Double sequential external shocks for refractory ventricular fibrillation.

OBJECTIVES: A technique for terminating refractory ventricular fibrillation is described. BACKGROUND: Refractory ventricular fibrillation can occur in up to 0.1% of electrophysiologic studies. Animal studies have shown that rapid sequential shocks may reduce ventricular fibrillation threshold. METHODS: Five patients of 2,990 consecutive patients in a 3-year period experienced refractory ventricular fibrillation during 5,450 routine electrophysiologic studies. Multiple shocks were delivered by means of a single defibrillator. Double sequential shocks were delivered externally 0.5 to 4.5 s apart by means of two defibrillators with separate pairs of electrodes. RESULTS: In all patients, standard defibrillation was unsuccessful, but all were successfully resuscitated using the double sequential shocks. CONCLUSIONS: This report stresses the importance of an additional defibrillator being readily available during electrophysiologic testing. This technique of rapid, double sequential external shocks may have general applicability, providing a simple and potentially lifesaving approach to refractory ventricular fibrillation.

A new system for classification of cardiac death as arrhythmic, ischemic, or due to myocardial pump failure.

Existing classifications of cardiac death fail to incorporate current understanding of the pathophysiology of sudden cardiac death. We developed a new scheme for classifying cardiac death that defines 3 categories of underlying mechanism: primary arrhythmia, acute myocardial ischemia/infarction, and myocardial pump failure. Using this new system, we classified the mechanism of 106 definite cardiac deaths from the Recurrent Coronary Prevention Project. Fifty deaths (47%) were classified as arrhythmic, 46 (43%) as ischemic, and 9 (8%) as due to myocardial pump failure (1 death was not classifiable). All 36 witnessed arrhythmic deaths were sudden and 8 of 9 witnessed myocardial pump failure deaths were nonsudden. The 38 witnessed ischemic deaths were split evenly between sudden and nonsudden. Interrater agreement for the classification of mechanism was 100%. This classification scheme, if validated in subsequent studies, will provide a useful algorithm for classifying deaths by underlying mechanism.

Equine arch vessel anomaly associated with coarctation of the aorta.

Angiography in a 30-year-old man revealed the unique combination of aortic coarctation and an unusual arch anomaly. Proximal to the coarctation, a single arch vessel trifurcated into the brachiocephalic, left common carotid and left subclavian arteries. This anomalous arch vessel is a normal equine variant.

Early changes in material properties of rabbit articular cartilage after meniscectomy.

We have correlated early material and biochemical changes in articular cartilage in a surgical model for cartilage degeneration. Medial meniscectomy was performed on the left knee of 17 adult, female New Zealand white rabbits. The equilibrium Young's modulus of cartilage was assessed by an indentation test in situ at defined sites on the medial and lateral tibial plateaus of the operated and control knees; the cartilage was then excised and analyzed biochemically. Focal changes were consistently observed in the medial surface of the operated knee. The equilibrium modulus and the glycosaminoglycan content fell rapidly, reaching a minimum by 2 weeks after surgery; the lateral tibial surface was essentially unaffected. Six months after surgery, the glycosaminoglycan content had returned to normal and the modulus to near normal. Independent measurements on cored plugs from the medial surface 2 weeks after surgery revealed a significant decrease in both the dynamic stiffness and the streaming potential in the operated knee compared with the control. The findings suggest that normal ambulatory loads in vivo will deform the affected medial cartilage much more than normal. It remains to be seen if altered mechanical stresses are solely responsible for initiating and sustaining matrix remodeling by the chondrocytes.

Tachycardias of right ventricular origin.

Ventricular tachycardia arising from the right ventricle usually has a left bundle branch morphology and occurs in a variety of disorders. Uhl's anomaly and right ventricular dysplasia may represent a spectrum of one disorder and are a cause of right heart dilatation, failure, and premature sudden death due to ventricular arrhythmias. Familial forms of the disorder may account for focal clustering in some geographic areas. Management should involve aggressive stratification of arrhythmia risk and may include medical, surgical, or device therapy. In contrast, the syndrome of right ventricular outflow tract tachycardia, including nonischemic exercise-induced and repetitive monomorphic ventricular tachycardia, is a more benign entity. Management often involves beta- and calcium channel blocking drugs or type IC antiarrhythmic drugs. Catheter ablation of the arrhythmia focus in the right ventricular outflow tract has been used in selected patients. In this syndrome the right ventricle is normal, and noninvasive testing as well as electrophysiologic studies can be helpful in distinguishing it from the more malignant right ventricular dysplasia. Ventricular arrhythmias may also be seen after right ventricular incision, as in surgical repair of tetralogy of Fallot and ventricular septal defects. Significant ventricular ectopy associated with an abnormal right ventricle (enlarged or depressed systolic function) is associated with an increased risk for sustained arrhythmia and sudden cardiac death in this group. The optimal indicator(s) of highest risk in these patients remains under investigation but will likely include electrophysiologic testing. Bifascicular block occurs commonly after repair of tetralogy of Fallot, but is usually benign. Isolated right ventricular infarction is rare. Most right ventricular arrhythmias associated with ischemia occur in the setting of iatrogenic catheter manipulation for pacing or hemodynamic monitoring. In conclusion, right ventricular arrhythmias involve an unusual and interesting group of clinical entities and appear to span the spectrum of arrhythmias mechanisms. A macroreentrant activation ring around the ventriculotomy scar may account for the arrhythmias following repair of tetralogy of Fallot. Microreentry at sites of morphologic abnormalities results in the arrhythmias associated with right ventricular dysplasia and ischemia. Triggered activity related to DADs or, less likely, abnormal automaticity, produce repetitive monomorphic ventricular tachycardia and nonischemic exercise-induced ventricular tachycardia, both of which usually originate from the right ventricular outflow tract. Iatrogenic ventricular tachycardia associated with catheter manipulation is especially likely to occur in the presence of right ventricular ischemia and infarction. It is important to recognize these clinical entities because treatment is specific.(ABSTRACT TRUNCATED AT 400 WORDS)

Advances in syncope: a combined approach utilizing head-up tilt testing and electrophysiologic evaluation.

