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You Don’t Have to Die Of a Heart Attack

My maternal grandfather, Zelig Levitt, was a role model whose lifelong dedication to hard work and persistence reflected his immigrant background. His strength and vitality never waned, until the day he suffered a myocardial infarction — a heart attack. There were no warning signs. One day, he was hard at work – he died in the hospital two days later. The man who was larger than life, always so full of strength and vitality, died in a narrow white hospital bed. He never knew what hit him.

In addition to losing my dear grandfather to a heart attack, I later watched my father suffer the devastation of congestive heart failure. I became a doctor because I wanted to help people, but I also wanted answers. Thus, I entered the world of cardiovascular research.


Heart attacks occur because a part of the heart stops squeezing after there is sudden loss of blood supply to that area. After a heart attack, modern treatments employ different approaches to resolve the problem of a completely closed artery.

Cardiologists use drugs to dissolve the clots in the arteries, or open the artery with a catheter and balloon (angioplasty) to restore normal blood flow.

Alternatively, cardiac surgeons may perform a bypass graft, like the one my dad had, to carry the normal blood supply around the blockage. This is done by taking a portion of a healthy artery or vein from elsewhere in the body – and inserting one end into the healthy artery or aorta that exists before the stoppage, and inserting the other end into the unobstructed part of that vessel beyond the narrowing – so that it passes by the blocked segment to provide unrestricted flow.

To appreciate the value – and limitations – of these approaches, it helps to understand what typically occurs when someone is brought in with a heart attack.

It is not what most people believe (including many cardiologists and cardiac surgeons).

Customarily, sirens are blaring as the heart attack victim is rushed to the hospital in an ambulance or paramedic’s van. The doors of the Emergency Room burst open as a team of paramedics wheel in a gurney carrying a prone man, his face awash in fear, as the EMT rattles off all known information about the patient to the attending physician: patient is in his 60s, slightly overweight; he has severe chest pain and shortness of breath, rapid heart rate, with a blood pressure of 100/80 (normal being 120/80).

The patient is evaluated and then hurried into the cath lab. A catheter is placed into his pulmonary artery to find that his heart-filling pressures are elevated and the amount of blood ejected by the heart is lower than normal. The ejection fraction (the percentage of blood in his heart getting pumped out to the body per beat) is reduced from a normal 60% down to 35%.

This is what they can measure.

What is occurring inside is that the damaged heart muscle area immediately loses its capacity to pump. This causes the heart’s structural anatomy to change. Every time the heart contracts, this injured region of the ventricle will expand and thin – as some of the blood in the chamber does not pump out, but rather stretches or billows the damaged region, making the heart shape look like it has a blister. This bulge is called an aneurysm.

In addition to the pain felt by the patient, this bigger ventricle may develop arrhythmias (abnormal heart rhythms) – or it may contract inefficiently.

To counteract the dysfunction of this now bulging region, the remaining still-functioning muscle areas (called the “remote muscle” – away from the damaged muscle) must also stretch or expand to help the heart pump more forcibly – to ensure the body has adequate circulation.

The result is that as the dead heart attack region develops its new bulging form, the heart’s overall shape becomes more circular – like a basketball – instead of its natural elliptical or football-like appearance.

 So what treatment will counter these effects?

At first glance, coronary angioplasty seems like a perfect remedy, since blockage of blood flow caused the heart attack in the first place. Cardiologists insert a catheter into the artery, push it beyond the blockages, and then deploy a balloon to stretch the narrowed vessels… a maneuver that will dramatically provide the patient with new blood supply. To assess this, the monitors are promptly checked by the treatment team:

“His blood pressure is back to 120 over 80.”

“Pulse rate has dropped from 110 to 80 beats per minute.”

“His pulmonary blood pressure is down… his cardiac output is better… his ejection fraction has increased from 35% to 50%.”

The conscious patient chimes in by reporting, “Thanks, my chest pain is gone.”

With his vessels once again cleared and his heart action improved, the patient is sent to the cardiac ward for observation and recovery. The treatment team congratulates themselves on another life saved.


Without question, the initial results support the conclusion that this patient’s life has been preserved. His chest pain is immediately relieved. His blood pressure increases, heart rate falls, and heart-filling pressures decrease.

