Praise for A Strong and Steady Pulse
“Dr. Chapman, through his patients’ histories, shares his experiences and insights across three decades of caring for patients with cardio- vascular disease. I highly recommend his well- written, easy-to-read narrative not only to health care providers and their students but also to patients. All will benefit from a better understanding of their care.”
—F. Andrew Gaffney, MD, professor of medicine, Vanderbilt University
“Can using cocaine cause a heart attack? Will indulging in an all-you- can-eat breakfast buffet result in a torn artery? Do we die from broken hearts? Greg Chapman answers all these questions in A Strong and Steady Pulse, a collection of vignettes about his years as a practicing cardiologist. Here, bits of medical knowledge are artfully woven into stories of real life. While patients’ lives hang in the balance, readers are transported into the center of the action in the emergency department or the hospital room. Whether you are a practitioner or a patient, you will not put this one down easily.”
—Rachel Waide, JD, Tupelo, Mississippi, attorney
“Dr. Chapman uses patient stories as a powerful teaching tool for car- diology concepts. More importantly, his stories remind us of the priv- ilege and responsibility of caring for patients. It is a must read for all who care for patients, especially in the field of general medicine and cardiology.”
—Lisa Willett, MD, professor of medicine, vice chair for medical education, and director of Internal Medicine Residency Program, the University of Alabama at Birmingham
“Medicine is both an art and a science. These two realms merge reg- ularly in our conversations and interactions with patients and their families, oftentimes when we least expect it. In this wonderful book of medical vignettes, Dr. Chapman, an interventional cardiologist,
recounts poignant stories about his patients and his life that link the art and science of medicine, and in the end, generate wisdom that will be appreciated by patients and physicians alike.”
—Sumanth D. Prabhu, MD, professor of medicine, director of the Division of Cardiovascular Disease, University of Alabama at Birmingham
“Dr. Chapman provides readers with an inside view of medical prac- tice in a way that shares the ‘science of medicine’ while personalizing the stories of the people living through serious medical conditions.
Every scenario has an interesting twist with a medical response that is specific to the patient or is compared with others who have had sim- ilar experiences. These stories epitomize the art and science of medi- cine and why we respect individuals, like Dr. Chapman, who truly care about their patients. I recommend this book for aspiring health pro- fessionals as well as those who need to reach back to rediscover why they chose to serve in the health care field.”
—Martha Lavender, PhD, fellow of the American Academy of Nursing and member of the State of Alabama Nursing Hall of Fame
“A Strong and Steady Pulse is as instructive as it is fun to read. It won- derfully reflects Dr. Chapman’s wit and charm.”
—Marc G. Cribbs, MD, director of Alabama Adult Congenital Heart Program and director of the UAB Comprehensive Pregnancy and Heart Program
A STRONG
&
STEADY
PULSE
S T R O N G A
&
S T E A D Y P U L S E
S T O R I E S f r o m a C A R D I O L O G I S T
Gregory D. Chapman, MD
The University of Alabama Press Tuscaloosa
The University of Alabama Press Tuscaloosa, Alabama 35487-0380 uapress.ua.edu
Copyright © 2021 by the University of Alabama Press All rights reserved.
Inquiries about reproducing material from this work should be addressed to the University of Alabama Press.
Typeface: Arno Pro
Cover image: heart diagram; by Wende Berryhill, www.berryhillsartstudio.net Cover design: Lori Lynch
Cataloging-in-Publication data is available from the Library of Congress.
ISBN: 978-0-8173-2100-0 E-ISBN: 978-0-8173-9367-0
For Laura
Tact, sympathy, and understanding are expected of the physician, for the patient is no mere collection of symptoms, signs, and dis- ordered functions, damaged organs, and disturbed emotions. He is human, fearful, and hopeful, seeking relief, help, and reassurance.
To the physician, as to the anthropologist, nothing human is strange or repulsive. The misanthrope may become a smart diagnostician of organic disease, but he can scarcely hope to succeed as a physician.
The true physician has a Shakespearean breadth of interest in the wise and the foolish, the proud and the humble, the stoic hero and the whining rogue. He cares for people.
—Tinsley Harrison, introduction to Harrison’s Principles of Internal Medicine, 1950 Experience is fallacious, and judgment difficult.
—Hippocrates, Aphorisms, 1 And I said of medicine, that this is an art, which considers the con- stitution of the patient, and has principles of action and reasons in each case.
—Plato, Gorgias The Heart is a lonely hunter with only one desire! To find some last- ing comfort . . .
—Carson McCullers What wisdom can you find that is greater than kindness?
—Jean-Jacques Rousseau
Do not forget to entertain strangers, for by so doing some have un- wittingly entertained angels.
—Hebrews 13:2 I’m just trying to matter.
—June Carter Cash Whatever you are, be a good one.
—Abraham Lincoln
Contents
Author’s Note xi
1. A Five-Year-Old Girl Having a Heart Attack 1 2. The All-You-Can-Eat Breakfast at the Opryland Hotel 7
3. Lunchtime Stimulation 12
4. For Me to Live, Someone Has to Die 17
5. The Widow-Maker 21
6. Going Fishing 25
7. Casablanca 29
8. My College Boyfriend Had Ulcerative Colitis 34
9. Palpitations after Pregnancy 40
10. Fireflies, Gene Therapy, and Medicated Stents 45
11. Jack Sprat 52
12. The Crimson Tider 55
13. The Fog of War 61
14. Rachel Jackson and an Octopus Trap 66
15. Marathon Training 71
16. Don’t Mind Him, He’s an Engineer 78
17. My Heart Is Failing 84
x Contents
18. Jack Daniel’s 90
19. On TV They Say That Is a Bad Drug 96
20. I Hope You Are All Good Republicans 100
21. What Will It Be, Death or Mumva? 105
22. Joe Lieberman 110
23. Would Narcissus Wear an Apple Watch? 114
24. My Favorite Cation 120
25. The Troponin Is Abnormal 125
26. A Strong and Steady Pulse 134
Coda: A Life Lesson 143
Epilogue: The Coronavirus Pandemic 144
Disclosure Statement 148
Acknowledgments 149
Glossary and Acronyms 151
References 163
Further Reading 169
Index 171
Author’s Note
C
ardiovascular disease is a significant cause of death in the United States, and 50 percent of all Americans will even- tually deal with a cardiovascular condition. In this book I address car- diac problems prevalent in the twenty-first century, and aim to inform and advise on matters of the heart. A Strong and Steady Pulse is written for people with cardiac issues, as well as for the people who care for them. Cardiac textbooks and internet reference sources abound; this work illustrates concepts and practices with stories inspired by mem- orable patients in compelling situations. The wit, wisdom, courage, and humanity of these patients will be evident. I wish to honor them and, in the process, share beneficial information. In addition I reflect on training in medicine and cardiology in the 1980s and 1990s, a time of tremendous advances in cardiovascular care. It was also the time of the AIDs epidemic. Subsequent decades spawned epidem- ics in obesity and opioid drug use, and now we have the coronavirus pandemic. I comment on these and other issues, including Big Data in health care, the Apple Watch ECG feature, the use of statin drugs, and medical decision-making. These vignettes come from academic and private practice settings. Privacy concerns mandate the absence of patient identifiers. Names and identifying features of patients have been changed. Their characteristics, places, events, locales, and inci- dents are either the product of my imagination or used in a fictitious fashion. Any resemblance to actual people is coincidental.A STRONG
&
STEADY
PULSE
1
A Five-Year-Old Girl Having a Heart Attack
B
eep-beep-beep from my pager. The callback number was for the ER. Adam McDowel was paging me, which was a bit unusual, since he is a pediatric cardiologist.“Hello, Adam, what’s up?”
