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  2. Palavra-chave: Ventricular Fibrillation
IJCS
Case Report

Cardiocerebral Infarction: A Combination to Prevent

Margarida Cabral et al. Ana Ponciano Beatriz Santos João Morais

Background

The acute complications of myocardial infarction (MI), such as mechanical, arrhythmic, ischemic, and inflammatory sequelae, may be responsible for significant cardiovascular morbimortality.

Life-threatening arrhythmias, namely ventricular fibrillation or tachycardia, may be a challenging complication requiring a prompt approach. In some cases, acute ischemia leads to polymorphic ventricular tachycardia (PVT), and, rarely, to potentially lethal torsades de pointes ventricular tachycardia. –

[…]

  • Arrhythmias Cardiacs
  • Cerebral Infarction/complications
  • Myocardial Infarction
  • Stroke
  • Ventricular Fibrillation
Ler artigo completo
Creative Commons Attribution (CC BY) Creative Commons license
01/08/2022 DOI: 10.36660/ijcs.20210276
IJCS
Case Report

Commotio Cordis Secondary to Aggression

Luisa Gonçalves et al. Inês Pires João Santos Joana Laranjeira Correia … Davide Moreira Inês Almeida

Case report

A 35-year-old man was admitted following a recovered cardiorespiratory arrest. He was attacked by another man with multiples blunts by a wood stick in the chest and head. An eyewitness statement indicated that the victim had lost consciousness and collapsed after being hit in the chest. He was in cardiac arrest, and a nearby healthcare professional provided first aid with cardiopulmonary resuscitation. The first electrocardiogram (ECG) rhythm strip, fifteen minutes later, identified ventricular fibrillation (VF) (). Sixteen electrical shocks were delivered, always with VF, before restoration of sinus rhythm and circulation. A 12-lead-ECG revealed sinus rhythm without ST deviations and a corrected QT interval of 414 msec. On admission, he was under ventilatory support, with a heart rate of 80 beats per minute, blood pressure of 121/70mmHg, and no signs of shock. There was no previously known medical condition, besides being an active smoker and a binge drinker, and no family history of early coronary disease, cardiomyopathy, or sudden death. He was under the influence of alcohol, as was confirmed by blood tests (blood alcohol level of 1.31g/L), and had a discretely elevated cardiac troponin-T of 0.9ng/ml (normal range, 0 to 0.08 ng/ml). The remaining analyzes, cranial and cervical CT scan, chest X-ray, and abdominal eco FAST were normal. An initial echocardiogram in the emergency department demonstrated normal-sized chambers and global ventricular systolic dysfunction explained by a prolonged cardiac arrest. He was admitted to the intensive care unit for post-resuscitation care with therapeutic hypothermia and temporary ventilatory support. At 48 hours of admission, there was a normalization of systolic function with a normal ejection fraction by echocardiogram (). Coronary angiography excluded coronary disease (). Serial electrocardiograms were not suggestive of an arrhythmogenic substrate (). The sudden cardiac arrest was assumed secondary to a commotio cordis (CC), and for this reason, the patient was not proposed for an implantable cardioverter-defibrillator (ICD). The clinical outcome was favorable, and the patient was discharged. He remained asymptomatic during three years of follow-up, with normal ECG, echocardiogram with strain-rate imaging, exercise stress test, and 24-hour-Holter. During mid-term follow-up, a cardiac magnetic resonance imaging (MRI) showed normal-sized chambers, global and regional function, and no myocardial edema or myocardial scar by late focal hyperenhancement (-).

[…]

  • Arrhythmias, Cardiac/complications
  • atrioventricular block
  • Cardiovascular Diseases/complications
  • Commotio Cordis
  • Diagnosis, Dfferential
  • Heart Arrest
  • Ventricular Fibrillation
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Creative Commons Attribution (CC BY) Creative Commons license
09/08/2021 DOI: 10.36660/ijcs.20200356 Visualizações 1
ABC
Original Article

Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts

Guilherme Fenelon et al. Júlio Uchoa José Roberto Otobone Marcos Reis … José Luiz Gomes do Amaral Angelo A. V. De Paola

OBJECTIVE: To characterize the cardiac electrophysiologic effects of cocaine. METHODS: In 8 dogs (9-13 kg), electrophysiologic parameters and programmed stimulation were undertaken using transvenous catheters at baseline, and after cocaine intravenous infusion (12 mg/kg bolus followed by 0.22 mg/kg/min for 25 minutes). RESULTS: Cocaine plasma levels (n=5) rose to 6.73± 0.56 mg/mL. Cocaine did not affect sinus cycle length and arterial pressure. Cocaine prolonged P wave duration (54±6 vs 73±4 ms, P<0.001), PR interval (115±17 vs 164±15 ms, P<0.001), QRS duration (62±10 vs 88±14 ms, P<0.001), and QTc interval (344±28 vs 403±62 ms, P=0.03) but not JT interval (193±35 vs 226±53 ms, NS). Cocaine prolonged PA (9±6 vs 23±8 ms, P<0.001), AH (73±16 vs 92±15 ms; P=0.03), and HV (35±5 vs 45±3ms; P<0.001) intervals and Wenckebach point (247±26 vs 280±28 ms, P=0.04). An increase occurred in atrial (138±8 vs 184± 20 ms; P<0.001) and ventricular (160±15 vs 187±25 ms; P=0.03) refractoriness at a cycle length of 300 ms. Atrial arrhythmias were not induced in any dog. Ventricular fibrillation (VF) was induced in 2/8 dogs at baseline and 4/8 dogs after cocaine. CONCLUSION: High doses of cocaine exert significant class I effects and seem to enhance inducibility of VF but not of atrial arrhythmias.

