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A 74-year-old man with a history of hypertension, hyperlipidemia, and obstructive sleep apnea presented to his primary care physician for his annual examination. His only symptom was palpitations that started 6 months previously. The palpitations had been occurring several times per day, lasting only a few seconds on each occasion. They were not associated with activity or any particular time of the day. He had no other associated symptoms, including dyspnea, angina, or syncope. He reported no alcohol use and drank one cup of coffee daily. His medications included aspirin, losartan, hydrochlorothiazide, and simvastatin.
On examination, the patient was afebrile. His blood pressure was 142/70 mm Hg, and his pulse rate was 60 beats/min. Cardiovascular examination revealed a nondisplaced point of maximal impulse and irregular rhythm with frequent premature beats. Heart sounds were normal, no murmurs were heard, and jugular venous pressure was not elevated. The lungs were clear on auscultation bilaterally. His abdomen was soft and not distended, and no peripheral edema was noted.
Laboratory studies yielded the following results (reference ranges shown parenthetically): hemoglobin, 14.4 g/dL (13.5-17.5 g/dL); leukocytes, 7.0 × 109/L (3.5-10.5 × 109/L); platelet count, 184 × 109/L (150-450 × 109/L); potassium, 4.5 mmol/L (3.6-5.2 mmol/L); magnesium, 2.2 mg/dL (1.7-2.3 mg/dL); and thyrotropin, 1.6 mIU/L (0.3-5.0 mIU/L).
Electrocardiography (ECG) was performed to further investigate his palpitations (Figure).
Atrial fibrillation is an irregularly irregular rhythm with an absent P wave and a narrow QRS complex. The QRS complex on this patient's ECG was wide, which would only occur in atrial fibrillation if the electrical impulse was conducted aberrantly, ie, through an antegrade conducting accessory pathway or in the setting of bundle branch block (BBB). The American College of Cardiology/American Heart Association define NSVT as 3 or more wide QRS complexes, originating from the ventricles at a rate of more than 100 beats/min, that terminates spontaneously in less than 30 seconds.1 This would be the most likely cause of this patient's palpitations. Patients with panic disorder often, but not always, have palpitations. The diagnosis is usually made on the basis of a thorough history and psychiatric evaluation. In this patient, panic disorder would be a diagnosis of exclusion after organic causes were excluded. Patients with mitral valve prolapse may have palpitations. This diagnosis is confirmed via echocardiography, and ECG abnormalities may be absent. Atrioventricular nodal reentrant tachycardia is the most common form of regular supraventricular tachycardia. In atrioventricular nodal reentrant tachycardia, the ECG shows a narrow, complex, regular QRS configuration.
The patient's ECG demonstrated 4 wide complex beats at a rate of 150 beats/min without P waves, consistent with NSVT. This was followed by a slower wide complex idioventricular rhythm changing to a narrow complex rhythm with P waves for each QRS complex, consistent with sinus rhythm. Palpitations are a common, nonspecific symptom. They can be benign or associated with life-threatening arrhythmias. In this patient, the absence of syncope or presyncope, which would be concerning for hemodynamic instability, is reassuring. The patient was referred to the outpatient cardiology clinic for further evaluation and management later that day.
The presence of wide complex tachycardia on ECG is concerning for life-threatening arrhythmia such as sustained ventricular tachycardia (VT). Further evaluation is needed to identify the frequency and duration of the patient's rhythm disturbances as well as their etiology and any contributing factors. An external event recorder is useful in patients with paroxysmal symptoms to evaluate for an occult rhythm abnormality. In our patient, arrhythmia has already been documented, so an event recorder would have limited usefulness. A stress test is helpful in evaluating for exercise-induced ischemia. It can also determine whether an arrhythmia is exacerbated with exertion. If the patient had runs of sustained VT, this would be detected as well. Although VT associated with ischemia would more typically be polymorphic than monomorphic, in this patient with multiple cardiac risk factors, it is important to evaluate for ischemia and to further characterize the nature of his arrhythmia. A stress test is a reasonable method of obtaining this information and should be performed next. Coronary angiography is the criterion standard for the diagnosis of coronary artery disease as well as hemodynamic evaluation. However, more evidence of ischemia, such as a positive stress test result, would be prudent before performing such an invasive procedure. Although echocardiography would be useful in determining cardiac function as well as evaluating for structural heart disease, it cannot detect ischemia. Echocardiography would be helpful in this patient, but a stress test should be performed first. A 24-hour Holter monitor can provide evidence of the extent of the patient's NSVT. It would also identify any sustained ventricular arrhythmia, which would change management in this patient. Although Holter monitoring should be obtained in this patient, an ischemic etiology should be ruled out first.
