Stockholm, 8 October 1958
On 6 April 1964, while in Los Angeles filming the Billy Wilder comedy Kiss Me, Stupid, Peter Sellers had a massive heart attack and was rushed to hospital. At the age of thirty-eight the British actor was one of the biggest stars in Hollywood: Dr Strangelove, the film that would earn him his first Oscar nomination, had just been released, and his surprise marriage to Britt Ekland a few weeks earlier meant that his name was seldom out of the gossip columns.
When he arrived at Cedars of Lebanon Hospital, Sellers was still conscious and his condition appeared relatively stable, but over the next twenty-four hours he suffered eight cardiac arrests. Medical staff told journalists that he was near death, and a guard was posted at the door of the intensive care unit to deter unwanted visitors. At one point his heart stopped for almost two minutes; he was immediately whisked off to a room containing a gleaming new piece of equipment, a large metal cabinet covered with knobs and dials. The hospital’s chief of cardiology, Eliot Corday, picked up two leads, plugged them into the machine and attached them to the actor’s chest with small suction cups. Sellers’s unconscious body jerked periodically as pulses of electric current surged through it, and shortly afterwards his heart was beating once more; any longer and the result would have been brain damage or death.
This life-saving apparatus was an artificial pacemaker, and it supplied regular pulses of electricity which prompted his damaged heart to beat when it was unable to do so by itself. Sellers remained attached to it for three days, clinging tenuously to life, but he did eventually recover. After several months of recuperation he was well enough to return to work, though in later years he would suffer many more heart attacks – he once said that ‘I’m trying to give them up; I’m down to two a day’1 – before another finally killed him in 1980. But he had been lucky: without the pacemaker, invented only a few years earlier, that first cardiac arrest in 1964 would also have been his last.
A lot has changed in the half-century since those events in Los Angeles. Pacemakers are no longer a luxury owned by a few hospitals but the most common medical device in the world, with 250,000 given each year to American patients alone.2 The behemoth sitting by Peter Sellers’s hospital bed has been superseded by tiny objects that can be implanted into the body: the smallest available today is the size of a large pill and is inserted directly into the heart via a vein in the leg.3 They listen constantly to the heartbeat, correcting any disturbance in cardiac rhythm so subtly that their owners do not even know it is happening. And since the 1980s thousands of lives have also been saved by an implantable defibrillator, a device capable of reversing cardiac arrest by imparting a powerful electric shock, entirely automatically.
John Gibbon spent more than fifteen years perfecting the heart-lung machine, but his experience was relatively painless when compared with the tortuous development of the pacemaker and defibrillator. Both devices were conceived and then abandoned by visionaries who found that the world was not yet ready for their ideas, before being reinvented years later when medical thought had moved on. Though they differ fundamentally in their operation, the pacemaker and defibrillator are both predicated on the interesting fact that the heart is not merely a pump, but a pump controlled by electricity. This crucial insight was learned only after generations of scientists had tried and failed to answer a perplexing question: what causes the heart to beat?
In the first decade of the sixteenth century Leonardo da Vinci had suggested that the organ was made of muscle, an insight that explained its movements as nothing more than repeated muscular contractions. But whereas we can flex a bicep at will, the cardiac muscle contracts sixty times a minute without our telling it to; somehow it acts independently of the conscious mind. It was not at all clear why this should be the case. Several theories were put forward and then rejected: some believed that the brain stimulated the heartbeat via the nerves known to connect the two organs, while others suggested that an innate quality of the cardiac muscle, known as ‘irritability’, caused it to contract spontaneously.
The first inkling that there was a completely different mechanism at work came with the discovery that electric current affects the way the heart operates. In the eighteenth century, when the properties of electricity became a preoccupation of natural philosophers, it was not long before anatomists began to experiment with its effects on human tissues. Doctors (and a good many charlatans) attempted to cure all manner of disease with ‘medical electricity’, applying current to whichever part of the body was affected. A physicist from Geneva, Jean Jallabert, noticed that passing electricity through a muscle made it contract, and also found that it caused the heartbeat to accelerate.4 This observation was confirmed by John Wesley, the founder of Methodism, who as well as being a minister and theologian was an amateur physician and an enthusiastic proponent of electrical medicine. In his 1760 book The Desideratum: or, Electricity Made Plain and Useful, he recorded this messy sounding experiment: ‘Open a vein in a person standing on the rosin [an electrical insulator], and the blood will fly out to a certain distance. But let him be electrified, and it will spin out with a much greater force and to a far greater distance.’5
Wesley may even have performed the first electrical cure of a heart arrhythmia. In 1757 he was approached by Silas Todd, a forty-eight-year-old schoolmaster who had suffered from heart palpitations for seventeen years. Wesley passed an electric shock through his chest, noting that his patient ‘has been ever since perfectly well’.6 The episode is strikingly similar to the modern technique of cardioversion, in which an electrical impulse is used to correct certain types of tachycardia, disorders in which the heart beats too fast.
Still more dramatic was the story of Catherine-Sophie Greenhill, a three-year-old girl who on 16 July 1774 fell out of a first-floor window on to the pavement outside her parents’ London home. An apothecary called to the scene found that her heart had stopped and declared her dead, but a neighbour called Squires – apparently an amateur scientist – arrived twenty minutes later with an electrostatic generator, with which he passed electricity through various parts of her lifeless body. When he applied it to her chest the pulse reappeared, and the child began to breathe again – possibly the first use of cardiac defibrillation.7
Medical electricity fell out of favour in the 1850s, when doctors found that the extravagant claims made for the treatment were not supported by clinical results.8 But just as medics were abandoning its therapeutic use, researchers discovered that electricity played an essential role in the human body. In 1856 the Swiss anatomist Rudolf von Kölliker connected a galvanometer – an instrument for measuring current – to a frog’s beating heart and demonstrated that each contraction of its muscle was accompanied by a tiny pulse of electricity. He also noticed something even more significant: when he attached the nerves of a frog’s leg to the cardiac wall, the leg twitched just before the heart began to contract, suggesting that the electrical impulse not only preceded the muscle contraction, but also caused it.9
This hinted at a possible mechanism for cardiac action, but placing electrodes directly on the heart was not a practical method of studying electrical activity in living patients. Thirty years later the British physiologist Augustus Waller developed a way of doing so without breaching the skin. He attached electrodes to the front and back of a patient’s chest and connected them to a capillary electrometer, a device which used a thin column of mercury to measure electric potential. When he examined the mercury through a microscope he found that it moved slightly with each beat of the heart. These movements could be turned into a graph representing electrical changes over time, recognisable today as a rudimentary electrocardiogram. The first ever ECG, taken from a patient at St Mary’s Hospital in London, was published in a medical journal in 1887.10
One of those present on this historic occasion was a young Dutch doctor called Willem Einthoven. He immediately grasped its significance, while realising that the unwieldy apparatus gave results too inexact to be useful. After several years of research he unveiled a much-improved device, which he dubbed the ‘string galvanometer’. Signals from the chest electrodes were passed through a silvered quartz thread suspended in a magnetic field. Even tiny voltages would cause this to be deflected, and the degree of deviation was then measured photographically.11 This gave results far more precise than Waller’s mercury column, allowing Einthoven to observe features of the wave produced by the heartbeat that had never been seen before. His research was published in 1906, but few took much interest in his work until four years later, when he revealed that by installing a cable between the hospital and his laboratory he had been able to study the heartbeat of a patient a mile away.12 Einthoven won a Nobel Prize for his invention, which for the first time made it possible to describe the electrical activity of the heart – and to diagnose disturbances in its rhythm with great accuracy.
