The institutional review board (Chengdu Military General Hospital) approved this work and waived the need for informed consent.
In 2013, a 66-year-old farmer with a history of ventricular tachycardia (VT) and hypertension presented to the Emergency Department with continuous palpitation, chest tightness, profuse sweating and nausea with no obvious predisposing causes.
The patient experienced a sudden drop in blood pressure and acute confusion.
After an immediate electrical conversion, his consciousness was gradually restored, and symptoms relieved.
Then, this patient was transferred to the Department of Cardiology for further evaluations and treatments.
The patient's blood pressure was 105/75 mm Hg upon admission, with a heart rate of 75 beats/min, body temperature of 36.6°C and respiration rate of 18 times/min.
The heart border extended to the left, with the apical impulse located in the left 5th intercostal space, 1.0 cm lateral to the midclavicular line.
The patient had a history of hypertension over 30 years without regular antihypertensive medication.
The highest blood pressure was 170/110 mm Hg.
There was no family history of early coronary artery disease or sudden cardiac death.
He did not smoke cigarettes or use illicit drugs, and rarely consumed alcohol.
He also reported no known contacts with sick persons and no recent travel.
Twelve-lead surface electrocardiogram (ECG) of VT indicated that the origin of VT was at the boundary between right ventricular outflow tract (RVOT) and tricuspid valve.
When VT increased to 150 beats/min or higher, no epsilon waves were found in the precordial leads (Figure1A and B).
In contrast, when VT decreased to 120 beats/min or lower, epsilon waves appeared in leads V1–V2 (Figure1C).
Notably, the epsilon waves preceded QRS waves in leads V1–V2, while endocardiac tracing confirmed that the corresponding local potential originating from RVOT appeared prior to the ventricular rhythm (Figure ​(Figure1D).1D).
Sinus ECG in the year of 2013 suggested a slight left deviation of electric axis, with a heart rate of 87 beats/min and flat T waves in lead II.
T wave inversions were found in leads III, avF and V1–V3, meanwhile epsilon waves were found following QRS complex in leads V1–V3 (Figure ​(Figure2B).2B).
When the lead avR was amplified, epsilon waves were also found behind QRS waves (Figure ​2C).
Atrial premature beats appeared occasionally.
Moreover, ventricular premature beats were also found to originate from the right ventricular apex, with epsilon waves appearing behind QRS waves (Figure ​(Figure2B).2B).
In contrast, sinus ECG obtained in the year of 1999 revealed similar left deviation of electric axis, flat T waves and T wave inversions, but absence of epsilon waves (Figure ​(Figure2A).2A).
Data from biochemical assays were as follows: cardiac troponin I level was 0.714 μg/L (normal range, 0–0.06 μg/L), serum B-type natriuretic peptide level was 466.530 pg/mL (normal range, 0–100 pg/mL), serum d-dimer level was 8.14 mg/L (normal range, 0–0.55 mg/L), blood urea level was 11.69 mmol/L (normal range, 2.90–7.20 mmol/L), serum creatinine level was 144.00 μmol/L (normal range, 44–133 μmol/L), serum uric acid level was 611.40 μmol/L (normal range, 100–432 μmol/L), and endogenous creatinine clearing value was 57.90 mL/min (normal range, >80 mL/min).
Echo data revealed remarkably enlarged right atrium and right ventricle, and widened ROVT.
Uncoordinated motions of the left and right ventricular walls were also detected.
Moreover, we also found aortic valve degradation with slight regurgitation, slight mitral regurgitation, and moderate to severe tricuspid regurgitation.
The left ventricular diastolic function was reduced to 55% (Figure ​3A and B).
The coronary angiogram revealed no vascular stenosis (Figure ​3C–E).
Based on the above-mentioned examinations, this patient met at least 2 major criteria, the bilateral ventricular dilation and the existence of epsilon waves, providing diagnostic support for ARVC.
A diet with low salt and low fat was suggested.
The patient was also treated with metoprolol succinate sustained-release tablets (23.75 mg daily, p.o.), amiodarone (200 mg daily, p.o.), furosemide (20 mg daily, i.v.), and compound α-ketoacid tablets (2.52 g daily, p.o.).
Moreover, VTs with different morphologies and cycle lengths were found during radiofrequency ablation (Figure 4).
The substrate voltage mapping revealed that the anterior wall of RVOT was wrapped by circular scar (Figure 5A).
Considering the association of VT with scar areas, substrate ablation was chosen for this patient.
The residual potentials in the scar areas were searched, and then linear and focal ablations were performed (Figure ​5B).
Neither programmed stimulation nor induced stimulation could induce VT after the procedure was completed, indicating the success of operation.
The ECG after radiofrequency ablation showed sinus rhythm, with a heart rate of 61 beats/min, T wave inversions in leads III and avF, and epsilon waves and T wave inversions in leads V1–V3 (Figure 2D).
This patient was discharged from hospital on day 9 with a regimen of metoprolol succinate sustained-release tablets (23.75 mg daily, p.o.), amiodarone hydrochloride tablets (200 mg daily, p.o.), spironolactone tablets (40 mg daily, p.o.), and fosinopril sodium tablets (10 mg daily, p.o.).
The patient was followed up 3 months after discharge.
He had no recurrent palpitation, chest tightness, profuse sweating or nausea.
Although ARVC was the main diagnosis at the time of this patient's initial presentation, it is essential in such cases to perform a reassessment for the presence of structural heart disease, which can evolve over time.