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  • Despite potassium administration her serum potassium concent

    2019-04-11

    Despite potassium administration, her serum potassium concentration did not normalize until 56h after admission because she OG-L002 cost had taken hydrocortisone for pituitary adrenal insufficiency after surgery for a pituitary tumor. Under the persistent hypokalemic condition (K+=2.5–2.64mEq/L), alternans of J-wave amplitude and prominent TWA gradually decreased over time and disappeared after 38h (Fig. 3). Echocardiography performed 5 days after admission confirmed that left ventricular function had normalized. She was discharged without complications 18 days after admission. At the 1-month follow-up examination, she had hypokalemia (K+=2.6mEq/L) because she had not been taking a potassium supplement after discharge. Nevertheless, her ECG demonstrated an almost normal pattern (Fig. 3).
    Discussion Both hypokalemia and TC are known to cause QT prolongation and TWA. In spite of prolonged hypokalemia, the alternans of J-wave amplitude and TWA OG-L002 cost changed dramatically with the time course of the patient׳s recovery from myocardial stunning, which suggested that hypokalemia was not likely a cause of the J-wave and T-wave dynamic change. The J-wave alternans was prominently recorded in leads V2–V6, which lead positions were closely adjoining the area of the akinetic left ventricular segments. We hypothesize that myocardial stunning due to TC played a pivotal role in the J-wave alternans and TWA. To the best of our knowledge, this is the first report of a patient with TC who exhibited alternans of J-wave amplitude and TWA. Although QT-interval prolongation is relatively prevalent among patients with TC, they generally have good prognoses; however, development of torsade de pointes has been reported [3]. Patients with TC show QT-interval prolongation with a deep negative T-wave, the mechanism of which has not been explored in detail. A recent study indicated that a dynamic negative T wave and QT interval prolongation reflect edema-induced transient inhomogeneity and dispersion of repolarization between the apical and basal left ventricular regions [5]. This result may not be consistent with the fact that QT interval prolongation and deep negative T wave in patients with TC are observed broadly in the precordial leads rather than in the inferior leads, which reflect the apico-basal dispersion of repolarization. On the other hand, precordial leads, because of their proximity to the area, reflect the transmural potential gradient of the apical LV during the repolarization phase [6]. Visible TWA has been reported in patients with ischemia, long-QT syndrome, electrolyte disturbances, and post-tachycardia conditions, and is associated with the development of ventricular arrhythmias. It has been suggested that TWA results from alternans of the temporal dispersion of the action potential duration (APD), which is facilitated by the mechanism of steep APD restitution and calcium handling. APD restitution expresses the relationship between the APD and the preceding DI: a shorter DI is followed by a shorter APD. If APD restitution is steep, a small change in the DI causes large APD fluctuations and TWA. The alternans of cytosolic calcium also causes fluctuations in the APD; hence, TWA can be caused by calcium accumulation [7–9] and is linked with mechanical alternans [10,11]. A possible mechanism of TC is catecholamine-mediated myocardial stunning. Catecholamines induce myocardial injury via calcium overload [12], which may be related to alternans of cytosolic calcium. In addition to TWA, prominent J-wave alternans and mechanical alternans were observed in this case. The beats with shorter preceding DIs produced higher-amplitude J waves associated with lower systolic blood pressure, and the beats with longer preceding DIs produced lower-amplitude J waves associated with higher blood pressure (Fig. 2A). Further, a beat after a long pause showed an abbreviated J wave with increased ventricular pressure (Fig. 2B). With regard to the mechanism of J wave, the transient outward current (I) was assumed to play an important role. I is most prominently expressed in the ventricular epicardial cells and least in the endocardial cells. The prominent I-mediated action potential in the epicardium against the least developed one in the endocardium causes a transmural voltage gradient and produces a notch at the early phase of ventricular repolarization that registers as a J-wave on ECG [13]. The I current is reduced in a beat with a short coupling interval because of its slow recovery from inactivation [14]. According to the I theory, the beats with short coupling intervals or preceding DIs should cause small amplitude of J waves. In this case, the beats with shorter preceding DIs or coupling intervals had higher J-wave amplitude than those with longer preceding DIs, which does not agree with the above explanation of the I-mediated mechanism. During the repolarization phase of ventricular action potential, however, several different outward and inward currents overlap. The balance between them can determine the configuration of action potential repolarization and APD. Among these overlapped currents, the L-type calcium current (I), being one of the most important contributors for repolarization, also displays a recovery from inactivation during the diastolic period with a different time course from that of I. The balance between the recovery of I and I was shown to determine the action potential configuration and APD [15].