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Asymptomatic Nonsustained Ventricular Tachycardia During Routine Stress Echocardiography*

From the Department of Cardiology (Drs. Tavel and Olson), The Care Group, Indianapolis, IN; and the Department of Cardiology (Drs. Dixit and Callans), University of Pennsylvania Health System, Philadelphia, PA.

Correspondence to: Morton Tavel, MD, FCCP, 833 Naab Rd, Ste 400, Indianapolis, IN 46260

Key Words: hypertrophic cardiomyopathy • stress test • tachycardia • ventricular

	Introduction

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An asymptomatic, 54-year-old man was referred by his primary care physician for a treadmill stress echocardiogram. He had been asymptomatic from a cardiovascular standpoint. He denied chest pain, dizziness, syncope, shortness of breath, or palpitations. He occasionally has a "pulling sensation" in his chest related to positional changes but not exertion. He had a 30-year history of type I diabetes mellitus treated with subcutaneous insulin. He was recently started on simvastatin, and his only other medication was aspirin. He has a strong family history of diabetes mellitus and coronary artery disease (CAD) but no family history of sudden cardiac death (SCD). The patient remains active, is normotensive, and is not overweight. The treadmill stress echocardiogram was ordered for routine screening of CAD. Baseline ECG showed normal sinus rhythm, Q waves in leads V₁ and V₂, and nonspecific T wave changes in the lateral leads. Several episodes of nonsustained ventricular tachycardia (NSVT) developed; the longest run was 25 beats (50 beats/min) during the terminal portion of the stress test. The tachycardia had a left bundle-branch block morphology with a monophasic R wave in II, III, and aVF. The R wave transition point was in lead V₃ on the precordial leads. The rhythm was asymptomatic, resolved spontaneously, and did not occur at rest. Also, the patient showed good exercise tolerance (achieving a workload of 13 metabolic equivalents), experienced no symptoms, had a normal BP response, and showed no change in baseline ST segments. The resting echocardiogram showed a congenital bicuspid aortic valve, normal left ventricular function without segmental wall motion abnormalities, increased septal thickness (1.9 cm) without dynamic outflow obstruction, and a trace of mitral regurgitation. The stress echocardiogram showed no stress-inducible wall motion abnormalities and no ventricular dilatation.

The physical examination revealed a resting BP of 118/60 mm Hg and a heart rate of 70 beats/min. The cardiac examination disclosed normal first and second heart sounds, a fourth heart sound, and a short I/VI systolic ejection murmur along the left sternal border. Peripheral pulses were equal and symmetrical. There were no carotid bruits. Lung fields were clear, and the abdomen was unremarkable. Pertinent laboratory values included hemoglobin AIc, 8.1%; total cholesterol, 196 mg/dL; low-density lipoprotein, 107 mg/dL; high-density lipoprotein, 38 mg/dL; triglycerides, 256 mg/dL; BUN, 22 mg/dL; creatinine, 0.9 mg/dL; and potassium, 4.7 mmol/L.

	Questions for Consultants

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1. How would you proceed with further workup of this arrhythmia?
   
2. Given that the stress echocardiogram was unremarkable, would you proceed with a coronary angiogram to evaluate the NSVT?
   
3. Is the patient at risk for sudden death?
   
4. Would you add treatment with a ß-blocker?
   
5. Do you have any additional thoughts about this case?
   

	Response of Consultants

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Sanjay Dixit, MD, and David J. Callans, MD, University of Pennsylvania, Philadelphia, PA

This is the case of a 54-year-old man with long history of diabetes mellitus (reasonably controlled) and hyperlipidemia who underwent treadmill stress echocardiography to evaluate for the presence of CAD, during the course of which asymptomatic NSVT developed. The stress test, however, did not reveal any evidence for reversible ischemia (no ECG changes and/or wall-motion abnormalities), precluding the need for additional workup, although coincidental septal thickening was noted on echocardiogram that may explain the nonspecific T wave changes seen on baseline ECG.

