Solving the Mysteries of Heart Disease

by Gerald D Buckberg

The return of blood flow will make this bulge disappear — but the scar remains, now occupying 50 to 60% of the heart muscle’s inner shell. The scar’s extent changes (from whole muscle to just inner shell), but impaired performance within the scarred region does not. There is no recovery of contraction… regardless of whether the scar occupied either 100% or 50% of the injured muscle.

  To keep the patient alive, the remote muscle (that portion without a heart attack) must beat more strongly to compensate for the injured area’s lack of contraction. But the heart stretches as this is done, and as the ventricle widens over time, this dilation will wear down the remote muscle’s ability to function.

  Dor elaborated that this change in the heart’s geometry causes the heart’s normally elliptical or football shape to distort into a more spherical or basketball-like shape. (Figure 2) The result is its natural powerful twisting mechanism turns into a less efficient compressing piston (which ironically will now closely resemble the heart function that William Harvey described in the 1600s — mimicked by the clenched and opened fist.)

  As this remote muscle continues to weaken, heart failure symptoms appear and progressively worsen, and finalize in death.

  Until now, no one had ever talked about how the scar affects the ventricle or how it changes the heart’s geometry. Yet as I listened to Dor… clouds of confusion gave way to the exciting light of clarity.

  Figure 2: Cardiac shape of normal heart (left) is conical. Spherical configuration on right represents dilated heart in heart failure.

  How apparent things can become if we stop to truly see, and are not simply obedient to what has always been believed.

  I joined Dor’s new thinking and exclaimed, “Finally, this makes perfect sense!”

  The Grand Solution

  It was by listening to Dor that I finally began to understand that the solution to this post-heart attack dilemma could not be accomplished solely by the delivery of medications, or by surgeons performing coronary bypass grafts or mitral valve corrections. These are incomplete remedies.81, 82 The fundamental reason for poor outcomes arises from the medical world’s failure to address the geometric change from the elliptical heart to the ill-fated spherical shape.

  Part of the problem in understanding relates to an accepted medical objective called “muscle salvage.” This refers to the goal of keeping the muscle alive. Prompt use of angioplasty results in only 50 to 60% of the heart attack muscle becoming scarred, instead of 100%. Yet when this happens, the term “salvaged muscle” (referring to the other 40 to 50% of outer muscle that’s saved) creates a fundamental misconception. Despite the “saved muscle” now having a normal surface appearance — the area beneath it is dead and scarred, and the whole region does not function.22 Yet surgeons consider the normal surface to be healthy, and deem it “off limits” from getting cut into.

  It is essential to abandon this misconceived limitation, since the proper treatment of heart failure is to surgically rebuild the scarred ventricle. Dor’s work showed the solution was straightforward: operate on the spherical heart to get rid of the scar, and then reconstruct the natural elliptical shape. Only one other surgeon, Adib Jatene from Brazil, had simultaneously come to this conclusion.83

  Yet to me, this was the potential game-changer.

  Though some of us were aware that these thickened muscles after angioplasty were not able to squeeze, we never acted upon this. We too thought they were inoperable.

  But Dor had already performed these operations — with great success.

  Figure 3: The geometric changes described by Dor are shown in this image.

  Upper left is normal heart with conical shape. Upper right is dilated heart after a heart attack with the white area showing the scar, as the chamber dilates (expands) to compensate, and becomes spherical. Lower image shows ventricular restoration that excludes the scar and rebuilds the normal conical shape.

  He recognized that the scar nearly always involved half of the ventricular septum (a muscle that forms the curtain between the left and right ventricles), and knew that stitches in such a squeezing muscle may not normally hold well. So he developed a new procedure called an endoventricular circular patch plasty operation. It beautifully sews in a patch of synthetic material to safely exclude the scar.79 So to be clear, “excluding” the scar does not mean surgically removing it. Rather, we restructure the heart shape — so the area where the scar is located is excluded (isolated) from playing any role in the heart’s function. (Figure 3) Dor showed me videos of several of his operations. Each outcome was nothing less than amazing.

  I realized that while conventional surgical and medical protocols for heart failure focused on the “two Vs” — treating the blood vessels and the heart valves — we had ignored the third V — the ventricle. It was the “triple V” — vessels, valve, and ventricle — which together played the vital roles that needed to be dealt with simultaneously in treating congestive heart failure.

  Confronting the Culprit

  While I had learned all of this some years before my trip to Argentina, I had been fully occupied with my cardiac operations and research activities. Yet my interest in exploring this avenue blossomed at the end of my depression.

  A number of years had passed since we showed that giving controlled reperfusion after a heart attack (described in Chapter 8) prevents the culprit scar from ever occurring, thus avoiding subsequent heart failure. Yet this approach to treating a heart attack had not yet been widely adopted, so I now turned my focus directly toward addressing the scar causing heart failure in these large dilated (stretched beyond normal size) hearts. In other words, I shifted my pursuits from trying to avoid the detrimental scar… to learning how to exclude it.

