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    • In focal coronary spastic angina intravascular ultrasound wa

    2019-06-11

    In focal coronary spastic angina, intravascular ultrasound was reported to detect intima–media complex thickening and an increased sonolucent zone [16,17], and OCT can detect intimal thickening with low lipid and calcium deposits [18], which are believed to reflect neointimal hyperplasia subsequent to intimal disorders found on histopathology [19]. The OCT findings in the present case were similar. Although stenting is an option for local stenotic lesions following continued treatment with calcium blockers for refractory coronary spastic RG-108 [20], its use appears to be limited in cases of multiple vessel spasms, as in the present case.
    Conclusion
    Conflict of interest
    Acknowledgment
    Introduction J waves are electrocardiographic findings defined as slurs or notches at the terminal portion of the QRS complexes in contiguous leads (>2), with an amplitude>0.1mV from the electric baseline [1,2]. Recent studies have confirmed that J waves are closely related to ventricular fibrillation (VF) or sudden cardiac death [2–6] and found in ischemic heart diseases [7–11]. Whether J wave is due to a repolarization abnormality or depolarization is controversial.
    Case The patient was a 64-year-old man who was admitted to our hospital because of a severe anterior chest pain. On admission, an electrocardiogram (ECG) showed ST-segment elevation in the inferior leads, with slurs at the terminal portion of the QRS complexes, which were suspected as J waves (Fig. 1A, arrow). Emergency coronary angiography (CAG) revealed total occlusion of the proximal portion of the right coronary artery, and angioplasty was performed immediately after written informed consent was obtained from the patient. After partial recanalization of the right coronary artery, the ST-segment elevation returned to baseline (Fig. 1B, arrow), but the J waves disappeared only after full revascularization (Fig. 1C). The J-wave amplitude was augmented, as measured in the conducted atrial premature beats (Fig. 2). The patient\'s clinical course was good, and no ventricular tachyarrhythmias developed. On the follow-up CAG 8 months later, restenosis was absent, as well as no CAG-induced ST-segment elevation was observed. However, J waves developed in the inferior leads after the injection of contrast media into the right coronary artery (Fig. 3A and B, arrows). Then, the frontal electrical axis was shifted toward the right (from 58° to 72°), as in during the acute phase ST-elevation MI. J waves did not appear during the left CAG. The configurations were notches and slurs in the acute and chronic ischemic J waves, respectively.
    Discussion In the present case, J waves were denoted but resolved only after full reperfusion, whereas the ST elevation returned earlier to the baseline. On the follow-up CAG, the J waves reappeared but without ST elevation. These findings suggest that J waves are more sensitive than ST-segment elevation and are associated with an altered electrical axis, indicating a depolarization abnormality for the genesis. Contrast media were shown to induce an alternation in the electrical axis, a widening of the QRS duration, or an ST-T segment elevation [12]. All these changes were considered to be due to contrast media-induced transient myocardial ischemia. However, J waves have not been focused on during CAG. Recently, J waves have been reported in relation to myocardial ischemia or VF [7–10] and demonstrated to be a useful predictor of myocardial ischemia or ventricular tachyarrhythmias. As to their mechanism, J waves, the slurs or notches at the terminal portion of the QRS complexes, can represent a conduction delay [11,13]. In a previous report [11], we observed a high prevalence of J waves in post-MI patients, and the J wave amplitudes in these patients were augmented at a higher heart rate, suggesting a tachycardia-dependent augmentation. The concomitant changes in the electrical axis in the present study suggest a conduction delay in the inferior wall, which was caused by contrast media-induced myocardial ischemia [12]. However, conduction delay would result in an altered activation pattern over the ventricle, which in turn, results in J waves. Masking or unmasking of J waves is also known to occur during preexcitation in patients with Wolff–Parkinson–White syndrome [14,15].