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Biomedical subjects

N J Linker

Publications and source records attributed to N J Linker.

24 records · Page 2Linked to original sources
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.

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PubMed1989

Myopotential interference in unipolar rate responsive pacemakers.

The effects of myopotential interference on unipolar rate responsive pacemakers were assessed in 22 patients. Six types of pacemakers (from four manufacturers) were studied: five TX2 (QT sensing), seven Biorate (five RDP3 and two MB-1, respiratory rate sensing), seven Activitrax (activity sensing), two Medtronic 2503 (dP/dt sensing), and one Sensolog P703 (activity sensing). Provocative tests using arm exercises were performed in both VVI and rate responsive modes. At nominal sensitivity settings (1.8-2.5 mV), 55% of these patients were myopotential positive for at least 1 provocative test. Pressing the palms together was found to be the most sensitive provocative test. Rate response was achieved with treadmill exercise (all patients), hyperventilation (RDP3 and MB-1) and tapping (Activitrax) or wobbling the pacemaker in its pocket (Sensolog). During continued rate acceleration, myopotential interference was induced by arm exercises. The duration of inhibition was shorter when the provocative tests were performed during rate response compared to that occurred at rest. Short periods of myopotential interference resulted in temporary inhibition of pacing but rate response continued immediately on removal of the interference. In one patient with a RDP3 pacemaker, a prolonged episode of myopotential interference during treadmill exercise resulted in reversion of the pacemaker to the interference mode. Appropriate adjustment of the sensitivity setting effectively controlled the symptoms in most patients. However, one patient with a QT sensing pacemaker and symptomatic myopotential interference required programming to the VVT pacing mode. Two out of five patients with RDP3 required pacemaker replacement because of uncontrolled myopotential interference.(ABSTRACT TRUNCATED AT 250 WORDS)

Equipment Design↗
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

Drug effects on the sinus node. A clinical perspective.

The direct and indirect effects of drugs on the sinoatrial (SA) node are described in relation to basic cellular mechanisms and clinical applications. The effects of the different classes of antiarrhythmic agents are considered in terms of their direct depressant and excitatory actions. Indirect actions, particularly autonomic effects, are also discussed. Clinical aspects of the pharmacologic management of disorders of sinus node function such as the bradycardia-tachycardia syndrome, inappropriate sinus tachycardia, sinus bradycardia, and the identification of sinus node dysfunction by drug effects are considered in detail.

Humans↗
PubMed1987

Chronic sinoatrial disorder (sick sinus syndrome): a possible result of cardiac ischaemia.

Postmortem angiography was used to examine the blood vessels supplying the sinoatrial node in 25 subjects with chronic sinoatrial disorder (group 1). The results were compared with similar studies in 54 subjects who died of heart block and in whom sinus node function was normal (group 2). Although no significant lesion obstructing the blood flow to the sinus node was seen in the majority of those in group 1, there were abnormalities in seven cases, with reduced filling of the sinus node artery in five. In group 2 the sinus node artery filled normally in all cases despite major disease of the parent vessel in three. The combination of contralateral coronary artery disease with extensive atrial anastomoses was actively sought because this arrangement might predispose to a steal phenomenon. Such conditions were fully met in three cases in group 1 and two cases in group 2, and were found to a lesser extent in a further two cases in group 1 and three in group 2. Although coronary artery disease was unlikely to be the principal cause of sinus node dysfunction in most of the cases studied it was relatively common and may have been a factor in about one third. Improved survival after myocardial infarction may increase the number of patients with chronic sinoatrial disorder of ischaemic origin.

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