and other endangered northern creatures. His job requirements ran from the delicate surgery of installing satellite transmitters in spectacled eider ducks to the bravura choreography involved in collaring a half-ton polar bear as part of a worldwide team monitoring and trying to preserve these animals’ disappearing hunting grounds.

When we met, we quickly discovered that we shared a professional and personal fascination—with the ways death lurks in the interplay of the heart and the mind. We bonded, as only two doctors can, by trading ghoulish yet exciting tales of fear-based sudden death we’d seen and treated.

Mulcahy’s interest had a poignant and frustrating root: every once in a while, an animal—especially, for some reason, certain birds—would silently die in his hands after being chased, captured, and handled. Sometimes they seemed to get through the medical procedure just fine, only to weaken and die the minute they were reintroduced to a new habitat. Mulcahy knew it wasn’t anything he was doing wrong. In fact, his supervision made these important surveys carried out by field biologists much safer for the animals.
^‖

Veterinary textbooks describe a heartbreaking yet eerily predictable reality: animals consistently die from the stress of chase and handling. Veterinarians call it capture myopathy.
The term describes a syndrome
of illness and death seen in animals who are terrified, captured, or running for their lives from predators, hunters, or well-intentioned but underinformed wildlife biologists. Sometimes the affected animals expire on the spot, crumpling to the ground like a maiden in a gothic novel. Sometimes they endure for a few hours after the stressful incident before expiring. Other times they linger for days or weeks, listless and depressed, unable to walk or even stand, refusing food and water, until they die. In any case, postcapture death rates are disturbingly consistent.
^a
It’s usually about 1 to 10 percent of a population, sometimes as high as 50 percent, depending on the species.

Capture myopathy was first noticed by human hunters a hundred or so years ago. It was initially thought to be an exclusive syndrome of big prey, like zebra, buffaloes, moose, and deer. These animals often died mysteriously after a hearty chase, even when the hunters’ weapons had left no mark on their bodies.

But then ornithologists started noticing capture myopathy’s fingerprint on the muscles of birds from tiny parakeets to lanky whooping cranes to brawny, ostrichlike rhea. Marine biologists described cases in dolphins and whales.
Fishermen trawling for wild Norway lobsters off the coast of Scotland saw it pinch their bottom line. The meat of chased lobsters was discolored and had an unappealing, watery texture. It looked spoiled—in a way, it was deader than dead. It rotted faster. At the market, it was rejected on sight.
^b

Soon wildlife veterinarians realized that pursuit—chasing without rest—was killing animals from every corner of the food web. In South Africa, where animals frequently need to be moved around to accommodate national park boundaries and human encroachment, capture myopathy is a serious health threat and a major cause of death.
Special
care is taken when capturing sensitive giraffe, which aren’t as a rule accustomed to running long distances and are also known for their anxiety.
Deer, elk, and reindeer in North America have capture myopathy mortality rates from relocation and hunting as high as 20 percent. The Bureau of Land Management’s
yearly helicopter roundups of wild mustangs in Nevada result in the deaths of a certain number of horses every year from capture myopathy.

Fueling an animal’s escape from threat is a powerful neurochemical response: a catecholamine dump. Pushed beyond a safe limit, though, catecholamines can overwhelm the skeletal and cardiac muscles and cause them to break down. When significant chunks of skeletal muscle are degraded, massive amounts of their proteins are released into the bloodstream. These proteins can overpower and eventually shut down the kidneys. The medical name for this muscle damage is rhabdomyolysis. “Rhabdo”—as it’s widely known in clinical shorthand—can be fatal, but if it is caught early, it can be effectively treated with hydration and supportive care. In people, it’s most often seen in extreme cases of trauma and immobility: an earthquake victim pinned under steel beams and rubble, for example, or a motorcyclist thrown from his bike with multiple skeletal fractures and overwhelming soft-tissue injuries. Veterinarians and physicians alike know that a telltale sign of rhabdo is rust-colored urine—tinged that shade by the overflow of toxic muscle enzymes that the kidneys couldn’t filter out.