Cox v. Fatemi

Dr. William Rogers Details Timeline of Patient’s Fatal Heart Attack, Clearing Defendant Physician in Med Mal Trial

The Expert: Dr. William Rogers, a cardiologist and professor at the University of Alabama Birmingham testifies for the defense, explaining his belief that the patient did not suffer from acute coronary syndrome at the time he saw the defendant and concluding the physician appropriately treated the patient.

In this 2017 Georgia medical malpractice trial, plaintiff claims the defendant physician failed to diagnose acute coronary syndrome that a man allegedly suffered from when he visited the physician complaining of weakness, nausea, sweating, and pain. The patient ultimately suffered a fatal heart attack days later.

The trial centered on whether the defendant was negligent in failing to order heart tests when she diagnosed the patient with a viral illness. The defense argued that the doctor acted appropriately and the patient did not suffer from acute coronary syndrome, or ACS, at the time of the encounter. Dr. William Rogers, a practicing cardiologist from Birmingham, Alabama, testified for the defense.

In this clip, the expert initially confirms that the patient did indeed suffer a heart attack several days after he was seen for the viral illness. He based this opinion on the patient’s classic symptoms and EKG results. However, Rogers feels that this was a “very, very fresh” heart attack and he’s certain that this was quite recent, since an acute clot was demonstrated within the right coronary artery on the angiogram performed at that time.

The doctor discusses the significance of the cardiac enzymes measured in the bloodstream at the time of the patient’s second presentation, four days after the first, in determining the timing of the heart attack. The CKMB, an enzyme found primarily in heart muscles, has not yet risen, and it would be the last to rise among the three markers being discussed. The myoglobin typically is elevated in the bloodstream first, being the smallest of the protein molecule markers, Rogers explains to the jury. It rises within 2 hours of the cardiac injury, peaks at about 9 hours and becomes normal at 24 hours. A significantly elevated myoglobin result, as in this case, would therefore be an indication that the cardiac damage occurred more recently. Additionally, the troponin elevation rises early after a heart attack and goes down slower than the other values. These facts, and the three values taken together, support the conclusion that an acute event occurred rather than something happening four days before when the patient had viral symptoms.

Rogers then walks jurors through an easy to understand, yet elegant explanation of how an acute coronary occlusion occurs. Using marking pen and paper, he draws a cross-section of a coronary artery and demonstrates a 40-50% occlusion of the lumen of that artery by plaque formation. He notes the plaques causing the occlusion to that degree are prone to rupture from the blood rushing into them, resulting in the sudden, complete occlusion of the artery. These are called “vulnerable plaques.” A plaque like this has a large fatty core, and a thin fibrous cap. These can break off at their attachment to the sidewall of the artery. This disruption exposes the undersurface of the plaque to the bloodstream. That undersurface, the fatty area, then attracts blood clots, and those clots attract more clots until the entire lumen becomes acutely filled. In this patient’s case, it was the right coronary artery that was affected by this series of events. When this artery became completely blocked, the heart became starved for oxygen resulting in the symptoms that make up ACS.

The cardiac expert goes on to explain that we now understand that most plaques that rupture and acutely occlude the coronary arteries, causing myocardial infarction, or heart attack, occur in vessels that were only 40-50% narrowed before the rupture. Rogers states plainly that the patient likely had such a narrowing when he was first seen and correctly diagnosed with a viral illness. This narrowing is not enough to cause ACS, or pain from a cardiac origin. However, four days later, the plaque in the narrowing ruptured, completely occluding the artery in a very short period of time, and causing pain and damage to the heart from ischemia.

The attorney raises what may be in the jury’s mind: that the expert’s explanation seems counterintuitive because one would think that a significantly narrowed artery, rather than a partially narrowed artery, would be the one to suddenly clot off.

The expert says that up until recently, doctors thought that same thing. However, he explains, they now understand that it is these partly narrowed vessels that are asymptomatic one day and dangerously blocked the next by the series of events he described. This explains the lack of evidence of acute coronary syndrome in this patient’s initial presentation, and the overwhelming evidence four days later. Rogers concludes that there is no doubt in his mind, even looking retrospectively, that this is the case.

This testimony was unequivocal and convincing. The defendant physician, Rogers says, was not obligated to obtain tests for acute coronary syndrome on the first visit because those tests could not be justified without symptoms or signs indicating that this was likely.

The jury found for the defense.