PubMed HealthSearch

Biomedical subjects

R W Campbell

Publications and source records attributed to R W Campbell.

At least 19 recordsLinked to original sources

The management and outcome of late post-infarct ventricular tachycardia presenting to a district general hospital.

A review was undertaken of late post-infarct ventricular tachycardia in a district hospital cardiac care unit in order to study the clinical course of a total population of such patients from initial presentation to ultimate outcome. Thirty-six patients with this diagnosis were identified over a 3 1/2-yr period. Twelve were treated by empirically chosen antiarrhythmic drugs. Twenty-four were referred for electrophysiologically guided treatment, of whom 16 were treated by antiarrhythmic drugs, 3 by anti-ischaemic measures alone, and 5 by non-pharmacological antiarrhythmic treatments (antiarrhythmic surgery, percutaneous ablation, defibrillator implantation, cardiac transplantation). Of those treated empirically, 4 died in hospital of their arrhythmia, 1 died suddenly at home, and 2 suffered non-fatal arrhythmia recurrences during mean follow-up of 20 months. There were no arrhythmic deaths in those whose treatment was guided by serial electrophysiology studies, although 4 patients died of cardiac failure or reinfarction, and 3 were hospitalised with a recurrence of ventricular tachycardia during mean follow-up of 16 months. Age, concomitant medical problems and the apparent response to initial antiarrhythmic therapy were the main factors influencing management decisions. The apparent superiority of more intensive management strategies based on electrophysiology studies must be interpreted in the context of the selection processes applied to the total population initially presenting.

Aged

Surgery for ventricular tachycardia associated with right ventricular dysplasia: disarticulation of right ventricle in 9 of 10 cases.

Ten patients (nine men, one woman; mean age 39 years) with arrhythmogenic right ventricular dysplasia underwent surgery to control life-threatening drug refractory ventricular arrhythmias. All had ventricular tachycardia causing syncope and six had a history of cardiac arrest. In all a minimum of three antiarrhythmic drugs (mean five) had been ineffective. At operation, the right ventricle was grossly diseased in all patients. Ventricular tachycardias were induced and mapped intraoperatively in all patients. The surgical plan was to ablate the arrhythmogenic focus if it was less than 4 cm2; one patient was so managed. Of the remaining nine, four underwent partial (approximately 40% of the right ventricular free wall) and five underwent total right ventricular disarticulation. All survived the operation and are alive at a mean follow-up interval of 24 months (range 5 to 67). Two patients developed new sustained ventricular tachycardias. These were well tolerated and, unlike the original arrhythmias, were easily controlled by drug treatment. All patients who underwent right ventricular disarticulation manifested signs of right heart failure in the early postoperative period, but these lessened progressively with the development of systolic septal movement into the right ventricular cavity. All 10 patients are in New York Heart Association class I or II at last review. In selected patients with arrhythmogenic right ventricular dysplasia, surgery offers a curative treatment for ventricular tachycardia and should be considered for patients whose arrhythmias are life-threatening and refractory to drug treatment.

Adolescent

QT dispersion in sinus beats and ventricular extrasystoles in normal hearts.

OBJECTIVE: Recent studies have suggested that QT interlead variability (dispersion) on the surface electrocardiogram may have potential as a measure of recovery time dispersion. To test this hypothesis further QT dispersion occurring in sinus beats was compared with that in ventricular extrasystoles. DESIGN: Simultaneous electrocardiograms were recorded at 50 mm/s during sinus rhythm in a drug free state while ventricular extrastimuli were introduced by programmed right ventricular stimulation at different coupling intervals. QT dispersion, defined as the difference between the maximum and minimum QT, was calculated separately for the extrasystoles and preceding and following sinus complexes. To correct for the influence of the number of measurable leads on QT dispersion, an "adjusted" QT dispersion calculated as QT dispersion/square root of the number of measurable leads, was used to compare sinus complexes and extrasystoles. PATIENTS: Nine patients were studied who were undergoing electrophysiological study for investigation of palpitation and were found to have electrically normal ventricles. RESULTS: At all coupling intervals tested "adjusted" QT dispersion was significantly greater in the ventricular extrasystoles than in either the preceding or following sinus complexes. For the coupling interval 350 ms, the 95% confidence intervals for the difference between means was 52 to 78 ms (preceding sinus complex) and 56 to 82 ms (following sinus complex) (p less than 0.00001). There was no correlation between the coupling interval and the magnitude of the "adjusted" QT dispersion. CONCLUSION: These results accord fully with expected differences in ventricular recovery time dispersion and offer further support for the hypothesis that QT dispersion reflects regional variation in ventricular recovery. If substantiated by invasive studies, these findings have wide implications for both the usefulness and the method of QT measurement.

