Ventricular Premature Complexes Clinical Trial
Official title:
Effects of Carvedilol on Suppressing the Premature Ventricular Complex/Ventricular Tachycardia From Outflow Tract
Carvedilol is known to be effective in reducing ventricular arrhythmias and mortality in patients with heart failure. It is suggested that one of the mechanisms is its ability to block store overload-induced Calcium release which activates spontaneous calcium release by Ryanodine receptors. Ventricular outflow tract tachyarrhythmia is known to be associated with calcium overload due to activation of Ryanodine receptors. The aim of this study is to evaluate the efficacy of Carvedilol on premature ventricular complex(PVC)/ventricular tachycardia(VT) originating from outflow tract.
Carvedilol is one of the third-generation beta-blockers effective in reducing ventricular
arrhythmias and mortality in patients with heart failure. Antioxidative and alpha - blocking
effects, along with nonselective beta - blockade, have been described as a mechanism of
effect in various diseases.
The antiarrhythmic effect of carvedilol inhibiting atrial fibrillation or ventricular
arrhythmia has been reported, but its mechanism is not yet clear. Among them, inhibition of
store overload-induced Ca2+ release (SOICR) is suggested as an antiarrhythmic mechanism of
carvedilol.
Stimulation of the beta receptor leads to the entry of calcium into the sarcoplasmic
reticulum (SR) by opening the L-type calcium channel. The influx of calcium through the
L-type calcium channel also increases the calcium release through the Ryanodine receptor
(RyR) in the sarcoplasmic reticulum. This is called Ca-induced Ca release and is known as a
normal physiological response. However, when calcium overload in the myofibrillar body
occurs, spontaneous calcium release, known as SOICR, can occur through RyR, which can make
triggered activity by inducing Na+/Ca2+ exchanger present in myocardium, leading to severe
arrhythmia. Among several beta-blockers, only carvedilol has been known as a drug that can
directly inhibit SOICR in combination with beta-blockade effect.
Ventricular tachyarrhythmia originating from the ventricular outflow tract is an arrhythmia
occurring in a patient with normal cardiac function. The mechanism of the arrhythmia is known
to be triggered activity which is caused by activation of RyR due to increased cyclic
adenosine monophasphate, resulting in calcium overload, eventually causing activation of
Na+/Ca2+ exchanger. The aim of this study is to evaluate the efficacy of Carvedilol on PVC/VT
originating from outflow tract.
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