inappropriate sinus tachycardia


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'Inappropriate' Sinus TachycardiaDoes the 100 Beats per min Cut-off Matter?Rashmi U Hottigoudar, Rakesh GopinathannairFuture Cardiol.2013;9(2):273-288.Abstract and IntroductionAbstractSinus tachycardia is commonly encountered in clinical practice and when persistent, can result in significant symptoms and impaired quality of life, warranting further evaluation. On the other hand, a growing body of epidemiological and clinical evidence has shown that high resting heart rate (HR) within the accepted normal range is independently associated with increased risk of all-cause and cardiovascular mortality. However, higher HR as a risk factor for adverse cardiovascular outcomes is frequently underappreciated. In this review, we focus on two challenging problems that span the spectrum of abnormally fast sinus HR. The first section reviews inappropriate sinus tachycardia, a complex disorder characterized by rapid sinus HR without a clear underlying cause, with particular emphasis on current management options. The latter section discusses the prognostic significance of elevated resting HR and reviews clinical evidence aimed at modifying this simple, yet highly important risk factor.IntroductionHeart rate (HR) is perhaps the most frequently monitored vital sign and affects medical decision-making in everyday clinical practice. It is a key determinant of myocardial work and metabolic requirements.[1,2] Of the cardiac arrhythmias, sinus tachycardia (ST; sinus rate >100 bpm) is perhaps the most frequently encountered in clinical practice. The evaluation and management of ST involves careful assessment to determine whether tachycardia is an appropriate response to an underlying illness. This appropriate ST can be secondary to a variety of pathological conditions whose discussion is beyond the scope of this article.However, a small proportion of patients, mostly young adults, have marked resting ST without underlying secondary causes or structural heart disease. This can often lead to debilitating symptoms and is referred to as inappropriate ST (IST). IST is an often under-recognized problem with significant morbidity. There is a paucity of knowledge with regards to the pathophysiology of IST and this, along with identifying effective management options, remains an active area of research.Animal studies first noted that increased HR is associated with detrimental vascular effects and decreased survival.[3] Epidemiological, as well as human, clinical trials have provided further evidence for a strong association between elevated HR and adverse cardiovascular outcomes.[410] Over the course of the past few years, high resting sinus HR within the normal range of 60100 bpm has become an exciting area of investigation as more and more data have emerged supporting its role in predicting hard clinical end points,[9,1113] and has led to suggestions that it is time to redefine tachycardia.[14,15] This has resulted in the trial of pharmacological approaches at ameliorating this risk.[16,17] In this review, we focus on the pathophysiology, clinical characteristics, diagnosis and management of IST. We also review the prognostic significance of high resting sinus HR, as well as outcome data on the ability to modify this important clinical variable.ISTClinical VignetteA 29-year-old female with no prior cardiac history presented for evaluation of a 2-year history of palpitations associated with significant nausea, dyspnea and dizziness that were exacerbated with minimal activity. These symptoms started after her second pregnancy and had been progressively worsening over the preceding few months, significantly impairing her quality of life. A 12-lead ECG during an episode of symptomatic palpitations showed a narrow complex tachycardia at 187 bpm. P-wave morphology was difficult to characterize (Figure 1A). Upon gradual slowing of the tachycardia, a second ECG obtained clearly shows p-wave morphology similar to sinus rhythm (Figure 1B), suggestng ST as the culprit rhythm for the patient's symptoms. Total blood count, hematocrit and thyroid function were normal. Extensive evaluation failed to disclose any underlying acute or chronic illness contributing to tachycardia. A transthoracic echocardiogram showed a structurally normal heart. A 24-h Holter monitor revealed an average resting sinus HR of 130 bpm (range: 102213 bpm) (Figure 2).

Figure 1. 12-lead ECG during tachycardia.

(A) 12-lead ECG during tachycardia in the patient presented in the 'Clinical vignette' section. This shows a narrow complex tachycardia with a ventricular rate of 187 bpm and difficult-to-characterize p-waves. (B) Tachycardia gradually slowed without any sudden transition and a second ECG now shows sinus tachycardia (upright p-waves in leads 1, aVL, II, III, aVF, biphasic p-wave in V1 and negative p-wave in lead aVR) at 115 bpm.

Figure 2. Holter monitor showing persistent sinus tachycardia.

