A. R. Denniss

Prognostic significance of ventricular tachycardia and fibrillation induced at programmed stimulation and delayed potentials detected on the signal-averaged electrocardiograms of survivors of acute myocardial infarction.

The relative prognostic significance of ventricular tachycardia and ventricular fibrillation inducible at programmed stimulation within 1 month of acute myocardial infarction was compared in a prospective study of 403 clinically well survivors of transmural infarction who were 65 years old or younger. The prognostic significance of delayed potentials on the signal-averaged electrocardiogram was also examined in a subset of 306 patients without bundle branch block. Among the study patients, 20% had inducible ventricular tachycardia, 14% had inducible ventricular fibrillation, and 66% had no inducible arrhythmias. The 2 year probability of remaining free from cardiac death or nonfatal ventricular tachycardia or fibrillation was 0.73 for those with inducible ventricular tachycardia, 0.93 for those with inducible ventricular fibrillation, and 0.92 for those with no inducible arrhythmias. The cycle length of inducible ventricular tachycardia was 230 msec or more in 70% of the patients with inducible tachycardia who died. Of the patients studied by signal-averaged electrocardiography, 26% had delayed potentials. At 2 years, the probability of remaining free from cardiac death or nonfatal ventricular tachycardia or fibrillation was 0.73 for patients with delayed potentials and 0.95 for patients with no delayed potentials. There was a significant correlation (p less than .001) between the presence of delayed potentials and the ability to induce ventricular tachycardia. In conclusion, in survivors of recent infarction who have not had spontaneous ventricular tachycardia or fibrillation, inducible tachycardia (but not inducible fibrillation) at programmed stimulation predicts a significant risk of death or spontaneous tachycardia or fibrillation. A similar risk is found for patients with delayed potentials on the signal-averaged electrocardiogram.

Ventricular electrical instability: A predictor of death after myocardial infarction*

The results of a prospective study of ventricular electrical instability after myocardial infarction (MI) are presented. Ventricular electrical stability was assessed using a standardized protocol of programmed stimulation in 165 hemodynamically stable patients 6 to 28 days after acute MI. Ventricular electrical instability was defined as induction at programmed stimulation of ventricular fibrillation (VF) or ventricular tachycardia (VT) lasting at least 10 seconds. Of 165 MI survivors, 38 (23%) had ventricular electrical instability. No significant differences were noted between stable and unstable patients in terms of coronary prognostic index, elevation of serum creatine phosphokinase, coronary anatomy, site of MI, or frequency of VT within 48 hours of MI. The mean follow-up period was 8 months (range 0 to 12). There were 7 deaths in stable patients (5 from cardiogenic shock, 1 from septicemia, and 1 unwitnessed) and 10 deaths in unstable patients (8 instantaneous, 1 from cardiogenic shock, and 1 unwitnessed) during the subsequent year. In addition, 2 of 127 stable patients and 4 of 38 unstable patients had spontaneous VT from which they were satisfactorily resuscitated. Thus, the sensitivity of ventricular electrical instability as a predictor of instantaneous death or spontaneous VT was 86% and the specificity 83%. The predictive accuracy of the absence of ventricular electrical instability as an indicator for the absence of instantaneous death or spontaneous VT was 98%. The predictive accuracy of the presence of ventricular electrical instability as a predictor of instantaneous death or spontaneous VT was 32%. Thus, patients with ventricular electrical instability after MI have a high risk of instantaneous death within 1 year; patients without ventricular electrical instability after MI have a low risk of instantaneous death within 1 year; prospective studies of antiarrhythmic therapy and measures to prevent reinfarction and optimize left ventricular performance are required to determine whether instantaneous death can be prevented in unstable patients; and therapy to prevent reinfarction and optimize left ventricular performance may offer the best chance to improve prognosis in stable patients.

