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A new algorithm (St. George's algorithm), based on the polarity and morphology of QRS complexes rather than delta waves, was developed for localizing accessory pathways to 1 of 9 sites on the atrioventricular annuli. This was compared with algorithms previously proposed by Skeberis et al (localizing to 1 of 7 sites) and Milstein et al (localizing to 1 of 4 sites). The preexcited 12-lead electrocardiograms recorded during sinus rhythm in 106 consecutive patients (including 60 retrospectively analyzed patients and 46 prospectively analyzed patients) who underwent successful radiofrequency catheter ablation of a single accessory pathway were analyzed by 3 blinded observers using all 3 algorithms. The results were compared with the actual localization of accessory pathways as derived from endocardial mapping during catheter ablation. In all 106 patients, the accuracy of the 3 algorithms for 4 sites on the atrioventricular annuli (as considered by Milstein's method) was 72%, 79%, and 92% for Milstein's, Skeberis', and St. George's algorithms, respectively. For 7 sites (as considered by Skeberis' method), the accuracy was 65% (Skeberis' algorithm) and 88% (St. George's algorithm), and for 9 sites (as considered by our method) the accuracy was 86% (St. George's algorithm). In 46 prospectively analyzed patients, the accuracy of the 3 algorithms for 4 sites was 70% (Milstein's), 67% (Skeberis'), and 87% (St. George's); for 7 sites the accuracy was 61% (Skeberis') and 85% (St. George's), and for 9 sites the accuracy was 85% (St. George's). The reproducibility of St. George's and Skeberis' methods was better than that of Milstein's method. It is concluded that our algorithm allows localization of a single accessory pathway from the preexcited 12-lead electrocardiogram with sufficient precision and greater accuracy than other methods. (Am J Cardiol 1994;74:161-165)

Immediate responses to head-up flit were determined in 78 consecutive patients with unexplained syncope undergoing 45-minute tilt tests at 60[degrees]. Thirty-four patients developed neurally mediated syncope (mean time to syncope 18 minutes), 40 tolerated the full duration of tilt, and 4 were unable to complete the study but did not develop syncope. Blood pressure, heart rate, forearm blood flow and forearm vascular resistance were measured at baseline and after 2 and 5 minutes of tilt. Syncopal and nonsyncopal patients were well-matched for age and baseline hemodynamic parameters. There was no difference between the groups in heart rate or blood pressure at 2 minutes, but there was a small but significant difference in percent reduction in mean arterial pressure at 5 minutes. After 2 and 5 minutes of tilt, mean forearm blood flow was 2.4 and 2.6 ml/ min/100 ml, respectively, in syncopal patients compared with 1.6 (p 15 minutes were included in the analysis. Patients with neurally mediated syncope have clearly demonstrable abnormalities in vascular control immediately after assumption of the upright posture. The results shed new light on the pathophysiology of neurally mediated syncope. (Am J Cardiol 1993;71:72-76)