“Thanks for calling me back, Greg. I need your help. I have a five- year- old girl here in the ER having a heart attack, and I’m not sure what to do.”
I dropped everything to go to the ER, not without some trepi- dation. Years had passed since my pediatric rotation as a medical stu- dent, and I had no specialized training in the care of children. I did know that children were not supposed to have heart attacks.
Amy Cho was in bay 6. Her parents, valued researchers who had come to the university from Japan seven years ago, were at her side, as was Dr. McDowel, who reviewed with me Amy’s illness and presentation.
Two weeks earlier, her parents reported, Amy began to have a fever of 102 degrees F. She developed red eyes from conjunctivitis and had swollen lymph nodes in her neck. Her lips cracked and her tongue turned strawberry red. Her hands and feet swelled. Today she had developed a rapid heart rate. When Amy complained that her chest hurt, her parents brought her to the ER. Dr. McDowel diag- nosed Kawasaki’s disease. Her ECG showed ST- segment elevation in the anterior leads. Amy was having a heart attack.
Chapter 1
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Kawasaki’s disease is an illness that affects young children. It is rare in newborns and adolescents. Its exact cause is unknown. It occurs most often in winter months, when infections are more common, but no definite infectious source has yet been identified. Coronaviruses may play a role; Kawasaki- like disease is an emerging complication in the young with COVID-19 infection. Kawasaki’s disease is the most common cause of vasculitis in children. White blood cells invade the walls of arteries throughout the body, including the coronary arter- ies, weakening collagen and causing intense inflammation. The artery wall may be damaged to the point that pathological enlargement oc- curs. Blood flow within an enlarged artery segment can be like a slug- gish, stagnant eddy pool adjacent to a rapidly flowing river. Sluggish flow in this aneurysmal artery leads to formation of a blood clot. If large, the blood clot spills out, obstructing the coronary artery and cutting off oxygen downstream. The cause of a heart attack in a child with Kawasaki’s disease is different from the cause of heart attack in an adult. In adults, a heart attack is usually due to plaque rupture at the site of a blockage in a coronary artery, which also triggers clot for- mation, but not from an enlarged aneurysmal segment with stagnant flow. An echocardiogram done at the bedside showed that Amy’s left anterior descending coronary artery had a 5- millimeter aneurysm at its proximal segment. The normal part of her artery was only 1 mil- limeter in diameter. The anterior wall of the heart was stunned and not contracting. Amy’s signs and symptoms, the diagnosis of Kawa- saki’s disease, the ECG findings, and the echocardiogram results left no doubt: she had an obstructing blood clot causing a heart attack.
Cardiologists (as well as EMTs, other medical workers, police offi- cers, firefighters, and parents) are often called upon to make type 1 decisions. These require quick action to ensure survival. Heuristics (rules of thumb) are helpful, such as telltale findings on the ECG that guide lifesaving treatments. For example, if a cardiac patient passes out, and the ECG monitor shows that the heart rhythm is ventricular fibrillation, that patient only has a few minutes to live unless a shock
Five-Year-Old Girl Having a Heart Attack
is applied to the chest to restore normal heart rhythm. Recognizing ventricular fibrillation and immediately giving a shock is an action based on a type 1 decision. A type 2 decision allows more time to fully research the problem over days or weeks, considering every possible cause in the differential diagnosis, with help from the literature or con- sultants, and then definitively determining the diagnosis and the best treatment. Ideally, all diagnoses would be made as type 2 decisions.
Amy could not wait days or weeks. She was losing heart muscle cells with each passing minute. She required a type 1 decision.
That was why Dr. McDowel paged me. As a pediatric cardiolo- gist, he had never treated a child having a myocardial infarction. As director of the Vanderbilt CCU, I cared for adult patients having an MI on a weekly, sometimes daily, basis.
Dr. McDowel and I considered treatment options. If Amy had been an adult with adult- size arteries, an emergency cardiac catheter- ization with angioplasty was indicated. But there were no catheters and devices available that were small enough to treat Amy’s occluded artery. We could call our cardiac surgery colleagues for a bypass op- eration. But even if a cardiac surgeon were immediately available and an operating room were open, it would take precious time (at best one to two hours, perhaps longer) to perform the surgery and restore blood flow to her heart. Every elapsed moment would cost more heart cells, leading to irreversible damage. There was a third option: give clot- dissolving medicine (thrombolytic therapy) through an IV to re- store blood flow.
“I have never given thrombolytic therapy to a child,” I said.
“Neither have I. How do we do it? What dose would we use?”
This all took place in 1994. We had no Google, no internet, and no website to guide us. Since thrombolytic therapy was rarely admin- istered to children, its complication rate in them was unknown. We had multiple questions to quickly consider. Would we be harming Amy with this treatment? Would she have a lethal bleed if we gave it?
Would she have a lethal heart rhythm or crippling cardiomyopathy if we didn’t get her artery open as soon as possible?
Chapter 1
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As part of my fellowship training at Duke, once a month I staffed an outreach clinic in a rural North Carolina hospital three hours north of Durham by car. Like most rural hospitals, the facility did not have a local cardiologist or a cardiac cath lab program with the equipment and personnel to perform emergency angioplasty and stent placement. While there, I treated patients having an acute myo- cardial infarction with thrombolytic therapy because it was the only option available.
“In adults, the loading dose of tissue plasminogen activator is 0.75 mg per kilogram IV, followed by 0.25 mg per kilogram IV over the next hour.”
Dr. McDowel thought for a moment.
“Do you think it’s the best thing to do?”
“Yes. I think it is what we should do,” I replied.
Dr. McDowel agreed. We discussed all this with Amy’s con- cerned parents, who voiced understanding of the potential risks and benefits. They gave their consent for us to proceed with thrombolytic therapy.
We administered tPA, a thrombolytic drug, with the dose ad- justed for Amy’s weight in kilograms. Fifteen minutes passed . . . the heart rate came down and Amy looked more comfortable. We re- peated the ECG. The ST segments on her ECG had returned to nor- mal, and an echocardiogram of the anterior wall of the heart showed that it was pumping normally again.
Our plan had worked. Amy had no bleeding or any other compli- cation from the thrombolytic therapy. We started her on medicines that improve survival after myocardial infarction in adults, adjusted for her age and weight. Over time, the enlarged segment of her coro- nary artery healed and returned to normal size.
One of the cardiology fellows thought Amy’s case would be instruc- tive. (A cardiology fellow is an advanced trainee who has completed medical school, as well as an internship and residency in internal med- icine.) I presented it at a Division of Cardiology weekly conference.
Five-Year-Old Girl Having a Heart Attack
After I presented the case, including the outcome, my division chief, Dr. Douglas, began asking questions. Why had I done what I did?
Was it not dangerous? Where were the data to support my actions?
Those were fair questions, part of the give- and- take of practic- ing medicine. We all have accountability, as we should. Our actions should be based on data, best practices, and whenever possible, re- sults from randomized controlled trials. I readily agreed that I was in uncharted territory.
The questions kept coming in an extremely critical fashion. The message from the chief was clear. In his opinion, we had practiced reckless cowboy cardiology, and we were lucky to have gotten away with it.
