Heart--A History

by Sandeep Jauhar

  Vessels filled with water were hung at each of the four bedposts and set up to drip in a basin on the floor. The water began to drip into the containers, initially fast, then progressively slowing [mimicking bleeding]. By degrees the prisoner grew weaker, a condition reinforced by the physician’s intoning in a lower and lower voice. Finally the silence was absolute as the dripping of water ceased. Although the prisoner was a healthy young man, at the completion of the experiment, when the water flow stopped, he appeared to have fainted. On examination, however, he was found to be dead, despite not having lost a single drop of blood.

  These types of “emotional” deaths have been observed for at least a century. In 1942, the Harvard physiologist Walter B. Cannon published a paper called “‘Voodoo’ Death” in which he described cases of death from fright in primitive people who believed they had been cursed, such as by a bone-pointing witch doctor or as a consequence of eating “taboo” fruit. In his book The Australian Aboriginal, published in 1925, the anthropologist Herbert Basedow wrote:

  The man who discovers that he is being boned by an enemy is, indeed, a pitiable sight. He stands aghast with his eyes staring at the treacherous pointer, and with his hands lifted to ward off the lethal medium, which he imagines is pouring into his body. His cheeks blanch, and his eyes become glassy, and the expression of his face becomes horribly distorted. He attempts to shriek but usually the sound chokes in his throat, and all that one might see is froth at his mouth. His body begins to tremble and his muscles twitch involuntarily. He sways backward and falls to the ground, and after a short time appears to be in a swoon. He finally composes himself, goes to his hut and there frets to death.

  What these deaths had in common was the victims’ absolute belief that there was an external force that could cause their demise and against which they were powerless to fight. This perceived lack of control, Cannon postulated, resulted in an unmitigated physiological response in which blood vessels constricted to such a degree that blood volume acutely dropped, blood pressure plummeted, the heart acutely weakened, and massive organ damage resulted from a lack of transported oxygen. Cannon believed that voodoo deaths were limited to primitive people “so superstitious, so ignorant, that they feel themselves bewildered strangers in a hostile world.” But over the years these types of sudden deaths have been shown to affect all manner of modern people, too. A host of sudden-death syndromes have been identified today, including sudden death in middle-aged men (usually after myocardial infarction), sudden infant death syndrome, sudden unexpected nocturnal death syndrome, sudden death during natural catastrophe, sudden death associated with recreational drug abuse, sudden death in wild and domestic animals, sudden death during alcohol withdrawal, sudden death after a major loss, sudden death during panic attacks, and sudden death during war. Almost all occur because of a sudden stoppage of the heart.

  This is what happened to my grandfather. His sudden death was likely caused by the intense fright he experienced when he saw the snake that bit him. But stress can have both acute and chronic effects, and so I believe the emotional conditions for his cardiac death were laid much earlier, during the tumultuous partition of India in the summer of 1947. My grandfather lived in a district in the Punjab province of what is today Pakistan, where he owned a land management business, hiring laborers to tend to large estates. With the end of British rule in August 1947, the long-standing animosity between Hindus and Muslims in Punjab, as in the rest of the Indian subcontinent, exploded. That year, six years before my grandfather died, the country was partitioned into India and West and East Pakistan (now called Bangladesh), along largely sectarian lines. The result was the largest mass migration in recorded history. Millions of Hindus trekked into India (my grandfather’s family among them). Millions of Muslims went in the opposite direction. The violence on both sides was unimaginable, with massacres, rapes, abductions, and forced religious conversions. One victim was my grandfather’s family’s priest, whose throat was cut by a Muslim gang when he refused to say “Allahu akbar.” “We had Oms,” my father explains, pointing to a gray tattoo on his hand. “No question they would have killed us, too.”

  My grandfather and his family escaped to the border in bullock-driven carts along rutted roads, taking whatever they could bear. There was terrible bloodshed along the way. Villages were in flames; families left behind small children because they could not carry them. The Indian government had issued special armed escorts for teenage girls. Even so, some killed their own daughters to keep them from being raped.

