Thallium imaging after ligation of an anomalous left coronary artery from the pulmonary artery.
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
J M McComb
Publications and source records attributed to J M McComb.
Surgery for control of recurrent life-threatening ventricular tachyarrhythmias within 2 months of myocardial infarction.
Twenty-seven patients (mean age 57 +/- 7 years) underwent surgery for control of recurrent drug-refractory ventricular tachyarrhythmias (uniform ventricular tachycardia alone in 9 patients, ventricular tachycardia and ventricular fibrillation in 15 and ventricular fibrillation alone in 3) within 2 months of acute myocardial infarction. The mean number of major arrhythmic episodes per patient was 15 (range 2 to 200) and of drug failures 4 +/- 2. Left ventricular function was severely impaired in the majority (ejection fraction 29%; range 14% to 47%) and 18 patients (66%) had a left ventricular aneurysm. Endocardial resection guided by a combination of endocardial activation mapping during tachycardia and fragmentation mapping during sinus rhythm was performed in all patients. All electrically abnormal left ventricular endocardium was excised. Eight patients (29.6%) died within 30 days of surgery. Death was not related to age, time of surgery after infarction, ventricular function, bypass time or type of arrhythmia. Patients requiring emergency surgery had a higher early postoperative mortality rate than did those undergoing planned surgery (43% versus 15%). During a follow-up period of 32 +/- 20 months, there have been no arrhythmic deaths and only three patients (16%) have required antiarrhythmic drug therapy. When required in the early weeks after infarction, surgery for ventricular arrhythmias offers a high cure rate at a risk related to the patient's preoperative arrhythmia frequency, which in turn relates to the risk of arrhythmic death.
Adult↗
Atrial antitachycardia pacing in patients with supraventricular tachycardia: clinical experience with the Intertach pacemaker.
During a 3-year period, 22 patients with recurrent supraventricular tachycardia have been treated with antitachycardia pacemakers (Intermedics Intertach, 262-12, n = 17, and Intertach II, 262-16, n = 5). Eighty-two percent were female, the mean age was 44 +/- 14 years; 86% had atrioventricular node reentrant tachycardia. Symptoms had occurred over 11.8 +/- 7.1 years, with 3.6 hospital admissions per patient, despite 4.7 +/- 2.1 antiarrhythmic drugs. Following pacemaker implantation, during a follow-up of 14.8 +/- 11.5 months, only two patients have been readmitted to a hospital because of supraventricular tachycardia (mean 0.1 per patient). One patient is taking an antiarrhythmic agent, and four are taking beta adrenergic blocking agents. Thus, 23% are taking cardioactive drugs (it was anticipated that two patients would continue on drugs after pacemaker implantation). There have been no serious complications. Atrial antitachycardia is thus an effective therapy in carefully selected patients with recurrent supraventricular tachycardia, reducing hospital admissions for supraventricular tachycardia and reducing the need for antiarrhythmic drugs.
Adrenergic beta-Antagonists↗
QT dispersion: an indication of arrhythmia risk in patients with long QT intervals.
Homogeneity of recovery time protects against arrhythmias whereas dispersion of recovery time is arrhythmogenic. A single surface electrocardiographic QT interval gives no information on recovery time dispersion but the difference between the maximum and minimum body surface QT interval may be relevant. This hypothesis was tested by measuring the dispersion of the corrected QT interval (QTc) in 10 patients with an arrhythmogenic long QT interval (Romano Ward and Jervell and Lange-Nielsen syndromes or drug arrhythmogenicity) and in 14 patients without arrhythmias in whom the QT interval was prolonged by sotalol. QTc dispersion was significantly greater in the arrhythmogenic QT group than in the sotalol QT group. In patients with prolonged QT intervals, QT dispersion distinguished between those with ventricular arrhythmias and those without. This supports the hypothesis that QT dispersion reflects spatial differences in myocardial recovery time. QT dispersion may be useful in the assessment of both arrhythmia risk and the efficacy of antiarrhythmic drugs.
Adolescent↗
Surgery for ventricular tachyarrhythmias based on fragmentation mapping in sinus rhythm alone.