  I knew that Dor’s method of treating heart failure (by excluding the scar and making the ventricle look normal again) needed to be proven to the surgical cardiac community, if we were to galvanize a new approach to correct the ventricular cause of heart failure. To ignite such a fundamental change in thinking requires a major study to confirm that other surgical teams could match Dor’s results. To achieve that goal, I intended to create a new international team.

  Our primary objective would be to prove that the cause of heart failure is the scar, and then correct it. This concept would be tested by restoring the normal size and shape of the ventricle with the Dor procedure.

  A totally new surgical solution for treating heart failure would emerge if this was successful.

  Changing the Game

  As noted, I needed to pursue this new ventricular approach to solving heart failure because until now, the use of controlled reperfusion after an acute heart attack (that would keep the culprit scar from forming, as discussed in Chapter 8) was not generally accepted. Said most simply, the primary treatment goal needed to change from preventing the scar, to correcting the abnormal ventricular shape that is caused by the scar’s presence.

  Despite the inherent shortcomings of normal blood reperfusion after a heart attack, the enormous contributions of conventional angioplasty or drugs that dissolve the clot should not be disregarded. Each treatment achieves the powerful common goal of opening the closed artery, and such success yields a reduction in how often sudden death and / or early heart failure can develop. This treatment lowers the high mortality that would otherwise occur if the closed artery was not reopened. Angioplasty contributes a dramatic finding because it reduces initial mortality from 20% to 5%.

  Yet despite these improvements, the culprit scar in the ventricle remains, and its presence causes the later development of heart failure. The timing of this ill-fated complication? That depends on when the remote muscle stretches enough to make the ventricle develop a spherical shape.

  At Great Cost

  The importance of finding answers becomes greater as we realize a dire truth: the frequency of heart failure has continued undiminished.

  The incidence of cardiovascular disease fell 30% between 1995 and 200984 — but the incidence of congestive heart failur
e remains unchanged. There certainly has been progress in treating congestive heart failure through improvement in drug therapies, including agents that alter calcium metabolism and relax arterial blood vessels, and specialized diuretics that limit potassium loss. While we are grateful for these support medications that reduce symptoms and prolong life, we also note the challenge to cardiologists who continue their search for drugs to counter heart failure’s many effects. This quest seems impossible when one considers the broad spectrum and sheer number of different body processes that are negatively affected. This also points to the ineffectiveness of trying a “one by one” approach to offset each of these numerous symptoms, which result from the body receiving profoundly inadequate nourishment due to a poorly functioning heart.

  Aside from the physical and emotional costs, there are substantial financial costs associated with this as well. Present treatments for heart attacks and heart failure make up this nation’s and the world’s largest health care expenditure. It may reach $1 trillion per year by 2030 in the U.S. alone.38

  The bottom line is we are not solving the problem. Instead, we are finding ways to make sick people live sicker longer, taking one expensive drug after another.

  Who Will Get Heart Failure: The Secret of Volume

  The debilitating symptoms and continuing high costs stemming from this terrible disease lead the patient or their family to ask a natural question: “Is there a way to predict who will get heart failure?” This is a thoughtful question, because not every heart attack results in heart failure.

  There is an answer, and it again relates to the scar. Progression to heart failure begins if more than 20% of the heart muscle is dead, as this area forms the scar.77 When that occurs, an increase in the ventricle’s volume (the ventricle size, determined by the amount of blood in the ventricle at end of contraction) results as it dilates… with the heart sometimes progressing to become spherical in shape rather than elliptical.

  Figure 4: Athletic analogy, with spherical / basketball shape (left) and normal conical / football shape on right. I went to Ohio State, where the spherical Michigan shape represents our enemy.

  Again, from a sports perspective, the elliptical heart is like a football (having a spiral twisting motion) and the failing abnormal one is more like a basketball (having a squeezing motion). (Figure 4)

  I had never paid attention to — or measured — ventricular volume until Dor finally revealed this information to me in Monaco. But I learned there is a five-fold greater chance to develop heart failure when the size of the ventricle starts to more than double, from the normal 25 ml/m2… to 60 ml/m2.85 Subsequently, death from congestive heart failure also correlates to these increasing volumes. The larger the volume, the more often and more quickly one succumbs. For instance, people with 150 ml/m2 will perish much faster than those with 70 ml/m2. (Video 1)

  Video 1: The normal efficient ventricle with an elliptical shape is shown first, followed by a failing dilated heart with a spherical form, which also makes the mitral valve leak due to stretching of its parts.

  www.vimeo.com/buckberg/failing-normal-heart

  Nobody can predict exactly how long it will take in a particular person. This depends on how much the ventricle volume enlarged after the initial heart attack. But it has been shown that if the volume is more than 60 ml/m2 after the initial attack… heart failure and ultimately death rates can rise to 40% during the first year.86 The reason is that larger ventricle volumes require the remote muscle to function in an increasingly abnormal way, wearing it out faster.

  It should be noted that these dilated hearts that cannot contract efficiently — are the cause of heart failure in only about half of our patients. Congestive heart failure can also be due to another cause. The other 50% of patients develop this condition when ventricular size and geometry are normal, but the heart does not relax easily. This second issue will be addressed later in Chapter 22.

