SummaryRecent evidence suggests an association between vasospastic angina and Brugada syndrome. Here we present two cases of coronary artery disease who presented with ECG abnormalities which might have been provoked or enhanced by ischemia of the conus branch of the right coronary artery. The 12-lead ECGs demonstrated normal sinus rhythm in these two cases. Interestingly, a saddle back or coved type ST segment elevation in leads V1-V3 was documented either in the percutaneous transluminal angioplasty procedure of the proximal right coronary artery or with an intracoronary acetylcholine (Ach) administration into the right coronary artery. These Brugada type ECG changes were restored to the baseline ECG waveform after improvement in the ischemia. In the second case, vasospasms of the conus branch of the right coronary artery were associated with a coved type ST segment elevation in leads V1 to V2. We discuss the possible interaction between ischemia caused by conus branch lesions and Brugada type electrocardiographic changes. ( and Brugada syndrome has been reported in several cases. 1,2) According to Noda, et al, the coexistence of vasospastic angina and Brugada syndrome was not rare (11%) and they hypothesized that mild ischemia and vagal influences act additively with the substrate responsible for the Brugada syndrome reported in the literature. 1)When Brugada syndrome and vasospastic angina coexist, the risk of inducing life-threatening ventricular fibrillation caused by Brugada syndrome or coronary vasospasms would be high.3) On the other hand, the therapeutic strategy for the two diseases is quite different since Ca channel blockers may cause deteriorative effects in Brugada syndrome. In fact, Chinushi reported a case with Brugada syndrome and vasospastic angina in which there was shortening of the ventricular fibrillatory interval after the administration of verapamil.4) Thus, the interaction between Brugada type ECG abnormalities and vasospasms or ischemia is very important from the therapeutic point of view.It is well known that the conus branch of the right coronary artery supplies the right ventricular outflow tract, and there are some reports regarding ischemia caused by conus branch lesions that may have induced Brugada type ECG changes. 5) Recent experimental evidence has also suggested that acute global ischemia in right ventricular wedge preparations can cause a loss of the action potential dome, leading to ST-segment elevation similar to that in Brugada syndrome. 6) Furthermore, a recent paper has shown that the occurrence of a J wave in the 12-lead ECG may be a marker for acute ischemia. 7) In this paper, we present two cases with coronary artery disease who presented with ECG abnormalities which might have been provoked by ischemia of the conus branch of the right coronary arteries, and discuss the possible interaction between these two phenomena.

We describe a case of early repolarization syndrome in which augmented J waves were documented during an electrical storm associated with hypokalemia. The patient was referred to our hospital for therapy to treat recurrent ventricular fibrillation (VF). The 12-lead electrocardiogram showed giant J waves associated with hypokalemia during multiple episodes of VF. Although antiarrhythmic agents or deep sedation were not effective for the VF, an intravenous supplementation of potassium completely suppressed the VF with a reduction in the J-wave amplitude. Our report discusses the possible relationship between hypokalemia and VF in early repolarization syndrome.

ERS patients had a continuously depressed diurnal and nocturnal adaptation of the QT interval to the heart rate. Such abnormal repolarization dynamics might provide a substrate for reentry and be an important element for developing ventricular fibrillation in the ERS cohort.

We describe a case of a myocardial infarction, in which prominent ischemic J waves were documented during recurrent ventricular fibrillation attacks. The patient was referred to our hospital to treat an out-of hospital cardiac arrest. Although the 12-lead electrocardiogram obtained just after the first cardioversion did not show any apparent J waves, a J wave-like steep downsloping type ST-segment elevation associated with q waves in the inferior leads was documented during multiple episodes of ventricular fibrillation. Our report revealed the appearance of J waves as an important marker for lethal arrhythmias in acute ischemia.

The pro-arrhythmic triggers in Brugada and early repolarization syndromes (BrS, ERS) have not been analyzed systematically except for case reports. We clinically investigated the circumstances which precede/predispose to arrhythmic events in these syndromes during long-term follow-up. A detailed history from the patients/witnesses was taken to investigate the antecedent events in the last few hours that preceded syncope/ventricular fibrillation (VF); medical records, ECG and blood test from the emergency room (ER) were reviewed. 19 patients that fulfilled the investigation criteria were followed up for 71 ± 49 months (34-190 months). Prior to the event (syncope/VF), the patients were partaking different activities in the following decreasing order; drinking alcoholic beverage, having meal, and getting up from sleep, exercise. 3 patients reported mental/physical stress prior to the event and 2 patients developed VF several days after starting oral steroid for treatment of bronchial asthma. In the ER, elevated J-wave amplitude (0.27 ± 0.15 mV) was found with 58 % of the patients having hypokalemia. After electrolyte correction and cessation of steroids, the following day plasma K (4.2 ± 0.3 mEq/L, P < 0.001) was significantly increased and J-wave amplitude (0.13 ± 0.1 mV, P < 0.001) was remarkably reduced. Three patients were kept on oral spironolactone/potassium supplements. During follow-up for 71 ± 49 (34-190) months, among 4 patients with VF recurrence, one patient developed VF after taking oral steroid. In ERS and BrS, hypokalemia and corticosteroid therapy add substantial pro-arrhythmic effects, but potentially treatable. Stopping steroid therapy and avoiding hypokalemia had excellent long-term outcome.