Intraoperative arrhythmia activation mapping underlies the impressive success of surgery for sustained uniform ventricular tachycardia. Unstable arrhythmias and those intraoperatively noninducible, however, are not amenable to activation mapping and strategies for dealing with them are poorly defined. We propose that fragmentation mapping in sinus rhythm can be used to direct surgery in such situation. In 21 (33%) of 64 patients operated upon at this unit, intra-operative arrhythmia mapping was impossible because of non-inducibility in 17 (27%) and unstable morphology in 4 (6%). Endocardial resection was performed in all areas showing 'fragmented' local electrograms (greater than 100 ms duration at 30-300 Hz filtering). Mean patient characteristics included: age 51 years; LV ejection fraction 32%; major arrhythmic episodes 16 (range 2-200); antiarrhythmic drug failures, 4. There were 5 (24%) early postoperative deaths (heart failure 3; sudden 1; metabolic 1) and 1 early arrhythmia recurrence. There were 3 late non-arrhythmic deaths and 1 further arrhythmia recurrence during follow-up of 23 +/- 19 months. Both patients with documented postoperative arrhythmic episodes were controlled on previously ineffective antiarrhythmic drug therapy. Fragmentation mapping in sinus rhythm successfully extends the surgical option to arrhythmias previously considered inoperable. The results compare favourably with those for arrhythmias in which surgery was directed by activation mapping.
Adolescent↗
Latent functional duality in an accessory pathway.
Accessory atrioventricular pathways classically possess neither decremental conduction nor functional duality. This report details an accessory pathway in which functional longitudinal dissociation, with decremental ventriculoatrial conduction in each component, was observed after, but not before, administration of the antiarrhythmic drug recainam.
Adult↗
Recurrent ventricular tachycardia associated with anomalous left coronary artery from the pulmonary artery in a child managed by revascularisation and map-guided endocardial resection.
A 13 year old girl with recurrent ventricular tachycardia that occurred in association with anomalous origin of the left coronary artery from the pulmonary artery is described. Such an arrhythmia has not been described before. Ligation of the anomalous left coronary artery led to more frequent episodes of ventricular tachycardia with evidence of myocardial ischaemia. She was successfully managed by revascularisation (to establish a two coronary system) and map-guided left ventricular aneurysmectomy.
Adolescent↗
Electrically induced ventricular arrhythmias in acute myocardial infarction treated with thrombolytic agents.
Ninety-two patients underwent programmed ventricular stimulation 12 +/- 3 days after acute myocardial infarction (AMI) treated with thrombolytic agents (streptokinase, recombinant tissue plasminogen activator, or both). Cardiac catheterization was performed in all patients on admission to hospital and was repeated in 97% of them 13 +/- 5 days later. Sustained ventricular arrhythmias--either tachycardia (VT) or fibrillation--were induced in 20 (22%) patients, with nonsustained VT induced in another 12 (13%). Multivariate analysis was used to identify predictors of induction of sustained VT, with short right ventricular effective refractory period (p = 0.0061), site of AMI (inferior or posterior, p = 0.008), infarct-related artery (right or circumflex coronary artery, p = 0.018), multivessel coronary artery disease (p = 0.043) and male sex (p = 0.028) being significant predictors of sustained VT. Neither successful reperfusion, time to reperfusion, nor residual stenosis in the infarct-related artery was significant. All patients in whom VT was induced were treated with electrophysiologically guided antiarrhythmic therapy. Cardiac mortality after hospital discharge was 1% over 30 +/- 16 months.
Cardiac Catheterization↗
Predictors of automatic implantable cardioverter defibrillator discharge for life-threatening ventricular arrhythmias.
Data from 100 patients with life-threatening ventricular arrhythmias and automatic implantable cardioverter defibrillators (AICDs) were analyzed to determine if clinical, angiographic and electrophysiologic variables are predictive of AICD discharge. During a median follow-up period of 18 months, 45% of patients experienced greater than or equal to 1 device discharge during a documented ventricular arrhythmia or in association with presyncope or syncope ("appropriate" AICD discharge). Univariate predictors of appropriate AICD discharge included depressed left ventricular ejection fraction (p = 0.0007), inducible sustained ventricular arrhythmia at electrophysiologic study performed in the absence of antiarrhythmic drugs (p = 0.009), fewer number of extrastimuli required for induction at this study (p = 0.001), inducible sustained arrhythmia at electrophysiologic study performed on the discharge antiarrhythmic regimen (p = 0.0005) and fewer extrastimuli required for this induction (p less than 0.0001). Multivariate analysis identified the induction of a sustained ventricular arrhythmia by 1 or 2 extrastimuli during electrophysiologic study performed on the discharge regimen as the only independent predictor among the variables analyzed (p less than 0.0001). The probability of appropriate AICD discharge at 18 months was 86% for patients who had a sustained arrhythmia induced with 1 or 2 extrastimuli versus 15% for those requiring 3 extrastimuli for arrhythmia induction and 13% for patients without inducible sustained arrhythmias.
Arrhythmias, Cardiac↗
Spontaneous and electrically induced ventricular arrhythmias during acute ischemia superimposed on 2 week old canine myocardial infarction.
