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Anesth Analg 1999;89:609
© 1999 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Wolff-Parkinson-White Syndrome Simulating Inferior Myocardial Infarction in a Cocaine Abuser for Urgent Dilation and Evacuation of the Uterus

Stewart J Lustik, MD, Jacek Wojtczak, MD, PhD, and Ashwani K. Chhibber, MD

Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York

Address correspondence and reprint requests to Stewart Lustik, MD, University of Rochester Medical Center, Strong Memorial Hospital, Department of Anesthesiology, Box 604, 601 Elmwood Ave., Rochester, NY 14642. Address e-mail to SLUSTIK{at}CCMAIL.ANES.ROCHESTER.EDU


   Introduction
Top
 Introduction
Case Report
 Discussion
 References
 
We describe the case of a patient presenting for urgent surgery who had symptoms and an electrocardiogram (EKG) consistent with a recent myocardial infarction. The inferior Q waves on her EKG were negative delta waves of Wolff-Parkinson-White (WPW) syndrome, and her chest pain was caused by a rapid tachycardia. We discuss methods to differentiate WPW from myocardial infarction and the anesthetic management of WPW.


   Case Report
Top
 Introduction
 Case Report
Discussion
 References
 
A 34-yr-old woman at 17 wk conception presented for dilation and evacuation, after earlier placement of laminaria. During her preoperative anesthesia assessment, she mentioned that 2 wk before she had experienced palpitations, lightheadedness, and chest pain that resolved with treatment in the emergency department. She claimed that she left the emergency department against medical advice. She admitted to occasional cocaine use but denied use at the time of the emergency department visit and in the last 2 wk. The patient described several episodes of substernal chest pain that were nonexertional and lasted hours in the last few years. She denied orthopnea or postural nocturnal dyspnea. She smoked 46 packs per year and drank three beers once or twice weekly. Preoperative blood pressure was 100/50 mm Hg with a heart rate of 80 bpm.

The preoperative EKG showed large inferior Q waves and a short PR interval (Figure 1). In light of the patient's recent chest pain and EKG indicating a possible inferior myocardial infarction, a cardiology consultation was arranged. The cardiologist concluded that the patient's symptoms and EKG findings were consistent with WPW syndrome rather than a myocardial infarction. The patient underwent successful uterine dilation and evacuation under spinal anesthesia.



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  		Figure 1. A, Preoperative electrocardiogram. Note short PR interval (0.10 s), large Q waves in II, III, and aVF, and slurred R waves in V2 and V3. B, After successful catheter ablation, there is a normalization of the PR interval and absence of inferior Q waves (loss of delta waves).

 
Postoperatively, the patient agreed to further evaluation of her symptoms. An echocardiogram revealed no wall motion abnormalities, a normal ejection fraction, and mild mitral regurgitation. Electrophysiologic testing confirmed the presence of a posteroseptal accessory pathway. The patient underwent successful catheter ablation using radiofrequency current. Her posttreatment EKG (Figure 1B) revealed resolution of the inferior Q waves.


   Discussion
Top
 Introduction
 Case Report
 Discussion
References
 
We were concerned that our patient had a recent inferior myocardial infarction because of her recent chest pain and deep Q waves in leads II, III, and aVF. The patient's EKG revealed a short PR interval in addition to the inferior Q waves. The differential diagnosis included WPW, inferior myocardial infarction, or both.

WPW was confirmed in our patient by the presence of delta waves (slurred upstroke of R waves) in leads V2 and V3. In addition to activation of the ventricles from the normal bundle branches, this patient had activation from an accessory posteroseptal bypass tract. This resulted in negative delta waves in the inferior leads, which are morphologically identical to infarction Q waves and are present in 16% of patients with WPW (1).

In most young patients with WPW and no cardiac risk factors or symptoms, it is not likely that the Q waves would have suggested a myocardial infarction; however, our patient's cocaine use and chest pain increased our concern. Cocaine prevents the uptake of norepinephrine, epinephrine, and dopamine at postsynaptic junctions, and it stimulates the presynaptic release of norepinephrine. This results in excess catecholamines at the postsynaptic receptors, which cause tachycardia and hypertension that may lead to cardiac ischemia (2). Cocaine also causes coronary artery vasospasm (3) and increased platelet aggregation (4), which probably account for cocaine's association with acute myocardial infarctions in young patients (5).