  That year, as the country was torn apart, more than one million people died, and fifty million Hindus, Muslims, and Sikhs were uprooted. The epicenter of the violence was in Punjab, but the shock waves resounded across the subcontinent. My grandfather and his family survived, but months of squalor in border camps, where cholera and dysentery were rampant, would claim the lives of my grandfather’s mother and his one-year-old son.

  The struggle and upheaval during the summer and fall of 1947 no doubt contributed to my grandfather’s premature demise six years later. Reeling from the loss of his business, the family eventually settled into a one-bedroom flat in rural Kanpur. They had no furniture, electricity, or running water. My father did his homework under streetlamps; my grandmother prepared meals on a wood-and-dung-burning stove. My grandfather eventually scraped together enough money to open a small convenience shop that sold rice and other foodstuffs, where he worked virtually every waking hour. He was at that shop on the day he died.

  * * *

  The heart’s physiological responses to emotions such as fright, fear, or joy are controlled by the autonomic nervous system, which regulates unconscious movements such as heartbeat and breathing. The autonomic nervous system has two divisions: the “sympathetic” system, which mediates the fight-or-flight reaction, using adrenaline to speed up the heart and increase blood pressure; and the “parasympathetic” system, which has the opposite effect, slowing respirations and heartbeat, lowering blood pressure, and promoting digestion. Both sympathetic and parasympathetic nerves travel along blood vessels and terminate in nerve cells within the heart to help regulate the heart’s emotional reactions.

  However, there is still a lot we do not understand about the effects of the autonomic nervous system on the heart. For instance, in 1957, Curt Richter, a scientist at Johns Hopkins, described experiments on wild rats in which the animals were dunked in a glass jar filled with water and sprayed by a narrow jet that precluded the animals from floating—in essence, waterboarding them. Wild rats are fierce, suspicious animals that react very negatively to any form of restraint. Not surprisingly, most rats rapidly drowned within minutes (though a few amazingly were able to swim for eighty or more hours before drowning).

  When Richter measured the heartbeat of the drowning rats by means of electrodes inserted under the skin, he discovered to his surprise that the rate was not rapid, as would be expected from sympathetic overactivity. “Contrary to our expectations, the EKG records indicated that the rats succumbing promptly died with a slowing of the heart rate rather than with an acceleration,” Richter wrote, suggesting parasympathetic activation. Moreover, drugs that increased parasympathetic activity accelerated these deaths; drugs that blocked this activity prevented them. Therefore, Richter concluded that the rats died as the result of parasympathetic, not sympathetic, overactivation. “The situation of these rats scarcely seems one demanding fight or flight—it is rather one of hopelessness; whether they are restrained in the hand or confined in the swimming jar, the rats are in a situation against which they have no defense.” Richter further noted that teaching the rats that their situation was not hopeless—by releasing them from the jar at certain intervals, for example—caused them to become aggressive again and try to escape. He conjectured that hopelessness, leading to parasympathetic overactivity, was the reason that aborigines succumbed to voodoo death.

  It is now believed that the seemingly contradictory conclusions of Cannon and Richter ar
e both true and that life-threatening stress unleashes an autonomic storm on the heart that has both sympathetic and parasympathetic components. Both mechanisms have now been implicated in takotsubo cardiomyopathy. Which one predominates depends largely on the time elapsed after the stress. Early on, sympathetic effects are most important (cardiac arrhythmias, elevated blood pressure), while parasympathetic effects (slowing of the heartbeat, lowering of blood pressure) come to the fore later.

  Interestingly, takotsubo cardiomyopathy can develop after a happy event, too, but the heart appears to react differently—ballooning in the midportion, for instance, rather than at the apex. Why different emotional precipitants result in different cardiac changes is a mystery. But today—perhaps as an ode to our ancient philosophers—we can acknowledge that even if our emotions are not located inside our hearts, the biological heart overlaps with its metaphorical counterpart in surprising and mysterious ways.

  2

  Prime Mover

  The six planets orbit the sun, as though around their heart, and give power to the sun and draw power from it: as life winds around the heart and penetrates into it.

