AT 4.30 AM on 17 January 1994, millions of people in Los Angeles were
sleeping peacefully in their beds. One minute later, they were bolt upright as
the ground began to heave with a force that terrorised even the most jaded and
earthquake-weary West Coasters. One of the worst earthquakes to strike the US
rose up near Northridge, California, and sent shock waves ripping across the
state, twisting highways and crumbling buildings with horrifying ease. The walls
of houses undulated, chimneys collapsed and shattered windowpanes flew across
bedrooms as people in their nightclothes scrambled for the shelter of doorways.
“I live about eight miles from the epicentre,” remembers Robert Kloner, a
cardiologist at the Good Samaritan Hospital in Los Angeles. “There are only a
few times in my life when I thought I was going to die. This was one of
ٳ.”
Over a hundred other Californians had the same awful thought, but unlike
Kloner, they actually did die. Not because they were crushed by houses or struck
by debris, but because they literally died of fright. Two years ago, Kloner and
his colleagues reviewed the records of the Los Angeles county coroner’s
department for the week before the earthquake, the day of the earthquake and
corresponding control periods in 1991, 1992 and 1993. They found that on the day
of the quake, the coroner recorded five times more sudden cardiac deaths than
would ordinarily be expected, and this wasn’t because people were physically
exerting themselves as they dug themselves out of the rubble. “The typical story
was that a patient clutched his chest, described chest pain, and dropped over
dead,” says Kloner.
When Franklin D. Roosevelt said “the only thing we have to fear is fear
itself”, he meant it in a philosophical sense. But physicians know that the
fight-or-flight response that protects the body from harm can sometimes
backfire. “If you are terrorised by a God-awful stress, it can take you out,”
says Richard Verrier of Deaconess Hospital in Boston. “I don’t think you would
find a cardiologist who thinks it’s impossible to die of fright.”
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Most people who die from fear have a predisposing condition, such as unstable
cholesterol plaques on their blood vessel walls that can break open and cause a
fatal blood clot. These heart attacks can be sparked by fear but are
indistinguishable from those induced by, say, digging the garden or having sex.
But sometimes, in a tiny minority of cases, the terrorised brain of a healthy
person triggers the release of a mix of chemicals so potent that it induces a
cataclysmic influx of calcium into the heart cells, causing the heart to
contract so fiercely that it never relaxes again.
Accounts of death from fear fill the anthropological literature, as Walter
Bradford Cannon pointed out more than forty years ago in a remarkable paper
called “Voodoo Death” (American Anthropologist, vol 4, p 1). Cannon, a
Harvard Medical School physiologist, described how in many primitive cultures, a
curse from an all-powerful wizard or medicine man was enough to kill a believer.
Mostly, the death was slow and lingering, but sometimes the person simply
dropped down dead. So in New Zealand in 1845, a Maori woman died hours after
being told that the fruit she ate came from a taboo place. While more recently,
anthropologists in Haiti reported seeing witch doctors hold a hen atop a
possessed boy’s head. A circle of villagers then chanted, beat drums and pointed
bones at the hen, which drew the evil spirits out of the boy when it suddenly
squawked and died. Animals, it seems, can also be frightened to death.
When it comes to people, however, Cannon thought that fear-induced death was
limited to superstitious societies. Few people now agree with that view. And
given that millions of people suffer heart attacks each year, and around
one-third are sudden and fatal, anything that was responsible for even a small
per cent of these sudden death cases would still be a significant public health
threat.
Cat and mouse
“This is not a phenomenon which is buried in the ancient past,” says
neurologist Martin A. Samuels of Harvard Medical School in Boston, who is
researching the way the brain affects the heart and collects newspaper accounts
of death from fright as a hobby. Samuels recalls his cat coming across a field
mouse. The cat simply put its paw on the mouse’s tail and batted it about a bit.
Within twenty minutes the mouse died despite having no serious injuries.
“Animals commonly drop dead under these circumstances,” says Samuels, who wanted
to put the mouse in the freezer to save it for a cardiologist friend. (His wife
vetoed the idea.)