My thoughts turned to Theodore Roosevelt. He once said, “It is not the critic who counts; not the man who points out how the strong man stumbles, or where the doer of deeds could have done them better. The credit belongs to the man who is actually in the arena, whose face is marred by dust and sweat and blood; who strives valiantly; who errs, who comes short again and again, because there is no effort without error and shortcoming; but who does actually strive to do the deeds; who knows the great enthusiasms, the great devotions; who spends himself in a worthy cause; who at the best knows in the end the triumph of high achievement, and who at the worst, if he fails, at least fails while daring greatly, so that his place shall never be with those cold and timid souls who know neither vic- tory nor defeat.”
“Dr. Douglas,” I said, “if you had been called to the ER by Dr.
McDowel to help him care for this five- year- old girl, what would you have done?”
He looked at me for a long time. And said nothing. There were no more questions from him about this case.
Today, if you research the recommended treatments for children like Amy, Dr. McDowel and I didn’t do too badly.
Twenty years went by. I returned to Nashville for a wedding. At the reception, I ran into Adam McDowel.
Chapter 1
6
I asked him about Amy Cho.
“She lives near me in Belle Meade, is married, and recently gave birth to a beautiful baby girl,” he said. “She’s a successful writer and has published two children’s books.”
A server with a tray of champagne came by, and Dr. McDowel and I each took a flute.
“To Amy!” We toasted, and as our glasses clinked, we nodded, sharing a savory moment of sublime satisfaction.
We had been in the arena. We had made a type 1 decision.
Somewhere, Teddy Roosevelt was smiling.
2
The All- You- Can- Eat Breakfast at the Opryland Hotel
M
y first job after completing an interventional cardiol- ogy fellowship at Duke was on the faculty at Vanderbilt Univer- sity in Nashville. I had not been there long, and I was on call for acute cardiac cases. Paged to take a sick patient in transfer from a hospital in Carthage, Tennessee, I activated the medical helicopter service, and its pilot and medical crew immediately took off to go pick him up.Ray Watson was dying. He had severely low blood pressure and was on life support with a ventilator. Six weeks before, he had under- gone a coronary artery bypass operation in Waco, Texas, where he worked as a general contractor. I was concerned. The description of his condition by the doctor in the emergency department in Car- thage indicated that he was in cardiogenic shock, with his heart un- able to supply sufficient cardiac output to his brain and body. At best, his chances of survival would be 50:50 if we could quickly reestablish blood flow to blocked vessels or could correct an acute problem of the heart valves or chambers.
Mr. Watson and his wife, on their way to Myrtle Beach, South Carolina, for a vacation, were traveling east through Tennessee on I- 40. While driving, he suddenly passed out. His wife managed to get their pickup truck stopped. A passing motorist called 911. An ambu- lance came and took him to the ER in Carthage.
Chapter 2
8
The Life Flight helicopter crew brought Mr. Watson and his wife directly to the Vanderbilt cardiac cath lab. A cardiology fellow and I were expecting them. Mr. Watson was intubated and sedated. He still had dangerously low blood pressure and was unable to talk with us. I asked Mrs. Watson what had happened.
“Ray and I stopped this morning in Nashville at the Opryland Hotel,” she said. “We had the all- you- can- eat breakfast there. Ray was determined to get his money’s worth. He went back several times for more food. Then we got back on the interstate, and Ray passed out while driving. I got our truck stopped and an ambulance came and took us to the ER in Carthage. I’m so worried. He has done so well since his bypass operation, until this morning.”
Mrs. Watson provided the name of the hospital in Texas where her husband had his coronary bypass operation. I asked the staff to have the operative report of his bypass surgery from there faxed to us stat. The operative report details exactly which vessels were bypassed and what type of bypass grafts were placed by the cardiac surgeon.
This information would tell us where to look for occluded grafts that might be causing cardiogenic shock.
Given Mr. Watson’s critical condition, the cardiology fellow and I could not wait for the report before starting his case. We accessed Mr. Watson’s circulation by placing a hollow needle and then a sheath into the right femoral artery. His blood from the needle was thin and bright red, not the usual crimson color. It looked like red Kool- Aid.
We sent a sample off for stat lab results. I placed an intra- aortic balloon pump via the femoral artery in his left leg. This device uses a catheter with a long balloon at its end. I positioned it in the aorta. During the relaxation phase of the heartbeat the balloon inflates, pushing needed blood flow into the coronary arteries. During the contraction phase of the cardiac cycle the balloon deflates, which reduces the work of the heart and promotes forward flow to the body. This would support and improve Mr. Watson’s blood pressure.
I then placed catheters in the various native coronary arteries and in the bypass grafts, looking for acute occlusions. As expected,
All- You- Can- Eat Breakfast
the native coronary arteries had severe blockages, and these block- ages were the reason for Mr. Watson’s bypass operation. Next, I checked the bypass grafts. The left internal mammary artery graft to his left anterior descending artery was open. Likewise, a vein graft to the left circumflex artery was clear, as was a vein graft to the right coronary artery.
This was puzzling. All three of the major coronary arteries were well supplied by bypass grafts, with good blood flow to all parts of Mr.
Watson’s heart. I placed a catheter across the aortic valve into the left ventricle (LV) and took a picture. The heart was contracting well, if not super- well, in a dynamic fashion. The heart valves were intact and functioning normally. There was no evidence for a ventricular sep- tal defect, an abnormal hole between the main pumping chambers, which if acute causes cardiogenic shock.
I measured the pressure in the left ventricle: 0 mm of mercury (Hg). I turned to the fellow. “This is not cardiogenic shock at all.” In cardiogenic shock, the pressure in the LV is severely elevated, 30 to 40 mm Hg or higher. A pressure of 0 is seen if a person is “dry,” due to hypovolemia from severe dehydration—or if a person is in hemor- rhagic shock from acute blood loss.
Lab work results and the faxed operative report from Texas ar- rived simultaneously. Mr. Watson’s hematocrit, a measure of red blood cells, was 18 percent, about a third of what it should be. He was bleed- ing—almost bleeding to death. The operative report mentioned the three grafts that I found, and a fourth graft rarely utilized in the United States: the gastroepiploic artery was used as a bypass graft and had been attached to a small posterolateral branch of the right coronary ar- tery. The gastroepiploic artery usually supplies the stomach and greater omentum, a tissue that supports the abdominal organs. For Mr. Wat- son, this artery had been rerouted to his heart by the cardiac surgeon.
I suspected that the surgeon had trained in Korea or Japan, where this graft is done more often than in the United States.
My thoughts flashed to William of Occam, a fourteenth- century English Franciscan friar and philosopher. Occam’s razor is often
Chapter 2
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invoked in medicine. Referred to as the law of parsimony, its medi- cal application states that the patient benefits most if a single diagno- sis can account for all the signs and symptoms of a patient’s illness.
Treating this one condition yields the best outcome. Occam’s razor is sometimes in dynamic tension with Hickam’s dictum: Patients can have as many diseases as they damn well please.
This was an Occam moment.
Vanderbilt University Hospital was a level 1 trauma center, able to care for patients suffering severe trauma, accidents, or gunshot wounds.
We ordered a stat CT scan of Mr. Watson’s abdomen and called the trauma surgeons for an emergency consultation. The CT scan showed that Mr. Watson’s belly was full of blood. The trauma surgeons took Mr. Watson to the operating room and opened his abdomen. They found that the gastroepiploic artery had torn off from the heart. It was spewing blood into the abdomen like an unattended garden hose on full pressure. A simple stitch stopped the bleeding. The next day Mr. Watson was off life support and talking to us. Shortly thereafter he and his wife resumed their vacation.
