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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 1  |  Issue : 2  |  Page : 91-92

Therapeutic hypothermia after out-of-hospital cardiac arrest - Should we keep platelets in mind?


Cardiovascular Clinic Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Catalonia, Spain

Date of Web Publication16-Nov-2017

Correspondence Address:
Rodolfo San Antonio
Cardiovascular Clinic Institute, Hospital Clinic, 170 Villarroel Street, 08036 Barcelona, Catalonia
Spain
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/hm.hm_1_17

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  Abstract 

Therapeutic hypothermia has been associated with an increase in thrombotic events, but this point has not been fully clarified. Most patients undergoing therapeutic hypothermia in a cardiac ICU receive antithrombotic treatment, usually in the context of ischemic heart disease. But, what should we do if our patient does not need antithrombotic treatment for any reason? After this case, doubts arise on the need to use an anti-thrombotic treatment on all patients subjected to therapeutic hypothermia in the context of aborted cardiac arrest

Keywords: Antiplatelet therapy, cardiac arrest, hypothermia, thrombosis


How to cite this article:
Antonio RS, Flores-Umanzor EJ, Pujol-López M, Caldentey G. Therapeutic hypothermia after out-of-hospital cardiac arrest - Should we keep platelets in mind?. Heart Mind 2017;1:91-2

How to cite this URL:
Antonio RS, Flores-Umanzor EJ, Pujol-López M, Caldentey G. Therapeutic hypothermia after out-of-hospital cardiac arrest - Should we keep platelets in mind?. Heart Mind [serial online] 2017 [cited 2019 Jul 16];1:91-2. Available from: http://www.heartmindjournal.org/text.asp?2017/1/2/91/218514



From 2002, several randomized clinical trials in the setting of cardiac arrest have validated the clinical applicability of therapeutic hypothermia (TH) in patients who have survived after an out-of-hospital cardiac arrest secondary to shockable rhythms.[1],[2] However, TH has been related to a disturbingly high rate of cases of stent thrombosis despite antithrombotic therapy.[3],[4] In the same way, several authors have observed a high rate of systemic venous thrombosis in patients treated with endovascular catheters for hypothermia induction.[5] On one hand, increased platelet activation and a potential inefficiency of antiplatelet therapy may explain the increased risk of thrombosis in TH. On the other hand, recent data suggest that other etiologic mechanisms may play roles in thrombotic events.[6] Thus, experimental models have been developed and have demonstrated a relationship between TH and endothelial dysfunction.[7] Endothelial disorders have been associated with coronary flow impairment and therefore thrombotic events.[8],[9]

We present the case of a 19-year-old man who was admitted after suffering a resuscitated cardiac arrest. A computed tomography (CT) brain scan was initially performed, and no changes were seen in morphology or density at the encephalic structure level. An initial echocardiogram showed diffuse left ventricular hypokinesis with mild systolic dysfunction (ejection fraction 45%) in the context of postarrest syndrome. Laboratory studies revealed normal platelets (310,000/mm 3) and normal prothrombin time.

TH at 33°C was initiated using a noninvasive method (hydrogel-coated pads). After 24 h, the patient developed hemodynamic instability and pupil asymmetry. A subsequent CT scan showed a subsegmental pulmonary thromboembolism and bilateral cerebral ischemic strokes. A transesophageal echocardiogram revealed the presence of atrial thrombi on the right side [Figure 1]a, ruling out the presence of interatrial communication [Figure 1]b. A thrombophilia study was requested and was negative. In spite of intensive medical support, the patient died as a result of neurological damage [Figure 1]c and [Figure 1]d.
Figure 1: (a) Transoesophageal echocardiogram showing two mobile masses (red arrows) in the right atrium, well defined and with increased echogenicity, 8.6 mm × 5.2 mm and 10 mm × 9 mm, adhered to the eustachian valve. (b) Transoesophageal echocardiogram showing the presence of spontaneous echo contrast (*) and integrity of the interatrial septum. (c and d) Brain computed tomography showing established regional lesions suggestive of a right frontal-temporal-parietal subacute ischemic infarction (middle cerebral artery, yellow arrows) and a left temporal-occipital level infarction (posterior cerebral artery, blue arrow). Diffuse cerebral edema is evident.