The arrhythmogenic effect of acute reversible myocardial ischemia before and 2 weeks after experimental myocardial infarction was investigated in 37 dogs that underwent reversible 10 min occlusion of the first major marginal branch of the left circumflex coronary artery. Subsequently, 24 of the dogs underwent experimental myocardial infarction with permanent left anterior descending coronary ligation, and 13 dogs served as sham-operated controls. Two weeks later, an open chest programmed electrical stimulation was performed in the 13 sham-operated and 24 postinfarction dogs to determine its accuracy in predicting the ventricular arrhythmias that develop during a subsequent episode of acute reversible ischemia. After programmed electrical stimulation, the left circumflex marginal branch was reversibly occluded for 10 min at the same site. The incidence of spontaneous ventricular fibrillation during reversible left circumflex marginal coronary occlusion did not differ from the first to the second study in sham-operated dogs, whereas in the postinfarction dogs, it increased from 13% before infarction to 54% after infarction (p = 0.005). The outcome of programmed electrical stimulation predicted spontaneous ventricular arrhythmias during coronary occlusion in only 21% of the postinfarction dogs. The accuracy of programmed electrical stimulation was 42% and its predictive value was 47% in detecting the dogs with spontaneous ventricular fibrillation. Regional myocardial blood flow measurements by microsphere technique identified the severity of reversible ischemia in the infarct border and periinfarction zones as a correlate of spontaneous ventricular fibrillation during coronary occlusion. In contrast, total infarct size correlated with electrically induced but not with spontaneous ventricular arrhythmias.
Acute Disease↗
Electrophysiologic effects of d-sotalol in humans.
Sotalol is a beta-adrenergic blocking agent that prolongs the duration of the cardiac action potential in humans, without affecting the upstroke velocity of depolarization. The dextrorotatory isomer, d-sotalol, retains these class III effects, but has little beta-blocking activity in vitro. d-Sotalol has not been studied extensively in humans. The electrocardiographic (ECG) and electrophysiologic effects of d- and d,l-sotalol were therefore assessed in a prospective randomized study of 20 patients. Each patient received either d-sotalol (1, 1.5 or 2 mg/kg body weight) or d,l-sotalol (1 mg/kg) by intravenous infusion. The QT and QTc intervals were prolonged and refractoriness increased in the atrium, atrioventricular (AV) node, His-Purkinje system and right ventricle after both d- and d,l-sotalol. After d-sotalol, the increases in both QT and QTc intervals and in atrial and ventricular effective refractory periods were dose dependent. Highly significant linear correlation was demonstrated between the plasma sotalol level and the change in QT (r = 0.86, p = 0.001) and QTc intervals (r = 0.79, p = 0.002), and between the plasma sotalol level and the effective refractory period of the right atrium (r = 0.75, p = 0.005) and ventricle (r = 0.70, p = 0.025). This study confirms that d-sotalol has effects consistent with class III properties. It demonstrates these effects in humans, and suggests that d-sotalol may prove to be a useful antiarrhythmic agent.
Adolescent↗
Management of refractory supraventricular tachyarrhythmias using low-energy transcatheter shocks.
Alteration of atrioventricular (AV) conduction was attempted in 7 consecutive patients with severely symptomatic, drug-refractory supraventricular tachyarrhythmias using low-energy, direct-current transcatheter shocks of between 20 and 50 J. A single shock of 50 J or less delivered at the AV junction resulted immediately in complete AV block in 6 of the patients. Complete AV block has persisted in 3 patients, and in another who received a second shock 24 hours after the first. AV conduction was altered in the 3 patients in whom conduction either persisted or returned in such a way that supraventricular arrhythmias no longer occurred or were associated with a much slower ventricular response. After a follow-up of 20 to 37 months (mean 27 +/- 8), all 7 patients have improved symptomatically and 6 are taking no antiarrhythmic drugs. Thus, single low-energy transcatheter shocks can be used to ablate AV conduction. Such shocks may also modify AV conduction without production of complete AV block, but with changes in anterograde or retrograde conduction that may favorably influence recurrent symptomatic supraventricular tachyarrhythmias.
Aged↗
Survival to leave hospital from ventricular fibrillation.