As Einthoven was preparing his first results for publication the mystery of what makes the heart beat was finally solved. A decade earlier the Swiss cardiologist Wilhelm His had spotted a previously unnoticed bundle of muscle fibres which extended through the septum between the two sides of the heart. He realised that the purpose of this specialised tissue was to conduct electrical impulses from the right atrium to the two ventricles, causing them to contract – the first physical evidence of a conduction circuit inside the heart.13 By 1906 a number of similar fibres had been identified, but the source of the electrical signals remained unknown. It was finally discovered that summer by a medical student, in the unlikely surroundings of a farmhouse in the Kent countryside. Martin Flack, the son of the local butcher, was assisting the anatomist Arthur Keith in his research in an improvised laboratory in his drawing room. While Keith and his wife were on a bicycle ride one afternoon Flack dissected the heart of a mole, and found a ‘wonderful structure’ high in the right atrium.14
The tiny bundle of nerves Flack saw through his microscope was not much to look at, but it represented the final piece of a puzzle that had mystified the greatest scientific minds for centuries. His ‘wonderful structure’ was the sinoatrial node, the heart’s natural pacemaker and the origin of the signals that make it beat. Once or more a second the SA node fires out an electrical impulse that propagates through the heart muscle, causing the atria to contract. A fraction of a second later the electrical signal reaches a similar bundle located in the wall between the two sides of the heart, the atrioventricular node, which in turn sends out an impulse that makes the ventricles contract and eject their load of blood.
The sinoatrial node is the heart’s orchestral conductor, and the muscle fibres contract in time to its beat. Like a real maestro, it can change its tempo as circumstances demand: responding to nerve impulses from the brain and hormones in the bloodstream, the pacemaker increases the heart rate when we exercise, and reduces it when the body’s oxygen needs have returned to normal.fn1 The network of electrical connections responsible for the heartbeat is complex – so complex that it is still not fully understood. Disease or old age can cause the conduction pathways to break down or make new, anomalous connections, disrupting the electrical signal and provoking arrhythmia – a disturbance in heart rhythm. The voltages involved are tiny, measured in millivolts, but this microscopic electrical system regulates the cardiac rhythm with precision. Finding out what makes the heart tick was a crucial breakthrough that helped doctors understand the manifold ways in which it can go wrong; but it would be some years before they found a way of translating this knowledge into an effective treatment.
The Australian Mark Lidwill is perhaps unique among medical pioneers in being better known for catching a fish. On 8 February 1913 he became the first person in the world to land a black marlin, a powerful saltwater species capable of swimming at 80 mph and much prized by game fishermen. The 70-pound specimen he caught that day in the waters off Port Stephen was donated to the Australian Museum, where its skeleton still resides today.15 His monster catch managed to overshadow his invention the same year of an anaesthetics machine that was used in most of Australia’s hospitals – and, fifteen years later, his creation of the world’s first artificial pacemaker.
What interested Lidwill was what happened to the heart as it failed. He was one of the first to use the ECG to find out how its electrical signals changed as a patient died, and noticed that death was often preceded by a breakdown in the cardiac conduction system. He knew that applying electricity to the heart muscle made it contract, and concluded that it might be possible to help an ailing heart by artificial means.16 With a colleague from the University of Sydney he designed a machine intended to provide an artificial stimulus for the heart in cases where the sinoatrial node had stopped producing its electrical signal. His device, which was plugged into a lighting socket, had two electrodes: one was attached to a pad on the skin, and the other was a needle which was plunged into the heart. Regular pulses of electricity were then passed through this circuit to stimulate the cardiac muscle. His first patient was a baby born without a heartbeat at the Crown Street Women’s Hospital in 1926; after the usual resuscitation methods had been tried without success, Lidwill thrust the needle of his pacemaker into the ventricle and switched it on. The heart immediately responded, and ten minutes later when the machine was turned off it was beating normally. The child made a full recovery, and when Lidwill reported his research at a medical conference in 1929 he expressed confidence that his device could save many lives: ‘There may be many failures, but one life in fifty or even a hundred, is a big advancement where there is no hope at all.’17
It is curious, then, that Lidwill’s advance did not lead anywhere. His research went almost unnoticed, and seems to have come to a halt when his collaborator left the Sydney maternity hospital. One of the few investigators aware of his work was Albert Hyman, an American cardiologist whose interest in the problem of cardiac resuscitation began during his first week as a surgical intern in 1918. The twenty-five-year-old doctor was on duty when a middle-aged man was admitted to his hospital in Boston with a broken leg. As Hyman examined him the man’s heart stopped beating. The emergency-room medics inserted a long needle through his chest to inject adrenaline directly into his heart – a technique that had recently been adopted to treat cardiac arrest. The heart began to beat again, but a few minutes later its rhythm became unstable and then stopped entirely, with further injections proving futile. Hyman was desperate to understand what had happened in the minutes leading up to his patient’s death, and in particular why the heart had restarted and then stopped again. For the next five years he kept meticulous notes every time he witnessed a similar case, hoping to spot something that might lead to an effective treatment.18
Adrenaline was not the only substance injected into the heart on these occasions: many others, including caffeine and camphor, were also tried. Hyman noticed that the choice of drug made no difference to the chances of success, and inferred that it was the prick of the needle, rather than the chemical injected, which prompted the muscle to contract.19 His first thought was that a simple puncture with an empty needle would be as effective as any other method, but this rarely kept the heart beating for more than a few minutes. To keep it going for any length of time several pricks would often be required, which might cause serious damage. Instead he conceived the idea of an electrical stimulus conveyed to the heart muscle through a needle. A pulse of electricity would have the same effect as a needle prick, and it could be repeated once a second or more, until the muscle had recovered enough to produce its own contractions.
With his brother Henry, an electrical engineer, Hyman constructed a machine which he called the ‘artificial pacemaker’. Like Lidwill’s device, it was intended as a temporary stand-in for the patient’s own sinoatrial node in cases where the cardiac conduction mechanisms had broken down. It was powered by a small generator, which had to be hand-cranked every six minutes, and used two electrodes, one of which was a needle inserted into the heart. The device could be adjusted to various rates, providing between 30 and 120 electrical impulses per minute.20 It was tested on a dog called Electra, whose heart was artificially stopped and restarted no fewer than thirteen times. ‘The dog that died thirteen times’ became a minor celebrity, and was adopted as a pet by one of Hyman’s assistants.
