This validation of Brad’s results, which paralleled the successes of controlled reperfusion in other organs, led me to present my thoughts on this issue at a special conference at UCLA. The intent was to develop a Controlled Reperfusion Theme at our university. I provided an overview of the established benefits to this innovative approach for restoring blood supply after ischemia in different organs. Representatives from every department that did clinical transplantation attended, as each had experience with patients who had suffered ischemic reperfusion injury.
Everyone listened raptly, especially when Ron described his astonishment at observing mental normality in pigs who received controlled reperfusion after liver ischemia. He contrasted this to the metabolic chaos (and sometimes coma) that can typically follow normal blood reperfusion. Ron was taken aback, because the clinical appearance of mental normality meant that there was no washout of toxic substances from the liver. This included an absence of the generation of ammonia, a chemical that causes hepatic coma during the near terminal end-stage liver disease.
While the transition to using controlled reperfusion of the liver in patients has yet to happen at UCLA, its seeds have been sown into the mindsets of those in attendance. Again, from my perspective, it is not a matter of if it will happen… but when such truth will win.
It was gratifying to watch Friedhelm Beyersdorf and Brad Allen mount new steps on the scientific ladder. They used controlled reperfusion concepts to protect the diseased limb, the lung, and open the door to protecting the liver. Their capacity to identify, experimentally test, and then clinically implement a treatment that never before existed — provided the powerful foundation needed to allow controlled reperfusion to be tested in a spectrum of diseases — ones that had never before been solved in this manner.
It was everything a teacher could ever hope for.
Credit Where Credit is Due
The truest gauge for scientific accomplishment is how ideas become beacons to rethink problems, and lead to new solutions.
In all this, there is but one ultimate focus — the patient — who will benefit from the implementation of innovative changes. As I repeat to each incoming resident: personal acknowledgement is never the objective. The goal is the creation of ideas that transform action.
At UCLA’s annual Longmire Surgical Society Dinner, residents and faculty that trained with Dr. Longmire during his 40 years gather together. We typically recount endless amusing stories that had occurred within our hallowed halls. Traditionally, graduating residents who had done outstanding work would receive awards during this event. On rare occasions, other people are recognized as well.
I was there with my wife, sitting with friends, when to my surprise, it was announced that I would receive the Longmire Legacy Award. Only two or three of these awards have ever been given in the 20 years since these dinners began, and I had no idea I would be receiving it.
What happened next was equally unforeseen.
One of my prior research fellows, a cardiac surgeon, was the president of the Longmire Club. When he introduced me, he said to the audience, “I want to tell you a story about Gerry Buckberg that I’m not sure anybody has ever heard. It’s something that occurred when Gerry’s breakthrough concept of blood cardioplegia was to be presented at the American Association of Thoracic Surgery in 1978.”
At this point, I really had no idea what he was going to say.
He continued, “I happened to be present when Jim Maloney, the Division Chief of Cardiothoracic Surgery at UCLA, came to inform Gerry that he should present the paper. Maloney reasoned that it was Gerry’s idea, and his presence would make a positive impact on the over 4,000 surgeons who would be in attendance, especially since it was to be the first paper on the program due to its merit.”
My prior student smiled to himself a moment and resumed, “Gerry — being Gerry, then pointed to me and told Maloney, ‘Our research fellow did the experimental and clinical analyses and should make the presentation.’ Of course, Maloney being Maloney, persisted. ‘No, you have to present it.’
“Finally, Gerry looked Maloney in the eye and said, ‘Look, I won’t do it. Either my research fellow makes the presentation, or I will advise the meeting’s organizers that the paper will be withdrawn from presentation.’ Obviously, Maloney finally agreed.”
Several in the audience at the Longmire dinner laughed at this as they knew me quite well, thus fully appreciating my consistency in such decisions.
The dissemination of new medical information usually begins with a presentation at a major medical meeting, typically by the named leader of the study. Yet, everybody already knew it was my lab. Consequently, when the selected fellow demonstrates a superb effort, it elegantly reflects the leader’s presence. Besides, each research fellow is just beginning their career, so that presenting an important paper may boost their launching.
Rewards for Awards
Satisfying recognition comes from first discovering the truth, and then from others using your concepts to replace less successful treatments. This desired progression originates with our research presentations given at major surgical society meetings, where the work of those who have met these requirements is sometimes acknowledged.
In 2000, The Society of Thoracic Surgery established the Earl Bakken Award. It is named for the man who designed the first wearable cardiac pacemaker and co-founded Medtronic, which manufactures it. The award is intended to honor those who have made exceptional scientific contributions that notably improved the practice of cardiothoracic surgery and the quality of life for patients.
I was privileged to receive their first Lifetime Achievement Award for my work on myocardial protection, and needed to make some remarks at the ceremony. As I contemplated what to say, I was struck that it seemed miraculous I was even there. I said that “the kids on Clarke Place in the Bronx, where I grew up, could not have conceived that the guy who played stickball in the street with them would be receiving this organization’s first lifetime achievement award.”
