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Biomedical subjects

M J Griffith

Publications and source records attributed to M J Griffith.

At least 55 records · Page 3Linked to original sources
PubMed1992

A prospective study of the efficacy and safety of adjuvant metoprolol and xamoterol in combination with amiodarone for resistant ventricular tachycardia associated with impaired left ventricular function.

Combination antiarrhythmic drug therapy may be more effective than treatment with a single agent for control of refractory cases of sustained ventricular tachycardia (VT). In a prospective randomized crossover study of 20 patients with impaired left ventricular function (ejection fraction of 28% +/- 8%) and recurrent VT in spite of treatment with amiodarone, we compared the efficacy and safety of adjuvant therapy with metoprolol, 50 mg two times daily and xamoterol, 200 mg two times daily. Metoprolol caused hemodynamic deterioration in five patients, and only one also experienced intolerance to xamoterol. Sustained VT was inducible in all 20 patients who were receiving amiodarone alone but was suppressed or rendered nonsustained in 8 of 20 patients during treatment with amiodarone plus xamoterol and in 6 of 17 patients during treatment with amiodarone plus metoprolol. Addition of xamoterol restored sinus rhythm in four patients who presented with incessant VT, and metoprolol was effective for three of them. Neither beta-blocker significantly altered tachycardia cycle length or any electrophysiologic parameter other than the slowing of the sinus rate. Both beta-blockers suppressed exercise-induced VT in 3 of 4 patients, and addition of xamoterol significantly increased treadmill exercise duration (7.1 +/- 1.8 min) compared with administration of amiodarone alone (3.8 +/- 1.5 min; p < 0.01). Fourteen patients were discharged with prescriptions for amiodarone-beta-blocker combinations. During a mean follow-up period of 13 months (range, 2 to 24 months), there were three cases of recurrent VT (in all patients VT remained inducible) and no sudden deaths.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Difficulties in the use of electrocardiographic criteria for the differential diagnosis of left bundle branch block pattern tachycardia in patients with a structurally normal heart.

In patients with left bundle branch block pattern tachycardia, electrocardiographic criteria, based on leads V1, V2 and V6, have been shown to be effective for the diagnosis of ventricular tachycardia in patients with a previous myocardial infarct. To test these criteria on a wider population, we studied 53 consecutive patients with left bundle branch block pattern tachycardia. Seventeen patients had supraventricular tachycardia and 36 had ventricular tachycardia, 18 with a previous myocardial infarction, two with cardiomyopathy, and 16 with a normal heart. The sensitivity for the diagnosis of ventricular tachycardia in patients with a previous myocardial infarct of the combined criteria was 100% but was only 50% for the other patients, which was not significantly different from the patients with supraventricular tachycardia (29%). Two other criteria, right axis shift in tachycardia and ventricular ectopics during sinus rhythm with the same morphology as the tachycardia, were only seen in patients with ventricular tachycardia, and combined with the other criteria allowed the correct identification of 35/36 patients with ventricular tachycardia. To conclude, the electrocardiographic criteria based on leads V1, V2 and V6 are not sensitive for the diagnosis of a ventricular origin of left bundle branch block pattern tachycardia in patients with a normal heart and additional criteria are required for the diagnosis in these patients.

Adult↗
PubMed1992

Impact of the recommendations of the British Pacing and Electrophysiology Group on pacemaker prescription and on the immediate costs of pacing in the Northern Region.