In medical school, students are taught to take a detailed history from the patient. Eighty- five percent of diagnoses may be made from this inexpensive and efficacious practice. It goes back to one of Sir William Osler’s aphorisms. (Osler is considered the father of Amer- ican internal medicine after establishing high- quality care and med- ical education at Johns Hopkins University in the 1890s, as well as publishing a seminal medical textbook, The Practices and Principles of Medicine, in 1892.) Osler was fond of saying that if you talk to the patient long enough, he will tell you what is wrong with him. (How much time is long enough? Recommended are at least two uninter- rupted minutes for patients to describe their illness or concern when taking a history. One study found that doctors on average interrupt the patient after listening for seventeen seconds.)
In this case, Mr. Watson could not initially talk with us, but his wife did. The cardiac surgeon in Texas had run the gastroepiploic
All- You- Can- Eat Breakfast
artery graft over the fundus (main body) of the stomach when he per- formed the bypass operation. When Mr. Watson engorged his stom- ach at breakfast, the stomach expanded and strained the artery, caus- ing it to come loose from the heart, leading to massive bleeding and hemorrhagic shock. The small heart artery it was sewn to had sealed itself off and was not bleeding. During the surgery by the Vanderbilt trauma team, the disconnected gastroepiploic artery was sutured in a way to ensure no further bleeding in the belly—no matter how many times Mr. Watson got his money’s worth at an all- you- can- eat buffet.
Listening to patients describe their symptoms and concerns is all- important. Tinsley Harrison was the first editor in chief of Harri- son’s Principles of Internal Medicine, the standard medical textbook in use today. He said it takes twenty years to learn how to take a patient’s history. One must not only listen but also ask appropriate questions.
As I show in the next chapter, I was still learning how to take a good history, which is sometimes done indirectly, sometimes delayed, and sometimes facilitated by a clue from a mentor.
3
Lunchtime Stimulation
A
medical grand rounds conference at noon had just ended when my pager beeped. It was the emergency depart- ment alerting me that a patient was having a massive heart attack.Code STEMI blinked in the message section of my pager. For car- diologists, a Code STEMI is the equivalent of a five- alarm fire for a firefighter, a drowning child for a lifeguard, a woman requiring an ur- gent C- section for the obstetrician. Immediate action was mandated.
Time was of the essence.
The patient was Robert Lambert, a fifty- two- year- old liberal arts professor. During lunch in his office, he began to feel a heavy weight pressing down on his chest. Pain radiated to his jaw. He broke out in a heavy sweat, was short of breath, and his throat felt tight. He be- came nauseated and was dizzy. He had no history of heart disease or any other medical condition. He played racquetball regularly, often with his wife, Layla, who was twenty- eight. Except for a little graying around Dr. Lambert’s temples, he and Layla looked like models in a high- end fashion advertisement. Dr. Lambert continued to have chest pain and unease when I examined him in the ER. Layla was at his side, taken aback by this event and concerned for her husband.
They had been eating lunch in his office. When he began to feel ill, she had pleaded with him to proceed at once to the ER for evalua- tion. He was to benefit immensely from her insistence that he seek medical attention.
Lunchtime Stimulation
The ECG was classic for an acute heart attack. STEMI stands for ST elevation myocardial infarction. The ST segment on the ECG ab- normally elevates, in a characteristic fashion. A STEMI is the result of a total occlusion of a coronary artery. Depending on which of the 12 standard ECG leads shows ST-segment elevation, one may pre- dict which coronary artery is blocked. Dr. Lambert’s ECG showed marked ST elevation in the anterior leads, indicating an acute occlu- sion of the proximal left anterior descending artery, which in most people supplies 40 percent of the blood supply to the heart. If blood flow were not quickly reestablished, a large amount of heart muscle would die, putting Dr. Lambert at risk for lethal heart failure, cardiac chamber rupture, and fatal arrhythmias.
In the 1980s many studies established the efficacy of giving thrombolytic therapy through an IV to patients with STEMI. Such drugs dissolve the clots that cause most heart attacks. These clots form on diseased areas of the coronary arteries. This treatment was a major public health and lifesaving advance. It restored normal blood flow to the heart in approximately 80 percent of cases.
A possible complication with thrombolytic therapy, and greatly feared, is bleeding in the brain, which is usually fatal. Intracranial bleeds occurred 1 percent of the time in patients less than seventy-five years old, and 5 percent of the time in those seventy- five or older. Thrombo- lytic therapy remains the standard of care in rural areas where an expe- rienced cardiac cath lab team is not immediately available. Beginning in the 1990s studies showed that taking STEMI patients immediately to the cardiac cath lab and opening the blocked artery with balloon catheters and stents was successful in more than 95 percent of the cases. In addition, patients cared for with cardiac catheterization had essentially no intracranial bleeds. Thrombolytic therapy is not needed and intracranial bleeding is avoided. Primary percutaneous interven- tion (PCI) in the cardiac cath lab is now the standard of care for a STEMI if the patient can get to a hospital with experienced staff and have the procedure performed in a timely fashion.
The staff at academic medical centers like Vanderbilt, Duke, and
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the University of Alabama at Birmingham, as well as at many commu- nity hospitals, are experienced. They are committed to offering emer- gency cardiac catheterization and intervention twenty- four hours a day, 365 days a year. A well- run STEMI case looks like a NASCAR pit stop. The cardiologist, the nurses, and the techs know their jobs, perform those jobs quickly and expertly, and communicate well. If an acutely blocked coronary artery is opened within one hour of its closure, patient mortality is reduced to essentially 0 percent. “Time is heart muscle” is the watchword of the cath lab team. Because heart cells are saved, so are brain, kidney, and liver cells, which all suffer if the heart is dysfunctional.
Dr. Lambert gave his consent for our team to proceed with an urgent cardiac catheterization and possible balloon angioplasty. One distinct advantage of PCI compared to coronary artery bypass sur- gery is that the patient does not require general anesthesia. Patients having a PCI get what is called “moderate sedation” with IV medi- cations. When done correctly the procedure does not result in loss of respirations. He was wheeled on a gurney into the cardiac cath lab. By placing a catheter in his right femoral artery, I gained access to his circulation and performed coronary angiograms. The images confirmed that the proximal left anterior descending artery was the culprit, the infarct- related artery. Using X- ray guidance, I threaded a 0.14- inch wire from outside his body into a catheter and then across the blockage. Over this wire, I positioned a balloon catheter and in- flated it at the site of the occlusion, which restored normal blood flow.
Dr. Lambert’s chest pain ceased, and the ST segments on his ECG normalized. The door- to- balloon time was thirty- eight minutes. Not bad. I gave kudos to the cath lab staff for their performance, as well as to the ER staff and ER physician who had quickly recognized Dr.
Lambert’s STEMI. We estimated that his artery had been reopened within the golden hour before permanent damage ensues, and his prognosis was excellent.
Layla was visibly relieved when her husband smiled at her in the recovery area. Then the questions began.
Lunchtime Stimulation
“Dr. Chapman, Bob was in good health. Why did this happen?”
she asked.
It was an excellent question. Several known risk factors predis- pose a person to having a heart attack, and Dr. Lambert had none of them.
