I’m putting a new patient with chest pain in bed 31, the charge nurse yelled at me as she sped by the workstation. Looks pretty bad. Cardiac, I think. Could you have one of the doctors come in stat?
How old? I asked.
No. Anna Black. Forty-three-year-old female.
Relax--it’s not her heart! I replied. To calm the nurses, I assigned a senior resident to work up the patient but reminded him: Forty- year-old women don’t have heart attacks. Our patient’s chest pain would prove to be the result of some other condition--indigestion, perhaps even an ulcer, or maybe just a muscle pull.
From the first year of medical school, doctors endlessly recite the mantra of risk factors for coronary artery disease, or hardening of the arteries: male sex, age, family history, smoking cigarettes, high blood pressure, high cholesterol. And so, by these calculations, Anna Black was not at risk. Had she been a 43-year-old man who smoked, however, I would have rushed to her bedside. Had she been a 65-year-old man, I would immediately have notified the doctor from the cardiac intensive care unit.
Moments later the resident returned from bed 31, clutching a cardiogram and looking as if he had seen a ghost.
Take a look at this, he said, bending over and scrutinizing the sheaf of pink-checked papers that traced the electrical activity of the young woman’s heart. What do you think? Doesn’t it look like she has elevations in leads V1 through V3? He was referring to a series of rises in the cardiogram that are typical of a myocardial infarction--a heart attack.
With that, I jumped to attention. No way, I said. A woman my age? She couldn’t be infarcting.
As I rounded the corner to bed 31, I saw a young, dark-haired woman lying on the stretcher, sweaty and wincing in pain. Nurses had placed an oxygen mask on her face and were deftly inserting intravenous lines into her arms. The resident was slipping a tablet of nitroglycerin under her tongue to ease the cardiac pain.
On a scale of one to ten, how’s your pain? he was yelling.
A little better--but still maybe an eight, she said.
Hi, I’m Dr. Rosenthal, I said, feeling as though I should have introduced myself as Libby to a woman who was so clearly my contemporary. Tell me what happened to you today.
I don’t know--it was all so strange, she began. My husband and I had gone out to dinner, and while we were standing in the restaurant waiting for a table, I suddenly felt this great pressure in my chest, like there was a piano sitting on it. I sat down in a chair, but the pressure just got worse and worse. Before I knew it, my arms were aching, too, and my clothes were just drenched with perspiration.
It felt like what it must feel like to have a heart attack--and I guess I must have looked terrible because the restaurant manager wanted to call an ambulance. But that seemed silly to me and I said no. I thought, ‘I’m young. I’m healthy. It couldn’t be.’ So my husband got us a cab and we drove here instead.’’
When Mrs. Black said her pain was still an eight, the resident popped another nitroglycerin tablet under her tongue and asked the nurse to run another cardiogram. Again those ominous rises appeared.
I stared at the cardiogram, trying to believe that our initial reading had been wrong. After all, I told myself, reading cardiograms is far from an exact science. Plenty of patients with technically abnormal cardiograms have nothing wrong. And sometimes young patients will have small elevations as a normal variant on their ECG. Sure, the shape of the spike is generally slightly different from that associated with a heart attack, but it can be difficult to tell the two apart. In fact, doctors generally do not diagnose heart attacks based solely on an ECG. Because other kinds of chest pain can be mistaken for a heart attack, patients must also describe sensations that match cardiac pain. In addition, their blood tests must show enzymes associated with the destruction of heart muscle.
But all the evidence was pointing in one direction. Not only was Mrs. Black’s cardiogram alarming, but her symptoms were classic for a heart attack: the enormous pressure in the chest, the aching sensation in her arms, the sweats, the sense of impending doom. Oddly enough, such symptoms are statistically less likely to occur in women having heart attacks. They tend to experience atypical chest pain--a bit of indigestion or a nagging pain in the jaw that extends down into the throat. According to researchers, one possible explanation for this disparity is that women tend to have abnormalities in the smaller vessels of the heart rather than in the major conduits. But there was nothing atypical about Mrs. Black’s pain. The description she gave could have come straight out of a textbook.
Mrs. Black’s blood tests would give us the definitive answer, but they wouldn’t be back for hours, and we couldn’t wait that long. If this was indeed a heart attack, she desperately needed a dose of a drug that would restore the blood flow to her ailing heart. Every additional minute of pain meant more heart muscle irrevocably destroyed. And since she was only 43, I reminded myself, Mrs. Black would need those cells to sustain the second half of her life. Holding at bay the prejudices I had acquired in 15 years of training and practice, I paged the cardiologist to ask him to come by and check out my patient.
As I waited for an answer, I tried to piece together some explanation for why this young woman might fall victim to this unlikely foe. One by one, I went through the factors that could predispose a patient to heart disease.
