A 64-year-old woman presented to the emergency department with two days of severe nausea, numerous episodes of vomiting, and progressively worsening right upper quadrant/epigastric abdominal pain. She was continuously spitting clear secretions into an emesis bag on arrival in triage. Her 8/10 dull ”ripping” pain originated in the right upper quadrant and radiated in a band-like pattern to her epigastrium. She was not experiencing any chest pain or shortness of breath. Her medical history included hypertension, type 2 diabetes mellitus, recurrent acute pancreatitis secondary to hyperglycemia, peripheral artery disease, and gout. She smoked a pack of cigarettes daily.
Vital signs were blood pressure 123/79 mm Hg, pulse 86 bpm, respiratory rate 20 bpm, temperature 36.8°C, and SpO2 100%. She appeared quite uncomfortable. Her cardiac and chest exams were unremarkable. Her abdomen was soft but tender to palpation maximally in the epigastric region without rebound. Laboratory studies were ordered. An ECG is shown in Figure 1.
Figure 1. Presenting ECG.
This is a regular sinus tachycardia. The QRS axis is normal, but notable biphasic deep inverted T-waves are seen in the anterior precordial leads. The QTc is also very long at approximately 580 ms. These findings were noted to be different from a previous ECG obtained about three weeks earlier. (Figure 2.) The differential diagnosis of deep inverted T-waves is shown in Table 1.
Figure 2. Previous ECG.
If a patient presents with symptoms compatible with ischemic chest pain, there is a strong likelihood that deep inverted T-waves are an indication of reperfusion of a critically occluded LAD. Named Wellens’ syndrome, the inverted T-waves are seen in the anterior precordial leads, typically V2-V4. The QT interval is often prolonged. If Wellens’ waves are captured on ECG, it is usually after the LAD has reperfused and the chest pain has resolved, which is why the pattern is referred to as reperfusion waves. The initial troponins can be elevated because of a period of ischemia before reperfusion. A critical stenosis or ruptured plaque that remains in the LAD despite the reperfusion, however, that is at high risk of reoccluding. This warrants emergent angiography and PCI.
Her initial troponin I was 0.1 ng/mL. Labs were notable only for a lipase 194 IU/L, glucose 272 mg/dL, and WBC 17 k/mm3. Given the concern for acute coronary syndrome, she was given aspirin 325 mg orally and clopidogrel 600 mg orally, and started on heparin infusion. The patient was taken emergently to the cardiac catheterization lab for angiography with anticipation of PCI.
The patient was found to have a left dominant system and type III LAD. The left circumflex was chronically occluded, and she had pronounced left-to-left collaterals from the LAD. The right coronary artery had two areas of severe stenosis in the mid-portion. The patient had two-vessel coronary artery disease, but the LAD and diagonals had only mild diffuse irregularity, and no culprit lesion was suspected based on the ECG. No PCI was performed.
The naming convention for the LAD can be confusing. A type I LAD stops short of the apex of the ventricle. Type II goes to the apex. Finally, type III wraps around the apex and into the inferior interventricular groove to meet the PDA artery. (Figure 3.)
Figure 3. LAD naming convention.
An echocardiogram showed mild decreased left ventricular systolic function and a septal regional wall motion abnormality. The wall motion abnormality did not correspond to a vascular territory because the apex was preserved. This was felt to represent a stress cardiomyopathy (SCM), also referred to as Takotsubo cardiomyopathy. SCM is associated with severe physical (such as severe illness) or emotional stressors that generate a large catecholamine surge. Typically there is apical ballooning and hypokinesis, but it can also be seen as basal or septal hypokinesis. The effects of this wall motion abnormality can be seen on the ECG as ST-segment elevation (STEMI mimic), deep inverted T-waves, or prolonged QTc. Incidence is higher in women, and prognosis for recovery of systolic function is good.
Because no culprit lesion was identified, the dual antiplatelet therapy was stopped. The use of P2Y12 inhibitors in conjunction with aspirin have proven immensely valuable in treating acute coronary syndrome, largely supplanting the GIIb/IIIa inhibitors. Treating the patient in the ED before angiography (“defining the anatomy,” as cardiologists call it) may not be beneficial, however. A percentage of patients who undergo emergent angiography turn out not to have acute coronary syndrome. Treatment with dual antiplatelet therapy is not indicated, and subjects the patient to the risks of the medication, such as bleeding, without any benefit. Treatment with a P2Y12 inhibitor is a relative contraindication in our patient with acute pancreatitis because of the increased risk of hemorrhagic conversion of the pancreatitis. If a patient truly does have acute coronary syndrome, pretreatment with platelet inhibition with clopidogrel does not provide any anti-ischemic benefit, but does allow the time for the metabolism of the medication to its active metabolite.
The benefits of treating a patient with P2Y12 inhibitors are much smaller for the ACS group if there is a short interval between when a suspected diagnosis of acute coronary syndrome is made in the ED until angiography is performed, but the risks for the non-ACS group remain constant. This tradeoff has been shown not to be beneficial for upstream treatment with prasugrel and ticagrelor, though this is an open question for clopidogrel.
Our patient was placed on maximal medical therapy for atherosclerotic disease, and non-emergent PCI of the RCA was performed once the pancreatitis resolved. She had no complications from the antiplatelet therapy. The patient made a complete recovery from her stress cardiomyopathy with return of normal heart function.