A 24-h Holter monitor in the same patient presented in the 'Clinical vignette' section showing an average heart rate of 130 bpm (range: 102213 bpm).Over the past 2 years, the patient had tried lifestyle modification, as well as a variety of pharmacological agents, including -blockers, verapamil, diltiazem and digoxin at maximally tolerated doses without any significant improvement in resting sinus HR or symptoms. An electrophysiology study showed marked increase in sinus rate (from 100 to 170 bpm) with low-dose isoproterenol (2 g/min), with a gradual onset and offset, indicating an automatic mechanism for arrhythmia. No other supraventricular arrhythmias were inducible. The earliest atrial activation during tachycardia was from the high right atrium, near the anatomical location of the sinus node (Figure 3). What management options are available for this young lady with debilitating tachycardia?

Figure 3. Intracardiac ECG recordings during inappropriate sinus tachycardia.

Shown are surface leads II, aVF and V1, and intracardiac recordings from the electrophysiologic diagnostic catheters positioned in the high right atrium, His-bundle region, coronary sinus and right ventricular apex. P-waves are upright in inferior leads and atrial activation sequence is high-to-low (indicated by the arrow line) and similar to normal sinus rhythm. The earliest atrial activation (marked by the star) during tachycardia is recorded on the high right atrial catheter positioned close to anatomical location of sinus node. Stim: Stimulus.The sinoatrial node, the dominant cardiac pacemaker, is a spindle-shaped structure located epicardially at the junction of the superior vena cava and right atrium within the sulcus terminalis. The spontaneous diastolic depolarization of the sinus node pacemaker cells is a result of the interaction of several ion currents (I f , I k , T-type and L-type Ca2+).[18] The normal rate of sinus node depolarization is 6090 bpm. However, it is very dynamic and is modulated by autonomic tone, temperature, hypoxia, blood pH and hormonal influences. ST (HR >100 bpm) can be an appropriate or an inappropriate response to physiologic, pathologic or pharmacological triggers ().[19] Box 1. Common causes of sinus tachycardia. Fever Hypovolemia Hypoxia Infection/sepsis Anxiety Hyperthyroidism Pheochromocytoma Anemia Pulmonary embolism Myocardial ischemia/infarction Heart failure Chronic osbstructive pulmonary disease Stimulant drugs: Nicotine Alcohol Caffeine Salbutamol Aminophylline Atropine Catecholamines Illicit drugs: Amphetamines Cocaine Ecstasy Cannabis Anticancer drugs: Anthracycline compounds: Doxorubicin Daunorubicin

IST, a nonparoxysmal tachyarrhythmia, was originally described in 1939 by Codvelle and Boucher as a case of a healthy young adult man with a resting HR in the range of 160 bpm for more than 2 years.[20] In 1941, Wising reported a clustering of unexplained persistent ST of very long duration in a family of four members.[21] Bauernfeind et al., in 1979, performed electrophysiolgical studies on seven patients with IST and showed that a high-to-low right atrial activation sequence and atrial pacing neither terminated nor affected the tachycardia cycle length.[22] These findings suggested increased sinus node automaticity as the arrhythmia mechanism. In addition, HR response to pharmacologic autonomic blockade suggested an underlying defect either in the sympathetic or vagal nerve control of resting sinus HR, with or without an abnormality of intrinsic HR.[22] The sympathovagal influence in IST was further explored by Morillo et al. in 1994 who proposed that IST was characterized by high intrinsic HR, depressed efferent cardiovagal reflex and -adrenergic receptor hypersensitivity.[23] Over the years, this clinical entity has intrigued clinicians and researchers alike, and remains an active area of investigation to this day.IST is characterized by a persistent increase in resting sinus HR out of proportion to physiological or pathological stress. It is a diagnosis of exclusion and, hence, the patient needs to be evaluated for secondary causes of ST, such as endocrinopathies, hypovolemia, anemia, infection, autonomic dysfunction, orthostatic hypotension and drug effects (Box 1).[19] IST is predominantly seen in young adult females in their second to fourth decade of life and commonly in healthcare professionals.[19] Less frequently, the dysrhythmia is also encountered in elderly patients.[24] PathophysiologyThe pathophysiology of IST is complex and not well understood. Experimental and clinical studies have shown multiple pathophysiological mechanisms in IST. It is generally accepted that the pathogenesis of IST is multifactorial, with the principal mechanism potentially being enhanced intrinsic sinus node automaticity potentiated by altered sympathovagal balance. Other contributing mechanisms may include -adrenergic hypersensitivity, M2 anticholinergic hyposensitivity, abnormal barore


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