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Correspondence

Supraventricular Tachycardia

N Engl J Med 1995; 333:323-324August 3, 1995

Article

To the Editor:

We fully agree with the statement of Ganz and Friedman in their review article “Supraventricular Tachycardia” (Jan. 19 issue)1 regarding the efficacy of adenosine in the termination of supraventricular tachycardia. However, to counter their assertion that “bronchospasm triggered by intravenous adenosine remains a . . . clinically undocumented complication” in patients with asthma, we have observed a case of severe bronchospasm after a bolus intravenous injection of adenosine.

A 23-year-old man was admitted to our hospital for radiofrequency catheter ablation of a left free-wall accessory pathway causing frequent episodes of sustained atrioventricular reentry tachycardia. There was no history of overt pulmonary disease, and the patient denied having respiratory symptoms. We performed the ablation and then administered 12 mg of adenosine during right ventricular pacing to confirm the success of ablation. After the administration of the drug, persistent severe dyspnea and bronchospasm developed that necessitated aggressive intravenous bronchodilator therapy. Detailed reevaluation of the patient's clinical history and that of his parents revealed a vague history of asthma during early childhood.

This observation is supported by a report by Burkhart,2 who described a 54-year-old man with chronic obstructive pulmonary disease who presented with paroxysmal supraventricular tachycardia. A 12-mg bolus injection of adenosine aggravated mild bronchospasm, causing respiratory failure that required ventilatory support for nine days.

In contrast to Ganz and Friedman, we believe that bronchospasm triggered by intravenous adenosine is not only a theoretical complication, and we recommend caution in the use of adenosine in patients with a history of asthma or chronic obstructive pulmonary disease.

Florian Hintringer, M.D.
St. George's Hospital Medical School, London SW17 0RE, United Kingdom

Helmut Pürerfellner, M.D.
Josef Aichinger, M.D.
Krankenhaus der Elisabethinen, A-4010 Linz, Austria

2 References
  1. 1

    Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995;332:162-173
    Full Text | Web of Science | Medline

  2. 2

    Burkhart KK. Respiratory failure following adenosine administration. Am J Emerg Med 1993;11:249-250
    CrossRef | Web of Science | Medline

To the Editor:

Ganz and Friedman state, “In patients with asthma, bronchospasm triggered by intravenous adenosine remains a theoretical but clinically undocumented complication.” I believe the authors missed some recent case reports, one of which I coauthored, showing that there may well be documented cases of bronchospasm induced by the administration of intravenous adenosine.1

Curt G. DeGroff, M.D.
Oregon Health Sciences University, Portland, OR 97201

1 References
  1. 1

    DeGroff CG, Silka MJ. Bronchospasm after intravenous administration of adenosine in a patient with asthma. J Pediatr 1994;125:822-823
    CrossRef | Web of Science | Medline

To the Editor:

Drs. Ganz and Friedman state that the diagnosis of subtypes of supraventricular tachycardia on the basis of the 12-lead surface electrocardiogram may be incorrect in as many as 20 percent of cases. They do not mention the possible benefit afforded by the use of an additional esophageal lead.1 In patients with a history of recurring arrhythmia who are in sinus rhythm at the time of presentation, monitoring of an esophageal lead can provide reliable P-wave identification during 87.5 percent of the 24-hour monitoring period.2 The method is well accepted by patients,2 is easy to apply,3 and can contribute to a correct diagnosis of transient supraventricular tachycardia.4 An example of the use of the esophageal lead is shown in Figure 1Figure 1Atrial Tachycardia Registered by Means of an Esophageal Holter Electrocardiographic Monitor..

Werner Grille, M.D.
Frank Asbeck, M.D.
Community Hospital, 24116 Kiel, Germany

4 References
  1. 1

    el Sherif N, el-Ramly Z, Sorour AH. Oesophageal electrocardiography in the study of cardiac arrhythmias. Br Heart J 1969;31:414-425
    CrossRef | Web of Science | Medline

  2. 2

    Henke M, Grille W, Holst T, et al. Prospektive Untersuchung zur P-Wellen-Identifizierung und Patientenbelastung durch das Ösophagus-Langzeit-Ekg. Z Kardiol 1993;82:Suppl 3:24-24 abstract.

  3. 3

    Arzbaecher RC, Collins S, Jenkins J, Lorenzen S. Feasibility of long-term esophageal electrocardiography in the study of transient arrhythmias. Biomed Sci Instrum 1978;14:1-6
    Medline

  4. 4

    Schnittger I, Rodriguez IM, Winkle RA. Esophageal electrocardiography: a new technology revives an old technique. Am J Cardiol 1986;57:604-607
    CrossRef | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: We thank Dr. DeGroff and Dr. Hintringer and colleagues for sharing their experience1 with the triggering of bronchospasm by adenosine in patients with asthma who were treated for supraventricular tachycardia Such experiences and one other recent case report2 underscore the need to consider a history of asthma or obstructive lung disease when one is deciding which intravenous agent to use for the immediate termination of supraventricular tachycardia.

Grille and Asbeck point out the potential usefulness of esophageal electrocardiography in the differential diagnosis of supraventricular tachycardia. Because of its proximity to the left atrium, an esophageal lead can yield important clues about the relative timing of atrial and ventricular activation. We agree that this technique may help differentiate between atrial and atrioventricular junctional tachycardias. In cases in which a one-to-one relation between P waves and QRS complexes is absent, the esophageal recording can sometimes demonstrate this more clearly than the surface electrocardiogram or Lewis and Golub leads and, thus, can help to eliminate diagnoses such as tachycardias mediated by the accessory pathway. However, since the sequence of atrial activation is not always apparent from an examination of esophageal recordings of tachycardia, precise identification of the mechanism of tachycardia may still be difficult. Furthermore, in our experience, patients' acceptance of long-term esophageal electrocardiography is limited, particularly in the outpatient setting.

Leonard I. Ganz, M.D.
Peter L. Friedman, M.D., Ph.D.
Brigham and Women's Hospital, Boston, MA 02115

2 References
  1. 1

    DeGroff CG, Silka MJ. Bronchospasm after intravenous administration of adenosine in a patient with asthma. J Pediatr 1994;125:822-823
    CrossRef | Web of Science | Medline

  2. 2

    Burkhart KK. Respiratory failure following adenosine administration. Am J Emerg Med 1993;11:249-250
    CrossRef | Web of Science | Medline

Citing Articles (2)

Citing Articles

  1. 1

    Ivana I. Vranic, Mihailo Matic, Jovan Perunicic, Tijana Simic, Ljiljana Soskic, Natasa Milic. (2006) Adenosine cardioprotection study in clinical setting of paroxysmal supraventricular tachycardia. Prostaglandins, Leukotrienes and Essential Fatty Acids 74:6, 365-371
    CrossRef

  2. 2

    S. SERGE BAROLD. (1995) Bedside Diagnosis of Wide QRS Tachycardia. Pacing and Clinical Electrophysiology 18:12, 2109-2115
    CrossRef

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