Of course, I also talked about having my work applied in clinical care and how its use touched people’s lives, which was more gratifying than only publishing our findings in journals. I acknowledged the enormous contributions from my research fellows, and accepted the award with genuine gratitude. …Yet internally, I couldn’t help but think of all the discoveries we had made that still needed to be accepted and implemented.
Then the perfect illustration of the phrase “Rewards for Awards” arose after I received the Bakken Prize. The convention still had a couple more days to go. As I walked into meetings and visited cocktail parties, I was approached by person after person after person. Somewhere between 100 to 200 surgeons from all over the globe thanked me. Expressing appreciation for my helping their practices become safer — and making their patients better.
This was the true honor for my work on myocardial protection. These individuals were often not affiliated with universities, or in positions to influence the widespread approval of new treatments. Rather, they were in private practice where cardiac surgeons focus on a singular pursuit: “How do I make my patient better?” Their generous acknowledgments confirmed the success of my principal goal — helping others through my work. I experienced each of these unique rewards in a private, one-on-one setting… yet each conveyed to me that the power of my discovery had far transcended its public recognition.
I offered a grateful smile to each of those coming up, and told them how enriching their comments were to me. No more needed to be said.
Inside, I knew it was a job well done. My work had meaning.
CHAPTER 15
Unanticipated Interlude
As with science, life flows in waves. Surging us past troughs of uncertainty between the crescendos of new discovery. Both in professional undertakings… and within oneself. Such a pattern occurred to me in 1996, originating from the most unexpected of circumstances.
I was with my family in Missoula, Montana to present at a c
onference attended by prominent surgeons from all around the world. After completion of the event, I was scheduled to return to Los Angeles and operate on a high-ranking official in the Indonesian government, who was traveling to UCLA for this procedure.
The conference went well, and on the final day of our presentations, there was a special evening barbecue along the river. Before dinner, many of us planned to ride horses through the area. But when I mounted Il Nigro, my aging steed, it took one look at me — a rather large rider — and decided “Not a chance.”
He reared up… and bucked Uncle Bucky.
I landed hard on my arm and was in great pain. But mostly I remember thinking, “Damn it, I was supposed to operate on this important political leader and here I am flat on the ground.” My elbow was broken. They took me to a tiny private hospital in the area to check me over… and discovered I had atrial fibrillation (abnormally fast and irregular heart rhythm).
While most people with atrial fibrillation experience a rapid heart rate, sense a “flub-dub” in their chest, and encounter fatigue without much exertion, I’d had none of these symptoms. Because I was an athlete, my heart rate remained low, between 45 and 55, and I wasn’t tired. My condition only became evident when an electrocardiogram was taken prior to the expected brief surgical procedure to reset my bone. Yet once I knew I had atrial fibrillation, I could self-detect it by feeling my own pulse and sensing its irregularity.
The next morning, I returned to UCLA, where I saw a cardiologist who confirmed the diagnosis and reassured me it was not dangerous, and my elbow was fixed the next day. The subsequent treatment of my atrial fibrillation was straightforward. I was given a medical drug that would hopefully convert the rhythm back to normal (sinus) rhythm. In the meantime, I was placed on Coumadin, a blood-thinning drug used to prevent development of a clot on the surface of the heart’s atrium. This complication may happen because fibrillation causes a quivering of the atrium, instead of allowing the muscle covering the atrium to contract normally. Consequently, the entire wall of this non-functioning thin muscle now acts like a flat lake, becoming the ideal flaccid area where a clot can form. The biggest danger from such a clot is that it can break off and become an embolus that enters the blood stream and travels someplace to obstruct blood flow. The greatest hazard is its going to the brain, causing a stroke. Concern about this fearsome complication is why the patient is always given an anticoagulant — a blood-thinning drug.
Fortunately, return of my natural heart rate occurred in about two months — literally on the same day I was scheduled to be admitted to UCLA for electrical defibrillation, thereby canceling the need for such a treatment (which is best avoided if possible, since it entails a number of steps, including an anesthesiologist putting you to sleep while you undergo brief electrical shocking of your heart with a defibrillator to return normal rhythm). Self-detecting the return of my normal heart rate was easy, since I was evaluating its consistency by checking my own pulse rate.
Even though I was having no other symptoms, the change to a normal rhythm was very welcome. I was quite eager to have my regular heartbeat restored so that I could get off the Coumadin medication. There is a significant concern about bleeding complications in the brain while on this drug, should you experience an unexpected event, like a bump on the head. Such an incident during treatment with a blood-thinning drug may result in a 30% death rate.
Because of such concerns, I stopped taking Coumadin as soon as I developed a normal pulse rate, whose continued regularity (which I would self-check) confirmed an absence of atrial fibrillation. My customary activities continued: research and teaching, performing cardiac operations, and a busy travel schedule to present at national and worldwide centers where I’d be invited to speak about our work on myocardial protection.