  —Jakob Böhme, German theologian, The Threefold Life of Man (1620)

  My first few days in St. Louis were horribly muggy. Clothes clung to my skin like plastic wrap, and the air was like a thick meringue. So, the anatomy lab at the medical school was a welcome sanctuary: cold and dry, with limestone floors and twelve-foot ceilings and a giant multi-faucet sink in the middle of the room, where we assembled in green scrubs three mornings a week, like animals at a watering hole, to wash our hands. Hanging in a corner was a plastic skeleton, like a prop in a campy horror film. With the chill in the sterile chamber, I half expected its teeth to start chattering.

  It would be two years before we entered the hospital to do clinical rotations. Until then, we would have to satisfy ourselves with a human dissection. Our cadavers would soon be in sundry states of dismemberment, their vital organs soaking in buckets of formalin on the floor. But for those first few days after school opened in August, they lay there untouched.

  Mine rested on a steel gurney with rusted wheels, swathed in a white plastic bag containing a shallow puddle of reddish liquid. Sunken chest, light brown skin, distended belly: he was naked save for the tiny socks covering his feet like a baby’s bootees and the cloth mask over his face, which would slip off every now and then, revealing a morbidly serene visage. He was probably in his mid-eighties, faintly hominid in appearance, with a balding scalp, a Punjabi beak nose, and wrinkled leathery cheeks. His tongue partially hung out of his mouth, conferring a look of mild bemusement. Yellowish plaque, matching his pallid skin, caked his front teeth. Moldy-looking scabs pocked his eyelids. His contracted body raised unnatural bumps under the plastic.

  “Autopsy” means “to see for oneself,” and that was exactly what we were supposed to do. But before we got started—before we even applied scalpel to skin—our ponytailed anatomy professor had us do an exercise. What could we surmise about our cadavers, he asked, with an external inspection? What clues were available about how they might have lived or died? The most obvious thing about mine was that he died old. Surgical scars—most prominently a long track down the middle of his breastbone, a remnant of open-heart surgery—indicated that he’d had access to health care. His clean nail beds meant he had been well-off, at least well enough to take care of himself (or to pay others to take care of him). Callused hands generally suggest blue-collar work. My cadaver’s hands were smooth and polished. The feeding tube in his stomach implied his final days had been difficult, perhaps spent in a nursing home or some other full-time care facility. The edema in his limbs pointed to congestive heart failure. And the bulge in his abdomen? Probably a pacemaker.

  It was a fascinating exercise, a reminder to us aspiring doctors that even as we tried to figure out how our cadavers had died, we should not forget to think about how they might have lived. Reflect on their lives, our professor intoned, even as you cut. I took note to do that.

  Even from our first encounter, my cadaver confounded me. He was South Asian. In the culture I grew up in, people rarely donate their bodies to science; they belong to their loved ones. In his final decision—just before death—my cadaver likely defied the wishes of his family, his children, maybe even his wife. Why? I wondered. Of course, I would never know, but nonetheless I felt a sort of kinship to the body before me. The cadavers, our professor said, might remind us of a person we once knew—a close friend or relative who had passed away. Or perhaps a grandfather who lived only in stale stories.

  That semester, I felt closer to my paternal grandfather than ever. It was hard not to make a comparison between him and my cadaver. Both were Indian, probably born around the same time, and probably victims of the same disease. But there was at least one major difference. One man lived a full life, at least beyond what could reasonably be expected. The other died suddenly, leaving behind a distraught family without mooring. One life was terminated prematurely. My grandfather never got the chance to see my father off to college or watch him develop into a successful plant geneticist. The other lingered on into old age—in part because of where my cadaver had lived, because he had benefited from extraordinary scientific advances, many of them spearheaded in America. In a way, his life wasn’t over; he continued to leave a legacy as a physical textbook for the next generation of doctors. The most interesting thing about my nameless cadaver, I realized, was not why he had died but rather how he had managed to live for as long as he did, when for others the journey had ended so abruptly.

