Sudden death due to voluntary lighter fluid inhalation: A case report.

The abuse of hydrocarbon by inhalation in adolescent ages has increased in last year due to the euphoric effect it provokes. Butane, which is a kind of hydrocarbon compound, may be abused by inhalation and thus lead to addiction. Inhaling lighter fluid containing butane can cause lung toxicity, brain damage, myocardial effects, and neurologic problems. We reported, in parallel to literature, a 19-year-old patient who inhaled lighter fluid and who presented with lung haemorrhage, hypoxia and acute coronary syndrome.

The diagnostic significance of NT-proBNP and troponin I in emergency department patients presenting with palpitations

OBJECTIVE: This prospective study investigated the diagnostic significance of the N-terminal pro-brain natriuretic (NT-proBNP) and troponin I peptides in emergency department patients presenting with palpitations. METHODS: Two groups of patients with palpitations but without documented supraventricular tachycardia were compared: a group with supraventricular tachycardia (n = 49) and a control group (n = 47). Both groups were diagnosed using electrophysiological studies during the study period. Blood samples were obtained from all of the patients to determine the NT-proBNP and troponin I levels within the first hour following arrival in the emergency department. RESULT: The mean NT-proBNP levels were 207.74±197.11 in supraventricular tachyarrhythmia group and 39.99±32.83 pg/mL in control group (p<0.001). To predict supraventricular tachycardia, the optimum NT-proBNP threshold was 61.15 pg/mL, as defined by the receiver operating characteristic (ROC) curve, with a non-significant area under the ROC curve of 0.920 (95% CI, 0.86-0.97, p<0.001). The NT-proBNP cut-off for diagnosing supraventricular tachycardia had 81.6% sensitivity and 91.5% specificity. Supraventricular tachycardia was significantly more frequent in the patients with NT-proBNP levels ≥61.15 pg/mL (n = 44, 90.9%, p>0.001). The mean troponin I levels were 0.17±0.56 and 0.01±0.06 pg/mL for the patients with and without supraventricular tachycardia, respectively (p<0.05). Of the 96 patients, 21 (21.87%) had troponin I levels ≥0.01: 2 (4.25%) in the control group and 19 (38.77%) in the supraventricular tachycardia group (p<0.001). CONCLUSION: Troponin I and, in particular, NT-proBNP peptide were helpful for differentiating supraventricular tachycardia from non- supraventricular tachycardia palpitations. Further randomized, large, multicenter trials are needed to define the benefit and diagnostic ...

Efeitos agudos de levosimendana e dobutamina na duração do QRS em Pacientes com insuficiência cardíaca / Acute effects of levosimendan and dobutamine on QRS duration in patients with heart failure / Efectos agudos de levosimendana y dobutamina en la duración del QRS en pacientes con insuficiencia cardíaca

FUNDAMENTO: A levosimendana é um novo agente inotrópico que aumenta a contratilidade cardíaca sem aumentar a captação celular de cálcio, de forma a não causar sobrecarga de cálcio e arritmias relacionadas. Em pacientes com insuficiência cardíaca (IC), a duração prolongada do QRS está associada com um aumento no risco de mortalidade e morte súbita cardíaca. Mudanças estruturais no ventrículo esquerdo podem levar à contração assíncrona, causando atraso de condução e um QRS prolongado no ECG de superfície. OBJETIVO: O objetivo do presente estudo foi comparar os efeitos agudos de levosimendana e dobutamina na duração do QRS em pacientes com IC grave e ritmo sinusal. MÉTODOS: 60 pacientes consecutivos com IC isquêmica foram incluídos no estudo e randomizados em dois grupos para infusão de levosimendana (n=37) ou dobutamina (n=23). 67,2 por cento eram homens; a média da idade era 66,4 ± 9,2 anos para todos os pacientes. A duração basal do QRS nos grupos levosimendana e dobutamina foi 120,44 ± 23,82 ms vs 116,59 ± 13,80 ms respectivamente. A fração de ejeção do ventrículo esquerdo (FEVE) estava diminuída em ambos os grupos (23,15 ± 8,3 vs 24,56 ± 7,5 por cento). RESULTADOS: No grupo levosimendana, a duração do QRS diminuiu do valor basal para 116,47 ± 24,56 ms (p=0,006), enquanto não houve diferença significante no grupo dobutamina (p=0,605). Ambos os medicamentos causaram um aumento na FEVE, mas este foi significante apenas no grupo levosimendana (27,95 ± 8,9 por cento p=0,003 vs 26,67 ± 7,6 por cento, p=0,315). CONCLUSÃO: O estudo sugere que a administração de levosimendana, mas não de dobutamina, encurta a duração do QRS no ECG de superfície, possivelmente por causar uma contração coletiva nas fibras do músculo do ventrículo esquerdo. A base molecular desse efeito ainda precisa ser esclarecida.