He wasn’t especially old. He didn’t smoke. His father, mother, brothers, and sisters had not had any cardiac problems. He was not diabetic or hypertensive. His cholesterol was normal. He had none of the major risk factors. Some additional considerations, such as atrial fibrillation sending a clot from his left atrium to his coronary artery, didn’t apply because his heart rhythm was normal. He did not have end- stage renal disease requiring dialysis. He did not have psoriasis, rheumatoid arthritis, lupus, or scleroderma. His ancestry was not South Asian. He was not infected with HIV. He was not an organ recipient on immunosuppressive therapy. He had never had radiation therapy to his chest for cancer. An echocardiogram confirmed that he had no abnormal communication between the chambers of the heart such as an atrial septal defect or patent foramen ovale. If pres- ent, these would allow a blood clot embolizing from a vein in the leg to pass over from the venous circulation into the arterial circulation and into his coronary artery. His C- reactive protein level, a marker of inflammation and associated with cardiovascular disease, was nor- mal. His Lp(a), a lipoprotein associated with coronary thrombosis, was not elevated.
Dr. Lambert and Layla asked me again the next day on rounds why he had suffered the heart attack. I had no answer.
That afternoon I ran into my clinical chief, F. Andrew Gaffney, in the hallway and took the opportunity to “curbside” him about Dr.
Lambert, to see if he had any additional thoughts.
“Hello, Drew, may I run a case by you?”
“Certainly,” he said. “What have you got?”
I reviewed what had taken place with Dr. Lambert, including all test results.
My chief thought a moment and then said, “I know Dr. Lambert.
Chapter 3
16
Thirty years ago, Bob and I were fraternity brothers at Berkeley.” Then with a raised eyebrow and a soft chuckle, he asked, “Did you check a urine drug screen?”
“No, I did not,” I answered.
The next morning, Dr. Lambert and Layla again asked me why he had a heart attack. I again went over all the usual reasons, as well as unusual causes, and then mentioned that cocaine use may cause a heart attack. Cocaine, snorted or injected, may cause a flow- inhibiting spasm of a coronary artery. Cocaine may raise blood pressure to the point of either causing a coronary artery tear or inducing clot- producing plaque rupture, with resultant closure of the coronary ar- tery. Dr. Lambert and Layla quickly made eye contact with each other.
They asked no further questions on why he had had a heart attack.
The Lamberts had their answer. And so did I.
4
For Me to Live, Someone Has to Die
I
liked Gus Hendricks. He always had a joke for me. He ex- uded joie de vivre. Gus was forty- two years old and made his living as a stable hand in Shelbyville, where he trained Tennessee walking horses. He spoke of favorite horses past and present, and of his pride in his charges when they successfully learned the peculiar gait re- quired for walking horse competitions, a prancing and lifting of the hooves in quick succession, sustained around the track.“By the way, Doc, I’m really good at what I do. I’m an excellent trainer,” he said.
“Really?” I asked.
“Yes. I may be the best in the business. And just so you know, it’s my modesty that makes me great.”
He was constitutionally unable to suppress mirth.
He started smoking at age six. His uncle thought it was funny to see a kid smoking, and gave him cigarettes.
Gus’s heart was severely damaged from multiple heart attacks.
The left- ventricular ejection fraction is a standard measurement of how well a heart is working: it is a measure of the percentage of blood pumped from the left ventricle with each heartbeat. A normal per- centage is 55 percent or more. Mr. Hendricks was at 10 percent. If a heart is compared to a car engine with eight cylinders, his was down to one or two cylinders. Gus was not doing well.
A heart transplant was recommended.
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18
All surgical and medical treatments have been exhausted for a per- son placed on the heart transplant list. For several reasons, a heart transplant is a measure of last resort. First, it is a major operation with all attendant risks of surgery. Second, a patient is then committed to a lifetime of immunosuppressant drugs so that his immune system does not reject the transplanted heart. On these drugs, a patient is more susceptible to common, as well as rare, infections. A patient on such drugs is also more likely to get cancer. The transplanted cor- onary arteries, unfortunately, are at risk to develop blockages over time. A transplant candidate must pass a psychological evaluation showing that he has the temperament and insight to take these medi- cines. If he does not take them, the body will reject the donated heart, and it will fail. An unfortunate example, usually seen every summer, is the teenager who has had a heart transplant and decides to stop tak- ing the medicines when he goes to camp. Finally, hearts suitable for transplantation are in short supply. Many patients die before a donor heart with a compatible tissue type becomes available.
Gus had passed all tests confirming his suitability for cardiac transplantation, including the important fact that he had been a non- smoker for five years. With donor hearts in short supply, they are not given to patients who continue to smoke. He was in the cardiac care unit on IV medications to support his heart function, tethered there by his condition. He could not walk any distance without severe shortness of breath. A heart transplant was his last hope. Through all procedures, tests, and medications, he maintained his pleasant de- meanor. I had cared for him for three years. He was now on the heart transplant service in the cardiac care unit.
I came by one day to check on him, and he said, “Hey Doc, what is twenty- six inches long and hangs from an asshole?”
I didn’t know.
“A stethoscope,” he informed me.
We both laughed.
“You know it’s a strange business, this heart transplant situation.
For me to live, someone has to die,” he said.
For Me to Live, Someone Has to Die
“Yes,” I replied, “but they are going to die anyway, so it’s good if their organs are used to help someone else.”
He agreed. He asked me if I was an organ donor. I pulled my driver’s license from my wallet and showed him that I was.
A few days later, the transplant cardiologist in charge of Gus’s care called me. Gus had a new development. He was having severe chest pain and had ECG changes indicating acute myocardial ischemia—
his heart muscle was not getting needed oxygen and nutrients. He was on the maximum amount of IV medications that could be safely given, and he continued to deteriorate. Would I take him to the cardiac cath lab to see if a balloon or stent procedure could help him?
In the cardiac cath lab, the coronary angiograms were dire. Blood supply to the heart comes from two separate arteries and their subse- quent branches: the right coronary artery, and the left main coronary artery. The left main usually supplies 70 percent of the blood flow to the heart. For Gus, it supplied 100 percent, because the right coronary artery had a chronic occlusion at its origin. Even worse, his left main demonstrated a 95 percent, angry- appearing blockage. If it closed off, he would die. Usually, this situation called for urgent coronary artery bypass surgery, but Gus’s poor heart function, his dependence on IV medications to support his blood pressure, and gross fluid overload were problematic. The cardiac surgeon on call was concerned that Gus would not survive the operation. I agreed with her assessment.
The transplant cardiologist asked if I could place a stent in the left main and fix the 95 percent blockage there. It would be a high- risk procedure. Any mishap or poor stent placement would kill him. We talked with Gus there on the cardiac cath lab table. He was willing to go forward if the procedure gave him a chance to live. We decided to place an intra- aortic balloon pump, a support device, in his aorta.
This would maximally perfuse his left main. We would give him more diuretic medicine overnight to remove fluid from his lungs. I planned to stent Gus’s left main at seven o’clock the next morning.
“Doc, your expression reminds me of what the bartender said to the horse when it walked into his bar,” Gus said.
Chapter 4
20
“What did he say, Gus?”
“Hey, why the long face?”
I didn’t sleep well that night.
The next morning, I was up early and went to the CCU to see Gus be- fore he came to the cardiac cath lab for the procedure. My heart sank.
His room was empty, and the hospital bed was made up with clean sheets. An empty room usually means the patient has died.
A CCU nurse, seeing my reaction, hurried over and reported that Gus had not died. Overnight in Nashville, a man had not engaged the safety for his semiautomatic handgun. A bullet was chambered, and while removing the gun from his car, the trigger caught on a door lock.
