The Heart Attack on the First Tracing
How an ST-Elevation Pattern Was Read as “Nonspecific” Three Times in Four Days
Please read first.
Past results do not guarantee or predict a similar outcome. Every case is decided on its own facts, its own medical record, and its own expert testimony. The resolution described here says nothing about what any other case is worth or how it would turn out.
Reading this article does not create an attorney-client relationship with Lupetin & Unatin, LLC or any of its attorneys, and nothing here is legal or medical advice. It is published for general informational and educational purposes. A representation begins only through a signed written agreement.
Identifying details have been changed or removed. Names, dates, ages, locations, hospitals and health systems, physicians, and other identifying information have been omitted or generalized to protect client privacy. No quotations from medical records, depositions, or expert reports appear anywhere in this article; where testimony or an opinion is described, it is paraphrased.
The Error, Stated Plainly
A man in his sixties arrived at a Pennsylvania emergency department with a leg that was losing its blood supply. Outpatient imaging had just shown acute arterial occlusions, or clots, blocking several leg arteries below the hip. The patient was admitted for treatment of a threatened limb.
He also reported severe pain and tightness in his upper back and shoulders.
An electrocardiogram was obtained shortly after he arrived. It was read as showing a small amount of ST-segment elevation in a single lead with some T-wave changes. The conclusion recorded in the chart was that there was no concern for acute cardiac ischemia. No troponin was ordered. No cardiologist saw him in the emergency department. He was admitted to a surgical service for his leg.
Over the next three days the picture on his heart tracing never meaningfully changed. The interpretation of it changed twice after the fact. By the time anyone diagnosed a heart attack, the muscle of his left ventricle had been dying for days. On the fourth hospital day that wall gave way. He collapsed, went into cardiac arrest, and died. Autopsy found a rupture of the lateral wall of the left ventricle and the pericardial sac filled with blood.
He had hypertension, a smoking history, and a strong family history of coronary artery disease. He also carried a longstanding, well-documented chronic pain diagnosis involving his neck, upper back, and shoulders, treated by multiple specialists over a period of years. That history became the explanation for his symptoms rather than a reason to look harder at them.
Why This Tracing Was Missed — and Why That Is Not a Defense
Three points of medicine explain both how this happened and why it fell below the standard of care.
STEMI criteria are a rule for activating a protocol, not a rule for deciding whether a patient is having a heart attack. A standard electrocardiogram uses twelve leads, each viewing the heart from a different angle; leads that view the same region are contiguous. When a coronary artery closes, the injury typically shows as ST-segment elevation in the leads pointing at that region, often with mirror-image ST depression in the leads pointing at the opposite wall. This is called a reciprocal change. The formal criteria for declaring a STEMI generally require at least a millimeter of elevation in two contiguous leads. That threshold exists so hospitals do not activate a full cardiac emergency response for every minor squiggle. Infarctions of the high lateral wall are well recognized as easy to miss because they can produce elevation in only one or two leads, sometimes with subtle inferior depression. This pattern is readily dismissed as nonspecific on a quick look.
Heart attacks do not always present as chest pain. Pain in the jaw, neck, shoulders, upper back, or arm can be an anginal equivalent. Anginal equivalents are symptoms of cardiac ischemia in a patient who never uses the words “chest pain.” That is one reason the standard evaluation of a patient with cardiac risk factors and an abnormal tracing includes a troponin blood test, which detects injured heart muscle, and serial tracings, which show whether the picture is evolving.
The leg clot was itself a reason to examine the heart. A clot lodged in a leg artery has to come from somewhere. One well-described source is the heart: after an infarction damages a section of the left ventricle, blood can pool against the injured wall, form a clot, and later break loose and travel. An acute arterial occlusion of unexplained origin, in a patient with cardiac risk factors, is a reason to look closely at the heart rather than only at the limb.
Where Our Firm Came In
Brendan Lupetin and Greg Unatin of Lupetin & Unatin, LLC took the case. The firm limits its practice to medical malpractice and catastrophic injury, and delayed-diagnosis cardiac cases are among the most demanding categories of that work: the medicine is genuinely contestable, and causation is often harder to prove than negligence.
The first step was not a lawsuit. It was reviewing the medical records, including the emergency department and nursing documentation, every tracing and every reading of it, the laboratory results, the operative and procedural notes, and the autopsy materials including the tissue slides. Experts were retained by discipline: a board-certified emergency medicine physician on what the emergency department should have done with these complaints and this tracing; a board-certified cardiologist with interventional and vascular expertise on the cardiology standard of care, the interaction between the cardiac and vascular problems, and what timely intervention would have offered; and a board-certified forensic pathologist on the mechanism and timing of the fatal event.
