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A 55-year-old patient was found to have elevated high-sensitivity cardiac troponin (hs-cTn) and a shark fin electrocardiogram (ECG) pattern (triangular QRS-ST-T waveform) after presenting earlier that day with nausea, vomiting, and an altered mental status at an outside hospital, a case report in detailed.

The patient's medical history was notable for poorly controlled diabetes type 2 (treated with insulin) and use of several substances, including cocaine, cannabis, and tobacco, reported Lynda Rosenfeld, MD, and Katherine Clark, MD, MBA, both of Yale University School of Medicine in New Haven, Connecticut.

The patient had no history of heart disease. The patient also had low blood pressure, tachycardia, and tachypnea.

The referring institution reported that several lab tests had abnormal results:

• Potassium: 5.9 mEq/L
• HCO₃: 3.8 mEq/L
• Glucose: 1,472 mg/dL
• Creatinine: 4.7 mg/dL (normal range 0.4-1.3 mg/dL)
• Total creatinine kinase: 15,958 U/L (normal range 11-204 U/L)
• Initial hs-cTn level: 284 ng/L (positive >52 ng/L)

Based on the evidence of acute kidney insufficiency, clinicians treated the patient for diabetic ketoacidosis and intubation to provide airway protection. Toxicology report was positive for cannabis.

The ECG performed by the referring hospital at the time of presentation revealed sinus tachycardia with prominent T waves. Initially, this was thought to be related to the patient's metabolic derangement; however, a few hours later, there was a significant increase in the hs-cTn level to 820 ng/L. At that point, findings of a second ECG prompted the transfer of the patient to higher-level care.

Rosenfeld and Clark noted that "the ECG on transfer showed sinus rhythm with marked ST elevations in the inferolateral leads with a characteristic pattern entailing large R waves, loss of the ST segment, and massive ST elevation in the affected leads."

They pointed out that the pattern of downsloping ST elevations as opposed to more typical concave upward or "tombstoning" has been most commonly linked with injury due to left anterior descending coronary occlusion.

"This patient also had significant ST depression in leads aVR and V1 that overlie the base of the heart and may represent reciprocal apical injury," the case authors noted. When observed with the ST elevations, the affected area can be localized to the left ventricular apex inferolateral wall. Given the ECG findings, clinicians performed an urgent cardiac catheterization; however, this did not reveal any critical epicardial coronary lesions.

The patient underwent an endomyocardial biopsy and placement of a right heart catheter, which revealed a small increase in filling pressures and a reduction in cardiac output. Subsequently, case authors performed an echocardiogram that showed "a left ventricular ejection fraction of 32% with mid anterior, mid inferoseptal, mid anteroseptal, and apical akinesis. The remainder of the left ventricle was hypokinetic."

The presence of this ECG pattern in the absence of epicardial coronary disease caused clinicians to consider other causes, particularly stress cardiomyopathy or myocarditis.

"The patient was treated for diabetic ketoacidosis, cardiogenic shock, and rhabdomyolysis, and experienced dramatic improvement," the authors wrote.

There was no evidence of inflammation or granulomata detected in myocardial biopsy tissue, they noted. Total creatinine kinase level peaked at 43,300 U/L and hs-cTn peaked at 8,020 ng/L, while the ST elevation resolved over the following 2 days.

On hospital day 8, clinicians followed up with another echocardiogram and a cardiac MRI. Findings indicated that the patient's heart function had returned to normal, and there was no evidence of wall motion abnormalities. Although the cardiac magnetic resonance study was of poor quality, the results were suggestive of apical edema.

However, Rosenfeld and Clark noted that they were not able to determine exactly what had caused the patient's myocardial injury.

"The negative results of the endomyocardial biopsy specimen, the [cardiac MRI] showing edema, and the apical wall motion abnormality along with the rapid clinical recovery of the patient are consistent with a physically triggered stress cardiomyopathy. Although the patient's very high hs-cTn level may have suggested myocarditis, rhabdomyolysis probably contributed to it," they wrote.

Discussion

Rosenfeld and Clark observed that while the shark fin pattern is most commonly linked with STEMI, it also occurs in stress cardiomyopathy and myocarditis, which suggests that it may also signify a more generalized effect of myocardial injury.

The exact process that gives rise to the distinctive shark fin pattern is not well understood, the case authors noted. They reviewed several proposed theories, "all likely resulting in a mismatch of endocardial or epicardial repolarization and creating a transmural voltage gradient, the characteristic large R wave, and downsloping ST segment -- similar to the classic also thought to be associated with such a gradient."

Proposed explanations for shark fin pattern include:

• Epicardial or microvascular ischemia, possible increase by localized edema, as occurs with stress cardiomyopathy or myocarditis-related inflammation
• Mechanical effects of "localized abnormal wall motion and left ventricular cavity expansion, as seen with aneurysms"
• Catecholaminergic effects of an increase in metabolic demand or related to microvascular constriction

Case authors noted that the shark fin pattern on ECG in the presence of an elevated hs-cTn level requires immediate coronary catheterization, in order to rule out acute epicardial coronary obstruction before other etiologies can be considered.

In a 2018 of consecutive STEMI patients, the shark fin pattern was identified in 1.4% on the admission ECG. Compared with those with other ST-segment elevation ECG patterns, this subset of STEMI patients showed excess left main coronary artery involvement, ventricular fibrillation, cardiogenic shock, and in-hospital mortality.

Rosenfeld and Clark stated that "it is critically important to recognize this pattern that has been called the triangle, lambda (λ), or ."

Less commonly, the pattern has been observed in cases of stress (Takotsubo) cardiomyopathy, and more rarely, associated with acute myocarditis.

Case authors said aggressive treatment is required for the shark fin pattern. Furthermore, they added that diagnoses of stress cardiomyopathy or myocarditis should be considered in patients without the acute STEMI.

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