It has been suggested that QT dispersion recorded on the surface electrocardiogram may be a predictor of arrhythmic events in patients with congenital QT prolongation. To evaluate this, 9 patients (6 female, mean age 17.6 years) with congenital long QT syndromes, all of whom had syncope and documented torsades de pointes, were studied. Patients were studied off treatment and during therapy with [beta]-blocking agents. Three patients were also studied after left stellate ganglionectomy. An age-matched control group was also studied. Good quality 12-lead electrocardiograms were recorded from all patients. For each lead, QT and RR intervals were measured, and QTc value was calculated. QT and QTc dispersions were calculated for each patient. Patients had a significantly longer mean QT interval compared with that of the control group (450 [+ or -] 100 vs 359 [+ or -] 63 ms; p = 0.015) at similar mean RR intervals (736 [+ or -] 231 vs 783 [+ or -] 289 ms), with a longer mean QTc value (0.53 [+ or -] 0.08 vs 0.41 [+ or -] 0.02 [s.sup.1/2]; p = 0.004). Patients also had longer QT and QTc dispersions compared with those of the control group (110 [+ or -] 45 vs 43 [+ or -] 12 ms [p = 0.004], and 0.108 [+ or -] 0.03 vs 0.05 [+ or -] 0.02 [s.sup.1/2] [p = 0.002], respectively). QT and QTc dispersions on and off [beta]-blocking agents were not significantly different. Comparing patients with frequent and those with infrequent symptoms, there was no difference in QT or QTc dispersion either off treatment or during therapy with [beta]-blocking agents. There was an increase in mean QT interval and QTc value in patients with frequent symptoms on [beta]-blocking agents. On [beta]-blocking agents, patients with frequent symptoms had a significantly longer mean QTc value compared with that of those with infrequent symptoms. There was no change in QT or QTc dispersion, mean QT or RR interval, or mean QTc value after left stellate ganglionectomy. QT-interval dispersion is observed in patients with congenital long QT syndromes; however, the degree of dispersion is not related to the severity of symptoms, nor influenced by treatment with [beta]-blocking agents.

Percutaneous transluminal coronary angioplasty (PTCA) is a surgical technique used in the treatment of coronary arteries that have become blocked by fatty atherosclerotic plaques. In PTCA, a balloon-tipped catheter is inflated at sites of arterial stenosis (narrowing) until the diameter of the vessel is wide enough to allow adequate blood flow to the heart. The technique is usually successful, except in the case of completely occluded (blocked) coronary arteries. PTCA equipment has been amended in attempts to overcome this problem. In low speed rotational angioplasty, a battery-powered electric engine turns a thin drive shaft that runs through the catheter and rotates a rounded tip. The authors describe their initial experiences in using the low speed rotational angioplasty system (ROTACS) to treat 11 patients with complete occlusion or critical stenosis of a coronary artery. None of the patients were candidates for conventional PTCA because of the severity of the arterial lesions. Complete arterial blockages were opened in only two cases, while in another two, the device provided enough support for a guide wire to pass the lesion. In a fifth case, a passage was created for a balloon. In cases where ROTACS was not successful, the lesion was in the right coronary artery or in a curved area of a vessel, and the plaque was often dissected (split) within the artery. Subsequently, three patients were given medical treatment, three patients had coronary bypass surgery, one was symptom-free until angina recurred, and four remained free of symptoms. The study indicates that ROTACS has a low success rate and a high rate of complications. Simpler devices may be more useful. (Consumer Summary produced by Reliance Medical Information, Inc.)

Atrial arrhythmias are characterized by abnormal heart beats caused by malfunctions in the electrical conduction of the heart muscle. These malfunctions usually result from changes in the electrical properties of specialized heart tissue that conducts electrical impulses from the atria to the pumping chambers, the ventricles, and may be caused by damage to the heart from reduced oxygen supply (ischemia). Arrhythmias can often be treated with drug therapy, but some cases do not respond to this type of treatment. Electrical ablation (destruction of conductile function) may be used when drug therapy fails, and involves applying a shock to the patient's heart to destroy atrioventricular conduction and thus stop the arrhythmias. Once the ablation has occurred, a pacemaker can be installed to maintain normal heart rhythm. This ablation technique is not always successful, however, and can cause unwanted side effects. Other methods for ablation that might be more effective and safer are currently being studied. This study examined one of these new techniques, alcohol ablation. It involves placing a catheter into a coronary artery and introducing alcohol through it to destroy atrioventricular conduction. Fourteen men suffering from atrial arrhythmias were treated with this procedure. Results showed that catheterization was successfully performed in 10 patients. Four of these patients were given 1.0 ml of alcohol and the others were given 0.5 ml of alcohol. Atrioventricular block was achieved in all 10 patients immediately following the procedure, but only six maintained the condition four months later. All four receiving 1.0 ml of alcohol and two of six receiving 0.5 ml continued to have atrioventricular block. Overall, 6 of 14 patients (43 percent) were successfully treated using this technique. A large amount (three to four times above normal) of the cardiac enzyme creatine kinase was found to be released after the procedure was performed, indicating excessive damage to the heart muscle. The results show that this technique is less successful than other techniques for ablation and poses possible serious side effects caused by cardiac enzyme release. This technique should be limited to cases where other ablation techniques fail. (Consumer Summary produced by Reliance Medical Information, Inc.)