When he presented his work at a conference in 1932, Hyman had only used his pacemaker on a few patients, and his work aroused little enthusiasm. Though his colleagues remained unconvinced, the media took a close interest in a device that seemed to offer the possibility of bringing the dead back to life. By the following year Hyman had succeeded in reviving sixty patients from cardiac arrest,21 and a series of newspaper headlines reported his achievements to fascinated readers. Particularly sensational was the story of a New York millionaire in the final stages of heart disease who summoned Hyman to his bedside. He told the doctor that he knew he was about to die, but needed to live long enough to pass on some confidential information to his son, who was travelling from the other side of the country. A few hours later he went into cardiac arrest; the long pacemaker needle was inserted through his chest, the electric impulses switched on, and after fifteen minutes the patient regained consciousness. The son duly arrived, and was able to speak to his father while the machine continued to stimulate a heartbeat; twenty-four hours later the millionaire died.22
This anecdote has a whiff of journalistic embellishment to it, and some of the contemporary reporting seems even more dubious. Implausibly, it was claimed that three Cuban soldiers shot dead in battle had been restored to life by the pacemaker.23 In the 1930s, when a stopped heart was believed to be the very definition of death, recovery from cardiac arrest was nothing short of resurrection, and many people were eager to know whether Hyman’s patients had experienced any intimations of an afterlife. To answer such queries he commissioned a clergyman to interrogate those ‘raised from the dead’, who reported – disappointingly – that they remembered nothing about it.24 Nevertheless, suspicions lingered that there was something immoral, even sacrilegious, about Hyman’s work, and he received angry letters accusing him of interfering with God’s handiwork.25 Initial excitement at his invention turned to disapproval and horror: one possible reason was the release in 1931 of Frankenstein, starring Boris Karloff as an unnatural creature constructed from human corpses and given new life by the miracle of electricity. Another was the antics of Dr Robert Cornish, a young researcher who claimed to have resuscitated dogs after they had been asphyxiated, using artificial respiration, injections of heparin and a table that rocked like a seesaw to restore their circulation. In 1934 Cornish wrote to the governors of three US states asking for permission to revive the corpses of prisoners after execution in the gas chamber. His request – which was denied – aroused general disgust, and may have turned public opinion against those who claimed to bring the ‘dead’ back to life.26
Hyman persisted with his work despite the hostility directed against him, and in 1936 he replaced his original bulky apparatus with a battery-powered model the size of a large torch.27 His efforts to find a manufacturer failed, and a German researcher who tested the pacemaker found that he could not even use it to revive a rabbit.28 Although Hyman continued to use the device until the early 1940s, he could not persuade other doctors that it was safe and effective, and his invention faded into obscurity.
What exactly do we mean when we refer to ‘cardiac arrest’? Most people understand the term to mean a stopped heart, but it’s a little more complicated than that. A patient is in cardiac arrest if their heart abruptly ceases to pump blood around the body – a lethal condition unless speedily treated, often killing within minutes. It is not the same thing as a heart attack, in which an interruption to the organ’s blood supply causes sudden damage to part of its muscle. Heart attacks can lead to cardiac arrest, but there are many other possible causes, including blood loss, drug overdose, hypothermia or a pre-existing heart condition. Cardiac arrest does not necessarily mean that the heart is entirely motionless; the term is a rather vague one which encompasses several distinct eventualities. The pacemaker was developed in order to treat patients who were in a specific type of cardiac arrest known as asystole, in which there are no contractions and all electrical activity has ceased. This would not work in the majority of cases, however, since asystole is a comparatively rare form of cardiac arrest. Much more common is a type called ventricular fibrillation, in which the muscle goes into a sort of spasm, destroying the heartbeat and preventing the organ from pumping. To treat this condition required a rather more dramatic approach.
In 1849 two German physiologists, Carl Ludwig and Moritz Hoffa, performed an experiment which entailed passing a strong electric current through the heart of a live dog. To their surprise the powerful contractions of the cardiac muscle ceased and were replaced by a strange quivering which halted the circulation, killing the animal. This was ventricular fibrillation, but the significance of the observation did not become apparent until several decades later, when the introduction of electrical power to major cities provoked a new dread of electrocution – a strangely disproportionate fear, given that gas lighting caused far more fatalities.29 Little was known about the mechanism of death by electrocution, and so researchers set to work investigating how it killed, and whether the process could be reversed.
In the early 1890s Jean-Louis Prévost and Frederic Batelli, two scientists at the University of Geneva, made a useful discovery. They repeated Ludwig and Hoffa’s experiment, but instead of watching their experimental dog die, Prévost and Batelli managed to revive it. They found that imparting a second shock of much higher voltage banished the fibrillation from the heart – in other words, defibrillated it.30 Their work was repeated ten years later in the United States by Louise Robinovitch, a physiologist so devoted to the subject that her doctoral research had involved electrocuting a very large number of rabbits. She was the first to appreciate that the defibrillating electrodes should be applied only to the thorax, so as to exclude the delicate brain structures from the circuit,31 and even designed a portable defibrillator for use in ambulances.32 This was truly groundbreaking work, and yet it was largely ignored by the medical establishment: whether because of her sex or her temperament, Robinovitch was regarded as something of a maverick.33
Her findings had already been forgotten by 1925, when the managers of a large American electrical company became alarmed at the number of employees dying while working on high-voltage power lines, and asked a team at Johns Hopkins medical school to look into the problem. Their conclusions confirmed those of Prévost and Batelli thirty years earlier: when a dog was given an electric shock of around 110 volts, its heart went into ventricular fibrillation. This could be reversed by a much more powerful shock – they used 2,200 volts – which caused the heart to stop entirely for a few seconds before resuming its normal beat.34 One of the researchers, the electrical engineer William Kouwenhoven, designed a defibrillator to impart such shocks whenever needed, apparently unaware that Robinovitch had already done so twenty years earlier.
Kouwenhoven’s defibrillator and Hyman’s pacemaker, both invented in the early 1930s, were superficially similar, so it is important to distinguish between them. Each employed electricity to stimulate a heartbeat, but they performed very different functions. I’ve described the sinoatrial node as the heart’s conductor, in charge of an orchestra whose players are the organ’s muscle fibres, but it may help to extend that analogy a little. Imagine that an orchestra is in the middle of a concert when the conductor unexpectedly puts down her baton and walks off stage. The players suddenly have no beat to follow, so they stop playing and the music grinds to a halt. They are in a state of musical asystole – nothing is happening. But the situation is rescued by a member of the audience, who produces a metronome, places it on the absent conductor’s music stand and sets it going. This is all the players need to resume their performance: the loud and unvarying tick of the metronome may lack the fine nuance of a proper conductor, but it’s enough to keep the music going. Like the metronome, Hyman’s pacemaker provided an artificial beat that the cardiac muscle fibres could follow.
The defibrillator was designed to cope with another problem: ventricular fibrillation, in which the muscle fibres have lost all coordination and are contracting at random. This time the conductor is not the problem: the orchestra, rather than falling silent, have lost concentration and are now improvising wildly. Instead of playing as an ensemble they all do their own thing, resulting in deafening cacophony, while the conductor’s increasingly desperate gestures from the rostrum are ignored. Suddenly there is a blinding flash and a bang: a member of the audience has set off a firework in the auditorium. The players are so startled that they stop playing. There is silence for a moment, and the conductor finds that she now has their undivided attention; the performance can resume in an orderly manner. Kouwenhoven’s defibrillator, like the firework, offered a sudden shock to the system: a high-voltage pulse of electricity that abolished all muscle activity for a second, allowing the natural pacemaker rhythm to establish itself once more.
If you’ve watched a lot of medical dramas you might have been misled into thinking that a defibrillator can be used to reverse any type of cardiac arrest. We’re all familiar with the scene: a patient lies stricken in an intensive care bed, surrounded by worried faces. Suddenly an alarm goes off and the camera zooms in on the ECG, which briefly goes haywire before the trace settles into a featureless flat line, the machine’s regular ‘bip, bip, bip’ replaced by a monotone ‘beeeeee’. The medics spring into action, placing defibrillator pads on the patient’s chest, shouting ‘Clear!’ and unleashing a powerful shock that makes the whole bed jerk. Several more attempts are usually obligatory to wring every drop of suspense out of the situation, but eventually the heart springs back into life and everybody breathes a sigh of relief.
The scenario is not only hackneyed but utterly implausible. Medics distinguish between ‘shockable’ and ‘unshockable’ arrhythmias, and asystole – indicated by the flatlining ECG – is one of the unshockable varieties, so a defibrillator is no use in treating it.fn2 The more commonly encountered ventricular fibrillation, on the other hand, is shockable, so a defibrillator will often be effective in restoring a natural heart rhythm.