The gun fired, and the bullet entered his brain. He was an organ donor.
His heart was a perfect tissue match. It was transplanted into Gus, who was alive and well in the cardiac surgery recovery unit.
For the next several years, I did routine heart biopsy procedures for Gus at regular intervals. The biopsy device gained access to the heart via the large internal jugular vein in the neck. This was done to detect any subclinical rejection of the donor heart by Gus’s immune system. Tiny segments of the donor heart were reviewed under a micro scope by pathologists. If signs of rejection were seen, his immu- nosuppressive medications were adjusted. He returned to training walking horses.
“Doc, how do you get a million dollars in the horse business?”
“I don’t know Gus. How?”
“You start with two million.”
Sometimes, Gus would remind me that a heart transplant is a strange business. In order for him to live, someone had to die.
5
The Widow- Maker
I
was seeing a new patient in clinic, Samford Davidson, who had recently moved from Florida. He was fifty- two years old and managed a golf course. Six months ago, he had had an anterior MI and emergency stent placement in his left anterior descending cor- onary artery at a hospital in the Florida panhandle. He had been in the bleachers at his daughter’s softball game when he had his heart attack.“Hello, Mr. Davidson. It’s nice to meet you,” I said in introduction.
He barely looked up. He didn’t make eye contact with me, and his facial expression was flat.
“How are you, Mr. Davidson?” I asked.
“Not well, Doc,” he said. “I’m having a hard time sleeping, and if I do sleep I have terrible nightmares. I dread going to my daughter’s softball games now. I’m short- tempered with my wife, and I didn’t used to be that way. My work performance is suffering. I can’t stop thinking about what the cardiologist in Florida told me.”
“What did he tell you?”
“He told me I had the type of blockage that is called ‘the widow- maker.’ I can’t get that out of my mind.”
The “widow- maker” is a term some cardiologists use for a signifi- cant blockage in the proximal left anterior descending artery (LAD), which supplies 40 percent of the blood flow to the heart.
They shouldn’t.
Chapter 5
22
Using that phrase may make the patient a psychological cardiac- cripple. Mr. Davidson was exhibiting signs and symptoms of post- traumatic stress disorder (PTSD). In addition, each coronary artery and their branches, if they acutely occlude, may cause myocardial ischemia and lethal ventricular fibrillation. All coronary arteries are potential widow- makers. I once had a patient have ventricular fibril- lation when he acutely occluded a small (2 mm in diameter) obtuse marginal branch of the left circumflex coronary artery (LCx). Some of my patients who read copies of their cardiac cath reports that doc- ument LAD disease become alarmed after seeing postings on the web about the LAD being called the widow- maker.
In Mr. Davidson’s case, his blocked LAD was opened quickly, and his heart function remained normal. He had no post- MI compli- cations. He was on aspirin, Plavix, rosuvastatin, and metoprolol, all of which promoted his survival. He had no other significant lesions in his coronary arteries. His prognosis was favorable.
Why do cardiologists say to patients that they have the widow- maker? Is it to impress upon them the seriousness of a heart attack?
Patients already know that. Is it to help ensure that the patient will be compliant with taking medication and making lifestyle changes?
Or is it to make the cardiologist seem godlike in his ability to prevent death? Cardiologists do their job, like firefighters and police officers, in the line of duty. They should be recognized for their expertise and experience. That recognition should not come at the expense of the patient’s mental health.
I implore medical students and trainees not to use the term
“widow- maker.”
I had a difficult time in medical school deciding on a specialty. I en- joyed internal medicine, with its intellectual rigor, and the possibil- ity of long- term relationships with patients with chronic diseases. I also enjoyed surgery. To use physical and mental skills during pro- cedures to save lives and immediately alleviate suffering was appeal- ing. Psychiatry was also a consideration. The diagnosis and care of
Widow- Maker
patients with mental health conditions is challenging, fascinating, and gratifying.
I became an interventional cardiologist and got to do all three.
Psychosocial factors trigger cardiac events and significantly im- pact patients with cardiovascular conditions. Natural and man- made disasters increase the rate of heart attacks and cardiac death. For five days following the 1981 earthquake in Athens, there were on average 5.4 cardiac deaths per day, compared to the usual average of 2.6 per day. For sixty days after 9/11 there was a 49 percent increase in heart attack patients admitted to hospitals within a fifty- mile radius of New York City compared to the number admitted in the sixty days prior to the attack.
Chronic stress, whether related to problems at work or home, financial issues, or family illness, increases the incidence of acute cor- onary syndromes. MI patients, compared to a control group of pa- tients admitted for trauma, have a higher incidence of social isolation, self- blame, and avoidance. They also have more painful life experi- ences. Medical students who scored high on a survey assessing their degree of anger suffered cardiac death at a higher rate than their more mellow classmates over a thirty- year tracking period. A cynical, hos- tile, or angry personality is a cardiac risk factor.
A proposed mechanism for stress- induced cardiovascular events is sympathetic nervous system activation, with resultant elevated heart rate and blood pressure, facilitating vasospasm and reducing myocar- dial oxygenation. Coronary artery or carotid artery plaque rupture is more likely to occur with elevated blood pressure, leading to MI or stroke. Increased adrenaline increases platelet aggregation, making blood clots more likely.
A heart attack may be a person’s first serious medical condition, and it may prompt acute awareness of one’s mortality. One- third of heart attack patients have symptoms of depression, and one- fifth develop full clinical depression. A person’s likelihood of completing a suicide attempt is tripled in the five years after a heart attack. De- pressed patients are less compliant with medications and lifestyle
Chapter 5
24
changes, and they have poorer outcomes. Psychotherapy or antide- pressant medications, or both in combination, are helpful. The anti- depressants Lexapro and Zoloft are safe for patients with cardiac con- ditions. These medications do not prolong the QT interval on the ECG (which may cause arrhythmias), and they do not interfere with antiplatelet agents.
I offered reassurance to Mr. Davidson, emphasizing his overall favorable outlook. I recommended that he see a psychiatrist and start taking Zoloft. He agreed that something had to be done; his life was unraveling. My good friend and colleague Dr. Nathan, a talented and compassionate psychiatrist, provided psychotherapy and adjusted the dose of Zoloft for Mr. Davidson over the next six months.
Later, I saw him back in the office.
“How are you, Mr. Davidson?”
“Doc, I’m much better. I’m sleeping at night with no nightmares.
Things are better at work and with my wife. Last weekend I was at my daughter’s softball tournament, and in the finals she drove in the winning run in the last inning. I really enjoyed seeing that. Several college coaches are recruiting her. She hopes to play in the College World Series someday. And I plan to be there.”
Mr. Davidson was living life, and enjoying it.
His proximal LAD lesion was not a widow- maker.
It should never have been called one.
6
Going Fishing
M
y grandfather Nick had a large impact on my life, and I am thankful for his influence. Not going beyond eighth grade in school himself, he stressed the importance of learning and aca- demic achievement.“Get that education, boy,” he repeatedly told me. “They can’t take that from you.”
He was hard working and had earned a supervisor position at the local power plant. When he arrived home, coal dust painted his overalls and his face, which was usually smiling. He possessed joke and storytelling genes. His main passion in life was fishing. As a boy, I would accompany him in his small boat, and we caught bream, crap- pie, bass, and catfish on the Coosa River and at Weiss Lake.
The lessons I learned from him about fishing helped me stop a patient’s ventricular tachycardia.
