inappropriate sinus tachycardia

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inappropriate sinus tachycardia2016-11-08T06:30:02+00:00

inappropriate sinus tachycardia


A cardiopathy in which the sinus heart rate is inexplicably faster than expected and accompanied by tachycardic symptoms. The heart rate at rest, even in a supine position, can exceed 100 beats/min, a rate that is rapidly and substantially increased with minimal activity, thus restricting these patients’ physical activity.

Mechanism Unknown

DiffDx Appropriate sinus tachycardia, postural orthostatic tachycardia syndrome (overlap may occur).

Prognosis Long-term outcome seems benign

Management Treatment may be unnecessary, or require no more than exercise and training. For patients with severe symptoms, therapies include pharmaceuticals–e.g., β-adrenergic blockers, a first-line therapy, which may prove ineffective, as may other medications. Rarely, catheter- or surgically- based right atrial or sinus node modification may be effective, at the risk of limited efficacy and potential complications.

Reference J Am Coll Cardiol. 2013;61(8):793-801.


inappropriate_sinus_tachycardiaImage and caption taken directly from J Am Coll Cardiol. 2013;61(8):793-801.

Heart Rate Control via the Autonomic Nervous System

Predominant (not all-inclusive) regulators of the sinus rate are depicted. Sinus node activation is under the control of various cellular currents, including IKAch, If, INaCa, IKr, and the L-type calcium (Ca2+) channel, among others, regulated in part via G protein modulation (G). Additionally, the so-called calcium clock, involving ryanodine receptor (RyR) Ca2+ release from the sarcoplasmic reticulum (SR), has an important role in sinus rate determination. Further regulation and modulation of rate (particularly at rest) involves parasympathetic activation via acetylcholine (Ach) and nitric oxide (NO), in part via nitric oxide synthase (NOS). Parasympathetic nerve activation affects the muscarinic (M2) receptor via Ach and works by affecting intracellular cyclic GMP (cGMP) and cyclic AMP (cAMP) in part. Sympathetic activation stimulates β-1 receptors via norepinephrine to increase cAMP. Both limbs of the autonomic nervous system are regulated and interact at multiple levels, including the central nervous system and peripheral nerve terminals. There are multiple checks and balances throughout the entire regulatory system and, despite the simplifications shown here, they are extraordinarily complex. Presently, it is not clear what part(s) of the system is the predominant driver of increased rates in inappropriate sinus tachycardia. IKr = delayed rectifier K+ current; If = funny current; INaCa = sodium/calcium exchange current; NE = norepinephrine; + = stimulates; − = inhibits.Calcium clocks and cellular membrane voltage, driven by β-adrenergic sympathetic nervous system activation or extrinsic catecholamines, can be blocked, in part, by If blockade.

Although several drugs and ions can block the If current, their effects are nonspecific. Other If blockers have been developed, but only ivabradine is available commercially. Subsidiary pacemakers, residing in the superior portion of the sinus node, are activated by sympathetic stimulation such that a depolarizing shift in the If activation curve, a potentiation of ICa-L, a potentiation of IK, a hyperpolarized shift in IK activation curve, an acceleration of the deactivation of IK, and a potentiation of IST occur.Although phasic vagal (parasympathetic) activation supersedes sympathetic activation (called accentuated antagonism), tonic sympathetic activation overshadows intermittent vagal activation. Catecholamine excess or sympathetic activation, with or without vagal inhibition, could cause IST.

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