Kouwenhoven’s work attracted the attention of Claude Beck, Elliott Cutler’s former research student, who was now a surgeon in Cleveland. Like most members of his profession he was familiar with the problem of ventricular fibrillation, which sometimes arose when the heart was handled. Those unlucky enough to encounter this complication were helpless as they watched the cardiac muscle begin to seize: nothing they did would restore it to a natural rhythm. In its disordered state the heart could eject only a fraction of the usual volume of blood, and within a few minutes the patient would be dead.
In 1937 Beck outlined the advantages of the defibrillator to a meeting of surgeons, but his presentation made little impression. He installed one of the machines in the Cleveland Clinic and attempted to use it on a few patients, but by the time he applied the electrodes to their hearts the fibrillation was well established, and brain damage had already set in.35 It was not until 1947 that he had his first success. The patient was Dick Heyard, a fourteen-year-old boy who was undergoing surgery for pectus excavatum, a deformity in which the thorax has a concave appearance. After an uneventful operation the boy’s heart abruptly stopped as Beck was closing his chest. ‘The patient was apparently dead,’ he recorded. Outside the operating theatre Dick’s distraught mother was told that her son’s heart had stopped beating, and she sank to her knees in prayer.36
Beck hurriedly reopened the incision and began to massage Dick’s heart, squeezing it rhythmically with a gloved hand. He continued doing this for forty-five minutes; to get a sense of what this must have been like, imagine standing at a table squeezing a tennis ball every second for three-quarters of an hour – but with somebody’s life depending on it. After what must have seemed an eternity, the ECG finally showed that the heart was alive, but in ventricular fibrillation. Beck applied the defibrillator electrodes to the heart and passed a shock of 110 volts through it. It continued to quiver feverishly, so he tried again. Suddenly all activity ceased, and for a second it stood stock still. Then a rapid but feeble heartbeat appeared; as Beck continued to massage the heart the contractions grew stronger, and after twenty minutes he was able to close the wound in the boy’s chest.37 A month later Dick returned home. ‘Boy Who “Died” Is Alive Through Prayers’, read a headline in the local newspaper,38 which seems a little unfair on Beck.
While the defibrillator slowly became an accepted surgical tool, the pacemaker, which had been invented and abandoned twice, seemed a medical dead end – until 1949, when Wilfred Bigelow became the third person to stumble upon the idea. Then several years into his hypothermia research, he seemed to be making good progress, cooling dogs to well below their normal temperature in order to perform experimental open-heart surgery. But his team had encountered an infuriating problem. Sometimes when a dog was being cooled to the target temperature, its heart would stop without warning, and resist all attempts to restart it. Bigelow watched this happen in his basement laboratory one morning. His first feeling was exasperation: instead of operating on the dog, he and his team would have to spend the day trying (and probably failing) to revive it. As he looked at the quiescent heart, Bigelow was struck by how healthy it looked. He gave it an experimental prod, and to his surprise it responded with a vigorous contraction. Intrigued, he poked it repeatedly; each jab provoked an apparently normal heartbeat.39
Bigelow reached the same conclusion as Hyman: perhaps a small electric shock would have the same effect. He approached the Canadian National Research Council, who put him in touch with an electrical engineer, Jack Hopps. Hopps had been working on a new technique for pasteurising beer, a subject close to his heart, and accepted the new assignment reluctantly. But he soon became fascinated by Bigelow’s idea, and when another surgeon in his team, John Callaghan, came across a description of Hyman’s pacemaker they had confirmation that they were on to something. Hopps visited Kouwenhoven’s laboratory to learn about the defibrillator and what he had discovered about the conduction pathways of the heart, and not long afterwards he developed a pulse generator, a table-top unit that produced a regular electrical impulse.40 Bigelow hoped that the pacemaker would keep his dogs alive while they were being put in deep hypothermia, but the first trial was a failure: the first animal went into cardiac arrest at 17°C, and nothing would revive it. Disheartened, he tested the device on rabbits and dogs at normal temperatures and found that the pacemaker consistently succeeded in restarting a stopped heart. Once the heart was beating the device could even be made to override its native rhythm, giving the surgeon control over the heartbeat and allowing him to dictate its rate, between 60 and 200 beats per minute.41
In their early experiments they used a needle electrode similar to that used by Hyman, but Bigelow and his colleagues realised that this method was unnecessarily laborious. They developed a catheter electrode, a wire which could be inserted through a vein and navigated through the blood vessels towards the heart. This allowed the pacemaker to be used without opening the chest, considerably simplifying the operation. Bigelow became convinced that it was suitable for use on humans, and Callaghan employed it in treating five patients with severe cardiac arrhythmias. To their frustration the treatment had no effect; Callaghan later realised that the electrode had been placed in the wrong part of the heart. Two inches lower and it would have worked – a small distance, but one that made the difference between life and death.42
In October 1950 Callaghan gave a presentation about this work to a meeting of the American College of Surgeons. A week later he received a letter from Paul Zoll, a cardiologist at Beth Israel Hospital in Boston, asking for further details of the pacemaker apparatus.43 Zoll saw the device as the possible solution to a problem. Earlier that year he had treated a woman who was suffering regular Stokes–Adams attacks, episodes of unconsciousness caused by temporary cardiac arrest. These are a sign of heart block, a problem with the conduction pathways which prevents the electrical signal from the natural pacemaker from reaching all of the heart muscle. Zoll was unable to do anything for her, and was deeply upset when she died three weeks later.44
During the Second World War, Zoll had worked with Dwight Harken in his army hospital in Gloucestershire, watching him take fragments of shrapnel out of soldiers’ hearts, and had noticed how sensitive the cardiac muscle was to external stimulation.45 He reasoned that an electrical stimulus might prevent sudden death in heart block patients by keeping the organ pumping during periods when its natural rhythm disappeared. After animal experiments using a signal generator similar to that developed by Hopps and Callaghan, he discovered that it was not necessary to place electrodes directly on the heart: if a higher voltage was used, they could be attached to the skin of the chest. This was much quicker and safer, and still gave him full control of the animal’s heartbeat.
The first patient treated with the external pacemaker was a seventy-five-year-old man who arrived at the Boston hospital on 28 August 1952. His cardiac rhythm was unstable, resulting in regular Stokes–Adams attacks, and the medics struggled to keep him alive with adrenaline injections directly to the heart – thirty-four of them in just four hours. Eventually they decided to use the pacemaker, and electrodes were placed on his chest. It kept him alive for twenty-five minutes, but then his heartbeat faded to nothing and the doctors admitted defeat. The following month a second patient, a sixty-five-year-old man, was admitted to the hospital in severe heart failure. On his sixth day there he had the first of several episodes of cardiac arrest, and he too was connected to the pacemaker. Regular electric shocks of up to 130 volts were passed through his chest. At first the device was needed only occasionally, but on the fourth day the natural rhythm disappeared entirely and it had to be used continuously. For more than two days his heart was kept beating by regular shocks, ninety of them every minute, from the large box at his bedside.46
The subsequent recovery of this patient was a watershed. Physicians and the public alike were impressed: ‘Plug Failing Hearts into AC Outlet’, suggested one dangerously simplistic headline.47 But heart block was a fairly rare condition, so it was not immediately obvious that the pacemaker would often be needed. Zoll didn’t know it, but the development of open-heart surgery would soon make his device an essential item for all cardiac operating theatres.
The first person to appreciate this was a pathologist from Chicago, Maurice Lev. In the early 1950s, around the time that Walton Lillehei was performing the first of his open-heart operations using cross-circulation, Lev pointed out to him that working inside the organ was likely to provoke heart block. ‘What’s that?’ asked Lillehei. Lev explained that cutting and stitching cardiac tissue would probably disrupt its conduction pathways and affect the heartbeat. This was much like an orchestra trying to rehearse in a hall where the lighting only works intermittently: while the lights are on the players can follow the conductor’s beat, but as soon as they are plunged into darkness they can see nothing and stop playing.
