A Critical Period of Ventricular Fibrillation More Susceptible to Defibrillation: Real-Time Waveform Analysis Using a Single ECG Lead

Previous studies have suggested that variations in the underlying ventricular fibrillation (VF) waveform may be one of the factors responsible for the probabilistic nature of defibrillation. The heart appeared to be more susceptible to defibrillation at higher absolute VF voltages (AVFV). This study investigated in an open-chest canine model (n = 8), a newly developed system that analyzed the VF waveform in real-time, instantaneously determined the time to shock, and immediately delivered a fixed low energy DC shock. A two parameter tracking technique using a running long-term and short-term AVFV average was devised to automatically identify a high voltage peak area of the VF waveform, which has been hypothesized to represent a critical period susceptible to defibrillation. Using a DC shock estimated at the 50% success level, the performance using this technique in 58 defibrillation trials was compared to the performance of the conventional method of shocking at a fixed time (random shock method) in 62 trials. Patch size, electrode location, and discharge voltage were kept constant while VF duration, transmyocardial resistance (TMR), energy delivered, and AVFV at the point of shock were measured. Shock energy and current, TMR, and VF duration were similar with both shock methods. A significantly higher AVFV was observed for trials performed with the peak shock method (0.66 ± 0.02 mV) as compared to trials performed with the random shock method (0.25 ± 0.09 mV) (P < 0.003). Using lead II as the only sensing lead, the success rate was increased in 6 of 8 dogs (75%) with the new method. One animal showed identical performance, and one animal a worse performance. The overall increase in success rate was 24% using a single ECG lead (range 0%-100%; P < 0.04). Our data document that using this algorithm a period of high VF voltage can be detected in realtime. The improved success in the majority of animals supports the hypothesis that a critical period susceptible to defibrillation exists during VF. However, the high AVFV detected using a single ECG lead did not translate to an improved success rate in all animals. This suggests that other factors in addition to the VF voltage measured on a single lead of the ECG are important in characterizing this critical period.     

Radiofrequency Catheter Ablation of an Atriofascicular Pathway During Atrial Fibrillation:

Atriofascicular Ablation During Fibrillation. Introduction: A male patient with an atriofascicular pathway underwent catheter ablation of the atriofascicular pathway during atrial fibrillation.
Methods and Results: The patient had preexcited atrial fibrillation both clinically and repeatedly during electrophysioiogic study. A preexcited tachycardia with a 1:1 AV relationship and regular RR intervals was also induced. Catheter ablation of the atriofascicular pathway could only be performed during persistent atrial fibrillation, based on mapping of the pathway's insertion into the right bundle branch. Following successful ablation and cardioversion to sinus rhythm, a regular QRS tachycardia (atrioventricular [AV] nodal reentry) having (he same rate, atrial activation sequence, and His-atrial time as the regular preexcited tachycardia noted preablation was initiated. An AV nodal slow pathway modification eliminated this tachycardia. Neither atrial fibrillation nor AV nodal reentry has recurred on follow-up.
Conclusion: This is the first report of atriofascicular mapping and ablation performed exclusively during atrial fibrillation and illustrates the utility of mapping the pathway's ventricular insertion. Other unusual features ("bystander" pathway activation during AV nodal reentry, possible role of the pathway in genesis of atrial fibrillation) are discussed.     

Changes of hepatic and systemic haemodynamics following somatostatin administration in patients with hepatitis B-related cirrhosis

Abstract Somatostatin has been used to effectively control acute variceal haemorrhage, with conjectured mechanisms on portal hypertension. We, therefore, evaluated the effects of somatostatin on hepatic and systemic haemodynamics in 15 patients with hepatitis B-related cirrhosis and portal hypertension. All patients received an intravenous, continuous infusion of somatostatin 250 μg/h, following a bolus injection of 250 μg. In systemic haemodynamics, the mean arterial pressure (MAP) increased ( P < 0.05), associated with a reflex bradycardia within 3 min following bolus injections, compared with basal values. The right atrial pressure, pulmonary capillary wedge pressure, inferior vena cava pressure, cardiac index, and systemic vascular resistance remained unaffected after drug infusion. In hepatic haemodynamics, the wedge hepatic vein pressure remained unchanged after drug administration. However, there was an increase in free hepatic vein pressure (FHVP; P < 0.05), and a trend toward a decrease in the hepatic vein pressure gradient (HVPG; P = 0.063), within 3 min after bolus injection. Furthermore, the hepatic blood flow decreased significantly at 10 and 30 min after somatostatin infusion ( P < 0.05). The effective sinusoidal perfusion assessed by indocyanine green infusion also decreased progressively at 10 min ( P = 0.057) and 30 min ( P < 0.05). We concluded that somatostatin, at the dose used in this study, caused a transient and bolus-related vasoconstrictive effect, resulting in increases in MAP and FHVP, a decrease in heart rate, and a trend toward lower HVPG. In addition, somatostatin reduced the hepatic blood flow and effective sinusoidal perfusion which may be hazardous to cirrhotic patients during variceal haemorrhage.     

