Increases in P-Wave Dispersion Predict Postoperative Atrial Fibrillation After Coronary Artery Bypass Graft Surgery

Objectives Carbon monoxide (CO) poisoning frequently affects repolarization, resulting in abnormal electrocardiography findings. The goal of this study was to examine the effect of CO poisoning on the novel transmyocardial repolarization parameters T peak–T end (Tp-e), Tp-e dispersion, and Tp-e/QT and the relationship of these parameters to myocardial injury (MI). Methods This prospective study included 94 patients with CO poisoning and 40 healthy controls. Participants received an electrocardiography and had their blood drawn at admission and 6 and 24 hours after admission. The QT, Tp-e, Tp-e dispersion, and the Tp-e/QT ratio were calculated. Myocardial injury was determined based on an elevation in troponin any time during the first 24 hours. The patients were divided into 2 subgroups: those with and without MI. Results T peak–T end, Tp-e dispersion, and the Tp-e/QT ratio were higher at admission than after 6 and 24 hours of hospitalization and were higher than the control group ( P P P = .03). There were no any significant differences in the Tp-e dispersion or the Tp-e/QT ratio between the 2 MI subgroups. Receiver operating characteristic analysis showed that a Tp-e cutoff value for MI of 91.5 milliseconds had a sensitivity of 72.7% and a specificity of 67.2%. Conclusion Transmyocardial repolarization parameters indicative of arrhythmia were prolonged in patients with CO poisoning. T peak–T end was associated with MI.

A new marker for myocardial injury in carbon monoxide poisoning: T peak-T end

Background—The risk factors for ventricular arrhythmias in patients with coronary vasospasm have not been identified. We evaluated QT dispersion in patients with vasospastic angina and its relation to susceptibility to ventricular arrhythmias during myocardial ischemia and reperfusion. Methods and Results—We assessed the corrected QT (QTc) dispersion before induction of coronary artery spasm by intracoronary injection of acetylcholine (baseline) and 30 minutes after administration of isosorbide dinitrate in 50 patients with vasospastic angina and 50 patients with atypical chest pain. The baseline QTc dispersion was significantly greater in patients with vasospastic angina than in patients with atypical chest pain (mean±SD: 69±24 versus 44±19 ms, 95% confidence interval of mean difference [CI]: 16 to 33 ms; P<0.001). QTc dispersion decreased significantly, to 48±15 ms (CI: 15 to 26 ms; P<0.001 versus baseline), after administration of isosorbide dinitrate in patients with vasospastic angina but did not cha...

Increased QT Dispersion in Patients With Vasospastic Angina

Background: Myocardial injury is a frequent consequence of carbon monoxide (CO) poisoning. Oxidative stress affection seems to be a relevant mechanism in the patho-physiology of patients with acute CO poisoning.
Methodology: Cardiovascular system examination and Electrocardiography (ECG) were performed for fifty CO intoxicated patients admitted to Poison Control Center, Ain Shams university Hospital for whom some oxidative stress indices have been investigated through the assessment of plasma level of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO). Both cardiac enzymes; troponin I and beta natriuretic peptide (BNP) have been also assessed in addition to carboxyhemoglobin (COHb) levels. The investigated parameters were compared with those of 40 non-smoker healthy controls (comparable in terms of age and gender).
Results: ECG changes were present in 96% of patients, whereas only 4% had a normal ECG. In intoxicated patients, a statistical significant increase in plasma level of COHb level, MDA, NO, troponin I, and BNP peptide was reported compared to control individuals, while SOD enzyme was significantly decreased. BNP showed a significant positive correlation with COHb level and a negative correlation with SOD, while SOD showed a significant negative correlation with COHb level.
Conclusions and recommendations: Myocardial injury occurs frequently in patients hospitalized for CO poisoning. The oxidative stress indices are significantly affected after acute CO poisoning. We suggested that such affection could be partially mediated by CO. Patients admitted to the hospital with CO poisoning should have a baseline ECG and serial cardiac biomarkers.

