Intracoronary acetylcholine application as a possible probe inducing J waves in patients with early repolarization syndrome

Figures

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  Fig. 1. Electrocardiogram (ECG) recorded before (A) and under coronary spasm provocation test using the following incremental doses of acetylcholine (ACh): 10 μg (B), 30 μg (C), and 100 μg (D). J wave was absent before but was evident in the inferior leads of ECG during ACh administration (arrows). Short-coupled repetitive premature ventricular beats (PVBs) were observed in the precordial leads at the maximum dose of ACh (E). The origin of the triggering PVBs with superior-axis and left-bundle-branch-block morphology is not inconsistent with the area presenting with a J wave [41].

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  Fig. 2. Electrocardiogram (ECG) during the coronary spasm provocation test using acetylcholine (ACh). A persistent J wave was shown in lead II, whereas gradual fragmentation of the QRS complex and clear J wave formation were observed in lead III under the application of the maximum dose (100 μg) of ACh. The minimal amplitude of the S wave in lead I was not augmented according to the appearance of the J wave in lead III, indicating that this surface ECG does not indicate that a right bundle branch block was caused by ACh.

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  Fig. 3. Ambulatory electrocardiogram monitoring indicates nocturnal appearance of a J wave at the end of the QRS complex (arrows), associated with a transient sinoatrial conduction block recorded at 23:46 pm (A), and disappearance of the J wave in the early morning at 6:55 am (B) at the equivalent baseline heart rate, i.e., minimum RR interval in A is 1240 ms, and basic RR interval in B is 1160 ms.

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  Fig. 4. In arterially perfused canine myocardial wedge preparations (A), acetylcholine (ACh) (3 μm/L) reduces dome amplitude in the epicardial action potential (AP) and elevates the ST segment in a transmural electrocardiogram (ECG). In another preparation (B), flecainide (7 μm/L), a potent Na channel blocker, is applied. Thereafter, ACh (2 μm/L) causes loss of the AP dome in the epicardium, but not in the endocardium, and ST segment elevation in a transmural ECG under the presence of flecainide. Isoproterenol (0.5 μm/L) restores these epicardial AP configurations and ECG changes [46].

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  Fig. 5. A schematic illustration of the mechanisms of J wave formation from the viewpoint of epicardial transmembrane ionic currents as it relates to cardiac ischemia.