He had a whole battery of tests just a couple months ago. He couldn’t eat well and his legs ached. He had nearly every doctor at Emory look at him. They ended up prescribing him Vitamin A and Vitamin D. After all that. He got the full work over and really just needed vitamins. If a 28 year old heart is going to go out, shouldn’t they have found that? Maybe, but they didn’t.
Indeed. It’s a tragic death that raises many questions.
Most of time, when grieving families contact me, they’re not looking to file a lawsuit, they’re looking for answers. Doctors and hospitals rarely tell family members much about the circumstances, or about what could have been done differently, and so those family members start looking for answers. I made it my policy long ago that, even if I didn’t believe a lawsuit was warranted or would be successful, I would try to explain to everyone who contacts me about a medical malpractice case what actually happened and if something could have been done differently.
From the information Jeremy’s family has provided publicly, we can start to figure out what might have gone wrong. The coroner hasn’t determined the cause of death yet, and apparently is not going to conduct an autopsy, but the circumstances strongly suggest a heart attack.
Jeremy was only 28-years-old. Coronary heart disease is rare in individuals younger than 40, but it’s not unheard of. In the famous Framingham Study, acute myocardial infarction occurred in men 30 to 34 years old at a rate of 12.9 per 1,000. One of the few studies to look at risk factors for coronary heart disease in men under 40 found that the risk factors were roughly the same as for older men, i.e., “age, serum cholesterol level, systolic blood pressure, and cigarette smoking.”
Josh’s post makes a reference to cigarettes, so at least one of those risks is present. The vitamin A and D prescriptions strike me as a bit odd. In developed countries, vitamin A is typically only prescribed for measles, dermatology (e.g., acne), and leukemia. (There was some hope in the past that vitamin A supplementation could help with atherosclerosis, but a large study on the issue was stopped early when they found beta-carotene and vitamin A supplements “had no benefit and may have had an adverse effect,” including by increasing the risk of cardiovascular disease.) Vitamin D deficiency is correlated withan increased risk of “heart failure, sudden cardiac death, stroke, overall cardiovascular disease, and cardiovascular death,” but Jeremy was a young, active man from a background associated with a lower risk for cardiovascular disease. He was hardly your typical patient at risk for a vitamin D insufficiency, which is more common among “institutionalized elderly, osteoporotic individuals, chronically ill patients, African American patients, especially those with CVD.”
But something was obviously wrong with him. A 28-year-old who shows decreased appetite, leg pain, and produces whatever test results prompted the vitamins, surely has something going on. It has been well-known in the medical literature that young patients with myocardial infarction generally do not experience angina pectoris (i.e., chest pain), which should put doctors on guard when they see younger patients with an odd constellation of symptoms, particularly if they are smokers, as is the case in over 90% of young adults who suffer a heart attack.
To know if Jeremy Carter’s death was preventable, we’d need to know what the “battery of tests” he received included, and what those tests showed. Did his doctors:
- review biochemical markers of myocardial necrosis, like troponin and CK-MB?
- review his electrocardiogram (ECG) for pathologic Q waves?
- review his ECG for ST segment elevation or depression?
Those are the typical markers that show a patient is beginning an acute myocardial infarction. The question of treatment depends on what type of heart attack is occurring. Given that Jeremy apparently didn’t have chest pain, the key issue would likely be whether the ECG shows ST elevation (a “STEMI”) or if the ST is normal (“non-STEMI”). If it’s a STEMI, then the typical treatment is percutaneous coronary intervention, also known as angioplasty. If it’s non-STEMI, then medical therapy, coronary angiography, and perhaps re-vascularization.
Was Jeremy Carter having an acute myocardial infarction “a couple months ago” when he had the tests? Likely not. At the same time, however, we was showing a variety of unusual symptoms without a clear explanation, hence having “nearly every doctor at Emory look at him.” Who was in charge of his care? What was his follow-up schedule? Was he instructed to regularly see his family physician for any changes? What about regular visits with a cardiologist? As one article noted more than 15 years ago, “Despite advances in investigative modalities, a focused history and physical examination followed by an ECG remain the key tools for the diagnosis of MI.” Heart attacks will never be prevented if the doctors aren’t seeing the patient and using the tools available to spot them.
To me, the most disturbing aspect of Jeremy Carter’s death is that the doctors may have closed his case without ever reaching a clear diagnosis or treatment plan. Maybe they did, but Josh’s remark that Jeremy “got the full work over and really just needed vitamins” indicates to me that the doctors ran a lot of tests, never really reached any working diagnosis, and then sent him away with the belief that he was young and generally healthy, without any clear plan for followup.
Medical science isn’t perfect and never will be, but a doctor will never be able to see and cure a problem if they’re blinded by the person’s youth.