Scientists interested in understanding what causes death from fear have found
that it is a tricky subject to study. Obviously, you can’t do experiments
designed to scare people to death. In the past, such experiments have been
carried out on animals, but this is not acceptable today so researchers have had
to find other ways to explore this phenomenon. Sometimes they use “natural”
experiments such as the 1994 Los Angeles earthquake. Another of these was
provided by the Iraqi missile strikes on Israel during the Gulf War in 1991.
Almost the entire population took shelter in sealed rooms, gripped with fear as
they clutched their gas masks.
During the early hours of 18 January, when the first attack occurred, 147
deaths were recorded. In normal circumstances, based on previous years’ records,
only 93 deaths would have been expected during this time. Most of these deaths
were from heart attacks, and the increased mortality was limited to the first
day of missiles. Possibly this is because people who were highly susceptible to
sudden death succumbed right away.
In another study, coroners in Cleveland examined the hearts of 15 assault
victims who died even though their assailants hadn’t wounded them badly enough
to fatally injure their internal organs. “You’re kind of left wondering, how
exactly did the beating cause the death?” says Charles Hirsch, now chief medical
examiner for New York City. He and his colleagues looked at the hearts of these
victims during autopsies and compared them with age-matched controls. In 11 of
the victims, they discovered that many fibres from the heart muscles were
torn.
A typical heart attack from a cholesterol clog or blood clot would not have
torn those fibres. Hirsch recognised these as fear lesions because of some
rather sadistic animal experiments carried out in the 1950s and 60s. “People
actually did do these experiments, frightened animals to death, even primates,”
marvels Samuels. “If you read some of the old experiments, it’s quite
hair-raising.” In one experiment, a researcher forced rats to listen to
audiotapes of noisy fights between rats and cats, says Verrier, which was for
the rats “a horrible experience”.
Adrenaline rush
Terror, or indeed any extreme emotional response, including great joy, makes
the fight-or-flight response kick in. The brain’s hypothalamus tells the adrenal
glands to start pumping catecholamines such as adrenaline and noradrenaline into
the bloodstream. These constrict blood vessels and increase the ability of the
blood to coagulate and thereby reduce bleeding (in case you don’t run fast
enough and a wild beast chomps on your leg), dilate your pupils so that you can
see better, increase the heart rate, divert blood from the gastrointestinal
tract to the muscles, and so on. The brain also stimulates organs by causing
nerves to secrete catecholamines directly into them.
It is these nerves that have the potential to inflict the most damage. Heart
cells have a channel that lets calcium in, which is regulated by catecholamines.
When nerves release catecholamines directly into the heart, these channels open
like floodgates and the cells fill with calcium, triggering the contraction of
the muscle fibres. The theory is that a severe fright sometimes makes nerves
release massive amounts of catecholamine. This causes so much calcium to flood
into the fibres that they seize up completely. “The heart has contracted like a
little focal rigor mortis,” explains Samuels. “It has turned to stone in
seconds.” Death is almost instantaneous as the muscle damage sends the heart
into a chaotic arrhythmia.
That the brain’s emotional state can wreak such damage on a faraway organ is
a disturbing idea. Worse still, this can happen even in the absence of great
emotion, if a stroke or some sort of stimulus hits the right spot. Neurologists
have long noticed strange electrocardiogram readings in people with epilepsy or
brain damage from injuries such as strokes. Samuels remembers one epileptic
patient who would occasionally turn his head to the right and say mildly,
“something’s funny”. Although he otherwise seemed fine, brain scans showed he
was having an electrical seizure on that side of his brain. When physicians
hooked him up to an electrocardiogram, they saw that their patient was also
suffering intense cardiac arrythmias that subsided once the seizure stopped.
“This is a guy who was a millisecond from sudden death,” remembers an
incredulous Samuels.
In extreme cases, the brain releases so many catecholamines into the heart
that it bleeds. Samuels remembers one distraught young man who lingered on a
ledge on a hospital roof for hours negotiating with counsellors before finally
jumping. It was a personal tragedy for his friends and family, a public
relations nightmare for the hospital—and a fascinating autopsy case for
Samuels. “The cause of the death was trauma. Yet when we looked at the heart,
there were hundreds of haemorrhages,” he remembers. “The heart was just studded
with them. I thought I had the first such case in the world.” But when he
presented it at a scientific meeting, someone told him about similar findings
from a study years ago on a man who jumped off the Eiffel Tower. Fear of
contemplating jumping to your death probably causes these lesions.