Lev was soon proved right. Many of Lillehei’s early patients had ventricular septal defects, holes in the wall between the two ventricles. Repairing them entailed placing sutures perilously close to conductive tissue, and seven of his first seventy patients developed heart block as a result. All of them died.48 Lillehei found that a drug called Isuprel reduced the mortality rate to 50 per cent, but this was still unacceptably high. When he heard about Zoll’s work he realised that a pacemaker might be the answer, and tried the method on several of his patients. It did succeed in keeping them alive, but there was a problem. The device imparted a 60-volt electric shock every second that it was turned on. This could be exquisitely painful, and for patients reliant on the machine day and night it caused significant distress. One patient who was on a Zoll pacemaker for several weeks killed himself by disconnecting the device, preferring death to an apparently endless torture.49 Others developed skin burns and blisters at the electrode sites; given that Lillehei’s patients were mostly children, this was deeply unsatisfactory.50 In animal experiments his colleagues found that if the electrodes were placed directly on the heart a much smaller current was required, so small that the patient would not even notice it. Lillehei adopted this technique in early 1957, attaching electrodes to the heart after completing each operation. The results were striking: mortality from heart block dropped from 40 per cent to 2 per cent.51
As he soon discovered, there were some drawbacks to this life-saving therapy. Children who were wholly dependent on a device plugged into a wall socket could not easily be moved: a simple trip to the X-ray department entailed trailing an extension lead halfway across the hospital. That was inconvenient, but when a major power cut hit Minneapolis on 31 October 1957 the disadvantages of a mains-powered pacemaker became painfully apparent. For three hours, doctors ran around administering drugs to patients as they desperately tried to keep their hearts going. Miraculously all survived, but Lillehei knew he had to find a way to prevent the scenario from arising again.52
The obvious solution was a portable battery-powered device. Lillehei asked a physics student to design something, but several months later the undergraduate admitted that he had made no progress. Irritated, Lillehei bumped into Earl Bakken, an electrical engineer who was often in the hospital maintaining operating theatre equipment. He told him about the problem and asked whether he thought he could make one for him. Bakken accepted the challenge, and went home to do some tinkering in his garage. These unassuming premises were the headquarters of Medtronic, a two-man company he had founded with his brother-in-law a few years earlier. Business was slow, and as well as mending broken medical equipment Bakken often found himself moonlighting as a TV repair man. Rooting around in the messy workshop, he unearthed an old issue of Popular Electronics magazine. He remembered an article giving instructions for constructing an electronic metronome, a simple circuit using only a few basic components which when attached to a loudspeaker would produce regular clicks at an adjustable rate. Bakken realised this was just what he needed, made a few tweaks to the original circuit and put it in a small box with a battery.fn3 A few weeks after being given the commission he delivered the first portable pacemaker to a delighted Lillehei.53
Bakken assumed that the new device would require months of animal testing, so when he returned to the hospital the following day he was shocked to see a young patient already wearing his prototype on a strap around her neck, with wires poking through an incision in her chest. He sought out Lillehei, who told him that a quick test in the animal laboratory had shown that it worked, so he saw no point in waiting any longer before using it.54 Bakken was sent back to his garage to make more of them, and within a few months it became quite ordinary to see one of Lillehei’s young patients wandering the corridors with the vital equipment dangling from a holster over one shoulder.
The impact of this development was spectacular. ‘Not only has the threat of sudden death in these patients been removed, but their physical and emotional development has been dramatic,’ Lillehei wrote.55 Children reliant on the pacemaker could get out of bed and even go home. Most would only need it for a short period, until their heart rhythm returned to normal, but it could be left in place for many months if necessary. Although Lillehei had only envisioned it as a post-operative measure, he soon found it was effective in patients who developed heart block in old age or as the consequence of a heart attack. Bakken had to take on extra staff to meet the demand, and several thousand units were sold over the next few years. Many patients returned to work after years as invalids, and could lead active lives: one newspaper reported the story of Carl Baker, a thirty-eight-year-old engineer who was able to play golf and go hiking with his pacemaker strapped to his waist.56
But the device was far from perfect. Being permanently connected to a box of electronics is not terribly convenient if you want to take a shower or go for a swim. The pacemaker wires were fragile: one patient regularly turned up at Bakken’s office on a Monday morning having broken one while dancing at the weekend.57 The most serious problem was infection, since the leads emerged from the body through what was in effect a permanent wound in the skin. The only way to prevent this complication would be to implant the entire unit – electrodes, leads and the pacemaker itself – inside the body, though few researchers thought this practical, or even possible, in 1958.58
One person who did not share this pessimism was the Swede Åke Senning. A protégé of Clarence Crafoord, Senning was fascinated by engineering and helped to develop the first heart-lung machine and defibrillator in Scandinavia.59 His introduction to cardiac arrhythmia was a painful one: as a boy he managed to electrocute himself with a table lamp, causing a brief episode of ventricular fibrillation that caused him to feel as if his heart had stopped.60 Senning was a regular visitor to the US and had talked to Bigelow and Lillehei about their work. With the help of a technician from a local electronics company, Rune Elmqvist, he began his own pacemaker research at the Karolinska Hospital in Stockholm. Senning and Elmqvist began by constructing a device much like Bakken’s, but Senning was acutely aware of the drawbacks of an external pulse generator and wanted to create something small enough to implant under the skin.61
Such a thing would have been unthinkable only a couple of years earlier, but technology was entering an exciting new era. The pacemakers of Bigelow and Zoll had used vacuum tubes, large and unreliable components that had to be housed in a bulky casing. The transistor, an amplifying and switching device invented in 1947, consumed far less power and was a fraction of the size, making it possible to miniaturise electronic circuits. The first mass-produced transistor radio, the Regency TR-1, went on sale in late 1954; promotional material described it as smaller than a cigarette packet or martini glass, comparisons that surely say something about the preoccupations of advertising executives in this era. Using the silicon transistor, only just available in Sweden, Elmqvist was able to build a pacemaker that fitted in the palm of the hand.
Senning was in no hurry to use Elmqvist’s invention on a patient, but on 6 October 1958 he found himself with no other choice. That day Else-Marie Larsson, an ‘energetic, beautiful’ woman, walked into his laboratory and asked him to implant a pacemaker into her forty-four-year-old husband, Arne. Some weeks earlier her husband had contracted hepatitis after eating oysters in a restaurant, and the infection had spread to his heart. Now he was suffering up to thirty Stokes – Adams attacks a day, with Else-Marie watching helplessly at his bedside each time his heart rate dropped to a paltry twenty per minute. Senning explained that he was still conducting animal experiments and did not yet have a pacemaker for human use. ‘So make one,’ was her imperious reply.62
Her zeal was irresistible. To be on the safe side, Elmqvist assembled two pacemakers, simple electronic circuits each using a pair of transistors. He encased them in epoxy resin using a Kiwi shoe-polish tin as a mould, producing an object roughly the size and shape of an ice-hockey puck.63 On the evening of 8 October Senning operated, attaching electrodes to Arne’s heart muscle and tucking the pacemaker into a pocket behind the abdominal muscles. All seemed well at first, but at 2 a.m. it abruptly stopped working. After a frantic dash to Elmqvist’s lab to pick up the spare, Senning replaced the faulty unit the following morning, and this time there were no alarms: the pacemaker worked as expected, and Larsson suffered no more Stokes – Adams attacks. Every week or so the battery ran down and had to be recharged. In a futuristic touch this was done wirelessly: a coil strapped to Larsson’s chest transmitted power by electromagnetic induction to a smaller coil embedded underneath the skin.64
The pacemaker remained effective for only six weeks, but that was long enough to see Larsson through the crisis.65 He was well enough to manage without a pacemaker for the next three years, though the underlying heart block was still there. In 1961 his condition deteriorated again and Senning implanted a third device. There would be a further ten by the end of the decade, and when Arne Larsson died in 2002 he had received twenty-two pacemakers in total, and outlived the surgeon who saved him.66 His contribution to the development of the pacemaker went further than being its first guinea pig: a trained electrical engineer, Larsson also became involved in improving the device.67
At least half a dozen people have been described as the ‘inventor’ of the pacemaker, but Rune Elmqvist surely has a strong claim to the title. The simple device he constructed may have lasted little more than a month, but it was the first to be implanted inside the body; more to the point, it gave its first patient forty-four extra years of life. A few months later a slightly improved model was implanted into two patients in London by the surgeon Harold Siddons: one continued to work for ten months, an impressive demonstration of its capabilities.68 The fact that these successes predated the work of the American engineer Wilson Greatbatch – ‘inventor of the pacemaker’, according to the front cover of his memoirs69 – does nothing to diminish his achievement, for he was the first to produce a device which lasted not months, but years.