The patient underwent an exercise sestamibi scan, which was negative for stress-induced ischemia. He had exercise-induced NSVT of up to 8 beats. Subsequent echocardiography showed a left ventricular ejection freaction of 62%. The patient underwent 24-hour Holter monitoring. The device recorded 94,083 total beats, 22,080 of which (23%) were ventricular beats. There were 119 runs of VT; the longest run was 6 beats.
It is important to determine the underlying etiology of this patient's NSVT so that the correct treatment can be initiated. Nonsustained VT is commonly caused by structural or electrochemical abnormalities of the heart or in the setting of major stress such as recent heart manipulation or MI.
Cardiac arrhythmia can often present as a late manifestation of CHD, sometimes many years after diagnosis. The underlying cause is thought to be multifactorial, including structural abnormalities, longstanding abnormal cardiac hemodynamics, and fibrosis from corrective surgeries.2 Our patient has no history of CHD, no signs of structural abnormalities on echocardiography, and no history of cardiac surgery.
Brugada syndrome is caused by a sequence variation in cardiac sodium channels. There is no associated structural abnormality. It leads to an increased risk of sudden cardiac death (SCD), and patients who have had syncope or documented arrhythmia should be referred for placement of an implantable cardioverter-defibrillator. It is characterized by a pseudo right BBB pattern on ECG with persistent ST elevation in leads V1 through V3. This pattern was not evident on our patient's ECG.
Nonsustained VT often occurs in patients experiencing an acute MI. It is usually due to abnormal automaticity in the peri-infarct region and is most common within the first 48 hours. However, our patient has no evidence of ischemia. It is commonly seen in patients with CHF and is thought to be associated with increased mortality in patients with ischemic and hypertrophic cardiomyopathy. Our patient had no echocardiographic signs of CHF. In the absence of ischemia, any structural heart disease, or electrochemical abnormality, the most likely cause of this patient's arrhythmia is a focal ectopy causing episodic NSVT and premature ventricular contractions (PVCs). The monomorphic nature of the ectopy further supports a single focus of automaticity. In our patient, the QRS morphology showed an inferior axis, right BBB, and a predominant R wave in leads II, III, aVF, and V1 through V6, suggesting a focus in the left ventricular outflow tract.
Many patients with palpitations related to NSVT can be treated with medical management and achieve resolution of their symptoms. Others may require invasive treatment, but barring contraindications, conservative therapy should be attempted first. Metoprolol is a cardioselective β-blocker used in the treatment of hypertension, coronary artery disease, and CHF. It acts by antagonizing the β1-receptors and inhibiting sympathetic activation of the heart. It is an effective treatment to reduce symptoms in patients with palpitations related to NSVT and would be the first choice in our patient.
Flecainide is a class IC antiarrhythmic that acts by binding the intracellular portion of voltage-gated sodium channels. This causes a decrease in cardiac electrical conductivity. Flecainide is effective in suppressing ventricular arrhythmias; however, the Cardiac Arrhythmia Suppression Trial3 showed that early after MI, it caused an increase in mortality. Until ischemia is ruled out, class IC antiarrhythmics are contraindicated. If ischemia and structural heart disease are excluded, it could be used with caution. Radiofrequency ablation for monomorphic NSVT originating from the right ventricular outflow tract, as seen in our patient, has been shown to be effective in 75% to 100% of patients.4 There is limited long-term data regarding recurrence. An initial trial of medical therapy would be reasonable before contemplating ablation in this patient. Amiodarone is a class III antiarrhythmic that acts by inhibiting potassium channels and thus prolonging repolarization. Amiodarone has several highly active metabolites and is effective in suppressing ventricular ectopy. It has a significant adverse effect profile including pulmonary fibrosis and thyroid dysfunction, making it a less attractive therapeutic option.
Placement of an AICD has been shown to reduce mortality when compared with optimal medical management by preventing SCD in certain groups of patients with cardiomyopathy or life-threatening ventricular arrhythmias. Based on the available clinical data, there is no evidence to suggest that our patient would benefit from AICD implantation at this time.
Oral metoprolol tartrate, 25 mg twice daily, was prescribed for palpitations associated with NSVT.