Although it is not possible to reliably differentiate negative delta waves from myocardial infarction based solely on the EKG, the vector of the T waves may be helpful. Goldberger (6) found that 94% of patients with pseudoinfarct Q waves of WPW had isoelectric or positive T waves (Q wave-T wave discordance). Similarly, in a study of healthy aircrew, Q wave-T wave vector discordance was found in all 11 WPW patients with inferior Q waves (1). Although our patient had positive T waves in the inferior leads, Q-wave infarctions may occasionally have Q wave-T wave discordance; therefore, this does not rule out infarction.

If there is doubt whether the inferior Q waves represent infarction or negative delta waves, an echocardiogram may be obtained to study inferior wallmotion. The sensitivity of an echocardiogram is sufficient to rule out old inferior myocardial infarction if no wall motion abnormalities are seen (7). If the inferior wall is hypokinetic or akinetic, further testing is indicated to determine myocardium at risk. In patients with preexcitation, a regular exercise stress test is unreliable because there are many false positives (8); an exercise echocardiogram or stress thallium would be more useful in defining myocardium at risk.

Our patient's chest pain was most likely caused by the pounding sensation from the rapid tachycardia or, less likely, tachycardia induced ischemia. She had no exertional angina consistent with coronary artery disease. The chest pain was not a result of a myocardial infarction from cocaine use or coronary artery disease, as demonstrated by the absence of an inferior wall motion abnormality on echocardiogram. This was confirmed with resolution of the inferior Q waves after ablation of the accessory pathway.

Confusing the negative delta waves of WPW with a myocardial infarction is a common error. In one study, 34% of patients with WPW were erroneously diagnosed with myocardial infarction (9). In addition to simulating myocardial infarction, WPW may also mask the EKG abnormalities of acute myocardial infarction. It is difficult to recognize acute myocardial infarction in patients with WPW because preexcitation conceals the Q waves of transmural infarction (10).

Anesthesiologists should be expert at the perioperative care of patients with WPW, as the incidence is 0.25% of healthy patients (1). Patients presenting for elective surgery with a manifest accessory pathway should undergo electrophysiologic evaluation and catheter ablation in the presence of hemodynamically significant symptoms such as syncope, rapid rates of atrioventricular reentrant tachycardia (AVRT), or atrial fibrillation with rapid AV (atrioventricular) conduction during preexcited atrial fibrillation. Patients with WPW presenting for emergency surgery or at low risk of rapid AV conduction require continuation of antiarrhythmic drugs, which may include class IA (procainamide), IC (flecanide), or III (bretylium). The anesthetic should be modified to decrease the release of catecholamines, which may induce supraventricular tachycardias caused by shortening the refractory period and antagonizing the effects of antiarrhythmic drugs. If regional anesthesia is used as it was in our patient, the patient should be well sedated.

For general anesthesia, the anesthetic plan should reduce sympathetic outflow during periods of stress, such as induction and emergence. Ketamine should be avoided, as it may cause sympathetic nervous system stimulation. Pancuronium should be avoided for muscle relaxation because of its sympathomimetic activity, which reportedly caused a supraventricular tachycardia with ventricular rate of 280 bpm in a neonate with WPW (11). Mivacurium is an attractive choice if muscle relaxation is necessary because neither neostigmine nor edrophonium will likely be used; atropine accelerates conduction and shortens refractoriness in accessory pathways (12).

In a study on the effects of halothane, isoflurane, and enflurane on accessory pathway refractoriness in patients with WPW, the authors concluded the drug of choice is enflurane, and the least desirable drug is halothane (13). Although rarely used today, enflurane was believed to be least likely to facilitate tachyarrhythmias because it increases refractoriness without prolongation of the coupling interval (period of vulnerability). Halothane sensitizes the myocardium to catecholamines and increases the coupling interval.

