FARMACI ANTIARITMICI. Berne & Levy 1996. Indications for Treatment. One typically treats those arrhythmias that:. CO. - asynchronization (multifocal VT, VFib) - contractions too infrequent (bradycardia) - contractions too frequent (tachycardia).
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One typically treats those arrhythmias that:
- asynchronization (multifocal VT, VFib)
- contractions too infrequent (bradycardia)- contractions too frequent (tachycardia)
- AFlutter VTach - Sustained VT VFib
- AFib thrombus Cardioversion embolus (Rx: anticoagulate for 2-3 weeks prior to DC cardioversion)
- DC Cardioversion (AFib, VT, VFib)- Implantable Cardioverter-Defibrillators (ICD) (VT, VFib)- Pacemaker (SAN Dx., AVN Block)
- Rx. For PSVT (can also vagal tone by: occular pressure, diving reflex, ValSalva, phenylephrine, edrophonium)
-Rx. For AVN bypass tracts, WPW
- “Type A” behavior
- smoking, weight, hypertension, etc.
- C08D Calcioantagonisti selettivi con effetto cardiaco diretto
Results in rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output (CO)
To understand how antiarrhythmic drugs work, need to understand electrophysiology of normal contraction of heart
Repolarization of ventricles
Contraction of atria
(lidocaina, mexiletina, tocainide, moricizina)
(propranololo, metoprololo, atenololo...)
(amiodarone, bretilio, dofetilide, ibutilide, sotalolo*)
Mode of death
Type of beta blocker
Odds ratio (active:control)
(Yusuf et al. Prog Cardiovasc Dis 1985;27:335)
No CHF CHF
(modified from Eichorn & Bristow, AJC 79:794;1997)
ò34% all cause death
(95% CI: 0.54-0.81; P<0.0001)
ò44% sudden death
(95% CI: 0.39-0.80; P<0.0011)
Time after inclusion (days)
(CIBIS II, Lancet 1999;353:9)
(waldo et al., Lancet 1996; 348:7)
Proportion event free
95% CI= 1.15-2.36
Time from randomization (days)
Log rank test
Giorni dalla randomizzazione
Use-dependent binding (targets cardiac cells)
Voltage-dependent binding (targets smooth muscle)
APD ( ERP >CT)
Sustained V Tach:
Block IKrClass I & III Effects on Reentry (Ventricular)
Reentrant Circuit Established
Mechanism of Action:
Ca channel blockers inhibit L-type Ca
channels by the same State & Vm-
dependent mechanism as Na channel
blockers inhibit Na channels.
% Ca Channels Blocked
diltiazem (Cardizem ®) verapamil (Isoptin, Calan ®) propranolol (Inderal ®)
During Atrial Tachyarrhythmias - “Protect the ventricle”
diltiazem (Cardizem ®) verapamil (Isoptin, Calan ®) propranolol (Inderal ®) digoxin (Lanoxin ®) amiodarone (Cordarone ®)
Torsade de Pointes (Quinidine, Sotalol, Class III)
Quinidine: syncope, cinchonism, diarrhea
Procainamide: systemic lupus-like syndrome (20-25% of all patients after 1 year)
Amiodarone: pulmonary fibrosis, constipation, corneal deposits (100% >1 yr), bluish skin, hypo- or hyper-thyroidism, peripheral neuropathy, elevated transaminases.
The generation of pacemaker potentials relies on a complex interplay between different types of currents carried by cation channels.
I(f) is an inward current activated by hyperpolarization of the membrane potential and by intracellular cyclic nucleotides such as cAMP.
Specific agents have been developed for their ability to selectively reduce heart rate by lowering cardiac pacemaker activity where f-channels are their main natural target. These drugs include alinidine, zatebradine, cilobradine, ZD-7288 and ivabradine.
Drugs Fut 2007, 32(3): 245ISSN 0377-8282Copyright 2007 Prous ScienceCCC: 0377-8282DOI: 10.1358/dof.2007.032.03.1072639
Gap junction modifying antiarrhythmic peptides: Therapeutic potential in atrial fibrillationHaugan, K., Petersen, J.S.
Rotigaptide is a synthetic AAP* analogue that prevents metabolic stress-induced atrial conduction velocity (CV) slowing and rapidly reverts established atrial CV slowing in vitro. …
in dog models of ischemia-related AF and chronic atrial dilatation-induced AF, rotigaptide has significant antiarrhythmic effects. Rotigaptide also has a favorable safety profile.