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Biomedical subjects

C J Garratt

Publications and source records attributed to C J Garratt.

At least 55 records · Page 3Linked to original sources
PubMed1994

Effects of intravenous adenosine on verapamil-sensitive "idiopathic" ventricular tachycardia.

The mechanism of ventricular tachycardia (VT) that occurs in the absence of structural heart disease ("idiopathic" VT) is unknown, but may involve triggered activity or reentry through calcium channel-mediated conduction pathways. It has been suggested that termination of VT by adenosine is specific to ventricular arrhythmias caused by cyclic adenosine monophosphate-mediated triggered activity. The effects of vagotonic maneuvers, and intravenous adenosine (up to 0.25 mg/kg in incremental doses) and verapamil (0.145 mg/kg) administered to 9 patients with "idiopathic" VT were studied during electrophysiologic study. Seven patients had inducible fascicular VT and 2 had incessant right ventricular outflow tract tachycardia. Vagal maneuvers did not have any effect on any VT. Adenosine interrupted both right ventricular outflow tract tachycardias for a period (2 to 15 seconds) that was dependent on the dose of adenosine, but had no effect on VT in any patient with fascicular VT. Verapamil produced stuttering termination of right ventricular outflow tract tachycardia with no preceding change in RR interval in patients with this arrhythmia. Administration of verapamil to patients with fascicular VT was followed by gradual slowing of the arrhythmia (cycle length increased from 397 +/- 45 to 506 +/- 86 ms; p < 0.01) in all 7 patients and by termination of VT in 6. In conclusion, the differential response of fascicular and right ventricular outflow tract tachycardias to both adenosine and verapamil suggests that: (1) These 2 forms of idiopathic VT have different mechanisms. (2) Fascicular VT is unlikely to be due to cyclic adenosine monophosphate-mediated triggered activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Ventricular tachycardia as default diagnosis in broad complex tachycardia.

In the differential diagnosis of broad-complex tachycardia, the most important decision is whether or not the tachycardia is ventricular, since this type carries the worst prognosis. However, the rules for a diagnosis of ventricular tachycardia are so complex that they are not satisfied in many cases, and the default diagnosis, supraventricular tachycardia, is erroneously accepted. We sought to reverse this strategy; unless simple rules for a positive diagnosis of supraventricular tachycardia were satisfied, ventricular tachycardia was diagnosed by default. The criterion for a diagnosis of supraventricular tachycardia was electrocardiographic (ECG) findings typical of bundle branch block (left = rS or QS wave in leads V1 and V2, delay to S wave nadir < 70 ms, and R wave and no Q wave in lead V6; right = rSR' wave in lead V1 and an RS wave in lead V6, with R wave height greater than S wave depth). Twelve-lead ECGs were done for 102 consecutive patients with broad-complex tachycardia (QRS width > 110 ms). Two observers, who were unaware of definitive diagnoses validated by electrophysiology, by our diagnostic rules made correct diagnosis of ventricular tachycardia in 63 and 62 of 69 patients, respectively, and correct diagnoses of supraventricular tachycardia in 28 and 22 of 33 patients (sensitivity for ventricular tachycardia 90% and 91%, specificity 67% and 85%). One observer then sought independent P waves in cases diagnosed as supraventricular tachycardia; sensitivity for the diagnosis of ventricular tachycardia rose to 96%, with a specificity of 64%. These criteria, which require only knowledge of typical bundle branch block patterns, were highly sensitive for the important diagnosis of ventricular tachycardia.

Diagnosis, Differential↗
PubMed1994

Value of physical signs in the diagnosis of ventricular tachycardia.

BACKGROUND: Although the use of physical signs for the diagnosis of ventricular tachycardia (VT) was described in the early 1900s, their value in this role has never been systematically assessed. METHODS AND RESULTS: Using a blinded, randomized protocol, we examined the ability of 26 clinicians to detect ventriculoatrial (VA) dissociation during cardiac pacing in 21 patients with both atrial and ventricular pacing wires in situ after successful ablation of accessory pathways. In protocol 1 (10 patients), pacing was randomized to either ventricular pacing alone (simulating VT) or to atrioventricular sequential pacing (simulating supraventricular tachycardia or VT with intact VA conduction) at rates of 150 or 180 beats per minute. Each patients was examined by four clinicians blinded to the pacing mode. Clinicians were asked to make a diagnosis of "VA association" or "VA dissociation" after examining the patient for variability of the arterial pulse, jugular venous pulse (JVP), and first heart sound. In protocol 2 (11 patients), randomization of pacing mode was performed between examination of each of the three physical signs so that the value of each sign was assessed individually. In protocol 1, a diagnosis of VA dissociation (VT) was made in 21 of 40 observations, with a specificity of 75%, sensitivity of 70%, and a positive predictive value (PPV) of 71%. In protocol 2, from a total of 132 observations (44 for each sign), the sensitivity, specificity, and PPV for a diagnosis of VT were as follows: arterial pulse, 61%, 71%, 70%; JVP, 96%, 75%, 82%; and first heart sound, 58%, 100%, 100%. CONCLUSIONS: It is concluded that, in patients with a regular tachycardia of uncertain origin, clinically detectable variations in the first heart sound and JVP are highly specific and sensitive indicators, respectively, of a diagnosis of VT. Assessment of the arterial pulse is of little value in this role.