Another electrical engineer by training, Greatbatch began his career producing machines for an animal laboratory at Cornell University. He became interested in the problem of cardiac pacing after a chance conversation with two brain surgeons in 1951, and was immediately sure that electronics would provide a solution. A few years later he stumbled across one by mistake: while assembling a device to monitor heart rates in laboratory animals he accidentally inserted the wrong component, and found that the resulting circuit produced a periodic electrical pulse.70 This was not at all what he had been intending, but he immediately realised that it might be used as the basis for a pacemaker. Greatbatch struggled to interest clinicians in his idea until early 1958, when he finally met a surgeon who was receptive to his ideas.
William Chardack, the chief of surgery at the Veterans Administration Hospital in Buffalo, was instantly swayed by Greatbatch’s conviction that modern electronics made a long-term implantable pacemaker a realistic prospect. Chardack believed that a device using a mercury cell – a power source invented during the war – could last for at least a couple of years before needing to be replaced.71 Encouraged by the surgeon’s enthusiasm, Greatbatch left his job and sank $2,000, his life savings, into the project.72 His first pacemaker was, in appearance at least, similar to Elmqvist’s. Measuring 6 centimetres in diameter and just 1.5 centimetres thick, it was covered in epoxy resin which was then coated in a thin shell of silicone rubber.73 Its first success came in June 1960, when Chardack implanted one into the chest of Frank Henefelt, a seventy-seven-year-old with complete heart block. In the months before the operation Henefelt’s heart rate dropped to thirty-two per minute, causing regular blackouts. One particularly nasty fall resulted in a skull fracture, and he took to wearing a football helmet around the house.74 After implantation he was completely cured, with a healthy heart rate of fifty-five; the helmet was set aside and he was able to resume a normal life. The next two people to receive a pacemaker had similarly happy outcomes, and suddenly patients were beating a path to Chardack’s door and asking to have one of his ‘heart-stingers’ implanted.75 The wider medical profession, often slow to embrace such technology in the past, soon realised that a fully implantable pacemaker was a real step forwards, a treatment that allowed patients to put months or years of ill health behind them.
In October 1960 Greatbatch sold the patent for his invention to Earl Bakken’s firm, Medtronic.76 This was something of a gamble, since an independent expert had recently concluded that the potential market for the device was tiny, estimating that no more than 10,000 pacemakers would ever be needed in total.77 By the turn of the millennium 600,000 were being sold every year,78 and Bakken’s struggling business-in-a-garage had been transformed into a multinational corporation with more than 85,000 employees.79
After many false starts and much scepticism, the pacemaker was finally accepted as an effective therapy. But it was not without its deficiencies: in early patients the voltage required to stimulate the heart tended to increase over time until the device ceased to have any effect, a problem eventually solved by the introduction of a new type of electrodefn4. Another weakness was the leads, which tended to fracture until better materials and methods of construction were discovered. Battery life was a major concern: Greatbatch had estimated that his pacemaker would last five years or more,80 but early patients were lucky if their device lasted eighteen months. It would be another decade before a really durable power source became available; but in the meantime there was a still more formidable problem to be solved.
The first implantable pacemakers were unsophisticated objects that did only one thing: emit a pulse of electricity roughly every second to stimulate the ventricle, ticking away like a metronome until the battery ran down. The rate was preset and could not be changed, so the patient’s heart rate did not vary between rest and exercise. The device also took no account of the heart’s underlying rhythm, raising the possibility that the artificial pacemaker might ‘compete’ with the signals from the natural one. In the worst-case scenario this might even induce ventricular fibrillation and death. What was needed was a pacemaker which did not interfere with naturally generated muscle contractions. The answer was a beautifully ingenious piece of engineering, a device that listened to the heart as well as sending it instructions. The basic mechanism was invented as early as 1942, although without any idea of its application to pacing. Two New York cardiologists investigating heart block placed an electrode on the atrium to detect the natural pacemaker impulse. This was then sent to a circuit which amplified the signal and returned via another electrode to the ventricle.81 In cases of total heart block – where the electrical signals from the atrium never reach the ventricles – the device provided an artificial diversion, bypassing the electrical blockage.
In 1957 two researchers in Boston, Moses Judah Folkman and Elton Watkins, took the first step in turning this idea into a clinical solution. They experimented on twenty-four dogs, surgically producing heart block so that the atrial signals failed to reach the ventricles and giving them an unnaturally slow heartbeat. They then attached them to a miniature transistor amplifier, a device that picked up the tiny electrical signal from the atrioventricular node and magnified it fifty-fold. This amplified signal was enough to prompt ventricular contraction. It was like giving night-vision goggles to the members of an orchestra trying to play in a pitch-black auditorium: previously unable to see the conductor, they could now follow her beat. The beauty of the device was that it permitted a normal rhythm rather than imposing an artificial, unchanging one: the heartbeat varied with exercise, between 90 and 130 beats per minute. ‘The dog is frisky and eats well,’ they reported – it had been returned to full health.82
This was not a complete solution, since the device would only stimulate the ventricles if the natural pacemaker consistently produced an impulse. Some hearts are so damaged that the sinoatrial node fails to do this. To deal with this scenario, a Miami cardiologist, David Nathan, conceived a device that combined a pacemaker with an atrial-impulse amplifier. An electrode placed on the atrium ‘listened’ constantly for a signal, amplified it and passed it on to the ventricles; if no impulse was detected, an artificial pacemaker circuit stimulated the heart muscle until the natural signal returned.83 A New Jersey surgeon, Victor Parsonnet, hit upon an even better solution three years later: his ‘demand’ pacemaker monitored the ventricles rather than the atria, and only came into action if it noticed that the heartbeat had dropped below 69 per minute.84 Parsonnet’s device did not entail a potentially dangerous operation to attach electrodes to the heart: instead, they were passed up through a vein via an incision in the groin. This technique, originally described by Bigelow’s colleague John Callaghan, had been rediscovered in the early 1960s and soon became the method of choice when implanting pacemakers.
An extra level of complexity arrived in 1971 when a Massachusetts electrical engineer, Baruch Berkowitz, developed a pacemaker that acted not just on the ventricles but on the atria as well. This so-called ‘bifocal’ pacemaker monitored cardiac activity and, when required, stimulated both chambers in sequence, making the heartbeats more efficient by increasing the volume of blood ejected with each stroke.85 In little more than a decade the pacemaker had evolved from a simple metronome for the heart into something far more sophisticated.