  Size IS Everything

  Given this perspective, there needs to be a reassessment of the importance of volume. The knowledge gained from its measurement is vast — since a spherical cardiac shape (from an enlarged ventricle) becomes the constant factor that explains the development of heart failure from multiple causes. (Figure 5)

  Three such causes are described below (and in Figure 5 on the following page) — with shape again being the consistent factor in each:

  First, as we’ve discussed, in coronary artery disease, a scar forms where there has been a heart attack, and the remote, viable muscle expands to compensate by contracting more forcefully. This stretch will cause a spherical heart shape.

  Second, a spherical shape also occurs from valve disease when either the aortic or mitral valve leaks. Ventricular volume increases as the heart must pump extra blood to the body to compensate for the leakage from an insufficient heart valve.

  Third, a similar spherical form develops in patients who have a disease in the ventricular muscle (from a virus, for example), despite their having normal coronary arteries and valves.

  The ramifications from these examples are clear: the medical community needs to understand why enlarged ventricles are so detrimental to heart function, and that the solution is straightforward. They relate to the heart’s architectural structure.

  Figure 5: The three causes of a dilated heart include: on left, a heart attack due to a closed coronary artery; in center, a leaky aortic or mitral heart valve; and on right, direct damage of the heart muscle.

  The Right Fiber = Good Health

  This isn’t about dietary fiber.

  To truly understand why this spherical shape causes the heart to perform so much less efficiently, we need to visualize the heart not only from the outside, but also from within the ventricle. The external change to a sphere shape is obvious… but heart failure also changes the muscle fiber orientation (the angles of these fiber pathways) within the wall of the cardiac muscle. (Figure 6)

  As you see from the illustration, the slanted or sloping fiber pathways (at 60°) that exist in a normal elliptical heart… become more horizontal (extending from side to side, rather than at angles) when the ventricular shape becomes circular. Why is this important? Because this accounts for the decrease in the heart’s ability to function — as the twisting ability disappears — and is replaced by the inefficient, clenched fist version of pumping that also increases chances of a premature death.37

  Figure 6: Anatomy and muscle fiber arrangement in normal heart (upper) and dilated heart in heart failure (lower). Note the fiber angles are at 60° in normal heart, and more horizontal fibers at approximately 30° angles in failing heart.

  The dynamics of how the differences between the natural elliptical shape and the spherical contour account for the discrepancy in heart efficiency are shown in Video 2, taken in the operating room. It contrasts the performance of a normal heart with one that is dilated and failing.

  Drugs cannot fix this geometric problem responsible for poor heart function, but correcting the abnormal spherical structure to restore the natural elliptical shape will.

  Why was I so certain?

  The rationale for my confidence wasn’t limited only to what I had learned from Dor in Monaco. Or even my later discovering the additional vital contributions of Adib Jatene of Brazil, who had come up with a similar approach in 1984.83 The reason I was so convinced was that before I had flown to Argentina, before I composed my 70 pages on the plane ride back…

  I had performed this procedure in a patient with profound heart failure.

  Video 2: In these two sequential videos, the first shows the natural twisting motion of the normal heart with a natural elliptical shape. The second video component shows the inefficient performance of a failing dilated heart.

  www.vimeo.com/buckberg/twisting-and-dilated-hearts

  Hands-On Knowledge

  The circumstances leading to my conducting this operation arose out of a UCLA/Asian link we had established. We visited Asian countries to demonstrate our techniques
, and welcomed Asian teams to UCLA for learning. It was during a trip to Malaysia, not long after visiting Dor, when I told Yahya Awang, the Chief of Cardiac Surgery in Kuala Lumpur, about this new technique for heart failure that Dor had come up with — in which we change the geometry of the heart.

  Soon after I returned home, I got a call from Yahya, who asked me to see a patient in severe heart failure following a heart attack. The patient had been treated with angioplasty and no longer had an aneurysm or bulging segment. But he was in very bad condition, the situation grim enough to justify the patient traveling to UCLA for treatment.

  My thoughts immediately flashed on what I’d recently learned from Dor. This was my chance to see if his approach worked. But I had never performed this operation before… and needed to better understand how to do his procedure in this severely compromised patient. Dor had given me a videocassette showing his procedure, but it was not viewable at the hospital since it was recorded in the European PAL format. After many hurried phone calls throughout campus, I learned there was one PAL player in the Campus Library. Surprisingly, this was my first visit to Powell — the main college undergraduate library — and after some hunting, I found the machine and studied the tape.

  Armed with the certainty that this was the right procedure, and supported by Dor’s technical guidance, I embarked on my first treatment of heart failure by changing ventricular geometry in a patient.

  When the patient arrived at UCLA from Malaysia, he was not in good shape. Yet he trusted that I would help him. We scheduled the procedure.

  In the operating room, I informed the team, “We’re going to conduct an innovative kind of approach today, unlike anything we’ve ever done before. We will open the chest and shall find a ventricle that has a smooth, ordinary-looking surface, yet it camouflages the deeper internal scar that develops from the heart attack. The scar is why the ventricle dilates [enlarges] and causes poor function. We will exclude it and return the ventricle to its natural shape.”