Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • br Discussion In our patient series coronary

    2019-05-15


    Discussion In our patient series, coronary angiography was performed routinely prior to electrophysiological study, revealing a 9.1% (5/55) incidence of significant coronary artery stenosis in patients with Brugada syndrome/Brugada-type ECG. Although acute myocardial ischemia has been reported to cause right ventricular ST-segment changes similar to the Brugada-type ECG pattern [3–7] and coexistence of Brugada syndrome and vasospastic cyclooxygenase inhibitors has been reported [8–12], only a few individual case reports have suggested an association between significant coronary artery stenosis and Brugada syndrome [13–17]. Seow et al. [20] reported an interesting patient who presented with atypical chest pain, and the initial ECG showed a Brugada type 1 pattern. Subsequent ECGs depicted evolving anterior ST elevation myocardial infarction. The presence of a Brugada type 1 pattern masked the ECG changes indicative of acute anterior myocardial infarction, which made the diagnosis difficult. Hata et al. [21] described a patient who died suddenly due to VF documented by Holter monitoring, and a review of the patient\'s medical record revealed a Brugada type 2 ECG pattern. The autopsy revealed complete occlusion of the left main coronary artery. Ogano et al. [22] reported 2 asymptomatic patients with a saddleback Brugada-type ECG that dynamically converted to a coved-type pattern following ventricular arrhythmia episodes when myocardial ischemia occurred exclusively at the conus branch of the right coronary artery. These reports suggest that acute myocardial ischemia can mimic a Brugada-type ECG (and vice versa) and also that acute myocardial ischemia exacerbates the Brugada-type ECG pattern and has proarrhythmic effects. Therefore, coronary artery disease/ischemic heart disease should be considered when risk is being evaluated in patients with Brugada syndrome/Brugada-type ECG. According to the revised version of the “Guidelines for the primary prevention of ischemic heart disease” (JCS 2006 online only), the prevalence of ischemic heart disease in man was 8.13/1000 and 11.8/1000 in 2 cohort studies. It is very difficult to compare the prevalence of coronary artery disease between Brugada syndrome and non-Brugada syndrome because no data is available on the prevalence of coronary artery disease in the asymptomatic Japanese population, and many studies have indicated the annual incidence of ischemic heart disease in large cohort studies. As mentioned above, 2 studies have demonstrated the prevalence of coronary heart disease in Japanese men (8.13/1000 and 11.8/1000) [23,24]. In the present study, the incidence of coronary heart disease was 9.1%, which is almost 10 times higher than what was observed in previous studies. However, our study group included 2 patients with chest pain/oppression. Therefore, our results were slightly biased and could be merely coincidental. Unquestionably, age is related to risk, and remarkably, clinical, electrocardiographic, and electrophysiological characteristics were not statistically different in our patients with coronary artery disease compared to those without the disease.
    Conclusion
    Introduction Arrhythmic syncope is perhaps the most serious of all syncope types. Although syncope can result from many different diseases, [1–3] syncope due to cardiac causes is associated with a higher mortality than syncope due to non-cardiac causes [3]. Furthermore, even among cardiac causes, arrhythmias are associated with a high risk. The recently reported guidelines [1] and clinical scoring systems [4–6] for identifying high-risk patients include arrhythmia as a predictor. One study found that an abnormal electrocardiogram (ECG), history of congestive heart failure, and age >65 years predicted arrhythmia as a cause of unexplained syncope [7]. However, the positive predictive accuracy of those predictors was low, and better predictors are still needed.