Correspondence

Anaphylaxis and Coronary Disease

N Engl J Med 1996; 335:1925-1926December 19, 1996

Article

To the Editor:

In the Clinical Problem-Solving article entitled “The Domino Principle” (Aug. 1 issue),1 Jaffe and Zahger describe an assumed anaphylactic reaction that produced shock and subsequent myocardial ischemia. What is unusual in this case is the presence of sinus rhythm of 90 beats per minute in a patient who is assumed to be in anaphylactic shock and who is not receiving beta-adrenergic blockers. By virtue of the clinical presentation of shock, normal sinus rhythm without tachycardia is extremely unusual, especially in anaphylactic reactions.2 The release of histamine during anaphylaxis causes marked increases in sympathoadrenergic tone and directly stimulates histamine H₂ receptors, producing positive chronotropic effects.3 Multiple other mediators also produce direct and indirect reflex effects, all of which consistently produce tachycardia.2 The fact that this patient had a sinus rhythm of 90 beats per minute suggests she may not have had an anaphylactic reaction. Furthermore, the diagnosis of anaphylaxis is usually reserved for patients with immunospecific antibodies.2 The assumed reaction to diclofenac, a nonsteroidal antiinflammatory drug, is actually an anaphylactoid reaction caused by nonspecific activation of the inflammatory pathway, perhaps produced by the shunting of cyclooxygenase by-products into lipoxygenase pathways.2 Echocardiography performed in patients in acute anaphylactic shock can reveal evidence of low left ventricular end-diastolic volumes with ventricular obliteration during systole, changes suggestive of profound intravascular hypovolemia, low systemic vascular resistance, and normal ventricular function.4 The description of the echocardiogram did not discuss ventricular volumes. Finally, the patient's temperature of 35.5°C was never adequately explained.

Jerrold H. Levy, M.D.
Jack S. Shanewise, M.D.
Emory University School of Medicine, Atlanta, GA 30322

4 References

1. 1

   Jaffe R, Zahger D. The domino principle. N Engl J Med 1996;335:340-341
   Full Text | Web of Science | Medline

2. 2

   Levy JH. Anaphylactic reactions in anesthesia and intensive care. 2nd ed. Boston: Butterworth–Heinemann, 1992.
   

3. 3

   Levi R, Rubin LE, Gross SS. Histamine and cardiovascular function and dysfunction: recent developments. In: Uvnas B, ed. Handbook of experimental pharmacology. Vol. 97. Histamine and histamine antagonists. Berlin, Germany: Springer-Verlag, 1991.
   

4. 4

   Beaupre PN, Roizen MF, Cahalan MK, Alpert RA, Cassorla L, Schiller NB. Hemodynamic and two-dimensional transesophageal echocardiographic analysis of an anaphylactic reaction in a human. Anesthesiology 1984;60:482-484
   CrossRef | Web of Science | Medline

To the Editor:

The case of a 65-year-old woman who collapsed on the street and was then evaluated in an emergency room must have presented quite a challenge to the physician on duty. The interplay of a reaction to the previously injected nonsteroidal antiinflammatory drug and the subsequently discovered severe coronary artery disease presented a very confusing picture. Anaphylaxis is almost always accompanied by an elevated serum tryptase level, brought about by the activation of mast cells.1 I wonder whether serum tryptase was measured, since the results could have clarified the diagnosis. It is of interest that human heart tissue also contains mast cells, which may take part in anaphylactic reactions and have a role in myocardial disease.2

Alexander Roth, M.D.
Hawaii Permanente Medical Group, Honolulu, HI 96814

2 References

1. 1

   Schwartz HJ, Yunginger JW, Schwartz LB. Is unrecognized anaphylaxis a cause of sudden unexpected death? Clin Exp Allergy 1995;25:866-870
   CrossRef | Web of Science | Medline

2. 2

   Marone G, Patella V, de Crescenzo G, Genovese A, Adt M. Human heart mast cells in anaphylaxis and cardiovascular disease. Int Arch Allergy Immunol 1995;107:72-75
   CrossRef | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: Dr. Roth suggests that the finding of an elevated tryptase level might have facilitated the diagnosis of anaphylaxis. The assay is unfortunately not routinely available at our center and was therefore not performed.

Drs. Levy and Shanewise suggest that the absence of tachycardia and of hypercontraction and underfilling of the left ventricle argues strongly against the diagnosis of anaphylaxis. As discussed in our paper, the finding of normal ventricular function, rather than hypercontraction with cavity obliteration, should have raised the suspicion that factors other than anaphylaxis were operative. Our discussion focused on the interaction of the anaphylactic reaction and cardiac ischemia, and we believe that both the echocardiographic findings and the relative bradycardia may be explained by concomitant ischemia in a patient with severe triple-vessel disease. Myocardial ischemia was evident electrocardiographically on admission and could certainly have led to increased ventricular volumes and reduced contractility. Finally, the reaction may indeed have been an anaphylactoid rather than an anaphylactic one, although mast-cell degranulation and histamine release occur in both cases and may have precipitated the unstable coronary syndrome, as discussed in our article.

Doron Zahger, M.D.
Ronen Jaffe, M.D.
Hadassah University Hospital, Mt. Scopus, Jerusalem 91240, Israel