But the device still had an Achilles heel: its longevity. Wilson Greatbatch’s estimate of a five-year lifespan for the first implantable devices proved hopelessly optimistic. The weak link was the mercury-cell battery, which generally lasted no longer than eighteen months. Many patients only discovered this when their old symptoms recurred, and their doctors had no way of predicting when the units would fail. At one hospital in London, doctors took to placing a medium-wave radio next to their patients: regular clicks from the loudspeaker indicated that the pacemaker was still functioning.86 Many possible alternatives to the unreliable mercury batteries were tested: in 1960 a Birmingham surgeon, Leon Abrams, developed a pacemaker with a power pack outside the body, which transmitted power to its electrodes wirelessly via coils.87 Others tried to harness the natural movements of the patient’s body, using a mechanism like that of a self-winding watch to generate electrical power.88 Eventually the search for the perfect power source led to one of the odder innovations of medical history: a nuclear-powered pacemaker.
In 1968, Victor Parsonnet wrote to the United States Atomic Energy Commission, asking for help in developing a long-lasting power source. The Commission was keen to improve the image of nuclear technology by employing it in small-scale – and demonstrably safe – civilian applications, and had already developed plutonium-fuelled generators to power lighthouses and space probes.89 AEC scientists agreed that it should be feasible to design a nuclear battery small enough to power a pacemaker. The device they created was compact and simple: a thin wire of plutonium-238 was encased in a titanium capsule. As the plutonium decayed it threw out alpha particles which collided with the walls of the capsule, creating heat that was converted to electricity by a component called a thermocouple – the same technology that later powered the Voyager space probes. In 1969 a pacemaker containing a nuclear cell was successfully implanted into a dog called Brunhilde90 – the researchers apparently did not think it an ill omen to name her after a Wagnerian heroine who dies in a blazing inferno.
After exhaustive tests the nuclear pacemaker was finally implanted into a human patient in France in April 1970. Three months later Constance Ladell, a fifty-six-year-old mother of four from Barnet, became the first person in Britain, and the third anywhere in the world, to receive one of the devices. The day after her operation, which was reported in the Evening Standard under the headline ‘Atom Heart Mother Named’,91 members of the rock band Pink Floyd were in a BBC radio studio rehearsing for a live performance of their latest, as yet unreleased album. Mulling over possible names for the work, the lead singer Roger Waters was flicking through the evening paper when he spotted the story. ‘How about that, lads?’ he said, pointing at the headline. The LP was duly released as Atom Heart Mother – the first and only number one to be named in honour of a cardiac device.92
By 1975, around 1,400 nuclear pacemakers had been implanted without a single battery failure.93 In Britain the Atomic Energy Research Establishment at Harwell was awarded a government contract to produce pacemaker batteries, one of the largest civilian applications for nuclear technology.94 And the results were phenomenal; designed to have a ten-year lifespan, the devices proved even more durable. Dozens lasted for twenty years or more, and one implanted in 1973 was still working thirty-one years later.95
There were obvious concerns about placing a plutonium cell inside the human body. If just a millionth of a gram of fuel were to reach the bloodstream it would prove fatal, so it was necessary to take stringent safety precautions. The triple-walled titanium capsule was designed to withstand an aeroplane crash or the impact of a bullet, and every device was government-registered to ensure its whereabouts were known.96 Neither of these drastic scenarios was ever put to the test in real life, but when a nuclear pacemaker was inadvertently incinerated in 1998 the capsule survived intact, with no escape of radiation.97 In this respect they proved far safer than conventional devices, which had an unfortunate tendency to detonate when heated: in 1977 a crematorium in Solihull was badly damaged by a series of explosions caused by a mercury-cell pacemaker that had accidentally been left inside a body.98 As a result of that incident, regulations were introduced to ensure that devices were removed before cremation, but a survey in 2002 found that half of all UK crematoria had experienced explosions caused by cardiac pacemakers.99
The heyday of the nuclear pacemaker was brief, and the reasons for its decline were unrelated to its safety record, which was impeccable. In 1972 Wilson Greatbatch and his colleagues invented a lithium-iodine battery with a lifespan of ten years. It was smaller and far cheaper than the nuclear cell, and had none of the practical difficulties associated with radioactive substances. It was an obviously superior solution to the problem of battery life, and has remained the standard pacemaker power source ever since. It also made possible the development of another type of device that emerged in the 1970s: the implantable cardiac defibrillator, or ICD.
The science of cardiac resuscitation had come a long way since Claude Beck first defibrillated a patient during an operation in 1947. Eight years later Paul Zoll designed a defibrillator which could be used on the closed chest, without the need for an incision.100 But these early models used alternating current, which damaged and burned healthy tissue – to such an extent that, as Dwight Harken put it, ‘you could smell the patient’s heart cooking’.101 The Boston cardiologist Bernard Lown and Baruch Berkowitz showed that direct current was far safer, and their new type of defibrillator, first used in 1961, was a huge advance. It was not only able to resuscitate patients without a pulse (those in ventricular fibrillation), but could also be used to correct less serious types of arrhythmia in which the heart continued to beat, but in a disordered fashion.
Lown named this treatment ‘cardioversion’. The first patient to receive it was a sixty-three-year-old woman who arrived at Peter Bent Brigham Hospital after a heart attack. She had tachycardia (an unnaturally fast heartbeat) which failed to respond to drugs. Lown decided to attempt cardioversion, and the patient was given a powerful electric shock lasting 2.5 milliseconds. Her heart was immediately restored to its natural rhythm. ‘The patient was awake within two minutes and was quite startled by the newly found sense of well-being,’ Lown recorded.102
Another method of resuscitation that arrived at about the same time was, by comparison, startlingly low-tech. In 1960 William Kouwenhoven, the inventor of the modern defibrillator, wrote that ‘anyone, anywhere, can now initiate cardiac resuscitative procedures. All that is needed are two hands.’103 The technique he and two colleagues had discovered – or rather rediscovered, since similar research had been undertaken in Germany in the 1880s and then forgotten – entailed compressing the chest rhythmically with the hands. This was a vital addition, since it meant that heart-attack victims could be brought back to life even if they collapsed miles from the nearest hospital. In retrospect it is strange that such a simple method, one which is now taught to millions of amateur first-aiders every year, was introduced years after the invention of the defibrillator.
Another realisation dawned on the medical profession in the 1960s: some hearts were, as Claude Beck put it, ‘too good to die’. ‘Almost every physician has had experiences in which death occurred, and when the heart was examined the damage was inadequate to explain death,’ he wrote.104 A heart attack was not necessarily a fatal event, merely a process that could often be reversed. This was a profound insight that revolutionised the care of cardiac patients. In 1961 a senior registrar at Edinburgh Royal Infirmary, Desmond Julian, proposed a new type of ward for those who had suffered a heart attack, with twenty-four-hour nursing, electronic monitoring and resuscitation equipment.105 It was not long before these coronary care units started springing up around the world: first in Australia, then hospitals in America and Canada followed suit.106 Studies published a couple of years later showed that such wards drastically reduced mortality among cardiac patients. This was good news for those already in hospital; but many patients with serious arrhythmias were well most of the time and could not be kept permanently on a ward. What could be done for them?
This was the question the cardiologist Mieczysław Mirowski asked himself in 1966 when an old friend and colleague dropped dead from ventricular tachycardia while having dinner with his family.107 The condition from which he suffered had been diagnosed weeks earlier and responded to drug therapy, but everybody knew it could recur at any time. Mirowski wondered how his death could have been prevented, short of keeping him permanently in hospital. And then an idea occurred to him: would it be possible to miniaturise a defibrillator, make it work automatically and only when needed, and implant it in a patient?