Thomas Andrews had passed out at his machinist job. EMS was called, and he revived on the way to the hospital. An ECG performed in the emergency department showed that he was having runs of ventricu- lar tachycardia (VT), a serious abnormality of the heart rhythm. The abnormality originates from one of the two main pumping chambers of the heart, the right or left ventricle. If sustained, ventricular tachy- cardia can lead to ventricular fibrillation and sudden death.
Several disease processes may result in ventricular tachycardia.
Chapter 6
26
Coronary artery disease that leads to myocardial ischemia is a com- mon cause. A weak heart, one with cardiomyopathy, is more likely than a strong, healthy heart to have arrhythmias. Some people are born with extra pathways in their heart for the conduction of cardiac impulses, which can lead to VT. Others may have congenital abnor- malities of the heart chambers such as arrhythmogenic right ven- tricular cardiomyopathy or hypertrophic cardiomyopathy. Electrolyte abnormalities (low potassium or magnesium levels) may be present.
Inherited disorders such as the long QT syndrome, or ion channel abnormalities like that seen with Brugada syndrome may cause ven- tricular tachycardia.
The treatment of VT depends on its cause. If due to myocardial ischemia from severe coronary artery disease, then medication, cor- onary stents, or coronary artery bypass surgery are helpful. If due to cardiomyopathy, an internal defibrillator may be indicated. It can rec- ognize dangerous rhythms and give an internal shock to terminate them. Specialized cardiologists called electrophysiologists can ablate extra conduction pathways in the heart by disrupting them with cath- eters that emit radiofrequency energy.
None of these conditions applied to Mr. Andrews. The cause of his ventricular tachycardia was in full view on his chest X- ray.
He was twenty- nine years old. At twenty- six he had been treated for stomach cancer. He received many rounds of chemotherapy through a special intravenous catheter placed in his left subclavian vein in his chest. Called a Hickman catheter, it had a port just under the skin that allowed placement of an IV line with relative ease. That port was connected to a small tube about six inches long that resided in the vein and allowed the chemotherapy to be delivered to his body. He was in remission, with no signs of recurrent cancer for the past two years. Standard practice at that time was to leave the catheter in place;
it could be used again for future treatments, if needed.
He had a rare complication from the Hickman catheter, clearly visible on the chest X- ray. The tube had come loose from the port and
Going Fishing
migrated down the vein into the heart, where it lodged in his right ventricle. It was rubbing on the inside of the right ventricle with each heartbeat, and triggering VT. In order to fix the problem, that tube had to come out.
One way to remove it was to have open- heart surgery, with the surgeon sawing open the breastbone, cutting open the heart, and di- rectly removing the tube by grabbing it with his gloved hand. This option was presented to Mr. Andrews, who expressed concern about such a big operation.
“Is there another way to get the tube out, Doc?”
Yes, there was.
Foreign bodies—usually catheters that have broken loose—can mi- grate to the heart, and may be removed by snaring them with a re- trieval device. The retrieval device gains access to the heart via the large internal jugular vein in the neck or the large femoral vein in the leg. Mr. Andrews agreed to try this much less invasive procedure.
The staff helped him onto the table in the cardiac cath lab. The X- ray imaging source was rotated into place over his chest. The nurse gave him a mild sedative, and I injected a local anesthetic into the skin over the right internal jugular vein in his neck. A hollow needle in- serted into the vein allowed the insertion of a sheath. Via the sheath, a special retrieval catheter could be maneuvered into the RV and used to try to remove the dislodged Hickman tube.
The retrieval catheter acts like a lasso. It is a hollow catheter with a looped wire pushed into it; the loop exits the end of the catheter.
The goal was to snare the end of the Hickman catheter, cinch it fast, and pull everything out as one unit.
Using the retrieval device was similar to a fly fisherman casting his line. The heart was moving with each beat and the tip at the end of the Hickman tube was moving with each contraction. The trick was to time the position of the loop and tip so that the wire could lasso the wayward tube. Multiple casts are usually required to get the loop into proper position. The tube tip and loop were seen using live X- ray
Chapter 6
28
images from the cardiac cath lab imaging source. Monitors were just above the patient on the cath lab table, where we watched the results of the casts.
I say “we” because Mr. Andrews was awake enough to see what was happening on the monitor. The first cast was unsuccessful. So was the second. And the third. Five minutes went by, then ten, and then fifteen. It was like trying to spear a spaghetti strand in a boiling pot with a knife. I continued to make casts, turning the loop to differ- ent angles and positions, trying to lasso the tip of the Hickman.
“Don’t give up, Doc,” Mr. Andrews called out. “I’ve got all day.”
“Not giving up, sir,” I replied.
I channeled my Granddaddy Nick. I pictured him flicking his rod and placing his lure in the exact spot where a large bass would strike.
I angled the retrieval catheter—there! The loop slipped over the tip of the Hickman. I gingerly cinched the wire and the loop tightened around the Hickman tube. Slowly, carefully, I pulled everything out of the heart. Then I brought the tube up to the sheath in the inter- nal jugular vein. I removed everything as one unit and the scrub tech placed hand pressure over the vein to seal it. I held up the wayward tube as one would display a trophy catch. For the first and only time in my career, the cath lab staff and onlookers in the control room burst into applause.
I was smiling under my surgical mask.
But Mr. Andrews’s smile was bigger.
Thanks, Granddaddy.
7
Casablanca
I
was making rounds as the attending cardiologist with my team in the cardiac care unit. Overnight, several new patients had been admitted for chest pain—a common occurrence on the cardi- ology service.Outside the first patient’s room, we began a discussion of the causes of chest pain.
“We are going to invoke a well- known quote from a classic movie.
Do you remember Casablanca?”
The medical students, interns, residents, and fellow looked at me blankly.
“You know, the movie from 1942 with Humphry Bogart and In- grid Bergman?”
No response.
The CCU nurse and the social worker assigned to my team were closer to my age.
“Do you mean, ‘Of all the gin joints in all the world, why did she have to walk into this one?’” asked Julie, the nurse.
“No, not that one,” I replied.
“How about, ‘We’ll always have Paris’?” asked Casey, the social worker.
“No, not that one either,” I said.
“Play it again, Sam,” the two said in unison.
“No . . . the one I’m thinking of is ‘round up the usual suspects.’”
Chapter 7
30
There are “usual suspects” to round up when evaluating a patient with chest pain. I asked the team to list the cardiovascular causes of chest pain.
First, Amir Khan, a fourth- year medical student, raised his hand.
“Coronary artery disease with an obstructive blockage that limits blood flow causes chest pain, and the medical term for that is angina.
Patients may describe pressure, chest- squeezing, pain, or unease, even a sense of doom, sometimes with radiation of discomfort up to the jaw or down an arm. Initially, angina may occur when walking and putting stress on the heart. The most dramatic form of angina is that which occurs during a heart attack, with severe pain that is present and persistent at rest, when a coronary artery has suddenly occluded.”
“Very good,” I replied. “Have you heard of Dr. William Heberden?”
Another round of blank stares. Then the cardiology fellow, Kristy Spaniel, spoke up.
“William Heberden presented a paper in 1768 to the Royal Col- lege of Physicians and Surgeons in London about pectoris dolor, the first medical description of angina pectoris in English. Most of his pa- tients were over the age of fifty and initially experienced exertional discomfort. In the next five to ten years, the majority of them had sudden death.”