Ventricular Tachycardia/Ventricular Fibrillation Ablation in the Setting of Ischemic Heart Disease

Recurrent ventricular tachycardia (VT) in the setting of coronary artery disease is frequently a life-threatening electrophysiologic emergency. Even in patients with an implantable defibrillator, recurrent VT is frequently accompanied by repeated and disabling shock therapy. Catheter ablative therapy offers the ability to provide immediate control of recurrent VT. Long-term elimination of VT should be anticipated in most patients. This article reviews the strategies, tools, techniques, and expected outcome for catheter ablation of stable and unstable ventricular arrhythmias in the setting ischemic heart disease.     

Snake skin pattern gastropathy in cirrhotic patients

Gastric mucosal lesions are common in patients with cirrhosis. Among them, snake skin pattern gastropathy (SSPG) is the most distinguishing one. A prospective study was conducted to investigate the incidence of SSPG in cirrhotic patients, the relationship between the degree of portal pressure and SSPG, and the possible association of SSPG with serum levels of gastrin and pepsinogen I. SSPG was found to be significantly more common in 100 cirrhotic patients than in 100 age- and sex-matched healthy controls (41% vs 0%, P less than 0.0001). Hepatic venous pressure gradient and serum gastrin and pepsinogen I levels were measured in 21 cirrhotic patients with SSPG and 25 cirrhotics without SSPG. There was no significant difference in hepatic venous pressure gradient (16.1 +/- 4.4 mmHg vs 16.1 +/- 4.9 mmHg, P greater than 0.05), serum gastrin level (78.0 +/- 26.7 pg/mL vs 80.1 +/- 32.5 pg/mL, P greater than 0.05) and serum pepsinogen I level (69.5 +/- 26.6 ng/mL vs 65.2 +/- 26.1 ng/mL, P greater than 0.05) in cirrhotic patients with or without SSPG. In conclusion, SSPG is common in cirrhotic patients. Portal pressure per se may not be the only factor causing SSPG--other aggressive factors may be needed together to cause the gastropathy. There is no evidence of correlation between serum gastrin or pepsinogen I level and SSPG.     

Genesis of Sigmoidal Dose-Response Curve During Defibrillation by Random Shock: A Theoretical Model Based on Experimental Evidence for a Vulnerable Window During Ventricular Fibrillation

The sigmoidal dose-response curve (percent success vs shock energy) suggests a probabilistic nature of defibrillation. The mechanism is still largely unknown, however, random variation in the excitable state during ventricular fibrillation (VF) is suspected. A canine defibrillation study was designed to determine whether random variation in absolute VF voltage (AVFV) (a crude marker of number of excitable cells) was related to success of defibrillation, using a DC shock successful at the 50% level. The results were: (a) transmyocardial resistance (73.4 +/- 1.4 vs 73.6 +/- 1.5 ohms) and delivered energy (6.1 +/- 1.2 vs 6.2 +/- 1.2 joules) were similar; however, (b) AVFV 2 msec prior to DC shock was greater for successful as compared to unsuccessful attempts (0.5 +/- 0.1 vs 0.3 +/- 0.0 mV, P less than 0.01). A mathematical model was subsequently developed based on fluctuation in the number of excitable cells. Variation in the state of excitability resulted in a cyclic window potentially vulnerable to defibrillation. The vulnerable window occurred at a point when the number of excitable cells was low, i.e., a higher state of total depolarization, which was in agreement with the experimental finding. For a given VF pattern, duration of the vulnerable window was regulated by the shock energy. A larger shock energy generated a wider vulnerable window and, in turn, a higher success rate. Finally, the sigmoidal dose-response curve of defibrillation was theoretically constructed by calculating the variable chances of a random DC shock occurring either in a vulnerable window or elsewhere during VF. It is concluded that a vulnerable window susceptible to defibrillation can be demonstrated in the early stages (10 sec) of VF. The mathematical model provides a theoretical basis for the vulnerable window and helps elucidate the probabilistic nature of defibrillation.