Cardiac Complexes, Premature

Reduction in QT dispersion by sotalol following myocardial infarction.

Increased dispersion of ventricular recovery time is believed to be a substrate for serious ventricular arrhythmias. Class III antiarrhythmic drugs probably operate by decreasing dispersion through homogeneous prolongation of recovery time. A single surface QT value gives no information on recovery time dispersion but interlead variation in QT may be relevant. QTc dispersion was measured in 67 patients post myocardial infarction randomized to treatment with either sotalol or placebo. QTc dispersion was calculated as the difference between the maximum and minimum QTc in any surface electrocardiogram lead. Both maximum QTc and QTc dispersion varied considerably following infarction but throughout the 6-month follow-up period maximum QTc was significantly greater (P less than 0.05) and QTc dispersion significantly less (P less than 0.05) in patients on sotalol compared with placebo. These findings are in accord with expected changes in ventricular recovery time and provide strong support for the hypothesis that surface electrocardiogram QT variation reflects regional differences in ventricular recovery time.

Arrhythmias, Cardiac

Electrophysiologic effects and antiarrhythmic efficacy of recainam in patients with supraventricular tachycardia.

Recainam is a new antiarrhythmic agent with class Ic properties. To evaluate its electrophysiologic effects and antiarrhythmic efficacy in patients with recurrent supraventricular tachycardia (SVT), programmed electrical stimulation was performed in 10 patients before and after intravenous recainam (loading dose 0.8 mg/kg, infusion 1 mg/kg/h), and in four patients on oral recainam 1,200 mg/day. Five patients had atrioventricular (AV) node reentrant tachycardia; five had AV-reciprocating tachycardia. There were no significant changes in electrocardiographic and intracardiac intervals after either intravenous or oral recainam. After intravenous recainam, the ventricular effective refractory period (ERP) shortened (231 +/- 14-219 +/- 9 ms, p less than 0.05). The antegrade ERP of all three bidirectional accessory pathway markedly prolonged, but the effect on retrograde accessory pathway and AV node ERPs was unremarkable. SVT induction was prevented in three of 10 patients and SVT cycle length increased modestly in seven (357 +/- 44-374 +/- 42 ms, p = 0.07). On oral recainam, an increase in the frequency of spontaneous SVT occurred in two patients. At the doses given, recainam caused less electrophysiologic change than expected, had modest antiarrhythmic efficacy, and might have significant arrhythmogenic potential.

Administration, Oral

Acute and chronic hemodynamic impact of total right ventricular disarticulation.

Right ventricular disarticulation is a radical operation to control ventricular arrhythmias in patients with arrhythmogenic right ventricular dysplasia. This report describes the acute and chronic hemodynamic impact of the procedure based on our experience of five patients with life-threatening arrhythmias unresponsive to medical therapy who have undergone total disarticulation of the right ventricle. Although all patients suffered acute postoperative hemodynamic problems, all survived and returned to an excellent functional class. Right ventricular disarticulation should be considered in patients with drug refractory ventricular tachycardias due to arrhythmogenic right ventricular dysplasia when the arrhythmia either poses a life threat or results in chronic morbidity.

Adult

The deficiencies of current medical therapy for the management of angina pectoris.

The prime management need in angina pectoris is to abolish or to minimize pain. Nitrates, calcium antagonists and beta-blockers are indicated for this purpose but they are not a complete answer to the problem. Selection of therapy for individual patients is not guided scientifically and, at present, treatment of angina follows general protocols rather than a personalized approach based on the underlying patho-anatomy and physiology. Medical therapy offers palliation of the disease rather than a cure, although recent evidence raises possibilities that some anti-anginal therapy, notably the calcium antagonists, may favourably affect disease progression. Tachyphylaxis, dosing, unwanted effects, and optimal sequences and combinations of medical therapy are important clinical problems about which remarkably little is known. The greatest deficiency of current medical therapy, however, is that, despite the amelioration of angina, beneficial effects on mortality have not been established. Thus, for the foreseeable future non-pharmacological therapy in the form of surgery or angioplasty will dominate management of high-risk anginal patients. At present, it is only in unstable angina that there is evidence of prognostic benefit from medical therapy with aspirin and anticoagulants. In more stable forms of angina, medical versus surgical comparisons reflect 'old' drugs and strategies. The prospects of reducing death and infarction by medical therapy in anginal patients should be re-examined.

Adrenergic beta-Antagonists

Predisposing factors for ventricular arrhythmias.

