Congestive heart failure occurs when the heart has healed from the heart attack, but the tissue remains damaged. The injured heart muscle is so dysfunctional that the heart isn’t an efficient pump anymore. It can no longer get a good blood supply to the liver, kidneys, legs, and feet. Heart contraction is inefficient, and the blood in the heart backs up into the lungs. This makes it hard to breathe or perform physical activities.
It turned Dad into a cardiac cripple. His heart had been so damaged that the muscle had stretched and weakened. He maintained his mental acuity, but lost his physical vitality. He was a shell of the man I had known. It seemed like he spent more time in the hospital than at home. Grappling with the ongoing symptoms of heart failure became nearly unbearable.
Soon after, he broke his hip. He went in for an operation to have hip replacement, but the surgeon came out after to tell us that Dad wasn’t waking from the surgery. Initially they thought it was a stroke, but it became clear that Dad’s problem was an overdose of anesthesia.
The surgeon in me immediately began planning a course of care and strategies to save him. “Okay, Mom,” I said, attempting to rally my mother with forced optimism. “This isn’t permanent. He’s going to wake up, and there are a number of issues we’ll need to immediately address. First we have to….”
My mother laid her hand softly over mine. “No, Gerald. We can’t. It’s time to stop. Ever since Dad’s heart failure, he hasn’t been living the life he wants. He goes in the emergency room now every two weeks. He can’t do anything. It’s deprived him of all the joys of life. It’s over.”
“Over?” The word echoed in my mind. For once, my busy brain stopped and I had no plan or response. I felt empty as my mother acknowledged what I couldn’t: this was the end.
“Hospice,” she said quietly.
Dad passed away six days later.
It had been many years since my father’s passing when I turned the attention of our team toward heart attacks. I no longer felt the loss merely as a son; it was also impacting me as a doctor. Tracing my father’s journey was proof that when not treated proactively, the health of a heart attack survivor can go from good to bad to ugly in a relatively short time. Dad’s experience went like this:
acute chest pains (angina)
coronary artery grafting (weeks later)
loss of muscle from silent heart attack
devastating heart failure develops after the damaged heart dilates
death
It happened over a period of years, but for me and everyone else who loved my dad, the end still came way too fast.
If anything keeps me up at night, it’s the memories of my grandfather and father when they were hearty and hale, interrupted by their premature decline. For many, the grim reaper appears as an acute heart attack, like it did for my Grandpa Zelig. It strikes without warning, as half of its victims have had no prior symptoms.
Yet even those who survive a heart attack, like my dad, rarely escape unscathed. Damaged heart muscle may severely curtail activities, joys, and pleasures while it gravely shortens lives. I never will forget holding my Dad’s hand during his final moments in hospice when we said goodbye, watching life slowly leave his face as he drifted away.
Over a million people suffer heart attacks every year.
My family had to go through the loss of loved ones due to limited options for treating heart attacks and the secondary complication of congestive heart failure. I found this entirely unacceptable. I became determined to find a way for physicians to intervene in this process so others wouldn’t have to suffer as our family and so many others had.
I found a new mission.
The Weakened Heart
Many people believe that if you survive a heart attack, you’re one of the lucky ones. You might make some changes to your diet, begin exercising more, take better care of yourself, but you have your life back.
But the truth is hardly that simple… nor is your future that encouraging.
Heart attacks cause the death of the muscle region supplied by that closed artery. When your heart pumps too weakly, as it will commonly do after a substantial heart attack, no matter how much you improve health habits, it can cause ongoing inescapable fatigue. You may develop abnormal heart rhythms (called arrhythmia, where the heart beats irregularly, too fast, or too slow). What starts out as a nuisance all too often progresses to a debilitated heart that significantly impairs your life. It can become overwhelming, like in my father’s experience, where you have very little energy and the least amount of activity or exercise exhausts you. Where you have to rest all the time and can’t breathe unless you sit up in bed. Where your swelling is so bad that you cannot even put on your shoes and must go to the emergency room every two weeks to have fluid drained. Essentially, you’re incapacitated.
Frankly, the remaining life expectancy of patients in advanced stages of congestive heart failure is worse than those with terminal cancers — with a 50% chance of dying in one year and a 75% chance of dying in two years.
Dual Objectives
To counter such grim prognoses, I would develop two distinct goals. My first, the focus of this and the next chapter, was to offset these effects of heart attacks by returning function to the damaged muscle, ensuring that patients remain well until the natural end of their lives. The premise is that preventing the injured muscle from dying will prevent heart failure from developing after a heart attack.
I would later pursue another goal — to correct congestive heart failure in patients whose heart attack was not initially treated correctly. This will be the subject of subsequent chapters.
But at this point — I was directing all our efforts toward discovering a way to prevent heart damage from ever occurring in the heart attack victim. To do this, we needed to cast aside conventional views that heart muscle cannot be saved if treated more than two hours after a heart attack. Instead, we would consider something that had never been examined before: providing the injured area with a controlled reperfusion, rather than only delivering normal blood reflow after the attack.