  I’m embarrassed to admit it, but for those first few weeks I mostly watched as others dissected. Cadavers made me queasy, and my chatty fellow students’ poring over the body, like forensic pathologists, did nothing to lessen the discomfort with dissection that I’d carried ever since my frog experiment. So I stood at the periphery, peeking over green-scrubbed shoulders at the Indian man glistening under the ceiling lights. Multicolored pins were soon sticking into his various bodily structures. I imagined his last, bitter days in the hospital: swollen legs, boggy lungs, staring out the window as the death rattle of congestive heart failure began to set in. I pictured him, lips pursed, trying to resist as a nurse force-fed him medicated chocolate pudding, a documentary about the British East India Company playing muffled in the background. He must have scowled as the bittersweet dessert entered his mouth, resentful of the judgments the nurses were making of him, a shell of the man he once was. “I hope your father suffers like you are making me suffer,” I could hear him say.

  When we finally got to the dissection of the heart, I steeled myself and stepped up. It was the experience for which I had been waiting—for the better part of my life. The anatomy manual was terse: “Secure a handsaw and open the chest wall.” The skin overlying my cadaver’s ribs was like wet leather. Cutting through it was a team effort. With the chest opened, we did not see the heart at first. It was cloaked by the fleshy shroud of the lungs. For all its outward symmetry, the human body is not symmetric. The left lung, for example, has only two lobes, unlike its tri-lobed counterpart on the other side. (The left lung’s middle lobe atrophies during fetal development because the heart gobbles up its space.) Both of my cadaver’s lungs were speckled with black: smoker’s tar, I assumed, or perhaps just a remnant of city living. They felt like a waterlogged sponge, but when you squeezed them, no fluid seeped out. The cartilaginous airways were hard but pliable, like the end of a chicken bone.

  My cadaver’s heart was about the size of two hands clasped together in prayer, filling most of the mid-chest cavity from the breastbone to the spine and down to the diaphragm, the muscular drape that separates the chest from the abdomen. (Every time you take a breath, the beating heart, resting on the diaphragm, translates slightly downward.) The heart had the shape of a truncated ellipsoid, like a squat volcano tipped on its side. Its muscle—the myocardium—was stiff. Cardiac muscle utilizes energy to relax, not contract, so at death m
y cadaver’s heart went into a state of rigor mortis. The atria, the upper collecting chambers, sat behind the ventricles, the muscular pumping chambers. The right ventricle sat most forward in the chest. It was crescent shaped, its muscle fibers running circumferentially around its exterior. Our professor told us that if ever, as doctors, we had to insert a needle into a patient’s chest to drain fluid, the right ventricle is the first chamber we would hit.

  A few snips and we released the heart from its beige scaffolding. A lab mate placed it on the cadaver’s forearm. “This guy really wears his heart on his sleeve,” he said. Gripping the organ like a Rubik’s Cube, I poked my fingers into the thin-walled central veins. It was hard not to lapse into thinking that it was just a piece of meat, a rubberized toy. The left ventricle had thick walls, a sign of high blood pressure. The inside of the right ventricle was a dense morass of fibers. Maybe there were stories written in that mossy tangle, but I didn’t see any. By the time we’d cleaved all the chambers open—storing the heart between sessions in a circular aluminum pan, like the kind used for baking pies—it had the color and texture of cooked beef.

  Until then, it had been a mystery exactly how our cadaver had died. His ribs were just a bundle of sticks—thin and worn—so some in our group assumed he’d succumbed to one of the diseases that waste and ravage the body, such as tuberculosis or cancer. But when we finally dissected his heart, the answer was revealed. The aorta, the main artery that carries blood from the heart to the body, was marbled with a massive amount of hard, cholesterol-laden plaque. When we sliced open the left coronary artery, grit pushed back against the scalpel. Inside the artery was a long dark brown clot where an atherosclerotic plaque had ruptured. Blood-clotting platelets had surged like minnows to the site of injury, clumping together to form a thrombosis that blocked the artery, causing a heart attack and tissue death.1 This was the mechanism that probably killed my grandfather, too (and, I worried, would eventually claim another of the Jauhar men). Baked into those coarse arterial impurities, I couldn’t help but think, were my cadaver’s failures and sorrows.