Everything seems better. The treatment appears to have offset the heart attack. But this conclusion is incorrect.

The reality is it hasn’t helped the heart attack area’s ability to contract, since it remains non-functional. It has just helped the remote muscle (the muscle portion away from the damaged region). Things got better because the heart’s geometry improved – the reduced size of the bulging muscle (now smaller and thicker, instead of bulging and thin) permits the functioning remote muscle to get smaller. That is the only reason the heart recovered its performance.

But the injured (now rigid and thicker) heart attack muscle is still not squeezing. The inner half of the heart attack muscle has been damaged – yet the whole heart muscle simply cannot recover function if even 50% of its muscle is lifeless. (22) As a result, the dead muscle that existed before returning new blood flow – remains dead after blood flow is restored – and non-functional. The principal goal of returning this damaged heart muscle’s capacity to contract has simply not been achieved.

Consequently, the still-contracting remote muscle is now totally responsible for heart function. This responsibility began the instant the heart attack started – and it continues despite a successful angioplasty.

Now, cardiologists and surgeons know this inner half of the heart attack muscle has been damaged – yet nobody believes it can be helped. It is considered an unfortunate, but unavoidable and unfixable aspect of having a heart attack. This fait accompli conclusion has prevented progress being made toward finding another approach to treatment… but they don’t see the future.


While everyone celebrates the fact that opening the closed artery reduces the immediate loss of life from 20% to 5% after a heart attack… these treatments often only postpone the mortality.  The long-term aftermath is that 30% of surviving patients will develop heart failure within five years, despite having the artery successfully reopened.


If instead of initially returning normal blood to the damaged region as is traditionally done – we add specific ingredients to the nourishing blood and simultaneously control how it is delivered. Through this controlled reperfusion, the damaged region’s contraction returns immediately.

Following our procedure’s success in a laboratory setting, this technique was applied internationally in 1992 to 155 patients suffering an acute heart attack. The outcomes were successful: contraction immediately returned to the heart attack muscle, and the potential after-effects of heart failure and fatal arrhythmias did not happen.

Fortunately, both cardiologists, as well as surgeons, can apply this treatment, since the required equipment already exists in the cath lab, and needs only minor modifications.

But in order for our treatments to be adopted – cardiologists must recognize that our treatment works, since they are the gatekeepers that allow the emergence of new developments, and their acceptance will then become the starting place for the initial testing of a new pathway by their cardiac surgeons.

Our Treatment for Heart Attacks: The Three-Step Process

This new way to treat heart attacks requires cardiologists and surgeons to work together in a collaborative evolution of treatment that requires three steps:

  • First, the cardiologist must recognize the limitations of traditional angioplasty, and be open to a way to deliver controlled reperfusion surgically.
  • Second, surgeons in those same hospitals must learn to perform a new reflow method on acute heart attack victims. Their successes would show their cardiologists that this treatment works.
  • Third, the cardiologists must then adapt new strategies allowing them to use these approaches in their own catheterization labs.

Fulfillment of this cooperative process will initiate a new treatment for the heart attack patient, the true beneficiary – and save lives.


The intent for telling my story here is for the public to become aware that we have ways to counter the all-too-frequent misery and early death that still accompanies heart attacks.

As acclaimed astrophysicist, author, and recipient of the NASA Distinguished Public Service Medal, Neil de Grasse Tyson, once said: “The good thing about science is that it’s true whether or not you believe in it.”

The truth is, treatments solving these problems exist now.

Readers of my book, Solving the Mysteries of Heart Disease, may add their voices to mine and those of my colleagues who continue to push the rock up the hill, trying to encourage the larger medical community to transform. Frankly, we owe it to our patients, our colleagues, our loved ones, and the world at large to forward this long-overdue shift. Change and evolvement are inevitable. The answers are already here.

How long do we wait before we embrace them?


*Excerpted from, Solving the Mysteries of Heart Disease: Life-saving Answers Ignored by the Medical Establishment by the late Gerald D. Buckberg, M.D., D.Sc. REPRINTED WITH PERMISSION FROM THE PUBLISHER.


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