Aims: Although alcohol consumption is proposed to trigger electrographic abnormalities, acute changes in arrythmias and conductance disturbances have not been systematically studied in young adults who are the age group most likely to binge drink. The aim of this study was to determine if changes in breath alcohol content (BrAC) during an acute binging episode influence electrographic abnormalities in young adults. Methods: Fifty-five university students (20.6±2.1 years of age), who were not regular users of alcohol, consumed 60% mixer and 40% vodka until 0.08% BrAC was reached (6.4±1.9 standard drinks). Five-lead Holter recordings were analysed by a blinded cardiac technician. Electrographic abnormalities were identified and classified according to location (supraventricular or ventricular) and type (arrhythmia or conduction disturbance). Results: Although heart rate was elevated with BrAC beyond 0.05% compared to 0.00%, no differences existed in the relative incidence of electrographic abnormalities by location or type. Logistic regression revealed that baseline electrographic abnormality significantly contributed to predicting electrographic abnormality in 0.00% to 0.05% (p=0.02) and 0.05% to 0.08% BrAC phases (p=0.01). Conclusions: Alcohol consumption, resulting in BrAC of 0.08%, increased heart rate after BrAC reached 0.05% but did not acutely influence the relative incidence of electrographic abnormality by location or type in apparently healthy young people. These results do not support the hypothesis that a binge drinking episode causes electrographic abnormalities in young adults.

Purpose: Degenerative mitral stenosis (DMS) is an increasingly recognized cause of mitral stenosis. The goal of this study was to compare echocardiographic differences between DMS and rheumatic mitral stenosis (RMS), identify echocardiographic variables reflective of DMS severity, and propose a dimensionless mitral stenosis index (DMSI) for assessment of DMS severity. Methods: This is a single-center, retrospective cohort study. We included patients with at least mild MS and a mean transmitral pressure gradient (TMPG) ≥ 4 mmHg. Mitral valve area by the continuity equation (MVACEQ) was used as an independent reference. The DMSI was calculated as follows: DMSI = VTILVOT / VTIMV. All-cause mortality data were collected retrospectively. Results: A total of 64 patients with DMS and 24 patients with RMS were identified. MVACEQ was larger in patients with DMS (1.43  0.4 cm2) than RMS (0.9  0.3 cm2) by ~0.5 cm2 (p = <0.001) and mean TMPG was lower in the DMS group (6.0 2 vs. 7.93 mmHg, p=0.003). A DMSI of  0.50 and ≤ 0.351 were associated with MVACEQ ≤ 1.5 and MVACEQ ≤ 1.0 cm2 (p<0.001), respectively. With the progression of DMS from severe to very severe, there was a significant drop in DMSI. There was a non-significant trend towards worse survival in patients with MVACEQ ≤ 1.0 cm2 and DMSI ≤ 0.35, suggesting severe stenosis severity. Conclusion: Our results show that TMPG correlates poorly with MVA in patients with DMS. Proposed DMSI may serve as a simple echocardiographic indicator of hemodynamically significant DMS.

Purpose: Degenerative mitral stenosis (DMS) is an increasingly recognized cause of mitral stenosis. Echocardiographic evaluation of DMS severity is limited. The goal of this study was to compare echocardiographic differences between DMS and rheumatic mitral stenosis (RMS), identify echocardiographic variables reflective of DMS severity, and propose a dimensionless mitral stenosis index (DMSI) for assessment of DMS severity. Methods: This is a single-center, retrospective cohort study. We included patients with at least mild MS and a mean transmitral pressure gradient (TMPG) ≥ 4 mmHg. Mitral valve area by the continuity equation (MVACEQ) was used as an independent reference. The DMSI was calculated as follows: DMSI = VTILVOT / VTIMV. Results: A total of 64 patients with DMS and 24 patients with RMS were identified. MVACEQ was larger in patients with DMS (1.43  0.4 cm2) than RMS (0.9  0.3 cm2) by ~0.5 cm2 (p = <0.001) and mean TMPG was lower in the DMS group (6.0 2 vs. 7.93 mmHg, p=0.003) despite similar left ventricular stroke volume, left atrial volume index and pulmonary arterial systolic pressure. A DMSI of  0.50 and ≤ 0.351 were associated with MVACEQ ≤ 1.5 and MVACEQ ≤ 1.0 cm2 (p<0.001), respectively. With the progression of DMS from severe to very severe, there was a significant drop in DMSI. Conclusion: Our results show that TMPG correlates poorly with MVA in patients with DMS. Proposed DMSI may serve as a simple echocardiographic indicator of hemodynamically significant DMS. More extensive studies are needed to validate these findings.