Again, the brain can do this even in the absence of any great fear. The chess
master José Raúl Capablanca had a history of hypertension when he
died in 1942 at the Manhattan Chess Club of a massive stroke. At his autopsy,
the physicians noted numerous haemorrhages in his heart tissue, but no one
realised their significance. Last year, Orlando Hernándes-Meilán
at the Institute of Neurology and Neurosurgery in Havana reviewed the autopsy
notes and concluded that the stroke damaged his heart by activating the
sympathetic nerves.
Cocaine can also stimulate the brain to over activate these nerves, says
Samuels. “Cocaine imitates fright. Cocaine-induced deaths are almost certainly
due to this.”
Deadly debris
People might think of death by cardiac rigor mortis or bleeding as a sort of
heart attack. They wouldn’t be wrong, but there is an important difference
between these and other cases of heart attack: in most heart attacks, the muscle
fibres don’t break or bleed. Rather than seizing up, the heart is starved of
oxygen.
These more common types of heart attacks can also be triggered by fear. The
release of hormones causes arteries to clamp down, for example, and platelets
start to aggregate in readiness for clotting. Blood rushing through narrowed
vessels also generates shear forces against cholesterol plaques stuck to blood
vessel walls. A plaque is like a little bubble of collagen covering an inner
layer of cholesterol and macrophages. If it breaks, the debris can cause a clot
and block blood flow to the heart muscle.
For someone who already has risk factors such as narrowed arteries, this
increases the chance that their heart won’t get enough blood. And when the heart
is starved of blood and oxygen, its electrical system can become very unstable.
For some, these arrhythmias mean instant death. But often, they can be treated
at a hospital, if the person gets there in time.
Whether it is brought on by fear or physical exertion, doctors might be able
to prevent this type of heart attack if they could only identify the people with
risky plaques. Such people could then take drugs to strengthen the collagen cap
or have surgery to bypass the plaque, greatly reducing their risk of an
attack.
Researchers are putting enormous efforts into trying to identify people at
risk, using sonograms and infrared spectroscopy to examine the coronary
arteries. But so far, nobody has really found vulnerable plaques ahead of time,
says James Muller, who studies triggers of heart attacks at the University of
Kentucky in Lexington. “For the person who drops dead, it’s an easy way to die,
but it’s hard on loved ones who can’t say goodbye. It’s a failure of cardiology
that we can’t identify people who will have this problem.”
If it is proving difficult to work out who is walking around with a plaque
that is on the verge of breaking up, it is going to be even more difficult to
work out who is most likely to have their heart “turned to stone” by a terrified
nervous system. Starting in April, Muller and his colleagues will begin a study
of 2000 people who have cardiac defibrillators implanted in their chests because
they have already suffered one near-fatal heart attack. The aim is to get a
clearer picture of what types of physical and emotional stresses can induce
arrhythmias.
It would be difficult to even imagine a potential test for the general
population, however, when people’s fears are so personal. We don’t live in a
world like the one portrayed in George Orwell’s 1984, with a Ministry
of Love that knows everybody’s greatest fear and makes rebels face theirs in
Room 101. So how could anyone predict what might send the heart over the edge
before it actually happens?
“Personally, I think that’s hopeless,” says Samuels. “The human organism, by
definition, is at risk for this. It could happen to any of us.”
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Further Reading:
Voodoo Death Revisited: The Modern Lessons of Neurocardiology
by Martin A. Samuels,
The Neurologist, vol 3, p 293 (1996) -
Iraqi Missile Attacks on Israel
by Jeremy D. Kark, Sylvie Goldman and Leon Epstein,
Journal of the American Medical Association, vol 273, p 1208 (1995) -
Capablanca’s Stroke: An Early Case of Neurogenic Heart Disease
by Orlando and Manuel Hernández-Meilán and Calixto Machado-Curbelo,
Journal of the History of the Neurosciences, vol 7, p137 (1998)