Though not consciously aware of it, my driving force was knowing that if I had developed such a successful approach ten years earlier, it could have made all the difference for my dad, and, if it was available when I was age 14… would have helped my Grandpa Zelig.
While I was aware that was no longer possible, it wasn’t too late for the countless others who suffer from heart attacks every year. My hope was to catalyze a systemic change that ultimately could save many lives. We simply had to do better… because the adverse aftermath of conventional treatment was far too great.
More Than Observer
Our profession’s code, the Hippocratic Oath, states “Do no harm.” But it is often misused by today’s medical community, and unknowingly creates our greatest obstacles to making discoveries.
Why?
Hippocrates was an observer. To the ancient Greeks, disease was as much a normal part of life as health. From his perspective, the job of a physician was to understand and describe disease with as much precision as health. He didn’t believe that interventions could improve the patient’s standard of life.
But today, disease and disability are not for us merely to observe and certainly not to accept. Hippocrates would be at a loss in a modern hospital, where so much of what we do is in direct contradiction to his basic observational philosophy. His enormous contributions have formed the cornerstone for how we interact with patients, but as with all hallmarks, it was simply the first step. Therapeutic approaches and health care advances have allowed us to utilize a whole modern universe of ideas on our patients, taking us far beyond anything Hippocrates could have ever imagined.
Yet some conventional thinking has taken up his view that certain circumstances are inevitable and simply part of the disease process. Such has been the case with treating heart attacks. The lasting damage accompanying them was believed unavoidable — that the primary goal was to keep the patient from dying fro
m the heart attack — and was not aimed toward circumvention of the consequences that often came later.
Normality: The Shape of Things to Come
As Hippocrates wisely observed many centuries ago, disease is a departure from normality. I have stated in this book that in order to comprehend the abnormal heart, it is critical for us to first fully understand the proper functioning normal heart — which is linked to its proper shape.
Most physicians, and the general population itself, believe the heart simply squeezes (like closing a clenched fist) to circulate blood. But as we would discover — both in this study and later with even greater clarity (described in subsequent chapters) — a healthy heart has an elliptical shape, like a football, and actually twists to eject blood — and then recoils to fill efficiently.
This is important to know because one of the biggest problems with heart attacks is they change the geometry of the heart. This change in shape alters its ability to function — and not for the better.
As you read this, realize that you are about to know more about heart attacks than most people — including many cardiologists and heart surgeons who treat them.
With the heart, geometry is everything. Like so many of nature’s beautiful creations, the heart has a helical (spiral) formation, which is responsible for the twisting actions. While many people mistakenly think the normal heart is a pump that simply compresses (squeezes) to circulate blood and then dilates (expands) to fill — that motion is only the case for patients suffering from congestive heart failure. When the diseased heart stretches abnormally and its helix (spiral) shape becomes deformed, it appears and reacts more like a rotating basketball rather than an efficient spiraling football.
That’s a problem, because the spiral shape is the essence of efficiency in nature. Furthering the athletic analogy helps illustrate this process: a high school quarterback can throw an accurate 50-yard football pass, but even the best NBA guard cannot throw a basketball 20 yards with the same precision.
So how does this fundamental change in shape occur?
Anatomy of a Heart Attack
Heart attacks begin with narrowing of arteries — the large coronary blood vessels that nourish the heart muscle. They can narrow for a number of reasons. It can be from cholesterol and fatty deposits called plaque building up on their inner arterial walls (hardening of the arteries), which reduce the opening and restrict blood flow. This plaque can also develop a crack (or ulcer) that becomes an opening to allow blood to enter the inner surface of this arterial wall and become trapped, so a blood clot forms, obstructing the vessel. These sequences cause restriction of the blood supply to the muscular region of the heart. When the coronary artery is completely closed, a heart attack occurs.
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.
What Really Happened
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 looks good.
Indeed, these modern treatments have reduced the overall mortality that immediately follows a heart attack — due to abnormal heart rhythms (which can lead to dangerous ventricular fibrillation), or due to heart failure (causing lung congestion) — from around 20% down to about 5%. A powerful confirmation.
But it is essential to understand why the heart has improved — and after the patient leaves the hospital — how this “improvement” alters their future.
When the angioplasty restores blood flow, the bulging dead muscle in the heart attack region shrinks to a smaller, thickened — though still non-contracting region. (Figure 1) This heart changes shape in response to the now smaller size of the ventricle, so that the still-functioning (also called “viable” or “living”) remote muscle no longer needs to stretch as much to compensate for diminished function. The bulge disappears, and the now smaller heart size begins to reflect a more normal shape.
Figure 1: On left: cardiac shape of the normal heart in lighter gray color, showing its natural elliptical or V shape before a heart attack. The circular out
er form (darker shading) displays the effects of a heart attack where the injured muscle becomes spherical.
On right: cross section of heart attack region after angioplasty has successfully restored blood reflow. Note extensive damage (toward the right side) shown by the darkened area in the inner shell of deeper muscle. The outer muscle shell is undamaged so that the heart surface appears normal, yet this entire region does not function.
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 toward finding another approach to treatment… but they don’t see the future.
Solving the Mysteries of Heart Disease Page 12