  • cocaine
  • electrophysiology
  • Ventricular Fibrillation
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Creative Commons Attribution (CC BY) Creative Commons license
04/08/2003 DOI: 10.1590/S0066-782X2003000900002 Visualizações 1

Como citar este artigo

EndNote RIS

Formato de Documento Eletrônico (Vancouver)

Cabral M, Ponciano A, Santos B, Morais J. Cardiocerebral Infarction: A Combination to Prevent. International Journal of Cardiovascular Sciences 2022;36:e20210276.

Formato de Documento Eletrônico (ABNT)

Cabral, Margarida; Ponciano, Ana; Santos, Beatriz; Morais, João. Cardiocerebral Infarction: A Combination to Prevent. International Journal of Cardiovascular Sciences, v. 36, e20210276, jul. 2022.

Formato de Documento Eletrônico (APA)

Cabral, M., Ponciano, A., Santos, B., & Morais, J. (2022). Cardiocerebral Infarction: A Combination to Prevent. International Journal of Cardiovascular Sciences, 36, e20210276.

Formato de Documento Eletrônico (ISO)

Cabral, Margarida and Ponciano, Ana and Santos, Beatriz and Morais, João. Cardiocerebral Infarction: A Combination to Prevent. International Journal of Cardiovascular Sciences [online]. 2022, vol. 36, [citado 2026-10-14], e20210276. Disponível em: <https://journals.cardiol.br/article/cardiocerebral-infarction-a-combination-to-prevent-2/>. ISSN 2359-4802

EndNote RIS

Formato de Documento Eletrônico (Vancouver)

Gonçalves L, Pires I, Santos J, Correia JL, Moreira D, Almeida I. Commotio Cordis Secondary to Aggression. International Journal of Cardiovascular Sciences 2021;35(2):293-6.

Formato de Documento Eletrônico (ABNT)

Gonçalves, Luisa; Pires, Inês; Santos, João; Correia, Joana Laranjeira; Moreira, Davide; Almeida, Inês. Commotio Cordis Secondary to Aggression. International Journal of Cardiovascular Sciences, v. 35, n. 2, p. 293-296, ago. 2021.

Formato de Documento Eletrônico (APA)

Gonçalves, L., Pires, I., Santos, J., Correia, J. L., Moreira, D., & Almeida, I. (2021). Commotio Cordis Secondary to Aggression. International Journal of Cardiovascular Sciences, 35(2), 293-296.

Formato de Documento Eletrônico (ISO)

Gonçalves, Luisa and Pires, Inês and Santos, João and Correia, Joana Laranjeira and Moreira, Davide and Almeida, Inês. Commotio Cordis Secondary to Aggression. International Journal of Cardiovascular Sciences [online]. 2021, vol. 35, n. 2, [citado 2026-10-14], pp. 293-296. Disponível em: <https://journals.cardiol.br/article/commotio-cordis-secondary-to-aggression-2/>. ISSN 2359-4802

EndNote RIS

Formato de Documento Eletrônico (Vancouver)

Fenelon G, Uchoa J, Otobone JR, Reis M, Amaral JLG, Paola AAVD. Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts. Arquivos Brasileiros de Cardiologia 2003;81(1):29-34.

Formato de Documento Eletrônico (ABNT)

Fenelon, Guilherme; Uchoa, Júlio; Otobone, José Roberto; Reis, Marcos; Amaral, José Luiz Gomes do; Paola, Angelo A. V. De. Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts. Arquivos Brasileiros de Cardiologia, v. 81, n. 1, p. 29-34, ago. 2003.

Formato de Documento Eletrônico (APA)

Fenelon, G., Uchoa, J., Otobone, J. R., Reis, M., Amaral, J. L. G. , & Paola, A. A. V. D. (2003). Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts. Arquivos Brasileiros de Cardiologia, 81(1), 29-34.

Formato de Documento Eletrônico (ISO)

Fenelon, Guilherme and Uchoa, Júlio and Otobone, José Roberto and Reis, Marcos and Amaral, José Luiz Gomes do and Paola, Angelo A. V. De. Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts. Arquivos Brasileiros de Cardiologia [online]. 2003, vol. 81, n. 1, [citado 2026-10-14], pp. 29-34. Disponível em: <https://journals.cardiol.br/article/characterization-of-the-in-vivo-cardiac-electrophysiologic-effects-of-high-dose-cocaine-in-closed-chest-anesthetized-dogs-with-normal-hearts-2/>. ISSN 0066-782X

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