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Idiopathic Ventricular Tachycardia
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Jackson J. Liang, David S. Frankel
Long-term medical management Calcium channel blockers are most effective, followed by beta blockers and potassium channel blockers. Sodium channel blockers are least effective.
Antiarrhythmic Drugs
Published in Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 2, 2017
Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod
The sodium channel blockers exert their effects by blocking fast Na+ channels, therefore reducing the influx of Na+ into cardiac myocytes and increasing the time it takes the cell to reach threshold potential. By doing this they decrease the slope of Phase 0 of the AP and decrease cardiac conduction velocity. For this reason, they are effective at abolishing reentrant arrhythmias. These fast Na+ channels are not found in nodal tissue, where Phase 0 depolarisation results from the influx of Ca2+ ions.
Development of palliative medicine in the United Kingdom and Ireland
Published in Eduardo Bruera, Irene Higginson, Charles F von Gunten, Tatsuya Morita, Textbook of Palliative Medicine and Supportive Care, 2015
Systemic administration of sodium channel blockers may be analgesic. Â 29 Intravenous lidocaine at a dose between 1 and 4mg/kg infused over 30Â min to 1 hour has been used to treat severe neuropathic pains for many decades; this therapy is used by many pain specialists as a rapid-onset approach to address very severe neuropathic pain. The data supporting oral therapy with older sodium channel blockers, such as the antiarrhythmic mexiletine, are limited, and given their side effect profiles, a trial is considered only when sequential trials of other adjuvant analgesics have been ineffective. A new agent, lacosamide, has a unique mechanism involving sodium channel modulation. Although there are no data in populations with severe medically illness, its side-effect profile usually is acceptable and early experience suggests that it may be considered for a trial in refractory neuropathic pain. Â 30
Stiripentol for the treatment of seizures associated with Dravet syndrome in patients 6 months and older and taking clobazam
Published in Expert Review of Neurotherapeutics, 2023
Alejandra Vasquez, Elaine C Wirrell, Paul E Youssef
Several guidelines for DS diagnosis and management have been published [6–8], including a recent International Consensus statement which proposes valproic acid/sodium valproate (VPA) as first-line, either clobazam ± stiripentol (STP) or fenfluramine as first or second-line, pharmaceutical-grade cannabidiol as third-line, and topiramate or ketogenic diet as fourth-line therapy [9] (Figure 1). Importantly, sodium channel blockers typically exacerbate seizures and should be avoided for prophylactic use [9]. Despite optimizing current therapies, however, complete seizure control is generally not achievable, and the current treatments have minimal or no impact on comorbidities. More efficacious therapies which ideally would target the underlying pathogenesis and could be used very early in the disease course are clearly needed to improve seizure control, mitigate comorbidities, and improve quality of life.
Why are sodium channel modulators not yet pharmacotherapeutic trailblazers for neuropathic pain?
Published in Expert Opinion on Pharmacotherapy, 2021
The finding that mammals have 9 sodium channels and that in the main, three, namely, 1.7, 1.8 and 1.9 are rather selectively found in peripheral pain pathways, gives rise to the possibility of systemic yet pain selective sodium channel blockers [1]. A number of preclinical studies using transgenic approaches revealed key roles in pain, in particular neuropathic pain models. Generally, proof of concept arises when a drug has been developed, but here and rapidly, strong proof of concept arrived from recognition of a number of inherited pain disorders involving mutations in Nav 1.7 in particular where the abnormal sodium channel proteins caused a loss or gain of function and corresponding pain abnormalities [1]. Similar inherited changes in Nav 1.8 have been reported indicating that this channel could be an important target too [2]. This provided an impetus for the development of novel pain related 1.7 sodium channel blockers. But some important messages were not taken into account as the field progressed.
Drug-specific risk of severe QT prolongation following acute drug overdose
Published in Clinical Toxicology, 2020
Sharan L. Campleman, Jeffery Brent, Anthony F. Pizon, Joshua Shulman, Paul Wax, Alex F. Manini
An additional drug class with expected findings from this dataset was that of sodium channel blockers. Previously, patch clamp in vitro studies showed reduced hERG currents and disrupted hERG expression [20–23], while another retrospective case series of 13 tricyclic exposures suggested a risk of QT prolongation [24]. In the present study, sodium channel blockers with significantly increased risk of SQTP were overdoses from imipramine (aOR 21.3, CI 2.2–210), followed by nortriptyline (aOR 4.5, CI 2.1–9.9), doxepin (aOR 3.1, CI 1.8–5.6), diphenhydramine (aOR 1.97, CI 1.6–2.5), and amitriptyline (aOR 1.95, CI 1.3–2.9). Mechanistically, this was an expected finding because widening of the QRS via sodium channel blockade prolongs the QT interval, by definition. Interestingly, this suggests that the degree of QRS widening from the above sodium channel blockers follows the same order. Since this is speculative, investigations into the degree of QRS widening based on specific drugs in this class are warranted to help guide management.