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The diagnosis of Wolff-Parkinson-White syndrome is typically reserved for patients who experience ventricular pre-excitation and symptoms that are related to paroxysmal supraventricular tachycardia, such as chest pain, dyspnea, dizziness, palpitations, or syncope. Herein, we report the case of a 38-year-old woman who presented at our outpatient department because of exercise intolerance. Cardiac auscultation revealed a grade 2/6 pansystolic murmur over the left lower sternal border. Twelve-lead electrocardiography showed sinus rhythm at a rate of 76 beats/min, with a significant delta wave. Transthoracic echocardiography revealed abnormal left ventricular systolic function. The results of a thallium stress test were also abnormal. Coronary artery disease was suspected; however, coronary angiography yielded normal results. Electrophysiologic study revealed a para-Hisian Kent bundle and a dual atrioventricular nodal pathway. After radiofrequency catheter ablation was performed, the patient's left ventricular function improved and her symptoms disappeared.
In Wolff-Parkinson-White syndrome, left ventricular systolic dyssynchrony can yield abnormal findings on echocardiography and thallium scanning—even in persons who have no cardiovascular risk factors. Physicians who are armed with this knowledge can avoid performing coronary angiography unnecessarily. Catheter ablation can reverse the dyssynchrony of the ventricle and improve the patient's symptoms.
Wolff-Parkinson-White (WPW) syndrome is characterized by the presence of an accessory pathway. This pathway, when fused with the atrioventricular node, can lead the electrical stimulus from the atrium directly to the ventricle. Some studies have reported the finding of myocardial dyskinesia—on echocardiography1 and on nuclear cardiac stress tests2—in segments that have been precociously activated by the accessory pathway. Herein, we report the case of a 38-year-old woman with a para-Hisian Kent bundle who presented with exercise intolerance.
In October 2008, a 38-year-old woman presented at our outpatient department with progressive chest tightness, dyspnea, and dizziness, all of which had progressively worsened over 2 to 3 years and were exacerbated by exercise. She did not have hypertension, diabetes mellitus, or dyslipidemia. She had experienced no chest trauma or relevant disease and did not smoke or use cocaine. She reported no family history of premature coronary artery disease. On physical examination, she was in no outward distress. Her body temperature was 36.6 °C; heart rate, 89 beats/min; respiratory rate, 18 breaths/min, and blood pressure, 108/81 mmHg. Cardiac auscultation revealed a grade 2/6 pansystolic murmur over the left lower sternal border. Other physical findings were unremarkable. Laboratory tests, including troponin I, renal function, arterial blood gas, and coagulation, were all within normal ranges. Twelve-lead electrocardiography showed sinus rhythm (heart rate, 76 beats/min) with a significant delta wave (Fig. 1). M-mode echocardiography revealed global hypokinesia of the left ventricle (LV) and an ejection fraction of 0.40 (Fig. 2). Thallium myocardial scintigraphy revealed moderate, completely reversible perfusion defects at the anterior-to-apical wall of the LV. Coronary artery disease was suspected; however, diagnostic coronary angiography yielded normal results. Electrophysiologic study revealed a para-Hisian Kent bundle and a dual atrioventricular node. Radiofrequency catheter ablation was successfully performed. Five months after the procedure, TTE revealed normal LV function and an ejection fraction of 0.55 (Fig. 3). The patient was free of symptoms, and she remained well upon outpatient monitoring 12 months after the procedure.
The prevalence of an accessory pathway in the general population is reported to be 0.1% to 0.3%.3 In manifest WPW syndrome, paroxysmal supraventricular tachycardia is the most common arrhythmia. In WPW syndrome, the ventricles are electrically and mechanically pre-excited through an accessory pathway that connects the atria and ventricles, resulting in interventricular asynchronous contraction of the LV (due to an asynchronous spread of ventricular depolarization) and systolic dysfunction. In the mid-1970s, echocardiography in patients with WPW syndrome displayed an abnormal interventricular septal motion that was due to right septal or posteroseptal accessory pathways; in contrast, left-sided accessory pathways resulted in abnormal LV posterior wall motion.4,5 In particular, the presence of abnormal interventricular septal wall motion may provoke LV dyssynchrony and dysfunction.6
Individuals can have the accessory pathway but never experience tachycardia or any other symptoms of a WPW pattern. If symptoms do occur, they are related to the development of an irregular heart rhythm and a rapid heart rate. During tachycardia, palpitations, dizziness, lightheadedness, fainting, or, rarely, sudden death may occur. Fortunately, the incidence of sudden death in persons who have WPW syndrome is quite low, ranging from 0 to 0.39% per year.7
The treatment choices in WPW syndrome depend on the kind of arrhythmias, their frequency, and associated symptoms (if any). Options include observation, medication, electrical cardioversion, catheter ablation, or surgical intervention. In our patient, the diagnosis of WPW syndrome was well established by means of electrophysiologic study. After radiofrequency catheter ablation, her LV function improved and her symptoms disappeared.
In WPW syndrome, LV systolic dyssynchrony can yield abnormal findings on echocardiography and thallium scanning—even in persons who have no cardiovascular risk factors. Accordingly, physicians who are armed with this knowledge can avoid performing coronary angiography unnecessarily. Catheter ablation can reverse the dyssynchrony of the ventricle and improve the patient's symptoms.
Address for reprints: Wei-Shiang Lin, MD, Department of Medicine, Division of Cardiology, Tri-Service General Hospital, No. 325, Sec. 2, Cheng-Kung Rd., Neihu, Taipei 114, Taiwan, ROC