BACKGROUND: The report from the Working Party of the British Pacing and Electrophysiology Group recommends the use of more sophisticated pacemakers in most patients. These proposals were initially circulated in September 1990 and are likely to have major cost implications. Their impact on pacing practice and the immediate costs of pacemaker hardware in the Northern Region were retrospectively audited. METHODS: The pacing records of 550 patients undergoing a first pacemaker insertion at the Freeman Hospital between March 1990 and August 1991 were reviewed. The patient's age, indication for pacing, pacing mode, and the cost of generator and lead(s) were recorded. The cost was compared with the costs of pacing with the optimal and alternative modes recommended by the Working Party. The costs were calculated from the actual mean cost of the recommended unit over the 18 month period of study multiplied by the number of patients who would have received that unit. RESULTS: 96% of patients were paced for sinus node dysfunction, atrioventricular block, or atrioventricular block and atrial fibrillation. The mean (SD) ages of patients in each diagnostic group were: sinus node dysfunction 69.4 (14), sinus node disease and atrioventricular block 67.2 (17.6), atrioventricular block 73.9 (12.5), atrial fibrillation and atrioventricular block 74.0 (13.9), and carotid sinus hypersensitivity 74.6 (11.6) years. Over the 18 month audit period there was an increase in physiological pacing. AAI pacing in patients with sinus node dysfunction increased by 100% and DDD pacing in atrioventricular block increased by atrioventricular block increased by 56%. Over the whole 18 month period the adoption of the British Pacing and Electrophysiology Groups optimal recommendations would have increased expenditure on pacemaker hardware in the Northern Region by 94% and the use of the alternative mode would have increased it by 61%. For the last six months alone the excess would be 78% and 48%. CONCLUSIONS: The adoption of the recommendations of the British Pacing and Electrophysiology group in the Northern Region would greatly increase the cost of pacing hardware. The greater part of this increase would be attributable to the routine use of dual chamber pacing in patients with atrioventricular block and the increased use of rate responsive units. The benefits of sophisticated pacing in a predominantly elderly population need to outweigh the disadvantages of the increased cost and complexity of follow up.

Aged↗
PubMed1991

Echocardiographic left ventricular wall thickness: a poor predictor of the severity of aortic valve stenosis.

Echocardiographic left ventricular hypertrophy is thought to be helpful in grading the severity of aortic stenosis. This study compared M-mode echocardiographic left ventricular wall dimensions with Gorlin aortic valve area. Good quality echocardiograms were obtained in 294 patients with aortic stenosis who also underwent cardiac catheterization. Patients with grade 3 or 4 aortic regurgitation were excluded. The correlation was calculated between the aortic valve area and the left ventricular wall dimensions. Correlation coefficients were poor; r = 0.13 for the septum, r = 0.15 for the posterior wall, and r = 0.17 for the mean wall dimension. Correlation was not improved significantly if patients with poor left ventricular function or systemic hypertension were excluded. Correlation with other hemodynamic parameters was better, peak left ventricular systolic pressure having r values of 0.36 and 0.30 for posterior wall and septum. Mean and peak aortic valve gradient had r values approaching 0.30 for both dimensions. If the peak gradient was included in multivariate analysis, the wall dimensions then had no predictive power for severity of aortic stenosis. This study demonstrates that the degree of left ventricular wall hypertrophy is not related to the severity of aortic outflow obstruction and therefore cannot be used to grade the severity of aortic stenosis.

Aortic Valve↗
PubMed1991

Signal averaging of the electrocardiogram in the remote differential diagnosis of broad complex tachycardias.

The diagnosis of the origin of a broad complex tachycardia may be difficult, especially in the absence of a 12-lead electrocardiogram of the tachycardia. This study investigates the value of signal averaging in the differential diagnosis of broad complex tachycardia. Signal averaging during sinus rhythm was performed in 102 consecutive patients who presented with broad complex tachycardia (QRS width greater than 110 ms), in whom a definitive electrophysiological diagnosis was made. The presence of late potentials was determined on the basis of two definitions, the second including total QRS duration. The patients studied included 75 with ventricular tachycardia; 33 of these patients had suffered previous myocardial infarction, five had dilated cardiomyopathy, and 37 had a 'normal' heart. Of the 27 patients with supraventricular tachycardia, 22 had an atrioventricular accessory pathway (seven with a delta wave in sinus rhythm), three had atrioventricular nodal tachycardia and two had atrial tachycardia. The sensitivity of late potentials for the diagnosis of ventricular tachycardia was low utilizing both definitions (28% and 45%) although specificity was high (96% and 95%). The sensitivity for the diagnosis of ventricular tachycardia was higher for patients with ischaemic heart disease (43% and 70%) but very low for patients with ventricular tachycardia and a normal heart (16% and 22%). In conclusion, signal averaging in the remote diagnosis of broad complex tachycardia is specific but not sensitive for ventricular tachycardia, which limits its usefulness in selecting patients for electrophysiological study.

Coronary Disease↗
PubMed1991

Multivariate analysis to simplify the differential diagnosis of broad complex tachycardia.