The above description is fairly typical for outflow tract tachycardia, which is a subcategory of idiopathic ventricular tachycardia (VT) that is typically seen in patients with structurally normal hearts. In the majority of cases (approximately 85%), the site of origin of these tachycardias is from the superior aspect of the right ventricular outflow tract (RVOT) under the pulmonic valve, although less frequently they can also originate from the endo/epicardium of basal left ventricular (LV) and/or the aortic cusps. Mechanistically, these arrhythmias result from delayed after-depolarization-mediated triggered activity, which for reasons still unclear tends to cluster along the superior/septal aspect of the RVOT region, the bordering aortic valve cusps/LV epicardium, as well as the endocardium along the superior aspect of basal LV cusps (septum, aortomitral continuity and superior aspect of mitral valve). This narrow anatomic distribution results in characteristic ECG manifestations that comprise of an inferiorly directed axis (monophasic R waves in leads II, III, and aVF) with either a left bundle-branch block morphology (QS or rS pattern in lead V₁ for RVOT VT) or a right bundle-branch block morphology (R or Rs pattern in lead V₁ for basal LV VT). In addition to the above ECG features, subtle variations in the morphology of VT complexes in lead I, the presence or absence of notching in inferior leads, and early vs late precordial transition patterns can further help in accurately localizing the exact site of origin.

These arrhythmias are typically not life threatening, and treatment is directed primarily at achieving symptomatic relief. The most common symptom is palpitation with or without dizziness together with runs of ventricular premature beats (isolated or couplets) and short NSVT. Sustained VT is infrequently observed, and syncope is rare. ß-Blockers and calcium-channel blockers either alone or in combination are the initial agents of choice and can achieve symptomatic relief in 50 to 70% of patients. Other antiarrhythmic agents such as procainamide, flecainide, or sotalol are also quite efficacious. Lidocaine has also been shown to be effective in terminating these arrhythmias but is typically reserved for acute treatment of sustained symptomatic VT episodes. Radiofrequency ablation is another option especially since it can permanently cure the tachycardia in the majority ( 90%) of cases. This is typically offered to patients who have failed and/or are intolerant to antiarrhythmic agents. Implantable cardioverter defibrillators are generally not indicated for this group of patients unless they manifest structural heart disease (LV ejection fraction of 0.35) in association with syncope and/or CAD.

	Follow-up Information and Additional Comments

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Because the patient was asymptomatic and had no evidence of ischemia on either ECG or echocardiography, the NSVT was believed to be nonischemic in nature. We concluded that there was no need for additional evaluation for obstructive CAD. The ECG was consistent with RVOT tachycardia and was not believed to be secondary to ischemia or hypertrophic cardiomyopathy (HCM). The septal hypertrophy was thought to be coincidental and believed not to be related to the NSVT. There was no evidence for subaortic obstruction (ie, no subaortic pressure gradient or systolic anterior motion of the anterior mitral leaflet) on the echocardiogram.

The patient did have several risk factors for significant CAD; therefore, he was referred to an endocrinologist for improved glycemic control. In addition, we added an angiotensin-converting enzyme inhibitor to help prevent the progression of diabetic nephropathy. Follow-up laboratory assessment revealed excellent results with a total cholesterol of 110 mg/dL, low-density lipoprotein of 53 mg/dL, high-density lipoprotein of 51 mg/dL, and triglycerides of 32 mg/dL. His hemoglobin A1c also improved to 7.4%. The patient has remained asymptomatic and remains physically active.

This case presents three important problems confronting physicians evaluating patients for CAD: (1) When should an asymptomatic patient be evaluated with an exercise stress test to detect CAD? (2) How should one proceed when an asymptomatic exercised-induced NSVT with normal systolic function is identified? (3) When do we become concerned about HCM?

Current American College of Cardiology/American Heart Association guidelines state that there is no class I indication for screening asymptomatic patients.¹ Screening asymptomatic individuals without risk factors and those who are not planning to start a vigorous training program was given a class III indication, meaning it should not be performed. Therefore, routine screening of patients with multiple risk factors for CAD remains somewhat controversial. In the case described above, the indication to perform a stress test in this patient would be classified as IIb, meaning it is controversial and the efficacy of performing a treadmill stress test in such a patient has not well established. The patient has had diabetes mellitus for > 30 years and has a family history of CAD. Diabetic patients are somewhat unusual because they may not have classic symptoms of angina. Stress testing is not contraindicated to evaluate for obstructive CAD, but the predictive value in this population is unknown.