Forgotten Dreams
But my smooth routine soon became interrupted two months later in Tokyo, Japan, where I awakened one morning and found myself in my hotel bathtub. At first startled, I quickly deduced that the bruise on my cheek must have occurred from hitting a faucet on the tub, after having fallen in late at night when using the bathroom.
I checked my pulse — it was irregular. I thought I had gone into another bout of atrial fibrillation. That could vary my heart’s output and lower blood pressure enough to diminish the oxygen supply to my brain and cause a fall. I could detect no other neurological symptoms or injuries. So I visited Sapporo the next day to give another series of lectures and help one of my former UCLA fellows operate upon a patient at his clinical center, all without incident. My normal heart rate (beats per minute) promptly returned after taking a brief dose of heart medication.
Yet all was not the same.
Following my return to Los Angeles, my secretary observed that I was repeatedly asking the same questions of her and others, something she’d never witnessed before during our 15 years together. I immediately went to a neurologist, whose testing showed that my short-term memory was impaired. There were no other neurological problems, but a magnetic resonance imaging (MRI) study of my brain was performed that day.
Results were not good. My brain artery vessels were normal, but I had sustained a stroke. There was a loss of two-and-a-half centimeters (about one inch) of tissue in the brain region responsible for recent memory. Called necrosis, this tissue was now dead, likely caused by an embolus (traveling blood clot) that came from my heart.
This event was shocking to me, especially since I had remained in a normal heart rhythm for two months following my conversion (return to normal rhythm) from atrial fibrillation. I contacted a cardiology colleague, who astounded me further with information of which I was completely unaware. He told me that after an extended period of atrial fibrillation like I had experienced, the atrium does not immediately recover, even after the successful treatment. It does not contract at all — even though there is restoration of a regular ventricular heartbeat, which can be confirmed by checking the wrist’s pulse or with an electrocardiogram. The atrium chamber acts as if it was “stunned” — meaning it is like a motionless flaccid lake, despite allowing the return of uniform electrical ventricular impulses.
As I reflected on this new information, I realized it resembled what happens when the heart gets stunned as described previously in the chapter on heart attacks. Or the “daze” that a boxer or football player feels after a blow to the head causes a delayed neurological recovery.
This circumstance exposed a loophole in my knowledge. The consequence of this “stunning” after recovery from atrial fibrillation is that there continues to be a stagnant, non-contracting atrium — that provides a smooth non-moving surface that is perfect for clot formation. While I knew Coumadin was given to combat such clots, I thought this drug was discontinued as soon as atrial fibrillation was no longer present. I was not alone in this belief. Other surgical colleagues, including Jim Cox, a good friend and the surgical world’s expert on treatment of atrial fibrillation, were equally unaware of this “stunning” complication.
How could that be?
As surgeons, we only deal with very short periods of atrial fibrillation. It occurs in about 30% of patients after open-heart surgery, but this fibrillation usually stops after a few days, and Coumadin is promptly and correctly discontinued when heart rhythm becomes normal again. But when atrial fibrillation has continued for a prolonged period of time, as it had in my case, the return to normality is not so simple or quick. Though my cardiologist had said nothing about this to me, I learned that when there has been a long period of atrial fibrillation, Coumadin should continue to be taken for another couple of months, even after a return to a normal heart rhythm. It is then stopped only after a contracting atrium is seen and confirmed by echocardiogram.
Thoroughly understanding what happens is crucial because the heart is a pump, not simply something carrying electricity like a television set without moving parts. Despite absence of atrial fibrillation, it was still not squeezing properly. The union of electrical impulses and con
traction is essential for normality.
This dichotomy further emphasizes the importance of ensuring accurate communication between different medical specialties. Failure to do so has enormous impact upon people’s lives, by causing complications that may otherwise be prevented. It was unfortunate that this baseline knowledge was not known in the surgical community… especially by me.
My goal in seeing a neurologist, aside from his confirming the diagnosis and impact of the stroke, was to better understand my condition. My first question was whether I could operate. Fortunately, while I was advised not to undertake any new procedures, I could carry on with things I had done previously. I listened to this advice and all went well, as there was no impairment of long-term memory.
However, my limitations of short-term memory became increasingly apparent, particularly while reading newspapers. I was not able to remember headlines describing a story’s subject matter, and struggled to comprehend the articles as I could not recall the content of previous paragraphs. Wishing to counter these negative effects of my condition, I met with a cognitive therapist. She began by giving me a series of tests to challenge my capacities and judge my performance. The examinations turned out to be extremely perplexing and distressing, since she had me try a variety of things that I could not do. It candidly pointed out my present deficiencies, clarifying the depth of my brain damage that resulted from a stroke that impacted only a small region.
Solving the Mysteries of Heart Disease Page 25