Univariate analysis has identified several criteria that aid the differential diagnosis of broad complex tachycardia. In this study of 102 consecutive patients multivariate analysis was performed to identify which of 15 clinical and 11 electrocardiographic variables were independent predictors of ventricular tachycardia. These were shown to be a history of myocardial infarction, the QRS waveforms in leads aVF and V1, and a change in axis from sinus rhythm to tachycardia of more than 40 degrees. If none of the criteria was met, the diagnosis was almost certainly supraventricular tachycardia. If one criterion was met the diagnosis was probably supraventricular tachycardia. If two criteria were met then the diagnosis was probably ventricular tachycardia. If three or four criteria were met, the diagnosis was almost certainly ventricular tachycardia. The predictive accuracy was 93%. This was increased to 95% by including two other criteria--definite independent P wave activity and ventricular extrasystoles with the same QRS configuration as that in tachycardia. These criteria were not included in the multivariate analysis because though they were 100% specific they were seldom seen. These four criteria can be used as simple rules in determining the origin of a broad complex tachycardia.

Diagnosis, Differential↗
PubMed1991

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections.

BACKGROUND: Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated. METHODS AND RESULTS: We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261 +/- 41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17 +/- 0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252 +/- 44 msec to 224 +/- 35 msec, p less than 0.01) after adenosine, but no change in average RR interval was observed (360 +/- 59 msec to 357 +/- 60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 +/- 21 msec to 360 +/- 49 msec, p less than 0.05) due to shortening of flutter cycle length (207 +/- 10 msec to 180 +/- 24 msec, p less than 0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration. CONCLUSIONS: Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by beta-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin.

Adenosine↗
PubMed1990

Relative efficacy and safety of intravenous drugs for termination of sustained ventricular tachycardia.

The relative safety and efficacy of intravenous administration of adenosine, lignocaine, disopyramide, flecainide, and sotalol for termination of stable, induced ventricular tachycardia was assessed in serial trials. Ventricular tachycardia was terminated by pacing if it persisted 10-15 min after the end of drug administration. 24 patients with recurrent ventricular tachycardia were studied. Ventricular tachycardia was terminated by a drug in 35 of 105 trials. In 6 patients no drug terminated the arrhythmia. Adenosine did not terminate tachycardia or have any serious adverse effect in any patient; both flecainide and disopyramide were significantly more effective than lignocaine, but flecainide had significantly more severe adverse effects than lignocaine. Lignocaine was the safest drug and should continue to be used as first-line drug therapy for stable ventricular tachycardia. Disopyramide should be considered as second-line treatment. DC cardioversion is necessary for unstable ventricular tachycardia, and its availability must be ensured before attempted pharmacological intervention.

Adenosine↗
PubMed1990

Use of intravenous adenosine in sinus rhythm as a diagnostic test for latent preexcitation.

In a proportion of patients with left free wall accessory connections, preexcitation 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.

Adenosine↗
PubMed1990

Prospective evaluation of a protocol for induction of sustained ventricular tachycardia in patients referred to a tertiary centre.

All eight stages of a stimulation protocol that used one then two extrastimuli from the right ventricular apex in sinus rhythm and three ventricular drive rates (100, 120, and 140 beats/min) were performed in 24 patients with recurrent spontaneous sustained ventricular tachycardia despite drug treatment. Twenty two of the patients had sustained a previous myocardial infarct and 18 were on long term treatment with amiodarone. Sustained (greater than 30 s) ventricular tachycardia was induced in all patients. Two extrastimuli were significantly more likely to induce sustained ventricular tachycardia than one extrastimulus, both overall and individually for the three ventricular drive rates. A ventricular drive rate of 140 beats/min was significantly more likely to induce ventricular tachycardia than ventricular drive rates of 100 and 120 beats/min which were significantly more effective than sinus rhythm. A ventricular drive rate of 140 beats/min with one or two extrastimuli induced ventricular tachycardia in 23/24 (95%) of the patients in this study. The full eight stage protocol was progressive separately for both extrastimuli and ventricular drive rate but the last two stages (ventricular drive rate of 140 beats/min with one or two extrastimuli) were as effective as the entire protocol in inducing ventricular tachycardia.

Aged↗
PubMed1989

The effects of adenosine on sinus node reentrant tachycardia.

The effects of adenosine given during sinus node reentrant tachycardia were investigated in two patients. Both patients received intravenous bolus doses of 0.1 mg/kg and 0.15 mg/kg. Adenosine slowed the atrial rate in both patients and terminated the tachycardia in one. These effects of adenosine on sinus node reentrant tachycardia suggest that sinus nodal tissue (as opposed to perinodal atrial tissue) is involved in the tachycardia circuit and that these effects should be considered when adenosine is used as a diagnostic agent in narrow-complex tachycardia.