Findings That Drove the Case
The abnormality was on the very first tracing, and it never went away. The emergency department tracing showed ST-segment elevation in the high lateral leads with depression in the inferior leads. The tracings obtained on each subsequent day were, by the defense’s own description, essentially unchanged from it. That cuts in a direction the defense did not want: if the later tracings were diagnostic of an infarction, and the first tracing looked the same, then the first tracing was showing the same infarction.
No troponin was drawn in the emergency department. When Troponin was finally drawn after the patient reported chest tightness on the third hospital day it was markedly elevated. Every expert in the case, on both sides, agreed that a troponin drawn on arrival would have been abnormal.
The treatment for the leg carried a cardiac risk nobody was in a position to weigh. The patient was placed on full anticoagulation and then underwent catheter-directed clot-dissolving therapy for the limb. Aggressive anticoagulation and thrombolytic therapy in a patient with a recent, unrecognized infarction are associated with an increased risk of mechanical complications of that infarction, including rupture of the weakened ventricular wall. Because no one had diagnosed the heart attack, no one made a considered judgment about that trade-off.
The rupture occurred in the window the pathology predicts. Myocardial free-wall rupture is a mechanical complication of infarction. Dead heart muscle is infiltrated by inflammatory cells and loses tensile strength, leaving the wall at its weakest roughly three to seven days after the infarct while still bearing the same pressure with every beat. Transmural infarctions are the ones most likely to rupture, and the left ventricle is the most common site. The autopsy findings placed the age of this infarct within that window.
The Defense, and Why It Was Serious
This case was contested and by no means a foregone conclusion. The defense retained its own emergency physician, cardiologist, and cardiovascular pathologist. Their position, in substance, was that the initial tracing did not meet STEMI criteria and was properly characterized as nonspecific; that the patient repeatedly and explicitly denied chest pain and other cardiac symptoms; that his back and shoulder pain was chronic, longstanding, and documented as unchanged, so treating it as an anginal equivalent would have been unreasonable in context.
The defense also argued the infarction had largely occurred before the patient ever reached the hospital, so that much of the muscle damage was already done and the rupture would have happened regardless.
That last argument is why delayed-diagnosis cardiac cases are difficult. Proving that a physician should have acted differently is only half the work. Where the underlying injury has a head start, the defense will argue the delay changed nothing, and a jury may agree.
Resolution
The parties reached a negotiated resolution of the claims before trial. The terms are confidential.
What This Case Teaches
The lesson is not that the emergency physicians were careless people. It is that a patient can arrive with one urgent problem — a leg losing its blood supply — and have a second, more dangerous problem sitting in plain view on a tracing.
Anchoring is the enemy. Once a diagnosis is fixed, later information gets sorted into that box. Upper back and shoulder pain becomes “his chronic pain.” An abnormal tracing becomes “nonspecific.” The discipline is to ask what else could explain the findings, especially in a patient with multiple cardiac risk factors.
A chronic complaint is not automatically an old complaint. Patients with longstanding pain syndromes have heart attacks too, and their history can become a reason to stop asking questions rather than a reason to ask better ones.
A tracing that is hard to interpret is a reason to ask for help, not a reason to move on. In a patient with hypertension, a smoking history, a strong family history of premature coronary disease, an arterial clot of unexplained origin, and upper back and shoulder pain, the cost of a troponin and a call to cardiology is very small.
How Lupetin & Unatin Helps Families in These Cases
If someone you love suffered a heart attack, a stroke, or a death after a hospital or emergency department reported that the tests were normal, that record can be reviewed by someone whose job is to check the work.
Our practice is devoted to medical malpractice and catastrophic injury cases in Pennsylvania. In cases like this one, that means obtaining the complete record rather than a summary; having the actual studies re-read by qualified physicians rather than relying on the interpretations already in the chart; retaining experts in each discipline the case touches; and taking the sworn testimony of every provider involved.
We offer a free, confidential consultation to review what happened and to tell you honestly whether we believe there is a viable claim. We handle medical malpractice cases on a contingency fee basis, meaning our attorney’s fee is a percentage of any recovery and no fee is owed if there is no recovery. Clients may remain responsible for case costs and expenses, and we explain in writing how fees and costs work before you decide to hire us.
Pennsylvania has strict deadlines for filing medical malpractice claims, and they can be shorter than people expect.
Free Consultation — No Fee Unless We Win
Lupetin & Unatin, LLC represents Pennsylvania patients harmed by physicians who failed to meet the standard of care.