Cardiac anaphylaxis: searching for clari”>Correspondence

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American Journal of Emergency Medicine

journal homepage: www. elsevier.com/ locate/ajem

American Journal of Emergency Medicine 32 (2014) 86-106

Cardiac anaphylaxis: searching for clarity?,??

To the Editor,

We read the article by Tummala et al [1] with great interest. Apart from the type II Kounis syndrome and iatrogenic administration of excess doses of epinephrine, other mechanisms could contribute to Acute ST-segment elevation myocardial infarction in this patient. During anaphylaxis, there will be rapid shift of intravascular fluid into the extravascular compartment, which can trigger the rennin- angiotensin-aldosterone system resulting in compensatory catechol- amine release [2]. In addition, histamine could stimulate the release of catecholamines by a direct action on adrenal medulla [3], which initiates the coronary spasm or could rupture the atheroma plaque and causes platelet aggregation in patients with atherosclerotic coronary disease.

Likewise, one cannot disregard the recent systematic reviews and meta-analyses [4,5], which shed light on emerging evidence that not only selective COX-2 inhibitors but also traditional nonsteroidal anti-inflammatory drugs may be associated with atherothrombotic events such as myocardial infarction and stroke. The available evidence points to the fact that diclofenac, in particular, is likely to increase hazard ratio for Thrombotic cardiovascular events [6]. Diclofenac inhibits COX-2 to a higher level, which is coupled with an incomplete inhibition of COX-1, which alters the prostacyclin-thromboxane A2 balance, thus causing a prothrombotic situation [7]. The increased cardiovascular risk has been observed in patients with a prior high risk of cardiovascular disease and in previously healthy individuals. In addition, the prolonged systemic hypotension induced by vasoactive and inflam- matory mediators released during anaphylaxis probably caused further reduction of the myocardial perfusion, thus favoring in situ thrombus formation and subsequent coronary artery occlusion. In the present case, the patient is at high risk for coronary artery disease in respect with his age, sex, and smoking habit.

We can, therefore, deduce that prolonged Coronary vasospasm and thrombotic vascular occlusion on top of the preexisting coronary artery disease might have played a major role in addition to the hypersensitivity reaction in this patient. To overcome drug- induced morbidity and mortality in any case, the prescribers should look into patients’ health status and coexisting illness(es), and the status of medicines such as pharmacokinetics, Drug interactions, and contraindications. To bring these into reality, the health science education and training as well as accrediting bodies should enforce regular Prescription auditing and monitoring. Let our prescriptions be patient centered and value driven.

? Financial support: Nil.

?? Conflict of interest: Nil.

Subramanian Senthilkumaran MD Department of Emergency and Critical Care Sri Gokulam Hospital and Research Institute

Salem, Tamil Nadu, India E-mail address: [email protected]

Ritesh G. Menezes MD

Department of Forensic Medicine & Toxicology

ESIC-Medical College & PGIMSR

Bangalore, India

Syed Mohamed Mohamed Ibrahim MD

Department of Emergency and Critical Care

Apollo Speciality Hospital Madurai, Tamil Nadu, India

Ponniah Thirumalaikolundusubramanian MD

Department of Internal Medicine Chennai Medical College Hospital and Research Center

Irungalur, Trichy, Tamil Nadu, India

http://dx.doi.org/10.1016/j.ajem.2013.08.058

References

1. Tummala K, Maniyal VK, Chandrashekaran R, Mathew N, Ganeshwala G. Cardiac anaphylaxis: a case of acute ST-segment elevation myocardial infarction after IM epinephrine for anaphylactic shock. Am J Emerg Med 2013;31(7):1157.e1-3.
2. Hermann K, Ring J. The renin angiotensin system and hymenoptera venom anaphylaxis. Clin Exp Allergy 1993;23:762-9.
3. Marley PD. Mechanisms in histamine-mediated secretion from adrenal chromaffin cells. Pharmacol Ther 2003;98:1-34.
4. Trelle S, Reichenbach S, Wandel S, Hildebrand P, Tschannen B, Villiger PM, et al. Cardiovascular safety of Non-steroidal anti-inflammatory drugs: a network meta- analysis. BMJ 2011;342:c7086.
5. Krotz F, Struthmann L. A review on the risk of myocardial infarction associated with the NSAID diclofenac. Cardiovasc Hematol Disord Drug Targets 2010;10:53-65.
6. McGettigan P, Henry D. Use of non-steroidal anti-inflammatory drugs that elevate cardiovascular risk: an examination of sales and essential medicines lists in low-, middle-, and high-income countries. PLoS Med 2013;10(2):e1001388.
7. Struthmann L, Hellwig N, Pircher J, Sohn HY, Buerkle MA, Klauss V, et al. Prothrombotic effects of diclofenac on arteriolar platelet activation and thrombosis in vivo. J Thromb Haemost 2009;7:1727-35.

   Reply to the Letter to the editor

   To the Editor,

   Acute myocardial infarction is multifactorial in the setting of anaphylaxis. The relative risk of low- and high-dose diclofenac without medical prescription causing myocardial infarction is well described [1].

   This patient, with moderate Framingham risk score for cardiovas- cular events over 10 years [2], complained of chest pain immediately

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