BACKGROUND: Levosimendan is a novel inotropic agent that enhances cardiac contractility without increasing cellular calcium intake, so that it is not supposed to cause intracellular calcium overload and related arrhythmias. In patients with heart failure, prolonged QRS duration is associated with increased risk of mortality and sudden cardiac death. Structural changes in the left ventricle may lead to asynchronous contraction, causing conduction delay and a prolonged QRS on the surface electrocardiogram. OBJECTIVE: We aimed to compare the acute effects of levosimendan and dobutamine on QRS duration in patients with severe heart failure and sinus rhythm. METHODS: Sixty consecutive patients with ischemic heart failure were enrolled for the study and randomized into two groups for levosimendan (n=37) or dobutamine (n=23) infusions. 67.2 percent were male; mean age was 66.4±9.2 years for all patients. Baseline QRS durations in levosimendan and dobutamine groups were, 120.44 ± 23.82 ms vs 116.59 ± 13.80 ms respectively. Baseline ejection fractions were both depressed (23.15 ± 8.3 percent vs 24.56 ± 7.5 percent). RESULTS: In the levosimendan group, QRS duration shortened from baseline value to 116.47 ± 24.56 msec (p=0.006), whereas dobutamine group showed no significant change (p=0.605). Both drugs caused an increase in ejection fraction, but only the levosimendan group showed significance (27.95 ± 8.9 percent p=0.003 vs 26.67 ± 7.6 percent, p=0.315). CONCLUSION: We suggest that the administration of levosimendan, not dobutamine, shortens QRS duration on the surface ECG, possibly by means of providing collective contraction in the left ventricle muscle fibers. The molecular basis of this effect remains to be clarified.

FUNDAMENTO: La levosimendana es un nuevo agente inotrópico que aumenta la contractibilidad cardíaca sin aumentar la captación celular de calcio, de forma de no causar sobrecarga de calcio y arritmias relacionadas. En pacientes con insuficiencia cardíaca (IC), la duración prolongada del QRS está asociada a un aumento en el riesgo de mortalidad y muerte súbita cardíaca. Cambios estructurales en el ventrículo izquierdo pueden llevar a la contracción asíncrona, causando atraso de conducción y un QRS prolongado en el ECG de superficie. OBJETIVO: EL objetivo del presente estudio fue comparar los efectos agudos de levosimendana y dobutamina en la duración del QRS en pacientes con IC grave y ritmo sinusal. MÉTODOS: 60 pacientes consecutivos con IC isquémica fueron incluidos en el estudio y randomizados en dos grupos para infusión de levosimendana (n=37) o dobutamina (n=23). 67,2 por ciento eran hombres; la media de la edad era 66,4±9,2 para todos los pacientes. La duración basal del QRS en los grupos levosimendana y dobutamina fue 120,44±23,82 vs. 116,59±13,80 respectivamente. La fracción de eyección del ventrículo izquierdo (FEVI) estaba disminuida en ambos grupos (23,15±8,3 vs. 24,56±7,5). RESULTADOS: En el grupo levosimendana, la duración del QRS disminuyó del valor basal para 116,47±24,56 ms (p=0,006), en cuanto no hubo diferencia significativa en el grupo dobutamina (p=0,605). Ambos medicamentos causaron un aumento en la FEVI, pero este fue significativo apenas en el grupo levosimendana (27,95±8,9 p=0,003 vs. 26,67±7,6, p=0,315). CONCLUSIÓN: El estudio sugiere que la administración de levosimendana, pero no de dobutamina, acorta la duración del QRS en el ECG de superficie, posiblemente por causar una contracción colectiva en las fibras del músculo del ventrículo izquierdo. La base molecular de ese efecto aun precisa ser aclarada.