Echocardiograms, routinely used during open-heart surgery, sometimes reveal images of a dramatic change in normal septum performance — even though the heart seems to contract adequately after an operation. Yet a huge disparity exists if the septum is injured, as it does not contract, so that this midline muscle (between the ventricles) stretches to billow into the right ventricle. It now appears like an aneurysm inside of the heart. These adverse actions consistently take place after the septum is damaged (which is also called “septum stunning”), even though patients sustaining such dysfunction are consistently thought to be doing well.
Lesser damage will make the septum squeeze poorly or only a little — but a bulge is the worst injury of all. Surprisingly, this clear functional impairment caused by septum dysfunction, has continued to be considered an acceptable complication of cardiac surgery. This indifference to its presence may arise because the patient is discharged four to five days later, an end point that creates a sense of self-satisfaction for the surgical team about the operation’s success.
But this is not true.
Hidden in the background lurks an injured septum. Consequently, serious potential problems can arise — including right or left heart failure, or diastolic dysfunction — because this part of the heart is not working properly.
So how frequently does this septum injury occur?
Disturbingly often. A recent survey of 3,292 patients showed approximately 40% had bulging or “paradoxical motion” (the septum moving away from the left ventricle free wall during ejection, rather than its normal movement toward it). These incidences are even higher (about 60%) after valve surgery.134
Sometimes the septum never gets better. But even when it does, it can still be a significant burden to the patient. I have a friend that regularly swims with me, who had mitral valve repair and went home after five days. But then he could not swim for six months due to shortness of breath. He recovered, but unfortunately had to endure a preventable ordeal.
As we will discover, an ill-functioning septum has many ramifications. The ongoing failure to fully understand this septum problem has led to a unique fallback position for surgeons and their cardiology colleagues: it is disregarded and is conventionally judged as an acceptable post-operative complication.
Weighing the Reasons for Failure
My commitment to solve these “whodunit” mysteries of septum dysfunction grew after I asked a colleague, a legend of cardiac structure, about the size of the septum. I knew the answer when I posed the question, but wanted to find out what this leader thought. Carmine Clemente is a brilliant, world-renowned anatomist, whose textbook is used by over 1.5 million students worldwide. He guessed the septum occupied 10% of the total weight of the ventricles.
I had already weighed the septum after completing some experiments, and compared it to the weight of the free walls of the right and left ventricles. His guess was wrong, as the septum weighed almost 40% of whole heart ventricular weight (while it accounts for about 50% of just the left ventricular weight). (Figure 3)135, 136
This realization prompted me to accelerate my investigations, especially since the septum was often damaged during cardiac procedures, and this injury was simply accepted as a natural complication of heart surgery. It was astounding that incapacitating something that occupies nearly 40% of the whole heart’s ventricular weight was not thought to be important.
Figure 3: Upper image shows intact heart. Lower 3 images show separation of heart muscle into right ventricle (RV), septum, and left ventricle (LV). Note size of septum.
A trail of clues began to appear. I started by looking deeper into the previously described study of 3,292 patients. There was a tip-off right in front of me: the report indicated that septum bulging was most common when aortic clamping was prolonged while the heart was being repaired.
To me, that sounded exactly like a reperfusion injury.
My prior work showed our method of myocardial protection avoids reperfusion damage. I speculated that a surgical procedure shouldn’t cause damage to the septum — if our methods to protect against reperfusion injury were done correctly.
But this theory needed testing. So we studied 119 consecutive patients to see if this was true. The result: No septum damage developed in any of our patients, despite aortic clamping times that extended up to 155 minutes.136
We next gained an even more powerful clarification.
We compared results following operative procedures that employed our full approach — to those performed by others who had used the same cardioplegic solutions — but did not follow our delivery methods. The result: septum damage occurred if our delivery strategy was not followed, but was absent when it was.137
The conclusion: success involves two components — the cardioplegic solution and adopting a proper delivery strategy. Avoiding septum damage does not result from addressing just one part of an answer (like only selecting a single instrument of the orchestra), but rather by using an integrated approach that enhances its effectiveness (the whole orchestra).
I believed the surgical community needed to know and utilize this information. So I submitted a report, “Cardioplegia: Solutions or Strategies?” to the two major American cardiac surgery journals. It was rejected by both. Yet incredibly, not one of these seven reviewers stated that their methods of myocardial protection avoided septum injury.
The sweep-it-under-the-rug attitude persisted, unaffected by truth.
At issue was not a suggestion that they only follow our protection methods. Instead, I recommended that they must always examine whether the septum’s function was compromised. I advised that if there was no injury, then they should continue their current protection methods. However, if there was injury, their protection methods should change. The end goal is to avoid septum damage. The selection of what process to accomplish this is up to the surgeon. It seemed unconscionable to subject the septum, which comprises 40% of its ventricular muscle weight, to a preventable form of heart damage.