Aside from palpitations, the patient is completely asymptomatic without syncope, light-headedness, or signs of CHF. However, given his frequent PVCs and NSVT, there is a potential for development of tachycardia-induced cardiomyopathy. Close follow-up would allow early detection of any deterioration in his cardiac function and would be reasonable in this case. Repeated ECG is unlikely to be useful because the arrhythmia has already been diagnosed. It does not provide information regarding the frequency of his ectopy or his cardiac function. 24-Hour Holter monitoring would provide insight into the patient's ectopy and whether his NSVT has changed in frequency or duration. However, in order to detect any deterioration of cardiac function from possible tachycardia, an imaging study such as echocardiography is also required. A stress test would help evaluate for coronary artery disease; however, development of new ischemia is unlikely in such a short time interval. A stress test would detect whether the arrhythmia is exacerbated by exertion, but this could also be inferred from 24-hour Holter monitoring, and exacerbation was not observed on his previous stress test.
Premature ventricular contractions and NSVT are common cardiac rhythm disturbances that are frequently seen in clinical practice. They occur when a focus of automaticity causes premature depolarization in the ventricle. When found incidentally, they are often considered benign; however, the presence of such ectopy can be associated with increased risk of SCD, can be a sign of underlying cardiomyopathy, or in severe cases can lead to tachycardia-induced cardiomyopathy. One study found a greater than 50% prevalence of PVCs among healthy subjects, while the prevalence of NSVT was 2%.5 Primary care physicians should be familiar with the presenting signs and symptoms, know when further workup and treatment are indicated, and understand which patients are at increased risk of mortality.
Nonsustained VT can be monomorphic, suggesting that it emanates from a single focus, or polymorphic. It is common after cardiac injury such as MI, especially if an arrhythmogenic focus, such as a fibrin scar, is present. It can also occur in structurally normal hearts and in patients with hypertrophic or dilated cardiomyopathy. Obstructive sleep apnea has been associated with increased frequency of NSVT and other cardiac dysrhythmias.6 Some studies have shown improvement after treatment with nocturnal positive pressure ventilation; however, NSVT has not been shown to be associated with increased mortality in this population.7
Nonsustained VT is often asymptomatic, but some patients may experience palpitations, light-headedness, chest pain, or dyspnea. In asymptomatic patients, NSVT is often discovered incidentally when frequent premature beats are noted on routine physical examination or when a baseline ECG is obtained. In symptomatic patients with infrequent symptoms, a loop recorder may be useful to obtain ECG data during an episode. In patients with frequent NSVT, 24-hour Holter monitoring is helpful to evaluate for sustained VT as well as to quantify the number of ventricular premature beats. In such cases, the sites of origin as well as the frequency of ventricular ectopy are important because they may be useful for prognosis and in determining which patients will have progression to cardiomyopathy. One study showed that a focus originating in the right ventricular outflow tract was much more common than in the left ventricular outflow tract, as occurred in our patient.8 The authors also noted that a high burden of PVCs and right ventricular origin may be associated with a higher risk of cardiomyopathy. This can be important information because frequent NSVT can be an uncommon cause of cardiomyopathy and CHF.9 This is considered to be a reversible cause of heart failure inasmuch as patients who undergo radiofrequency ablation have been shown to regain systolic function.10 These patients must be distinguished from those with primary cardiomyopathies causing secondary arrhythmias. It is therefore helpful to document baseline systolic function on presentation.
The mainstays of NSVT treatment are medical management with β-blockers or, in refractory cases, with radiofrequency ablation. Rarely, antiarrhythmic drugs can be used. When NSVT is found, it is important to rule out associated structural heart disease that would put the patient at increased risk for SCD, such as ischemic, dilated, or hypertrophic cardiomyopathy. Such patients should be considered for AICD implantation. Primary prevention of SCD with AICD implantation is often a complex decision but is usually indicated in patients with hypertrophic cardiomyopathy who have at least 2 of 5 high-risk features: (1) maximum left ventricular wall thickness greater than 30 mm, (2) personal history of ventricular arrhythmias, (3) unexplained syncope in the past 6 months, (4) exertional hypotension, and (5) family history of sudden death. In patients with only 1 of these 5 risk factors, the risks vs benefits of AICD implantation are much more problematic. Several large studies have shown a mortality benefit in patients with ischemic cardiomyopathy and a reduced left ventricular ejection fraction, including the Multicenter Automatic Defibrillator Implantation Trials I11 and II12 and the Sudden Cardiac Death in Heart Failure Trial.13 The American College of Cardiology/American Heart Association guidelines from 2006 contain a class IA recommendation for AICD implantation to prevent SCD in such patients.1
Premature ventricular contractions and NSVT are common clinical entities. Stress testing and echocardiography in addition to a careful history and physical examination are useful investigations for risk stratification. If the results of these investigations are reassuring, patients can frequently be managed conservatively with medical therapy.
See end of article for correct answers to questions.
CORRECT ANSWERS: 1. b. 2. b. 3. e. 4. a. 5. d