This was a hugely ambitious project, but Mirowski was a man of exceptional tenacity. A Polish Jew, he grew up in Warsaw and was fifteen when the German army captured the city in 1939. Rather than submit to wearing the yellow star of David he set out on a six-year peregrination through eastern Europe and Russia, living on his wits and covering more than 6,000 miles. When he finally returned to Warsaw in 1945 his entire family, and their home, had disappeared. He went on to study medicine in Poland, France and America, where he worked for Helen Taussig at Johns Hopkins, before finding a job as a cardiologist in Israel. It was there that he conceived the idea of an implantable defibrillator, but his hospital lacked the requisite technical resources to get the project off the ground. It was not until 1968, when he moved to Sinai Hospital in Baltimore, that he was able to make any progress.108
There he joined forces with an electronics expert, Morton Mower, who had coincidentally had the same idea for an implantable device. Defibrillators were bulky objects, and Mower was at first sceptical that it would be possible to shrink one to the necessary size. But they soon realised that placing electrodes directly on the heart substantially reduced the voltages necessary to defibrillate, and hence the size of the electrical components involved. A rudimentary prototype was ready by 1969 and was implanted successfully in dogs.109 Like others before him, Mirowski encountered considerable resistance to the idea, and at least one journal rejected his first paper on the subject.110 When it was finally printed in 1970, Bernard Lown – the leading authority on defibrillation – was scathing in his response. He suggested that the device was likely to give unnecessary shocks, with possibly fatal results: ‘That the heart will be injured is certain; the only uncertainty is its extent.’111 Another specialist described the proposed device as a ‘bomb inside the body’.112
Prevailing opinion was so hostile that Mirowski and Mower were unable to raise funding for their project, and at first had to pay for their own equipment. Their situation eased somewhat after they reached agreement with a small medical technology firm, Medrad, to develop the device in partnership. The research was demanding and dangerous, involving electrical currents of thousands of volts. Mower narrowly escaped electrocution when one accidental discharge leapt from the electrode he was working on into a bowl of water six inches away.113
Making the device small enough turned out to be relatively straightforward; the main difficulty was how to make it recognise a serious arrhythmia. There was no room for error: a single unnecessary shock to the heart could kill the patient. At first Mirowski used a blood-pressure sensor, but this proved unreliable.114 The team eventually adopted a method that entailed continuous analysis of the heart’s electrical activity, using a mathematical formula called a probability density function to identify the chaotic state characteristic of ventricular fibrillation.115
By 1975 they had a working model, which was implanted in dogs. To convince the sceptics, Mower and Mirowski made a short film of the device in action. It showed a normal dog being put into ventricular fibrillation with an electric shock and collapsing as its heart stopped pumping. A few seconds later its unconscious body jerked as the automatic defibrillator went into action, zapping its moribund heart back to life. Shortly afterwards it was awake and got back to its feet.116 Long-term testing followed, with five dogs given the implantable cardiac defibrillator for periods of up to three years.117 By late 1979 Mirowski felt that they were ready to put the device into a human.
The first ICD was implanted in an operation at Johns Hopkins on 4 February 1980. The patient was a fifty-seven-year-old woman who had had a heart attack eight years earlier. She had suffered regular episodes of arrhythmia ever since, and on one occasion had only survived because she collapsed on the steps of a hospital, where a defibrillator soon brought her back to life.118 Mirowski watched as the surgeon, Levi Watkins, attached electrodes to her heart. One was passed through a vein to the right atrium; the other was a rectangular patch that was placed on top of the pericardium. The device itself was placed in a pocket under the skin of the abdomen and then connected to the two electrode leads. This first implantation was an unqualified success: when Mirowski reported the procedure five months later the patient was still alive and had suffered no more episodes of fibrillation.119
Within a year of this landmark operation sixteen patients had received an ICD. The device could be tested by artificially inducing a dangerous heart rhythm, and in the vast majority of cases the device quickly corrected the problem.120 Many cardiologists remained suspicious of the innovation, however, and over the next few years Mirowski and his colleagues produced an avalanche of clinical studies to demonstrate that it was both safe and effective. The earliest model was only able to detect ventricular fibrillation, but by 1983 Mirowski and Mower had produced a second-generation device – a cardioverter-defibrillator – which was also able to convert dangerous tachycardias into a normal heart rhythm.121
One early concern about the ICD was its effect on the patient – how painful would it be to receive a shock of several hundred volts to the heart? A few early units malfunctioned, imparting a series of shocks at regular intervals and causing great distress. But when the ICD functioned normally, patients reported that the sensation was generally no worse than being given a firm punch in the chest.122 And such temporary discomfort was certainly bearable if the alternative was cardiac arrest and death. When Mirowski began his research, most of his colleagues believed that there were few patients who would benefit from such a device. By the mid-1980s it was painfully apparent that sudden cardiac death was a problem of epidemic proportions – there were thousands of patients whose hearts were in danger of going into a life-threatening arrhythmia at any moment. By 1985 sufficient patients had received the device for researchers to establish whether it was effective in preventing death. The results were stunning. If left untreated, up to 66 per cent would be expected to die within a year; but mortality among those who had been implanted with a device was just 2 per cent.123 As evidence in its favour piled up, the medical establishment finally accepted the ICD without reservation. It had taken twenty years to convince them. The inventor was fond of quoting his ‘three laws of Mirowski’: ‘Don’t give up; don’t give in; and beat the bastards.’124 There could be no better vindication of his bloody-mindedness.
By 2009 more than 250,000 ICDs were being implanted every year worldwide.125 The current models are vastly more sophisticated than those of the 1980s, treating a greater range of arrhythmia and often combining the functions of an ICD and pacemaker in one unit. The latter has also been transformed: modern pacemakers are fully programmable, tailoring their response to the needs of the patient, and record all cardiac activity so that doctors can analyse it in detail, with data transmitted to a computer wirelessly or even over the internet.126
Today’s devices can even be controlled remotely, a fact that provided a chilling plot twist for the TV drama Homeland. In an episode broadcast in 2012, terrorists discover the serial number of the US vice president’s pacemaker and are able to hack into it, accelerating his heartbeat until he goes into cardiac arrest and dies. Astonishingly, the scenario is not as far-fetched as it at first appears. In 2008 a group of researchers investigated the security of wireless-enabled ICDs and discovered that they were able to take control of them using equipment available on the high street – though a would-be assassin would have to be standing next to their victim in order to be successful.127 Nor was this just a theoretical risk. Vice President Dick Cheney was given an ICD in 2001 after many years of serious heart trouble. Six years later the device was replaced with one with wireless capability, and his cardiologist Jonathan Reiner immediately became worried that it was vulnerable to malicious attack. At his request the manufacturer altered its software to disable the function, ensuring that the vice president would not be the first ever victim of a uniquely futuristic crime.128
The development of the pacemaker and then the ICD was a triumph of technology over disease. In the nineteenth century countless patients suffered from mysterious heart palpitations that eventually killed them. Today’s cardiologists do not use such vague terminology, and can identify specific arrhythmias and usually treat them – frequently by implanting an electronic device. This is often a palliative measure given to those who have already suffered a major heart attack. But – as the old adage goes – prevention is better than cure; what if it were possible to identify those at risk of such an event and somehow prevent it? Even as the pacemaker was being perfected in the 1960s another front was opening up against heart disease – one which relied on the old-fashioned virtues of the scalpel and superlative surgical skill.