If a patient with WPW develops a regular AVRT, treatment is dictated by the patient's hemodynamic response. If the patient does not tolerate the tachycardia, immediate electrical cardioversion is indicated. If the patient is hemodynamically stable and without symptoms, adenosine 6, 12 ,or 18 mg IV may be given in an attempt to break a reentrant tachycardia. IV verapamil is as effective as adenosine (14); however, because of adenosine's short half-life, adenosine is the preferred antiarrhythmic drug to terminate AVRT. Spontaneous degeneration of regular AVRT to atrial fibrillation in the presence of a manifest accessory pathway occurs in up to 30% of patients. In these instances, the physician should be aware that drugs that slow AV nodal conduction, such as verapamil, digitalis, or even adenosine may be potentially dangerous. Digitalis and verapamil are strictly contraindicated in patients with preexcited atrial fibrillation or atrial flutter with rapid conduction over an accessory pathway (15). In the presence of preexcited atrial fibrillation or atrial flutter with rapid conduction over an accessory pathway, antiarrhythmic class I drugs, such as procainamide, flecanide, or ajmaline (only available in Europe) are the treatments of choice to prolong the refractoriness and conduction of the accessory pathway. In addition, these drugs may terminate atrial fibrillation. In some cases, a combination therapy of a class I antiarrhythmic drug (i.e., procainamide) and a ß-adrenergic blocker (i.e., propranolol) are effective.

This case is an important reminder to anesthesiologists that EKG changes caused by WPW may be confused with a myocardial infarction.


   References
Top
 Introduction
 Case Report
 Discussion
 References
 

  1. Davidoff R, Schamroth CL, Myburgh DP. The Wolff-Parkinson-White pattern in healthy aircrew. Med 1981;52:554–8.
  2. Hollander JE. The management of cocaine-associated myocardial ischemia. J Med 1995;333:1267–72.
  3. Lange RA, Cigarroa RG, Yancy CW, et al. Cocaine-induced coronary artery vasoconstriction. N Engl J Med 1989;32:1157–62.
  4. Togna G, Tempesta E, Togna AR, et al. Platelet responsiveness and biosynthesis of thromboxane and prostacycline in response to in-vitro cocaine treatment. Haemostasis 1985;15:100–7.[Web of Science][Medline]
  5. Marzilli M, Goldstein S, Trivella MG, Palumbo C, Maseri A. Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis a hypothetical pathogenesis. Amer J Cardiol 1980;45:882–6.[Web of Science][Medline]
  6. Goldberger AR. Pseudo-infarct patterns in the Wolff-Parkinson-White Syndrome importance of Q wave-T wave vector discordance. Electrocard 1980;13:115–8.
  7. Siu S, Weyman AE. Left ventricle III: coronary artery disease-clinical manifestations and complications. In: Weyman AE, ed. Principles and practice of echocardiography. Media, PA:Williams & Wilkins, 1994:656–86.
  8. Gazes PC. False-positive exercise test in the presence of the Wolff-Parkinson-White syndrome. Am Heart J 1969;78:13–5.[Web of Science][Medline]
  9. Ruskin JN, Akhtar M, Damato AN, et al. Abnormal Q waves in Wolff-Parkinson-White Syndrome, incidence and clinical significance. JAMA 1976;235:2727–30.[Abstract/Free Full Text]
  10. Grayzel J. Electrocardiographic criteria in the differential diagnosis of pre-excitation (Wolff-Parkinson-White Syndrome) and arteriosclerotic heart disease. N Engl J Med 1958;259:369–74.
  11. Richmond MN, Conroy PT. Anesthetic management of a neonate born prematurely with Wolff Parkinson White syndrome. Anesth Analg 1988;67:477–8.[Free Full Text]
  12. Morady F, Kadish AH, Schmaltz S, et al. Effects of resting vagal tone on accessory atrioventricular connections. Circulation 1990;81:86–90.[Abstract/Free Full Text]
  13. Sharpe MD, Dobkowski WB, Murkin JM, et al. The electrophysiologic effects of volatile anesthetics and sufentanil on the normal atrioventricular conduction system and accessory pathways in Wolff-Parkinson-White syndrome. Anesthesiology 1994;80:63–70.[Web of Science][Medline]
  14. Goy JJ, Fromer M. Antiarrhythmic treatment of atrioventricular tachycardias. Pharmacol 1991;17:S36–40.
  15. Garratt C, Ward D, Antoniou A, Camm AJ. Misuse of verapamil in pre-excited atrial fibrillation. Lancet 1989;1:367–9.[Web of Science][Medline]
Accepted for publication May 5, 1999.





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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1999 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press