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TH has been shown to result in thrombocytopenia, slowing of coagulation enzymes, disordered fibrinolysis, and disruption of platelet function. It promotes platelet margination by increasing hematocrit, changing platelet shape, lowering blood flow rate, and increasing the expression of adhesion molecules.[10] Nevertheless, its consequences and the mechanisms behind the observed phenomena have not been fully elucidated.

In cardiac intensive care units, it is an usual practice to use antiplatelet drugs. Most patients receive antithrombotic therapy in the context of acute or chronic ischemic heart disease. In other cases, also very common, patients are treated with anticoagulant drugs due to atrial fibrillation, mechanical prosthesis implantation, or even after the implantation of an intra-aortic balloon pump. In patients undergoing TH, the scenario is similar, so very few patients are subjected to this type of treatment without associated antithrombotic therapy.

In the present case, our patient did not receive dual antiplatelet or anticoagulant treatment until thrombi were seen because no reason for antithrombotic treatment was presented. Although this is an isolated clinical case, we believe that this should be taken into consideration, being it critical to minimize this complication in the future. Doubts now arise about the need for antithrombotic treatment for all patients in the context of TH after aborted cardiac arrest. New research is needed to determine the optimal antithrombotic therapy and the exact cause of this type of episode.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Holzer M, Cerchiari E, Martens P, Roine R, Sterz F, Eisenburger P, et al. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549-56.  Back to cited text no. 1
    
2.
Takeuchi I, Takehana H, Satoh D, Fukaya H, Tamura Y, Nishi M, et al. Effect of hypothermia therapy after outpatient cardiac arrest due to ventricular fibrillation. Circ J 2009;73:1877-80.  Back to cited text no. 2
    
3.
Penela D, Magaldi M, Fontanals J, Martin V, Regueiro A, Ortiz JT, et al. Hypothermia in acute coronary syndrome: Brain salvage versus stent thrombosis? J Am Coll Cardiol 2013;61:686-7.  Back to cited text no. 3
    
4.
Ibrahim K. Increased rate of stent thrombosis due to clopidogrel resistance in patients in therapeutic hypothermia after sudden cardiac death. Eur Heart J 2011;32 Supp l:252.  Back to cited text no. 4
    
5.
Maze R, Le May MR, Froeschl M, Hazra SK, Wells PS, Osborne C, et al. Endovascular cooling catheter related thrombosis in patients undergoing therapeutic hypothermia for out of hospital cardiac arrest. Resuscitation 2014;85:1354-8.  Back to cited text no. 5
    
6.
Regueiro A, Freixa X, Heras M, Penela D, Fernández-Rodríguez D, Brugaletta S, et al. Impact of therapeutic hypothermia on coronary flow. Int J Cardiol 2014;172:228-9.  Back to cited text no. 6
    
7.
Zoerner F, Wiklund L, Miclescu A, Martijn C. Therapeutic hypothermia activates the endothelin and nitric oxide systems after cardiac arrest in a pig model of cardiopulmonary resuscitation. PLoS One 2013;8:e64792.  Back to cited text no. 7
    
8.
Muxel S, Fineschi M, Hauser ER, Gori T. Coronary slow flow or syndrome Y: Dysfunction at rest, preserved reactivity of the peripheral endothelium. Int J Cardiol 2011;147:151-3.  Back to cited text no. 8
    
9.
Tin-Hay EL, Poh KK, Lim YT, Low AF, Lee CH, Teo SG, et al. Clinical predictors of stent thrombosis in the “real world” drug-eluting stent era. Int J Cardiol 2010;145:422-5.  Back to cited text no. 9
    
10.
Zhang JN, Wood J, Bergeron AL, McBride L, Ball C, Yu Q, et al. Effects of low temperature on shear-induced platelet aggregation and activation. J Trauma 2004;57:216-23.  Back to cited text no. 10
    


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