Adult↗
PubMed1993

Ligand affinities in mutant metmyoglobins.

Ligand binding to the wild-type and a series of mutant porcine myoglobins, expressed and purified from Escherichia coli cells, has been studied using UV-VIS absorption spectroscopy. The proximal pocket mutation, F7 Ser-->Leu (F7), causes an increased affinity for OH- and N3- binding to metmyoglobin. A hydrogen bond between the F7 serine residue and the imidazole side-chain of the proximal histidine has been removed by this mutation. It is suggested that this allows the imidazole group to reorientate, reducing the steric clash between itself and the haem pyrrole nitrogen atoms and leading to a shortening of the bond between the proximal histidine and the haem iron. Other conformational changes further away from the haem pocket have also been induced, but the mutant still crystallizes under the same conditions as for the wild-type protein. A series of distal pocket mutants, E11 Val-->Thr (VT), E7 His-->Val (HV) and a mutant with both of these substitutions (M2) all have greatly reduced the OH- and N3- binding affinity. These effects have been interpreted by considering several factors: the changed stability of the aquometmyoglobin form, hydrogen-bond formation between the ligand and the E7 residue, and electrostatic repulsion between the ligand and the E11 threonine residue.

Animals↗
PubMed1993

The therapeutic and diagnostic cardiac electrophysiological uses of adenosine.

Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.

Adenosine↗
PubMed1993

Proarrhythmic effect of adenosine in a patient with atrial flutter.

Adenosine has been proposed as a useful diagnostic agent in patients with narrow complex regular tachycardia of uncertain origin. Its effects are usually transient owing to its extremely short plasma half life and, as a consequence, it is thought to be safer than other drugs used in the acute treatment of such arrhythmias. However, adenosine had a proarrhythmic effect when administered to a patient in order to confirm the diagnosis of atrial flutter. As expected, a transient increase in atrioventricular block was seen but this was followed by a doubling of the ventricular rate and haemodynamic compromise requiring immediate DC cardioversion. It is postulated that the secondary catecholamine-mediated effects of adenosine were responsible for this phenomenon.

Adenosine↗
PubMed1991

A comparison of intravenous propafenone and flecainide in the treatment of tachycardias associated with the Wolff-Parkinson-White syndrome.

UNLABELLED: We compared the electrophysiological effects of intravenous propafenone and flecainide on accessory pathway conduction by a randomized crossover study in 16 patients with Wolff-Parkinson-White syndrome. The antegrade refractory period of the pathway increased from 256 +/- 18 msec at baseline to 288 +/- 13 msec on propafenone (P less than 0.05) and to 296 +/- 27 msec on flecainide (P = 0.075). The minimum preexcited RR interval during atrial fibrillation or incremental atrial pacing was prolonged from 225 +/- 37 msec to 262 +/- 22 msec by propafenone (P less than 0.05) and to 301 +/- 31 msec by flecainide (P less than 0.005). The prolongation was significantly greater with flecainide than propafenone (P less than 0.05). Both drugs increased tachycardia cycle length (TCL) from 310 +/- 35 msec to 354 +/- 37 msec (propafenone P less than 0.005) and to 352 +/- 37 msec (flecainide P less than 0.01). Both propafenone and flecainide blocked antegrade conduction in the pathway in five patients. Both drugs rendered atrial fibrillation noninducible in seven patients and orthodromic tachycardia noninducible in five patients. CONCLUSIONS: (1) Flecainide causes a greater prolongation of minimum preexcited RR interval than propafenone; (2) There is no significant difference between propafenone and flecainide on the inducibility of arrhythmias, TCL, or incidence of antegrade conduction block.

Adult↗
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↗
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↗