In a proportion of patients with left free wall accessory connections, preexdtation is apparent only during atrial arrhythmias or atrial pacing (latent preexcitation). These patients may be at risk of a rapid ventricular response to atrial fibrillation despite the absence of preexcitation in sinus rhythm. The ability of intravenous adenosine to unmask latent preexcitation was evaluated in 22 patients with a history of documented supraventricular tachycardia and a normal electrocardiogram during sinus rhythm. Preexcitation was unmasked in response to adenosine in 4 patients: all 4 were shown to have latent preexcitation at electrophysiologic study. in 12 patients atrioventricular (AV) nodal conduction delay or block was induced without preexcitation after adenosine first-degree AV block in 8, second-degree block in 4): at subsequent electrophysiologic study none of these patients was found to have latent preexcitation. Five patients had little or no PR prolongation in response to adenosine: of these, 2 were shown to have latent preexcitation at electrophysiologic study. Atrial fibrillation was induced in 1 patient and a narrow complex regular tachycardia in another after intravenous adenosine. Intravenous adenosine during sinus rhythm is capable of producing AV nodal conduction delay or block in 73% of patients with a history of supraventricular tachycardia: in these patients adenosine provides a diagnostic test that is both 100% sensitive and 100% specific for latent preexcitation. in those patients in whom adenosine does not produce AV conduction delay or block, further investigation is required to establish or refute the diagnosis of latent preexcitation. (Am J Cardiol 1990;6S:868-873), Normal rhythmic contraction of the heart is the result of proper functioning of the heart's electrical conduction system, which involves special fibers in the heart muscle. Abnormalities of this conduction system can predispose the individual to sudden death if atrial fibrillation (AF) develops. AF is characterized by an irregular, random contraction of the atria, the chambers that receive blood from the body and lungs and transmit it to the ventricles. Abnormal accessory atrioventricular (AV) connections can exist, which are additional paths the electrical impulse can take as it moves from atria to ventricles. This can lead to preexcitation, or premature activation, of the ventricles, since the impulse that takes the accessory path may arrive at the ventricle before the impulse taking the normal path. Detection of preexcitation is important if treatment aimed at preventing ventricular fibrillation, a life-threatening development, is to be instituted. Some patients, however, in whom preexcitation exists, do not demonstrate it during sinus rhythm (the normal rhythm of the heart), and special techniques are necessary to diagnose the condition. Their condition is known as latent preexcitation. To investigate this matter, 22 patients with supraventricular tachycardia (rapid heart rate of more than 100 beats/minute) underwent electrophysiologic testing, during which electrical measurements were made at various locations in the heart using catheters carrying electrodes. Patients were given intravenous adenosine, a drug that can block the AV node, one of the major points in the normal conducting system. This made latent preexcitation, if present, more obvious. Of the patients tested, electrocardiographic records typical of preexcitement appeared in four patients, and the existence of preexcitement was confirmed by electrophysiology in all four. AV block was induced without preexcitation in 12 patients, and five other had little change in the large wave of the electrocardiogram. Of this latter group, two patients were found to have latent preexcitation upon physiological testing. It thus appears that intravenous adenosine can produce AV nodal conduction delay or block in 73 percent of patients with supraventricular tachycardia, and that it can aid in correct diagnosis of latent preexcitation. Since the incidence of people with supraventricular tachycardia is probably low, a less drastic diagnostic approach than invasive studies, such as the adenosine test reported here, may be more desirable. (Consumer Summary produced by Reliance Medical Information, Inc.)