A 68-year-old female with a past medical history of untreated hypertension was referred to the ED from an outside clinic for hypertension. She had been off antihypertensive medications for several months and had attempted to re-establish care with a PCP but was referred to the ED for a blood pressure of 200/120. At triage, she denied any symptoms. An ECG was obtained at 15:22, when the patient was asymptomatic.
She waited in the waiting room for several hours before being seen. Labs were initially drawn at 17:50 and resulted with a positive troponin-I of 0.07. On initial examination, the patient noted that, while waiting to be seen, she had developed epigastric pain. A repeat ECG was obtained at 18:30 (Figure 2), revealing new biphasic T wave changes most notable in V1-V3. The cath lab was subsequently activated.
Figure 2. Second ECG.
The cardiology fellow evaluated the patient and performed a point-of-care echocardiogram, which did not demonstrate any clear regional wall motion abnormalities. After discussion with the fellow, it was recommended that the patient be started on a nitroglycerin drip and obtain a CT scan of the abdomen and pelvis to assess for aortic dissection, which was negative. The patient’s symptoms improved with a nitroglycerin drip. A third ECG was obtained at 20:00 (Figure 3), with improvement in the biphasic changes in V1-V3.
Figure 3. Third ECG.
Interpretations:
First ECG: Normal sinus rhythm, normal axis, normal intervals. No significant ST elevations or depressions.
Second ECG: Normal sinus rhythm, normal axis, normal intervals. New biphasic T wave changes in V1-V3 initial positivity, terminal negativity, no precordial Q waves, +left ventricular hypertrophy (R wave in V5,6 + S wave V1 > 35).
Third ECG: Sinus tachycardia, normal axis, normal intervals. ST elevation in leads V1, no further biphasic T wave changes, no precordial Q waves.
Discussion:
The patient was admitted to the Cardiac ICU for hypertensive emergency. Ultimately, she had a CT of the coronary arteries completed during her admission, which revealed calcified atherosclerotic plaque resulting in minimal (1-24%) stenosis in the mid left anterior descending artery and distal left circumflex artery. She was discharged with prescription for nifedipine 60 mg ER PO daily, aspirin 81 mg PO daily, and atorvastatin 40 mg PO daily, with planned cardiology follow-up as an outpatient in several moths.
Wellen’s syndrome criteria are defined as (1):
Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
ECG pattern present in pain-free state
Isoelectric or minimally-elevated ST segment (< 1mm)
No precordial Q waves
Preserved precordial R wave progression
Recent history of angina
Normal or slightly elevated serum cardiac markers
Figure 4. LITFL https://litfl.com/wellens-syndrome-ecg-library/
The pattern is usually present in the pain-free state because biphasic T-waves are a reperfusion pattern and coincide with spontaneous opening of the affected coronary artery. That is why Wellen’s syndrome only occurs once chest pain (or anginal equivalent) resolves.
Wellen’s syndrome is highly specific for stenosis of the left anterior descending artery (LAD).
Our patient did have biphasic T waves in V1-V3 and her troponin was positive (0.07 at 1750, 0.04 at 2000). However, this ECG was obtained when the patient was having active epigastric pain and was not a pain-free state, so she did not meet the exact diagnostic criteria for Wellen’s syndrome. Nontheless, given the acute ECG changes in the setting of a positive troponin, and a patient with risk factors for CAD, the cath lab was activated for this patient.
What is hypertensive emergency?
Hypertensive emergency is defined as, “an acute, marked elevation in blood pressure that is associated with signs of target-organ damage” (2). Examples of hypertensive emergency include cardiac ischemia (type-2 myocardial ischemia), pulmonary edema, hypertensive encephalopathy (visual disturbance, seizure, delirium), and acute renal failure. The treatment for hypertensive emergency is generally dependent on the end-organ damage the patient is presenting with. For patients with cardiac ischemia, it is recommended to consider IV esmolol or IV nitroglycerin (3). The treatment should be titrated to a specific goal of decreasing mean arterial pressure by 20% to 25% within the first 1 to 2 hours (2).
Takeaway points:
Patterns concerning for occlusive MI (OMIs) should be brought to Cardiology’s attention immediately, including STE and Wellen’s syndrome patterns.
In patients with hypertensive emergencies with findings concerning for cardiac ischemia, consider IV nitroglycerin or IV esmolol, titrated to decreasing the MAP 20-25% in the first 1-2 hours.
In hypertensive emergencies with elevated troponin, consider possible aortic dissection both with point-of-care ultrasound and CT angiography of the chest, abdomen, and pelvis.
Repeat ECGs as the patient’s symptoms improve or worsen to monitor changes to the T waves for possible improving or worsening ischemic changes.
Authored by Iris Lawson-Seebaran, DO.
References:
Cadogan M, Buttner R. Wellens Syndrome. Life in the Fast Lane. September 8, 2021, accessed June 21, 2024. https://litfl.com/wellens-syndrome-ecg-library/
Alley WD, Schick MA. Hypertensive Emergency. [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470371/
Aronow WS. Treatment of hypertensive emergencies. Ann Transl Med. 2017 May;5(Suppl 1):S5. doi: 10.21037/atm.2017.03.34. PMID: 28567387; PMCID: PMC5440310.