In 125 consecutive patients with 173 arrests due to ventricular fibrillation, 53 survived to leave hospital. At the initial arrest and using univariate analysis, those who had primary ventricular fibrillation, had ventricular fibrillation less than 24 hours from the onset of symptoms, received the first DC shock less than 1 minute after the onset of ventricular fibrillation, who required less than 4 shocks to terminate the ventricular fibrillation, whose first established rhythm within the first minute of correction of ventricular fibrillation was atrial fibrillation, sinus rhythm or paced rhythm, or who were not receiving prior antiarrhythmic agents had a significantly improved survival to leave hospital (p less than 0.05). To predict survival to leave hospital using discriminant function analysis, the most significant factors ranking in order of importance at the time of the initial arrest were: less than or equal to 5 shocks to correct ventricular fibrillation, no prior antiarrhythmic therapy, primary ventricular fibrillation, and time from onset of ventricular fibrillation to first shock less than 1 minute. For the last arrest, the most significant factors were: no prior cardiac arrest, less than or equal to 5 shocks to correct ventricular fibrillation, no prior antiarrhythmic therapy, and primary ventricular fibrillation. The most significant factors measured at the time of the last arrest provided a better prediction of survival to leave hospital (sensitivity 77%, specificity 75%) than did similarly defined factors for the initial arrest (sensitivity 59%, specificity 89%).
Adolescent↗
Prophylactic lidocaine in the early phase of suspected myocardial infarction.
Four hundred two patients with suspected myocardial infarction seen within 6 hours of the onset of symptoms entered a double-blind randomized trial of lidocaine vs placebo. During the 1 hour after administration of the drug the incidence of ventricular fibrillation or sustained ventricular tachycardia among the 204 patients with acute myocardial infarction was low, 1.5%. Lidocaine, given in a 300 mg dose intramuscularly followed by 100 mg intravenously, did not prevent sustained ventricular tachycardia, although there was a significant reduction in the number of patients with warning arrhythmias between 15 and 45 minutes after the administration of lidocaine (p less than 0.05). The average plasma lidocaine level 10 minutes after administration for patients without a myocardial infarction was significantly higher than that for patients with an acute infarction. The mean plasma lidocaine level of patients on beta-blocking agents was no different from that in patients not on beta blocking agents. During the 1-hour study period, the incidence of central nervous system side effects was significantly greater in the lidocaine group, hypotension occurred in 11 patients, nine of whom had received lidocaine, and four patients died from asystole, three of whom had had lidocaine. We cannot advocate the administration of lidocaine prophylactically in the early hours of suspected myocardial infarction.
Adult↗
Myoglobin in the very early phase of acute myocardial infarction.
In this study of 35 patients with a definite or possible myocardial infarction seen within the first 5 h of the onset of symptoms and who could clearly define the onset of symptoms, the serum myoglobin was raised in 20% of those in whom blood was sampled within 1 h of the acute event. In 11 of the 35 (31%) patients the serum myoglobin was normal in the first blood sample. Of the nine patients seen within the first 2 h of the onset of symptoms who had frequent samples taken, the first raised serum myoglobin was recorded from 45 min to 3 h 15 min after the onset of symptoms. The serum levels started to rise 15-20 min before levels greater than 85 ng/mL were reached. In the absence of further chest pain more than one peak in serum myoglobin was recorded in 58% of the patients with acute myocardial infarction. The serum myoglobin level returned to normal within 24 h of the onset of symptoms in 44% of patients and within 36 h in 67%.
Female↗
Recurrent ventricular tachycardia associated with QT prolongation after mitral valve replacement and its association with intravenous administration of erythromycin.
Explore the source record for details and available documents.
Aged↗
Aortic valve endocarditis complicated by complete heart block.
A 34-year-old man with severe aortic incompetence caused by Streptococcus viridans developed severe central chest pain followed by complete heart block, multifocal ventricular extrasystoles, lengthening of the QTc and signs of cerebral emboli and pulmonary oedema. Early antibiotic therapy along with pacing, non-invasive investigations coupled with early surgery contributed significantly to the patient's survival.
Adult↗
Myoglobin and creatine kinase in acute myocardial infarction.
Serum myoglobin concentration and creatine kinase activity were measured serially in 70 consecutive patients presenting within four hours of the onset of symptoms of suspected acute myocardial infarction. Of 36 patients with definite or possible myocardial infarction (WHO criteria), the serum myoglobin concentration was raised (greater than 85 micrograms/l) one hour after the onset of symptoms in 25% and at four hours in 89%. Creatine kinase activity was raised (greater than 140 U/l) one hour after the onset in 25% and at four hours in only 56%. Within 12 hours of the onset of symptoms the myoglobin concentration reached a peak in 83% and the creatine kinase a peak in only 14%. Within 36 hours the myoglobin concentration fell to normal values in 67% while creatine kinase activity fell to normal values in only 3%. Four hours after the onset of symptoms the serum myoglobin concentration distinguished easily those patients with myocardial infarction from those without, whereas when creatine kinase values were used the sensitivity was poor but the specificity high. From the combined results of the two studies and using a single measurement of serum myoglobin concentration at six hours from the onset of symptoms to predict the diagnosis in 114 patients with suspected infarction, the sensitivity was 93% and specificity 89%.
Clinical Enzyme Tests↗