Resuscitation 85 (2014) e47–e48
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Letter to the Editor Therapeutic hypothermia after sudden cardiac arrest: Endothelial function evaluation Sir, Therapeutic hypothermia (TH) is now part of the treatment strategy for patients successfully resuscitated after cardiac arrest once it was demonstrated to improve neurologic outcome and increase survival rates.1 TH is associated with several cardiovascular effects. There is a decrease in heart rate and cardiac index and an increase in mean blood pressure and systemic vascular resistance. A variety of arrhythmias may be induced by hypothermia. However, it is unknown whether vascular reactivity is impaired during TH after cardiac arrest. We describe an evaluation of endothelium function in a case of an out-of-hospital survivor of cardiac arrest submitted to TH. During hypothermia and after rewarming brachial ﬂow-dependent vasodilation was evaluated. The patient was a 39-year-old male patient victim of ventricular ﬁbrillation who had been resuscitated at home after 20 min and remained comatose after the resumption of spontaneous circulation (ROSC). At hospital admission, Glasgow Coma Scale was 8. Cardiovascular risk stratiﬁcation was performed. Electrocardiography showed sinus rhythm with diffuse repolarization abnormalities. Angiographic study revealed no coronary obstructive lesions and moderate diffuse left ventricular dysfunction. Patient was admitted to the ICU and general management of post-cardiac arrest care was initiated, including TH for 24 h. After recovery, electrophysiological testing was performed and revealed ventricular ﬁbrillation triggered by the use of propafenone. An implantable cardioverter-deﬁbrillator was indicated. Patient was discharged from the hospital without neurological sequelae. Using a noninvasive approach, with high-resolution ultrasound, we measured brachial artery diameter and brachial artery blood ﬂow velocity at rest and during reactive hyperemia (RH) after a 5min occlusion of the brachial artery with a blood pressure cuff2,3 (Fig. 1) in two moments: ﬁrst at temperature of 32.6 ◦ C, after the cooling period, and second at 37.1 ◦ C, after rewarming. After the stimuli of RH, the % increases in brachial diameter, peak blood ﬂow and mean blood ﬂow during hypothermia were 20.8 ± 2.3%, 141.3 ± 14.9% and 416.7 ± 14.3%, respectively. After rewarming, these changes expressed as % were: 8.9 ± 3.5%, 84.5 ± 14.2% and 128.6 ± 18.9%, respectively. Flow-dependent vasodilation, that is secondary to endothelial NO release during RH, was maintained during TH suggesting an intact endothelial function. ROSC after prolonged whole-body ischemia and subsequent reperfusion that happens after successful cardiopulmonary resuscitation is a complex pathological process. The post-cardiac arrest syndrome is a multiple disorder process that causes brain injury, myocardial dysfunction and systemic ischemia/reperfusion response, including coagulation disorders, adrenal dysfunction, massive inﬂammation and microcirculatory impairment.4 The microcirculatory function is abnormal in post-resuscitation period 0300-9572/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.resuscitation.2013.12.018
Fig. 1. Acquisition of brachial artery diameter (D; mm) and brachial artery blood ﬂow velocity (BFV; m/s). (top) High resolution B-mode ultrasound image of brachial artery to calculate diameter. (bottom) Doppler ultrasound image of brachial artery blood ﬂow velocity during hyperemia reactive (HR).
and may be associated with the development of organ failure after cardiac arrest.5 Brachial vascular reactivity was preserved during TH. Our ﬁndings are relevant for future research investigation of possible vascular adaptive mechanisms involved in the maintenance of organ perfusion during TH. Conﬂict of interest statement None. References 1. The Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Eng J Med 2002;346:549–56. 2. Higa M, Pilon PE, Lage SG, Gutierrez MA. A computational tool for quantitative assessment of peripheral arteries in ultrasound images. Comput Cardiol 2009;36:41–4. 3. Corretti MC, Anderson TJ, Benjamin EJ, et al. Guidelines for the ultrasound assessment of endothelial-dependent ﬂow-mediated vasodilation of the brachial artery. J Am Coll Cardiol 2002;39:257–65. 4. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican
Letter to the Editor / Resuscitation 85 (2014) e47–e48
Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation 2008;118: 2452–83. 5. Kern KB, Zuercher M, Cragun D, et al. Myocardial microcirculatory dysfunction after prolonged ventricular ﬁbrillation and resuscitation. Crit Care Med 2008;36(Suppl.):S418–21.
Silvia G. Lage ∗ Liliane Kopel Claudia S.M. Bernoche Intensive Care Unit, Heart Institute (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Brazil
Sergio Timerman Laboratory of Training and Simulation in Cardiovascular Emergencies, Heart Institute (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Brazil Karl B. Kern Sarver Heart Center, University of Arizona, Tucson, AZ, USA ∗ Corresponding author. E-mail address: [email protected]
9 December 2013