Variants of Brugada Syndrome and Early Repolarization Syndrome: An Expanded Concept of J-Wave Syndrome.

BACKGROUND: The role of J-waves in the pathogenesis of ventricular fibrillation (VF) occurring in structurally normal hearts is important. METHODS: We evaluated 127 patients who received an implantable cardioverter-defibrillator (ICD) for Brugada syndrome (BS, n = 53), early repolarization syndrome (ERS, n = 24), and patients with unknown or deferred diagnosis (n = 50). Electrocardiography (ECG), clinical characteristics, and ICD data were analyzed. RESULTS: J-waves were found in 27/50 patients with VF of unknown/deferred diagnosis. The J-waves were reminiscent of those seen in BS or ERS, and this subgroup of patients was termed variants of ERS and BS (VEB). In 12 VEB patients, the J/ST/T-wave morphology was coved, although amplitudes were <0.2 mV. In 15 patients, noncoved-type J/ST/T-waves were present in the right precordial leads. In the remaining 23 patients, no J-waves were identified. VEB patients exhibited clinical characteristics similar to those of BS and ERS patients. Phenotypic transition and overlap were observed among patients with BS, ERS, and VEB. Twelve patients with BS had background inferolateral ER, while five ERS patients showed prominent right precordial J-waves. Patients with this transient phenotype overlap showed a significantly lower shock-free survival than the rest of the study patients. CONCLUSIONS: VEB patients demonstrate ECG phenotype similar to but distinct from those of BS and ERS. The spectral nature of J-wave morphology/distribution and phenotypic transition/overlap suggest a common pathophysiologic background in patients with VEB, BS, and ERS. Prognostic implication of these ECG variations requires further investigation.

Mid-term outcomes in patients implanted with cardiac resynchronization therapy.

We applied cardiac resynchronization therapy (CRT) for desynchronized heart failure patients. We evaluated clinical outcomes including morbidity, mortality, and echocardiographic parameters in 47 patients with implanted CRT in Korea from October 2005 to May 2013. The combined outcomes of hospitalization from heart failure, heart transplantation and death were the primary end point. Median follow-up period was 17.5 months. The primary outcomes listed above occurred in 10 (21.3%) patients. Two patients (4.3%) died after CRT and 8 (17%) patients were hospitalized for recurrent heart failure. Among patients hospitalized for heart failure, 2 (4.3%) patients underwent heart transplantation. The overall free rate of heart failure requiring hospitalization was 90.1% (95% CI, 0.81-0.99) over one year and 69.4% (95% CI, 0.47-0.91) over 3 yr. We observed improvement of the New York Heart Association classification (3.1±0.5 to 1.7±0.4), decreases in QRS duration (169.1 to 146.9 ms), decreases in left ventricular (LV) end-diastolic (255.0 to 220.1 mL) and end-systolic (194.4 to 159.4 mL) volume and increases in LV ejection fraction (22.5% to 31.1%) at 6 months after CRT. CRT improved symptoms and echocardiographic parameters in a relatively short period, resulting in low mortality and a decrease in hospitalization due to heart failure.

Circadian and seasonal variations of ventricular tachyarrhythmias in patients with early repolarization syndrome and Brugada syndrome: analysis of patients with implantable cardioverter defibrillator.

INTRODUCTION: The circadian and seasonal patterns of ventricular tachyarrhythmia (VTA) in patients with early repolarization syndrome (ERS) have not been determined. We compared the timing of VTAs in patients with ERS and Brugada syndrome (BS). METHODS AND RESULTS: We enrolled patients with ERS (n = 14) and BS (n = 53) who underwent implantable cardioverter defibrillator (ICD) implantation. The timing of VTAs, including cardiac arrest and appropriate shocks, was determined. During follow up of 6.4 ± 3.6 years in the ERS group and 5.0 ± 3.3 years in the BS group, 5 of 14 (36%) ERS and 10 of 53 (19%) BS patients experienced appropriate shocks (P = 0.37). Cardiac arrest showed a trend of nocturnal distribution peaking from midnight to early morning (P = 0.14 in ERS, P = 0.16 in BS). Circadian distribution of appropriate shocks showed a significant nocturnal peak in patients with ERS (P < 0.0001) but a trend toward a nocturnal peak in patients with BS (P = 0.08). There were no seasonal differences in cardiac arrest in patients with ERS and BS. However, patients with ERS showed a seasonal peak in appropriate shocks from spring to summer (P < 0.0001). There was no significant seasonal peak in patients with BS. The timing of VTAs (cardiac arrest plus appropriate shock) showed significant nocturnal distributions in patients with ERS and BS (P < 0.01, respectively). A significant clustering of VTAs was noted from spring to summer (P < 0.01) in patients with ERS, but not in patients with BS (P = 0.42). CONCLUSIONS: Incidence of VTAs showed marked circadian variations with night-time peaks in patients with ERS and BS.