The second issue about how to proceed with the evaluation of a patient with asymptomatic NSVT should be evaluated. The importance of this question arises from the fact that NSVT may be associated with an increased risk of SCD. The goal of further workup is to identify those patients at risk for SCD so that appropriate therapy can be initiated. The first objective should be to identify structural heart disease (LV dysfunction, valvular heart disease, and ventricular hypertrophy). In the absence of structural heart disease, NSVT carries a relatively low risk of SCD.² NSVT in this setting is typically due to one of two things: ischemia or idiopathic VT. In a study³ of healthy volunteers without structural heart disease, NSVT was found in approximately 1% of subjects and did not predict a worse outcome at 2 years. In patients with suspected CAD, NSVT was associated with a slightly increased risk but was not as strong a predictor as wall motion abnormalities by echocardiography.⁴ The second objective is to evaluate the morphology of the NSVT on 12-lead ECG. If the ECG findings are typical for RVOT or LV outflow tract VT, as outlined by our consultants, the patient has a low risk of SCD. The NSVT in our case described above was consistent with RVOT VT.

Finally, there was echocardiographic evidence for nonobstructive HCM. In the United States, HCM has an occurrence rate of 1:500 in the adult population. The risk of SCD in this population is < 3%⁵; however, a subset of patients have a significantly increased risk. Patients are considered at high risk if they have experienced cardiac arrest, a family history of sudden death, or sustained VT. NSVT is considered a minor risk factor, and the focus of the arrhythmia is typically different than RVOT or LV outflow tract arrhythmias. Other minor risk factors include severe (> 3 cm) septal hypertrophy, a drop in systolic BP with exercise, unexplained syncope, LV outflow obstruction, and microvascular obstruction. Patients with echocardiographic evidence for HCM should be screened for increased risk of SCD by having a 24-h Holter monitor to assess for NSVT and by following up the hypertrophy with a repeat echocardiogram every 5 years. NSVT on Holter monitoring is considered significant if it occurs on two separate occasions 6 months apart or if one episode lasts > 10 beats. These designations have been arbitrarily set, and validity is uncertain. In this particular case, the NSVT was characteristic for RVOT VT and was unrelated to the septal hypertrophy. We plan to follow up this patient with periodic echocardiograms to assess for progression.

	Footnotes

 
Abbreviations: CAD = coronary artery disease; HCM = hypertrophic cardiomyopathy; LV = left ventricular; NSVT = nonsustained ventricular tachycardia; RVOT = right ventricular outflow tract; SCD = sudden cardiac death; VT = ventricular tachycardia

Received for publication March 3, 2005. Accepted for publication June 9, 2005.

	References

TOP Introduction Questions for Consultants Response of Consultants Follow-up Information and... References

 

1. Gibbons, RJ, Balady, GJ, Bricker, JT, et al (2002) ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). Am Coll Cardiol 40,1531-1540[Free Full Text]
2. Lin, D, Callans, DJ Nonsustained VT during exercise testing: causes and work-up. Am Coll Cardiol Curr J Rev 2003;,Nov/Dec; 57–60
3. Fleg, JL, Lakatta, EG Prevalence and prognosis of exercise-induced nonsustained ventricular tachycardia in apparently healthy volunteers. Am J Cardiol 1984;54,762-764[CrossRef][ISI][Medline]
4. Elhendy, A, Chandrasekaran, K, Gersh, BJ, et al Functional and prognostic significance of exercise-induced ventricular arrhythmias in patients with suspected coronary artery disease. Am J Cardiol 2002;90,95-100[CrossRef][ISI][Medline]
5. Cannon, RO, III Assessing risk in hypertrophic cardiomyopathy. N Engl J Med 2003;349,1016-1018[Free Full Text]

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