As important as it was to solve this avoidable septum issue in cardiac surgery, I realized this surgical problem is only one example of many issues that can arise from a damaged septum. It was this appreciation that made me recognize that avoiding septum injury may “crack the case” — and resolve numerous causes of right heart failure.
Baby Heart Surgery… The Hidden Septum Role
My search to better understand issues with the septum intensified when I came across a revealing and unsettling problem.
As said, the inherent interplay between the septum — and right ventricle function — is linked to high resistance within the lung vessels against the blood flow that comes from the heart. This situation is dramatized by the tragic development of sudden right ventricular failure, which can develop unexpectedly… shortly after doing a successful heart operation in infants.
Before the baby’s operation, the beauty of the body’s ability to adapt to obstacles is clear — since right ventricle performance is normal — despite many of these infants having a high resistance to the flow of blood into their lungs. In other words, the uninjured septum had adjusted its function to fully compensate for this high lung blood flow resistance — enabling the right ventricle to readily eject blood into the lungs.
But that “adjustment” ceases as soon as the septum is acutely injured due to ineffective myocardial protection during a heart operation in infants. A new drama unfolds, as the infant may now experience the same septum problems that had confronted the adult. But the existence of this problem is initially hidden, since the infant’s right heart performance immediately after the operation may appear normal and satisfactory. Why? Because the surgical procedure had lowered the high resistance in those vessels going to the lungs by an operation that closed a congenital heart defect (a hole)… or one that opened a narrowed pulmonary valve to improve lung blood flow.
The infant looks fine at first, yet some babies, after they are in the intensive care unit, will quickly develop a problem called vasospasm, a
sudden narrowing of their small lung arteries. The right ventricle will fail, as this unexpected obstruction of its outflow of blood (to the lungs) cannot be overcome by the heart, when the septum is damaged. A dilemma evolves that can turn into a life-and-death crisis.
The bewildered surgeon asks, “What happened? I repaired everything that was wrong. The infant was fine yesterday!”
The culprit is the septum.
What happened is the heart is again confronted with high pulmonary resistance from this sudden narrowing of the small lung arteries (vasospasm). Septum twisting is needed to powerfully push the blood past this higher resistance, but it cannot do so because of its injury during the operation.
A false conclusion had buoyed the physician’s confidence on the first day — arising from the misguided thinking that the bellows action of the contracting wrap was all that was needed. While this is true with low lung vascular resistance — everything changes now if the cardiac twisting becomes compromised, as the septum can no longer be relied upon to combat the newly developed vasospasm.
Hopefully, understanding why this swift and sometimes life-threatening development of right heart failure evolves — may motivate selecting improved methods of protection that can avoid the aftermath of this awful complication.
Left Ventricle Assist Device Impairs Right Ventricle… But Why?
Spectacular advances have been made to support a failing left heart. Ventricular assist devices are put in left ventricles that are not ejecting blood well, their role being to suction blood from the heart and then pump it back into the arteries of the body. Impressive improvement frequently follows… but a major complication can also occur.
While the left heart performs better, the right heart now sometimes fails.
How can this be?
The problem is not with the device, but rather with the misunderstanding of how structure determines right ventricular (RV) function. The dilemma develops when the device may super-efficiently eject nearly all of the left ventricular blood — so that the left ventricle (LV) cavity shrivels to practically collapse. The septum (the muscular “wall” between the two ventricles) then bulges into the left ventricle to fill this now-empty space created inside it. The right ventricular cavity becomes more spherical as it stretches.
That expansion causes the septum’s oblique (angled) 60° fibers to become more transverse (horizontal) — a geometric change that makes RV function worsen.
The telltale clue to again deducing the septum as a culprit arose from my realizing that most of the critically-ill patients suffering this setback — had very high pulmonary resistance (from narrowed blood vessels to the lungs). The counterforce to this condition is a “fully functioning (twisting) septum” that will ensure an efficient and robust right ventricular performance. But this cannot happen until the septum fibers return to their natural oblique orientation.
Understanding this sequence leads to a straightforward action to counter this problem: all you need to do is decrease the suction on the left ventricle assist device, as this returns a normal LV chamber size and shape. The septum promptly returns to a midline position and right ventricle performance improves.138
Unfortunately, the septum’s role in this clear-cut solution has not yet been recognized, which needs to happen before better protocols for left ventricular assist devices can be developed to offset this problem. Yet anyone who has come to understand how the structure of the heart governs its function — including you, the reader — can easily grasp this need.
Electrical Ignition and Muscle Firing… Do We Have a “Concert?”
As you just read (and as I’ve often cited elsewhere as well), effective treatments are based upon comprehending normality, appreciating how disease distorts this, and finally using this knowledge to restore normality. For example, the septum that bulges is a serious dilemma, one that is solved by returning it to its natural midline position.
Yet the reason for abnormal septum bulging may be completely different from having a left ventricular assist device set too high. For example, problems due to uncoordinated electrical stimulation of the septum may cause it to billow. This happens when the septum’s electrical stimulus is delayed and the left side of the heart contracts before the septum. As a result, the non-contracting septum bulges into the right ventricle.