The electrophysiological evaluation of syncope of unknown origin yields a diagnosis in approximately 40% of patients. In the presence of structural heart disease ventricular tachycardia is the most common etiology accounting for 20% of cases. Over the past several years head-up tilt table testing with isoproterenol provocation has highlighted the syndrome of neurocardiogenic syncope. This syndrome accounts for an additional 30-40% of patients with syncope. There is compelling evidence that this syndrome involves the Bezold-Jarisch reflex with excessive stimulation of ventricular mechanoreceptors (C-fibers) located predominantly in the inferoposterior portion of the heart. Tilt table testing is now an established tool both for diagnosis of this syndrome and for guiding therapy with beta blockers, disopyramide, theophylline, or alpha-agonists. Tilt table testing combined with invasive electrophysiological testing significantly increases the diagnostic yield in the evaluation of syncope.

Neuropharmacological characterization of fragment B from tetanus toxin.

Tetanus toxin and Fragment B from tetanus toxin were assayed for activity on the mouse phrenic nerve-hemidiaphragm preparation. Both molecules produced blockade of neuromuscular transmission, but the parent molecule was at least two orders of magnitude more potent than the fragment. Experiments were done to determine whether the toxicity attributed to Fragment B was authentic or due to contamination with the parent molecule. Analysis of the fragment by high-performance liquid chromatography and by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate revealed trace contamination. Removal of the major contaminant (1-2%) did not abolish toxicity of the material. However, in pharmacological experiments with native toxin and its fragment, the latter behaved indistinguishably from the former. At equiactive concentrations, both were antagonized by Fragment C and both were antagonized by lysosomotropic agents (ammonium chloride and methylamine hydrochloride). In addition, monoclonal antibodies directed against epitopes in Fragment C neutralized both native toxin and the material presumed to be Fragment B. The studies with antagonists and antibodies suggest that the toxicity apparently associated with Fragment B was in fact due to trace contamination with the parent molecule. In experiments on planar lipid bilayers, Fragment B formed pH-dependent channels. This activity was not abolished by monoclonal antibodies directed against epitopes in Fragment C. The data indicate that Fragment B retains the ability to form channels in membranes, but in the absence of Fragment C it retains little ability to paralyze neuromuscular transmission.

Inappropriate discharges of an implantable cardioverter defibrillator secondary to automatic adjustable gain of atrial tachycardia.

Third generation implantable cardioverter defibrillators are capable of complex arrhythmia detection using sensing algorithms with automatic adjustable gain settings. We report a unique case where inappropriate sensing of atrial tachycardia in a patient with a His bundle ablation lead to satisfaction of ventricular fibrillation detection criteria.

Channels formed by botulinum, tetanus, and diphtheria toxins in planar lipid bilayers: relevance to translocation of proteins across membranes.

The heavy chains of both botulinum neurotoxin type B and tetanus toxin form channels in planar bilayer membranes. These channels have pH-dependent and voltage-dependent properties that are remarkably similar to those previously described for diphtheria toxin. Selectivity experiments with anions and cations show that the channels formed by the heavy chains of all three toxins are large; thus, these channels could serve as "tunnel proteins" for translocation of active peptide fragments. These findings support the hypothesis that the active fragments of botulinum neurotoxin and tetanus toxin, like that of diphtheria toxin, are translocated across the membranes of acidic vesicles.

Strategies in the surgical treatment of malignant ventricular arrhythmias. An 8-year experience.

Introduction of the automatic implantable cardioverter defibrillator (AICD) has dramatically affected the surgical treatment of malignant ventricular tachyarrhythmias. The authors continue to perform electrophysiologically directed subendocardial resection (SER) of left ventricular (LV) scars in selected patients, and we revascularize (CABG) those patients undergoing AICD implantation who have significant myocardial ischemia. In an attempt to define the optimal role of each procedure, this report analyzes our 8-year experience with 348 consecutive patients treated surgically for these arrhythmias (SER since 1983 and AICD since 1986). All patients undergoing SER had organized ventricular tachycardia (VT) as a result of myocardial infarction, and most had LV aneurysms; of those undergoing AICD or AICD/CABG, 60% had VT, 15% had ventricular fibrillation, and 25% had both or were noninducible. The thirty-day mortality rate was 1.5% (3/197) for AICD, 5.4% (5/93) for AICD/CABG, and 8.6% (5/58) for SER; these mortality figures are not significant different. Late deaths in all groups were predominantly due to congestive heart failure, and actuarial survival as well as freedom from sudden death was similar between the groups at 4 years. Recurrent VT occurred in 167 of 282 (59%) of long-term survivors of AICD or AICD/CABG during follow-up and in nine of 53 (17%) of those with SER. Forty-eight per cent of survivors of AICD or AICD/CABG required antiarrhythmic medications, whereas only 11% of those with SER required antiarrhythmics. Long-term survival in each group is much higher than that reported for comparable patients with severe LV dysfunction treated medically. In those patients with organized VT and LV aneurysm who are judged able to survive the procedure, SER offers a high likelihood of cure rather than simple prevention of sudden death.