Adenosine↗
PubMed1989

Inaccuracies in using aortic valve gradients alone to grade severity of aortic stenosis.

The severity of aortic stenosis is an important determinant of prognosis in patients with symptoms who do not undergo valve replacement. To assess the pitfalls of using valve gradients alone 636 patients with aortic stenosis in whom the aortic valve area had been calculated by the Gorlin formula were studied. The correlation between valve area and aortic gradients was poor. No gradient was found that was both sensitive and specific for aortic stenosis. The maximum predictive accuracy was 81% for a mean gradient of 30 mm Hg and 80% for a peak gradient of 30 mm Hg. A mean gradient of 50 mm Hg or a peak gradient of 60 mm Hg were specific with a 90% or more positive predictive value. It proved difficult, however, to find a lower limit with a 90% negative predictive value. Patients with severe aortic stenosis and low gradients (peak or mean gradient of less than 30 mm Hg) had small ventricles (on both angiographic and echocardiographic data) with good ejection fractions and so were unlikely to be detected subjectively. In comparison patients with mild aortic stenosis and low gradients tended to have more aortic regurgitation but have similar degrees of left ventricular hypertrophy on echocardiographic or electrocardiographic criteria. The aortic valve area should be measured in all patients with the suspicion of severe aortic stenosis with a mean gradient of less than 50 mm Hg (50% of patients in this study) or a peak gradient of less than 60 mm Hg (47% of patients in this study).

Age Factors↗
PubMed1989

Two new IgA1-kappa plasma cell leukaemia cell lines (JJN-1 & JJN-2) which proliferate in response to B cell stimulatory factor 2.

Two new cell lines with the phenotype of terminally differentiated B cells have been derived from the presentation bone marrow of a patient with plasma cell leukaemia. They express the same immunoglobulin (A1-kappa) as the original bone marrow cells. JJN-1 is an hypodiploid, slow-growing line with a plasmacytic morphology, which grows in medium with 15-20% fetal calf serum. When JJN-1 was stimulated with a supernatant ('ESG') containing B cell stimulatory factor 2 (BSF-2/IL-6), a hypotetraploid sub-line, JJN-2, was selectively stimulated. JJN-2 is dependent on ESG for survival. The stimulatory effect of ESG can be completely abrogated by an anti-BSF-2 monoclonal antibody. However, purified BSF-2 alone only produces sub-maximal stimulation of the lines. Both lines show complex karyotypic abnormalities, including 14q- and del(6q). JJN-1 and JJN-2 may be useful for the study of late B cell differentiation and for use as immunogens for the generation of anti-plasma cell monoclonal antibodies.

Antigens, Surface↗
PubMed1988

Adenosine in the diagnosis of broad complex tachycardia.

Adenosine, in incremental bolus doses up to 0.25 mg/kg, was given during regular broad complex tachycardia in 26 patients examined in an electrophysiological laboratory. In 8 of 9 cases of broad complex supraventricular tachycardia (SVT) the arrhythmia was terminated, converted into a narrow complex SVT, or atrioventricular block was induced. In all 9 cases of narrow complex SVT, the arrhythmia was stopped, or atrioventricular block was induced. The arrhythmia was stopped in only 1 of 17 cases of ventricular tachycardia. 6 patients with atrial fibrillation and ventricular pre-excitation were given adenosine, with no effect on mean ventricular rate (averaged over 3 s), although a significant, but short-lived, reduction in minimum RR interval was observed (from 242 ms, SD 45, to 217 ms, SD 39). The mean dose of adenosine required to stop the arrhythmia or to induce atrioventricular block in broad complex SVT (0.14 mg/kg, SD 0.04) was higher than in narrow complex SVT (0.11 mg/kg, SD 0.04). No adverse haemodynamic effects were observed in any patient, and large doses were tolerated by the patients with ventricular tachycardia. The data show that adenosine has a useful role in the diagnosis and treatment of regular broad complex tachycardia.

Adenosine↗
PubMed1988

Ventricular Wenckebach after intravenous therapy with class I antiarrhythmic agents.

Two unusual cases of Wenckebach-like conduction block in the infranodal tissues which developed after an intravenous dose of a Class I antiarrhythmic drug are presented. The first case shows infra-Hisian Wenckebach during sustained atrioventricular nodal reentrant tachycardia. The second case demonstrates rate-dependent Wenckebach-like exit block between the pacing catheter and the right ventricular tissues during pacing.

Adult↗