Enter the world of electrophysiology medicine and its use of a device called a pacemaker to provide programmed stimulation. This method is used in the over 5 million pacemakers implanted in patients in the United States alone. This is a common way of “pacing” when normal impulses through the natural wiring system within the heart are slow.
Aside from its common basic function of raising a low heart rate, one that most people are familiar with, a pacemaker can also be utilized when uncoordinated electrical stimulation causes the septum to bulge into the right ventricle. This treatment is called cardiac resynchronization therapy (CRT). Electrical leads are placed in the atrium and into the left ventricle and septum. Its goal is to stimulate both ventricles together to synchronize their beats, so that the outer left ventricular wall contraction is simultaneous with that of the septum. The septum returns to the midline position when this is effective.
Yet while pacemakers successfully increase the heart rate and return the septum to its proper position, the type of muscular contraction they create must be considered. Direct septum stimulation does not make the left ventricle twist. Instead, the muscle touched directly by the pacemaker lead develops an irregular local contraction, rather than the sequential full heart contraction generated by the normal flow of impulses that arrive from its natural wiring system — the prerequisite for producing the heart’s natural twisting action.
This difference motivated me to investigate how to use the natural wiring system to pace (electrically stimulate) the heart. I found this second approach had been established by other researchers, as pacemaker leads (wires) were instead placed into the area where the natural impulse starts — a site called the Bundle of His (pronounced “hiss”). The magnificence of nature reveals itself when this is done. These impulses travel ten times faster than those from direct muscle stimulation, and they produce twisting. The cardiac concert is restored by our pursuing normality instead of using the conventional pacemaker stimulation approach that cannot bring about the natural twisting beat.
While both types of pacing options are available, this second natural ignition pathway is rarely selected by physicians. It reflects a revolution in thinking, and very few cardiologists want to do it. Nor do the pacemaker manufacturers wish to redesign their currently widely used and profitable products.
Of the 5 million pacemakers implanted in the U.S.… the number of people who have been paced in this second manner is probably less than 1,000. (The possibilities of reproducing excellent normality with pacemakers will be further explored in Chapter 26).
Septum and Heart Valves… Leg Bone’s Connected to the Knee Bone
The heart has two atriums (to receive blood) and two ventricles (to pump blood). Cardiac valves are located between each atrium and ventricle. They open to let blood into the ventricles from the atrium, and close when the heart begins to contract. Today, the most common adult heart surgical procedure is to fix or replace these valves after they malfunction.
But in some cases, disappointing outcomes follow successful operations.
This is because those procedures are directed only at the valve. Understanding why this is a dilemma requires an appreciation that a heart valve does not live in isolation. Yes, it is the “doorway” between atrium to ventricle, through which blood flows. But the valve also has supporting structures — such as the collagen tissue that are struts that hold the valve leaflets as they open and close, and the papillary muscles that connect the valve to the ventricle’s muscular wall.
Leaky valves often happen because of issues with these supporting structures, and occur despite there being a normal valve configuration. So it isn’t always a valve problem. Th
is dilemma is common in patients with dilated hearts that are failing. Simply fixing or replacing the valve does not make the patient get better.114, 115
Why? Again, structure / function interaction becomes the crucial clue. The septum once more plays a pivotal role — since the valve’s supporting apparatus is physically connected to it.
This dynamic relationship of interdependence stirs vivid memories of my time in medical school when I failed that first anatomy test. My study habits were fine. I had memorized every muscle, nerve, artery, and bone, but I had not considered the relationships among them. Reminiscing back even further, I recall a song we sang as children, “Dem Bones,” the one that goes, “…the leg bone’s connected to the knee bone… the knee bone’s connected to the thigh bone….” It’s a lesson that remains relevant today, as the septum is connected to these valve structure components.
Just as Sherlock Holmes would find clues that were hidden in plain sight, the secret here involves seeing what you are looking at. For example, the papillary muscle (attached to the valve) is connected to the septum in the right ventricle — and it gets stretched when the septum bulges into the left ventricle. Similarly, when the septum bulges into the right ventricle, the left-side papillary muscle (located adjacent to the septum) is pulled downward. This form of tugging has a fancy name (tethering), and produces the dangerous action of causing a leaky valve (called valve insufficiency) by preventing the valve leaflets from fitting together.
The solution? As Holmes might say, “The answer is elementary.” Just take the stretching away — by bringing the septum back into normal position.
We followed this strategy in our studies to evaluate the interaction between the septum and the heart valves on the left and right sides of the heart. First, we made a test animal’s septum billow into the right ventricle by delaying the electrical impulse delivered to the left side of the heart. As expected, there was leaking from the mitral valve. Equally anticipated, returning the septum to a midline position by cardiac resynchronization therapy (CRT) — decreased mitral valve leaking.
Solving the Mysteries of Heart Disease Page 44