Ischemia-modified albumin is a highly sensitive serum marker of transient myocardial ischemia induced by coronary vasospasm.

BACKGROUND: Ischemia-modified albumin, a new marker of myocardial ischemia, is known to elevate during ischemia induced by percutaneous coronary intervention. It is, however, not known whether ischemia-modified albumin also elevates during transient coronary vasospasm. METHODS: We evaluated ischemia-modified albumin in patients undergoing intracoronary ergonovine spasm provocation test (n=26). For additional comparison, ischemia-modified albumin was also evaluated in elective percutaneous coronary intervention patients (n=18) and in patients with normal coronary angiography (n=10). Blood samples were taken from the arterial sheath before the procedure, just after procedural completion, or balloon inflation. RESULTS: Median ischemia-modified albumin level elevated significantly in patients with positive provocation test compared with baseline [n=16, 106.0 (interquartile range 96.5, 115.5) versus 128.5 (114.8, 171.8) U/ml, P<0.001], whereas it did not change in patients with negative provocation test [n=10, 109.5 (103.3, 115.0) versus 113.5 (104.0, 118.3) U/ml, P=0.108]. Ischemia-modified albumin was also higher after percutaneous coronary intervention [113.5 (101.0, 131.5) versus 151.0 (129.3, 231.0) U/ml, P<0.0001] and did not change in patients with normal coronary angiography [108.5 (99.3, 114.0) versus 110.0 (108.0, 114.0) U/ml, P=0.085]. Ischemia-modified albumin elevation higher than 9 U/ml after provocation test could detect the presence of coronary vasospasm, with an area under the receiver operating characteristic curve of 0.975 (95% confidence interval 0.921-1.000), with a sensitivity of 94% and a specificity of 99%. Serum albumin levels were within reference range for all patients and there was no significant relationship between albumin and baseline ischemia-modified albumin or postischemic ischemia-modified albumin. CONCLUSION: Thus, ischemia-modified albumin may have a role as a biochemical marker for transient myocardial ischemia induced by coronary vasospasm.

Conservative versus aggressive treatment strategy with angiographic guidance alone in patients with intermediate coronary lesions: The SMART-CASE randomized, non-inferiority trial.

BACKGROUND: Although coronary angiography is still the technique most widely used to guide percutaneous coronary intervention (PCI), the appropriate angiographic indication of revascularization for intermediate coronary lesions remains controversial. The aim of this study was to compare conservative versus aggressive strategies with angiographic guidance alone in patients with intermediate coronary lesions. METHODS AND RESULTS: A total of 899 patients with intermediate coronary lesions between 50% and 70% diameter stenosis by quantitative coronary analysis were randomly assigned to the conservative group (n=449) or the aggressive group (n=450). For intermediate lesions, PCI was performed using everolimus-eluting stents in the aggressive group, but was deferred in the conservative group. The primary end point was a composite of all-cause death, myocardial infarction, or any revascularization at 1year. The number of treated lesions per patient was 0.8±0.9 in the conservative group and 1.7±0.9 in the aggressive group (p<0.001). The cumulative rate of the primary endpoint was 7.3% in the conservative group and 6.8% in the aggressive group (the upper limit of the one-sided 95% confidence interval [CI], 3.4%; p=0.006 for non-inferiority with a predefined non-inferiority margin of 5.0%). The risk of death or myocardial infarction (hazard ratio [HR] 0.50; 95% CI, 0.19-1.33; p=0.17) and revascularization (HR 1.42; 95% CI, 0.80-2.52; p=0.23) was not significantly different between the 2 groups. CONCLUSIONS: Conservative revascularization was non-inferior to aggressive revascularization for intermediate coronary lesions. Revascularization of intermediate lesions can be safely deferred in patients undergoing PCI with angiographic guidance alone. CLINICAL TRIAL REGISTRATION: URL: http://ClinicalTrials.gov. Unique identifier: NCT00743899.

A case of postprandial hypotension in the intensive care unit treated with acarbose.

Postprandial hypotension (PPH) has not been described as a cause of hypotension after the return of spontaneous circulation (ROSC) in the intensive care unit (ICU). A 74 year old man underwent cardiopulmonary resuscitation (CPR) due to monomorphic ventricular tachycardia. After the ROSC, inotropic agents were not reduced but increased. PPH had occurred, according to the flow sheet, so a provocation test was performed. We noted hypotension but no serum hypoglycemia or tachycardia. The hypotension was diagnosed as PPH. We chose acarbose for treatment; thus, the inotropic agents were discontinued. This is the first case in which hypotension occurred in a patient recovering after CPR in the ICU and that the PPH was treated with acarbose. PPH should be considered and treated to manage hypotension in elderly patients in the ICU.