Some Biomarkers in Carbon Monoxide-Induced Cardiotoxicity

Se plantea un estudio de las intoxicaciones clinicas por monoxido de carbono con los siguientes objetivos: 1. Estudio epidemiologico de las intoxicaciones: distribucion por meses, dias de semana y hora. Evolucion anual. Relacion con numero de urgencias totales y con numero de intoxicaciones totales atendidas. 2. Perfil del paciente con intoxicacion por CO: edad, sexo, antecedentes personales, motivo de la intoxicacion, concomitancia con otros toxicos. 3. Constantes medicas al ingreso. 4. Manifestaciones clinicas presentadas en las intoxicaciones. 5. Niveles de COHb, correlacion con la clinica. Alteraciones gasometricas. 6. Alteraciones analiticas presentadas. 7. Toxicidad cardiologico: alteraciones ECG encontradas, marcadores de dano miocardico. 8. Toxicidad neurologica: manifestaciones clinicas, alteraciones en TAC. 9. Tratamiento administrado en el Servicio de Urgencias. Intervalo de tiempo hasta inicio de tratamiento (calidad). 10. Presencia de Sindrome Neurologico Tardio: incidencia, intervalo lucido, clinica presentada, secuelas. 11. Origen de la intoxicacion por CO. Medidas preventivas aplicadas en los lugares de intoxicacion 12. Conocimiento de los profesionales de urgencias sobre las intoxicaciones por CO. 13. Intoxicaciones inadvertidas por CO.

Intoxicaciones advertidas y ocultas por monóxido de carbono en el Área Sanitaria do Salnés

Objectives: Carbon monoxide (CO) is a potent myocardial toxin. We investigated the association between acute CO intoxication and electrocardiographic QT interval (QTmax/QTmin), corrected QT interval (cQTmax/cQTmin), QT dispersion (QTd) and corrected QT dispersion (cQTd), P wave duration (Pmax/ Pmin) and P wave dispersion (Pd), which were known as predictors of ventricular arrhythmias, atrial fibrillation and sudden death. Methods: Electrocardiography with 12-leads and blood gas were taken from 65 patients with CO intoxication as well as 65 control patients with similar age and gender distribution at the admission time to the emergency department and at the 4th hour post-therapy. The carboxyhaemoglobin (COHb) levels and the relationships with electrocardiographic parameters were studied. Results: The mean COHb levels were 21.43 plus or minus 6.85% and 1.37 plus or minus 0.98% in intoxicated patients and in the control group respectively. QTmax, QTd, cQTmax, cQTd, Pmax, and Pd were found significantly higher in intoxicated patients when compared to the control group (373.98 plus or minus 40.35 vs. 355.98 plus or minus 32.88, p=0.006; 49.29 plus or minus 22.66 vs. 20.43 plus or minus 11.16, p<0.001; 455.38 plus or minus 30.72 vs. 419.57 plus or minus 22.27, p<0.001; 60.88 plus or minus 25.99 vs. 25.75 plus or minus 13.13, p<0.001; 107.91 plus or minus 13.28 vs. 96.65 plus or minus 12.65, p<0.001, 46.85 plus or minus 13.49 vs. 35.22 plus or minus 10.07, p<0.001 respectively). In Pearson correlation analysis, there were significant correlations between COHb level and QTmax, QTd, cQTmax, cQTd, Pmax and Pd (r=0.211, p=0.016; r=0.610, p<0.001; r=0.599, p<0.001; r=0.628, p<0.001; r=0.458, p<0.001; r=0.414, p<0.001 respectively). Conclusion: A correlation between reversible increases in QTd, cQTmax, cQTd, Pmax and Pd in the electrocardiogram and COHb can be observed in acute CO intoxication patients.

Reversible Increases in Qt Dispersion and P Wave Dispersion during Carbon Monoxide Intoxication

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Reversible Increases in Qt Dispersion and P Wave Dispersion during Carbon Monoxide Intoxication