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Failure to treat myocardial infarction


At 6:51 p.m., a 62-year-old man came to the emergency department (ED) of a local hospital reporting pain in the “chest wall area.” After eating a large meal and mowing the lawn, the patient had indigestion that did not resolve after taking over-the-counter antacids. 

The patient’s history included colon cancer treated by colectomy 12 years earlier.  


Physician action

An emergency medicine (EM) physician treated the patient with aspirin, nitroglycerine, and a 250-cc normal saline bolus. The patient reported continuous pain in the sternal region with radiation to the arms. Pain intensity was reported as 6 out of 10. He also had bradycardia, hypotension, diaphoresis, nausea, vomiting, and shortness of breath. 

At 7:03 p.m., a 12-lead electrocardiogram (EKG) was performed that showed ST elevation and peaked T-waves (V2, V3). A second EKG at 7:36 p.m. showed “marked ST abnormality, possible subendocardial injury.”  

The patient’s chest pain continued throughout the evening. The EM physician’s impression was “acute chest pain/angina.” ST elevation myocardial infarction (STEMI), pneumonia, pericarditis, pneumomediastinum, pneumothorax, pulmonary edema, and pulmonary embolism appeared to be ruled out, according to notes in the clinical section of the EM physician’s evaluation.

At 12:25 a.m., the patient was admitted to the hospital. Hospitalist A was the attending physician, in consultation with Cardiologist A, who was on-call for the hospital.

Hospitalist A’s diagnosis was chest pain and to “continue to rule out MI.” She ordered hydromorphone and enoxaparin, along with lab work. A CT angiogram done in the ED showed no pulmonary embolism. The results of the first set of cardiac enzymes were negative. 

The patient remained in sinus rhythm with no reports of chest pain through the early morning. At 5:38 a.m., a nurse documented that she notified Cardiologist A — through his answering service — of a troponin level of 0.98 (normal level 0.00-0.03). 

At 6:15 a.m., Physician Assistant A (who worked with Cardiologist A) returned the phone call and was told of the patient’s troponin level. No new orders were given.

At 8 a.m., the patient reported nausea, vomiting, and intermittent pain in the sternal area. The pain radiated to his arms and was described as 3 out of 10. There was no documentation of a phone call reporting this information to Cardiologist A’s office, though Hospitalist A requested a consult from Cardiologist A at 8:17 a.m.

Hospitalist A ordered that the patient be kept on oxygen, and to start a proton pump inhibitor and nitroglycerine. She documented that although chest pain was present, there were two sets of negative cardiac enzymes. She also wrote that the patient would likely have a stress test or cardiac catheterization that morning. 

Throughout the morning and in to the afternoon, the patient continued to report chest pain. His blood pressure ranged from 140/77 mm Hg to 147/88 mm Hg. There were no calls made to Cardiologist A reporting the patient’s chest pain.

A 2:07 p.m., the patient’s troponin level was reported at 5.0. At 3:03, Cardiologist A was paged about the elevated troponin level. A woman from the office returned the call and was notified of the elevated troponin level at 3:27 p.m. The patient reported another period of chest pain at 4 p.m.

Cardiologist A saw the patient at 5:03 p.m. He noted that the patient’s troponin level was less than 0.05 in the first two draws. He also documented the 0.98 troponin level and that the patient was developing Q waves. His diagnosis was non-STEMI with EKG changes. He recommended urgent catheterization. 

The patient arrived in the catheterization lab at 5:32 p.m. and the catheterization began at 5:54 p.m. The patient had 100 percent occlusion of the proximal left anterior descending artery (LAD); the right coronary artery was described as “diffusely diseased”; and the left circumflex was 20 percent occluded in a proximal section. Cardiologist B deployed a stent to the LAD occlusion with an “excellent result.” The ejection fraction was 40 percent. 

The next day, an echocardiogram showed worsening left ventricular function and the presence of a new left bundle branch block. The patient was taken back to the catheterization lab where Cardiologist B and Cardiologist C placed a Swan Ganz catheter and Impella device. Cardiologist C’s assessment included cariogenic shock with a New York Heart Association Class III-IV classification. The patient’s ejection fraction after the second procedure was 20 percent. 

The patient was transferred to a regional hospital, where he underwent rescue temporal posterior ciliary artery (TPCA) to the LAD and experienced cardiogenic shock. His treating physician — Cardiologist D — reported, “we are beginning to workup for a transplant and possible long-term LVAD [left ventricular assist device] should that be necessary.”

The patient slowly improved and was discharged about two weeks later. Back at home, the patient was followed by Cardiologist D, who reported, “we began workup for heart transplant and unfortunately he appears not to have enough viability that he could avoid transplant. I don’t think he will need LVAD as a bridge.”

The patient continued to have symptoms of congestive heart failure, and was placed on the transplant list in June. He had a heart transplant in October, and was started on immunosuppressive drugs in November. At last report — three years after the transplant — the results of an echocardiogram were normal. The results of an endomyocardial biopsy were negative for evidence of acute cellular rejection.



The patient filed a lawsuit against the local hospital where he was first treated; the EM physician; Hospitalist A; Cardiologist A, Physician Assistant A, and their group. The allegations were improper and untimely management of the patient’s myocardial infarction, resulting in the need for a heart transplant. 


Legal implications

This was a complicated case with multiple defendants. Cardiology experts who reviewed this case stated that the EM physician should have recognized that the patient was experiencing a STEMI in the ED. A cardiology consult should have been requested at that time. Instead, the patient was placed on a non-STEMI track and Hospitalist A treated him for that condition.

Experts who reviewed this case also thought Hospitalist A should have monitored the patient more closely and ordered a cardiology consult. 

Communication errors made this case challenging to defend. Once the patient was admitted to the hospital, several chest pain episodes were either not documented or not reported by the nurses to Physician Assistant A or Cardiologist A. However, one nurse testified that she did report the patient’s chest pain, shortness of breath, and EKG results to Physician Assistant A. There was no mention of this in the medical record.  

There was also a misunderstanding about the patient’s cardiac enzymes. The 0.98 troponin value reported to Physician Assistant A was a Troponin T value and was considered more significant than a similar Troponin I value. It was Physician Assistant A’s understanding that the reported value was a Troponin I, though the hospital had used Troponin T values for more than 10 years. 

The plaintiffs developed the theory that Physician Assistant A should have obtained the additional data, recognized its significance, and consulted Cardiologist A or activated the catheterization lab. 



This case was settled on behalf of the EM physician, Physician Assistant A, and the cardiology group that employed her. The hospital also reached a settlement with the patient. The outcome of the case against Hospitalist A is unknown. 


Risk management considerations

Managing risk when determining how to treat patients with chest pain requires well-defined protocols that are followed by the hospital and the on-call physician’s staff. To reduce the risk of errors, verify that policies for on-call providers explicitly describe when the physician needs to be contacted. Protocols should be clearly communicated, and staff should receive regular training in following the protocols. In addition, confirm that ED staff are familiar with chest pain protocols and when to request a cardiology consult. 

In this case, a misunderstanding or miscommunication of lab values contributed to the alleged delay in treatment. Make sure your staff has a clear understanding of standards for lab reports. If not, ask for clarification from the lab or hospital.  

Communication between the caregivers in this case was not comprehensive. It was unclear whether the patient’s chest pain and other symptoms were reported to Physician Assistant A or Hospitalist A. It was also not clear if Hospitalist A was in contact with Physician Assistant A about the patient’s condition.