Do you smoke? I asked her. Perhaps if she had a three-pack-a- day habit, I could accept a woman of my generation suffering from heart disease.
Never, she said.
Do you have regular periods? Have you had your ovaries removed? Women are protected from heart disease through middle age by the high levels of estrogen that the ovaries produce during the childbearing years. After menopause, or if periods cease due to surgical removal of the ovaries, those hormone levels decline and, within a decade, women acquire the same level of risk as men. Heart disease is, in fact, the leading killer of both men and women.
But Mrs. Black said that her periods still came almost every month, although they had become somewhat irregular in the past two years. There was no way an early menopause could be blamed. And she had never had surgery of any kind.
How about your family? Are there others with heart disease? A strong family history of heart disease at an early age puts a patient at high risk.
I don’t know; I was adopted, she said. At last, here was a possible explanation. But it just didn’t seem enough.
Are you active? How’s your diet? I probed. I knew that neither of these factors alone would precipitate a heart attack in a young woman, but I was desperate to find any explanation.
I run every day and I’m really careful about my diet--if you can believe it, this happened in a macrobiotic restaurant, Mrs. Black answered, with a wry smile. That’s why I was certain it couldn’t be my heart.
Have you ever had this pain before? I asked.
Well, not this bad, she began. Over the past few weeks I’ve noticed a much lighter pressure under my chest bone a bunch of times, but it has always gone away if I just stopped and relaxed a bit. I was going to mention it the next time I saw the doctor, but it didn’t seem urgent.
I could deny the obvious no longer. Those smaller pains were clearly angina, an early warning signal from a heart in peril. Anginal pain is caused by short periods of inadequate blood flow through one or more narrowed arteries in the heart. When the body is resting, the narrowed arteries can deliver enough blood. But when the body is working, the heart requires more oxygen-filled blood--which the slender channel can’t deliver.
By now, after 15 minutes in the emergency room, Mrs. Black was on an intravenous drip of nitroglycerin, and still the pain lingered. We gave her a drug to slow her heart rate in hopes of reducing the demands on her ailing heart. We gave her heparin, a blood thinner, in hopes of allowing the blood to pass more easily through any narrowed arteries.
Although still in some pain, Mrs. Black remained remarkably calm for a woman who had gone from healthy to critically ill in the course of the past hour. So it is my heart after all, she said quietly, looking around in wonderment at the IVs, the monitors, and the small army of nurses and doctors who surrounded her.
Yes, I said, slowly. Your first instinct was right. I think you’re having a myocardial infarction.
But why? Why?
I don’t know, I answered--a very undoctorly answer, perhaps. Maybe your birth parents had a gene that gave you very high cholesterol. Maybe just bad luck.
The nurse mixed up a solution of a drug called TPA, which we hoped would dissolve the blood clot I now presumed was blocking a narrow coronary artery in Mrs. Black’s heart. As such drugs have become available over the past few years, they have vastly improved the outlook for patients suffering heart attacks. They work because most heart attacks require not only the gradual buildup of hard, fatty deposits that choke a coronary artery but also the formation of a blood clot. When that clot suddenly blocks the tiny remaining channel, it cuts off the blood flow, literally suffocating the heart muscle that the blood vessel supplies.
Because the clot-busting drugs--though very effective--can increase the risk of strokes or other bleeding complications, my hospital requires that a cardiologist supervise their use. When the cardiologist arrived, I directed him to the door, saying, Bed 31; the TPA is mixed.
He peeked inside, withdrew, and whispered to me, There’s a young woman in bed 31.
I know. That’s her. And it’s real.
After a brief talk with Mrs. Black and a quick glance at her cardiogram, he gave the go-ahead for the TPA. Three women--the two nurses and I--stood by, praying that the drug would work as it sailed down the intravenous tubing and into her arm.
Mrs. Black spent the following week in the cardiac care unit. By the end of her stay she had recovered fully from her infarction and was sent home with a drug that would lower her cholesterol. Her blood tests showed that she had indeed suffered a heart attack. Fortunately, the TPA had limited the damage and only a small amount of heart muscle had died. Cholesterol tests during her stay detected an unusually high level of LDL, the bad cholesterol that increases the risk of heart disease. And an angiogram found that while most of her coronary arteries were wide open, one--the circumflex artery, which winds around the heart--was tortuous and small. Mrs. Black had probably been born with the defect.
Although she was only in my emergency room for less than an hour, she has changed forever the mantra I recite to students seeing their first patients with chest pain. Risk factors for coronary artery disease? Male sex, age, family history, smoking cigarettes, high blood pressure, high cholesterol. And then there’s the story of Mrs. Black.