The majority of ventricular arrhythmias that affect humans are reentrant. Three components are then of relevance: the substrate, trigger, and facilitatory factors. The substrate comprises an area of slow conduction and unidirectional block. The anisotropic conduction of ventricular muscle is a contributory factor but, on its own, is unlikely to support a pathological arrhythmia. Ischemia and infarction are important but are not the exclusive disease mechanisms for creating patchy electrical conditions that will support reentry. Trigger factors are not well understood, but the perturbing influence of ectopic beats is important. Ectopic beat frequency correlates with risk, but variable coupling may be a more effective trigger, operating by "scanning" the cardiac cycle. Facilitatory factors act when both substrate and trigger are present and include autonomic tone, electrolyte imbalance, and biochemical influences. In the future, they may be important therapeutic targets. Substrate, trigger, and facilitators--all are interdependent. Separating their individual contribution is difficult and may be inappropriate. Sometimes the substrate is created by the trigger or facilitator and the facilitator may be the actual trigger. These issues raise exciting prospects for arrhythmia control but should not overshadow the fact that minimizing or preventing disease of ventricular muscle is the optimal clinical goal.

Animals

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

Heart failure--the options for therapy.

Diuretics and angiotensin-converting enzyme inhibitors currently are the mainstay of both acute and chronic heart failure management. They have earned their place by bringing measurable and reliable clinical benefit to patients with all grades and types of heart failure. Other treatments--digoxin, vasodilators and inotropes--offer less secure efficacy and their clinical role is at times controversial. The need for new remedies is inescapable. Despite current therapy, heart failure causes a distressing reduction in both quality and quantity of life. As knowledge of the pathophysiology of heart failure is gained, more selective treatment options may become available offering hitherto unknown specificity but demanding remarkable levels of diagnostic accuracy.

Cardiac Output, Low

Left posterior fascicular tachycardia due to localized microreentry.

Fascicular tachycardia in young patients without overt heart disease constitutes a rare but electrophysiologically distinct arrhythmia entity. Microreentry within the left posterior fascicle has been proposed as its mechanism, but evidence for this is inconclusive. This report details a patient with incessant fascicular tachycardia. The electrophysiological features, in particular the pattern of resetting response, provided strong evidence for reentry as the tachycardia mechanism. Satisfactory long-term arrhythmia control was achieved with flecainide.

Adult

Familial ventricular tachycardia: a report of four families.

Four cases of familial ventricular tachycardia are presented. In each family the proband was an adolescent girl. Twelve members in the four families were affected and all were female. The clinical and electrocardiographic features were relatively constant within each family but there were striking differences between families. These differences argue against a common electrophysiological or pathophysiological basis for the ventricular tachycardia.

Adolescent

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

Neural control of ANF release in hypoxia and pulmonary hypertension.

Hypoxia causes the release of atrial natriuretic factor (ANF), but the mechanisms are not yet understood. This study examined the relative contribution of pulmonary arterial hypertension, neural pathways, increased heart rate, or increased atrial size to the ANF response. Alveolar hypoxia [fractional concentration of O2 in inspired gas (FIo2) = 0.1] or pulmonary arterial hypertension (25-45 mmHg) was induced for 10 min in four series (n = 4-12 each) of anesthetized, mechanically ventilated pigs. During hypoxia, plasma ANF concentrations increased by 129 +/- 52 (SE) pg/ml (or 271 +/- 105%) over baseline (35 +/- 7 pg/ml; P less than 0.01) (series 1). There was also a significant increase of pulmonary arterial pressure, heart rate, central venous pressure, and pulmonary capillary wedge pressure. Repeated pulmonary hypertension induced by intravenous air infusion caused a repeated and reversible 125 +/- 14% increase (P less than 0.001) of plasma ANF, and this response was totally abolished by lesion of the cervical vagosympathetic trunks (series 2). Lesion of these nerves 1 h before hypoxia also decreased the ANF response to hypoxia by 45-58% (P less than 0.01), whereas responses of heart rate and atrial pressures were unchanged (series 3). The ANF response to hypoxia, expressed in percent of baseline, was not affected by 0.2 mg/kg propranolol (PR) (no PR: 145 +/- 63%; PR: 151 +/- 82%; not significantly different from series 1 and control, series 3), although the increase in heart rate (no PR: 61 +/- 15 beats/min) was almost abolished (PR: 17 +/- 5 beats/min) (series 4). Hypoxia caused no significant changes in right and left atrial peak volume regardless of propranolol, as measured with an electrical conductance catheter. The results indicate that a new neural reflex of probably pulmonary arterial origin mediates approximately 50% of the ANF response to hypoxia. The remaining ANF response remains to be explored further and cannot be explained by conventional release mechanisms such as atrial stretch and pulsatility alone.

Animals