Masked inherited primary arrhythmia syndromes in sudden cardiac death patients accompanied by coronary vasospasm

BACKGROUND/AIMS: Coronary vasospasms are one of the important causes of sudden cardiac death (SCD). Provocation of coronary vasospasms can be useful, though some results may lead to false positives, with patients potentially experiencing recurrent SCD despite appropriate medical treatments. We hypothesized that it is not coronary vasospasms but inherited primary arrhythmia syndromes (IPAS) that underlie the development of SCD. METHODS: We analyzed 74 consecutive patients (3.8%) who survived out-of-hospital cardiac arrest among 1,986 patients who had angiographically proven coronary vasospasms. Electrical abnormalities were evaluated in serial follow-up electrocardiograms (ECGs) during and after the index event for a 3.9 years median follow-up. Major clinical events were defined as the composite of death and recurrent SCD events. RESULTS: Forty five patients (60.8%) displayed electrocardiographic abnormalities suggesting IPAS: Brugada type patterns in six (8.2%), arrhythmogenic right ventricular dysplasia patterns in three (4.1%), long QT syndrome pattern in one (2.2%), and early repolarization in 38 (51.4%). Patients having major clinical events showed more frequent Brugada type patterns, early repolarization, and more diffuse multivessel coronary vasospasms. Brugada type pattern ECGs (adjusted hazard ratio [HR], 4.22; 95% confidence interval [CI], 1.16 to 15.99; p = 0.034), and early repolarization (HR, 2.97; 95% CI, 1.09 to 8.10; p = 0.034) were ultimately associated with an increased risk of mortality. CONCLUSIONS: Even though a number of aborted SCD survivors have coronary vasospasms, some also have IPAS, which has the potential to cause SCD. Therefore, meticulous evaluations and follow-ups for IPAS are required in those patients.

Clinical outcomes after recovery from severe asthma exacerbation: the third report

PURPOSE: Up to 10% of the mortality rate of asthmatics within a year from the near-fatal attacks has been reported. We previously reported that not a few patients with acute severe asthma died after discharge from the hospital. This study investigated whether our efforts to improve clinical outcomes of patients after recovery from severe asthma exacerbation did work or not. METHODS: Follow-up data from asthmatic patients who had been hospitalized due to severe exacerbation between 2007 and 2014 (present) were compared with that the previous one (1998–2006) (previous). RESULTS: Sex, age, near-fatal asthma, and mortality (9.8% vs. 9.6%) were not significantly different between the previous (n=225) and present (n=397) studies. However, rehospitalization rate was significantly lower in the present study (29.3% vs. 52.4%, P=0.000). The patients in the present study used inhaled steroid more frequently (78.5% vs. 68.0%, P=0.006), had better asthma knowledge (P=0.000), and higher proportion of regular hospital visitors to total subjects (75.6% vs. 64.9%, P=0.004) than did the previous patients. The regular hospital visitors (n=300) showed a significantly lower mortality (3.3% vs. 28.9%, P=0.000), better knowledge (P=0.000) and higher inhaled steroid use (85.8% vs. 54.1%, P=0.000) than did the other group (n=97) in the present study. CONCLUSION: Clinical outcomes after recovery from severe asthma exacerbation in the present study were better than the previous one. Our efforts to educate patients might contribute to these better results.