Left Ventricular Apex Ablation Decreases the Upper Limit of Vulnerability

Abstract

Background-After shocks with an Ϸ50% probability of success for the upper limit of vulnerability (ULV 50 ) of strength, the first few activations appear focally on the epicardium at almost the same site at the left ventricular (LV) apex in both successful and failed induction of ventricular fibrillation (VF). We tested the hypothesis that subendocardial ablation at this early site would decrease the shock strength required for the ULV 50 . Methods and Results-Ten S1 stimuli were delivered from the right ventricular apex at a 300-ms coupling interval in 5 pigs. Biphasic shocks were delivered from right ventricular-superior vena cava electrodes after the last S1 stimulus. The ULV 50 was determined using an up/down protocol with T-wave scanning. Radiofrequency ablation was performed endocardially at the apical LV. The ULV 50 was determined again 30 minutes after ablation. To determine the importance of the ablation region, this protocol was repeated in another 5 pigs with ablation at the LV base. Delivered voltage (401Ϯ60 versus 323Ϯ50 V) and energy (11Ϯ3 versus 7Ϯ2 J) for the ULV 50 were significantly decreased after LV apex ablation by 19% and 34%, respectively. However, no difference existed in ULV 50 before and after LV base ablation. Lesions at both the LV apex and base were subendocardial and ranged from 0.8 to 1.1 cm in diameter. Conclusions-Subendocardial ablation at the apical LV markedly decreases ULV 50 , which suggests that the activation originating from this postshock early site is responsible for VF initiation and that interventions to electrically silence this site can influence the outcome of VF induction by ULV shocks. (Circulation. 2000;101:2458-2460.)Key Words: ablation Ⅲ fibrillation Ⅲ shock S tudies on how ventricular fibrillation (VF) occurs and how a shock halts VF have been performed for decades. 1,2 Knowledge of VF induction and defibrillation has greatly increased with the advent of electrical and optical systems that can map activation simultaneously from hundreds of sites. 3,4 Several studies suggest that VF induction by shocks during the vulnerable period occurs by the same mechanism that causes VF to recur after shocks that fail to defibrillate. 3,5 Because VF induction is probabilistic and dependent on shock strength and timing, we recently compared the activation sequences after shocks of the same strength delivered at the same time during the vulnerable period that induced VF 50% of the time, ie, those that had a 50% probability of success for the upper limit of vulnerability (ULV 50 ). The activation pattern for the first few postshock cycles after shock-induced VF episodes did not differ from that of episodes in which VF was not induced. 6,7 These activations first and repeatedly appeared on the epicardium from the same site at the left ventricular (LV) apex, after which they either died out in episodes in which VF was not induced or arose progressively faster and degenerated into fibrillation in VF episodes. 6,7 These results suggest that this small arrhythmogenic region at the ...

Granulocyte colony-stimulating factor stabilizes cardiac electrophysiology and decreases infarct size during cardiac ischaemic/reperfusion in swine

“…The average value of these intervals was used as a coupling interval to deliver an S2 stimulus for VF induction (Kanlop et al. , 2008, Chattipakorn et al. 2000a,b,c).…”

Effect of sildenafil citrate on the cardiovascular system

“…It is most often caused by a lethal cardiac arrhythmia known as ventricular fibrillation (VF) (27,(30)(31)(32)(33)(34)(35). VF has been characterized as a rapid, disorganized, and asynchronous contraction of ventricular muscle, which causes the failure of the pumping function of the heart, leading to vital organ failure and causing death within minutes (36)(37)(38)(39).…”

Mechanisms of Clinical Arrhythmias

“…There is a lower limit of stimulus strength that can induce VF, and an upper limit of vulnerability, defined as a current strength at or above which VF cannot be induced. 24 Propagated graded responses may underlie the mechanisms of ventricular vulnerability to a single premature stimulus. A stimulus delivered during incomplete recovery evokes a gradual response that propagates slowly to neighboring recovered cells and, if its amplitude is large enough, can induce an all-or-none response.…”