“Excellent. Dr. Heberden experienced angina himself, and is remembered for saying, ‘I am at the mercy of any fool who chooses to annoy me,’ an example of situational angina caused by emotional stress or agitation.
“What are some other cardiovascular causes of chest pain?”
The team quickly listed them. Sean Gable, a second- year resident in medicine, named aortic stenosis, coronary vasospasm, spontaneous coronary artery dissection, takotsubo syndrome, pulmonary hyper- tension, systemic hypertension (when severe, it causes endomyocar- dial ischemia), and pulmonary embolism.
Caitlin Edwards, a first- year intern, added pericarditis, myocar- ditis, mitral valve prolapse, hypertrophic cardiomyopathy, vasculitis from Takayasu arteritis or Kawasaki’s disease, and the discomfort that
Casablanca
may occur with fast heart arrhythmias, sometimes due to drugs like cocaine or Adderall.
Next, I asked the team to recall the sailor who communicates with other ships by using signal flags. What does he do? Dr. Gable had been in the navy. He described the sailor’s use of semaphore, widely utilized before radio, and still used during radio silence. We dis- cussed the semiology, the signs and symptoms, of the various causes of chest pain. Patients signal their problems if we can but recognize them. Pain caused by deep inspiration, for example, may be present with pericarditis or pulmonary embolism. The triad of angina, short- ness of breath, and passing out, in the presence of a harsh crescendo- decrescendo systolic heart murmur, is characteristic of severe aortic stenosis.
We were standing in front of the room assigned to Samuel Evans, an eighty- eight- year- old Black man from Tuskegee, Alabama. Mr.
Evans had gone for a walk on the ward. We saw and heard him re- turning. As he approached we heard slap slap slap from his feet strik- ing the floor. He had foot drop. That abnormal gait was related to the cause of his chest pain.
“What other cardiovascular structure, when diseased, causes chest pain?” I asked.
Again, Dr. Spaniel spoke.
“Diseases of the aorta, the main conduit for delivering blood to the body as it exits the heart, may result in a ripping, tearing type of chest pain that radiates to the back and between the scapulae. Just as a balloon may pop if filled with too much air, the aorta may rupture or tear if it abnormally enlarges. The aorta may have a localized he- matoma in its wall or a discrete ulceration. An aortic dissection, or tear, in the wall of the aorta is perhaps the most ominous. A severe dissection can compromise the vessels that supply the brain and the arms and legs. If the tear is complete and the aorta has ruptured, fatal bleeding into the chest cavity is likely.”
“Good. Now let’s list the diseases and conditions that can affect the aorta.”
Chapter 7
32
The team responded well and rattled off atherosclerosis, hyper- tension, connective tissue diseases (such as Ehlers- Danlos syndrome), Marfan syndrome, bicuspid aortic valve with aortopathy, Loeys- Dietz syndrome, Turner syndrome, Takayasu arteritis, weakening of con- nective tissue with pregnancy, and trauma from a car accident.
“We have left out an important category,” I said. “It is the cause of the enlarged aorta in Mr. Evans. His gait is a clue.”
“Mycotic aneurysms due to infectious diseases,” Dr. Gable said.
“Mr. Evans must have syphilis.”
What happened to a cohort of young Black men in Tuskegee is a shameful and infamous chapter in medical research. They were diag- nosed with syphilis. There was a known cure available, penicillin. They were not given the cure. Instead, they were put in a research study to ascertain the long- term effects of syphilis, which include dementia, aortopathy, and peripheral neuropathy, the cause of Mr. Evans’s foot drop. Never mind that those sequelae had been extensively studied and known for more than two centuries. Mr. Evans had been part of that study. He was living in Oakland, California, when the study was discon- tinued. He was lost to follow- up and was never contacted about receiv- ing treatment. He returned to Alabama after retiring from the shipyards.
We called for infectious disease and cardiovascular surgery con- sults to help us address Mr. Evans’s enlarged and diseased ascending aorta.
“Okay,” I said, as we went down the hall to the next patient’s room.
“What are the noncardiovascular causes of chest pain?”
Amir Khan again responded, stating that gastrointestinal disease, including acid reflux, hiatal hernia, ulcers, pancreatitis, gall bladder disease, esophageal spasm, esophageal stricture, Boerhaave’s syndrome (esophageal rupture), and stomach tumors can cause chest pain.
Dr. Edwards listed pulmonary causes, including bronchitis, pneu- monia, pleurisy, pneumothorax, and lung cancer.
Dr. Gable mentioned musculoskeletal causes, such as costochon- dritis, back problems, herniated discs that impinge on nerves to the chest, and shingles.
Casablanca
“Well done,” I said. “Don’t forget that feeling you get when you see a flashing blue light in the rearview mirror.”
The next patient was April Salsbury, a forty- four- year- old mother of five, who had been admitted with chest pain. She told us she came to the hospital because of severe discomfort in her chest. The pain worsened when she went for long periods without eating. On physi- cal exam, she had severe tenderness just under her left ribcage when the left upper quadrant of her abdomen was touched firmly. The ECG and cardiac lab work were normal. Other lab work revealed that she was anemic. A stool sample was positive for blood.
“Now,” I said to the team, “we are going to apply Sutton’s law.”
Yet another round of blank faces.
“What is Sutton’s law?” I asked.
No response.
So I told them.
“Willie Sutton was a twentieth- century bank robber. A reporter asked him why he robbed banks. ‘Because,’ he replied, ‘that’s where the money is.’”
Dr. Edwards immediately said, “This patient has a bleeding ulcer and ‘that’s where the money is.’”
“Excellent application of Sutton’s law.”
Two hours later the gastroenterologist called me to say that the endoscopy revealed a bleeding gastric ulcer in Mrs. Salsbury. He cau- terized it, sealing the cause of her bleed. Mrs. Salsbury could expect a full recovery.
We completed our rounds. Dr. Spaniel’s pager beeped. She looked at the message console. “Another consult in the ER for a patient with chest pain.”
As our team headed toward the elevator I asked Amir how we would evaluate the new patient.
“We will round up the usual suspects,” he replied.
I gave him high marks on his clerkship evaluation.
8
My College Boyfriend Had Ulcerative Colitis
I
t was a clinic day on a Monday morning in October 2019, and I was seeing a new patient. Ralph Jemison was a fifty- five- year- old man with a history of intravenous drug abuse. He was infected with HIV. On antiretroviral therapy his lab work showed normal CD4 white blood cell counts and no detectable viral load. Mr. Jemison was referred to cardiology because of his elevated blood pressure. He had been HIV positive for ten years. With current treatments, he could expect to live for some time. HIV patients are at an increased risk of developing cardiomyopathy (a weak heart), as well as coronary ar- tery disease. They are more likely to get a pericardial effusion, a fluid collection in the lining of the heart. But for the most part, patients with HIV now live long enough to deal with common cardiovascular problems such as hypertension. It was not always so.In 1985, when I started my internship in internal medicine at New York Hospital–Cornell Medical Center, the AIDS epidemic was in full force. Fifteen percent of the patients admitted to the hospital had AIDS. Farther south in Manhattan, at NYU, 40 percent of the ad- missions to the medicine service were AIDS- related. There were no effective treatments for HIV at that time. AIDS was an almost certain death sentence.
My first patient with AIDS was Joseph Julliet. He was thirty- four years old and had an accounting degree. He was born and raised in Iowa. After college in Ames, he moved to San Francisco, where he
My College Boyfriend Had Ulcerative Colitis
often went to the bathhouses. He estimated he had a hun