Modification of salivary duct electrolyte transport in rat and rabbit by physalaemin, VIP, GIP and other enterohormones

The effects of various polypeptide enterohormones and the tachykinin secretogogue, physalaemin, on electrolyte transport by the main excretory duct of the mandibular gland of the rabbit were studied in vitro. Vasoactive intestinal peptide (VIP, 2×10−11 mol l−1) and gastric inhibitory polypeptide (GIP, 10−11 mol l−1) reduced nett Na+ movement from lumen to interstitium and VIP also reduced the transepithelial potential difference; the effective concentrations of the two hormones lay within the range of normal plasma concentrations. Gastrin (5×10−7 mol l−1) and synthetic secretin (2×10−7 mol l−1) had similar effects but only at concentrations well above the normal plasma levels. Caerulein, an analogue of the octapeptide of cholecystokinin, had no effect on duct function even at a concentration of 10−6 mol l−1. The potent salivary secretogogue, physalaemin (4×10−8 mol l−1), which is an analogue of SubstanceP, a putative mammalian enterohormone and neurotransmitter substance, caused a marked increase in ductal Na transport (in rat as well as rabbit). It is concluded that VIP and GIP would normally play a role in determining salivary electrolyte composition and it is postulated that their action may be antagonized by a tachykinin such as SubstanceP.

Electrophysiological and anatomic differences between canine hearts with inducible ventricular tachycardia and fibrillation associated with chronic myocardial infarction.

This study examined electrophysiological and anatomic differences between dogs with ventricular tachycardia (VT) and fibrillation (VF) inducible by programmed ventricular stimulation 7–21 days after left anterior descending coronary artery ligation. Of 106 dogs studied, 40 had inducible VT, 19 had inducible VF, and 47 had no inducible arrhythmias. Differences between these three groups of animals were examined with cardiac mapping (to determine ventricular activation time in sinus rhythm) and post-mortem pathology (to measure infarct size and to reconstruct the anatomy at the infarct edge). Animals with inducible VT had longer maximal epicardial activation time (127±8 msec) than did animals with inducible VF (91±8 msec, p<0.05) or animals with no inducible arrhythmias (75±2 msec, p<0.001). Delayed epicardial activation occurred in 90% of animals with VT, 42% of animals with VF, and in only 6% of animals with no inducible arrhythmias. Endocardial and myocardial activation times were similar for the VT and VF groups. Infarct size was 18±2% of the ventricles for the VT group, much higher than for the VF group (11±2%, p<0.001) or for the group with no inducible arrhythmias (9±1%, p<0.001). The maximum diameter of viable muscle bundles interdigitat- ing with scar tissue at the infarct edge was much larger in animals with VT (2.4±0.2 mm) than in animals with VF (1.8±0.2 mm, p<0.05) or animals with no inducible arrhythmias (1.7±0.1 mm, p<0.01). Thus, when compared with animals with inducible VF, animals with inducible VT had longer epicardial activation time, larger infarct size and viable muscle bundles of larger diameter at the infarct edge.

The action of neurotransmitter hormones and analogues and cyclic nucleotides and theophylline on electrolyte transport by the excretory duct of the rabbit mandibular gland.

SummaryThe effects of autonomic drugs on electrolyte transport by the main duct of the rabbit mandibular gland were studiedin vitro. Acetylcholine, in concentrations as low as 10−10 M, reduced nett Na+ reabsorption and partially depolarized the transepithelial potential difference (P.D.); the effects were blocked by atropine. Acetylcholine was relatively ineffective applied from the luminal rather than the interstitial surface of the duct. Noradrenaline and isoproterenol produced similar effects to acetylcholine but the minimum effective concentrations were much higher (10−7 M and 10−3M, respectively). It was concluded that the duct cells possessed specific muscarinic receptors on the basal cell membrane but that adrenergic receptors, particularly β receptors, were either scanty or lacking altogether. Theophylline (10−5M) could mimic the effects of the autonomic drugs and produced a dramatic potentiation of the action of acetylcholine. Both cAMP and cGMP (4×10−5M) mimicked the acetylcholine response but cAMP was only effective when applied to the luminal cell membrane. It is proposed that cAMP is the intracellular mediator of the acetylcholine response and that it produces some of its effects by acting on an enzyme system close to the apical cell membrane.

Technique for maximizing the frequency response of the signal averaged Frank vectorcardiogram.

This system for signal averaging of the Frank vectorcardiogram incorporates several important features: 1, simultaneous analogue to digital conversion of three orthogonal leads; 2, interactive editing of the data; 3, optimization of the fiducial timing point using a template derived from the calculated QRS vector magnitude; and 4, simultaneous display of both the averaged recording and the noise level at high amplification, which facilitates the assessment of low amplitude signals in the ST segment. The effective frequency response of the system approached theoretical expectation and background noise was low. The effect of exclusion versus inclusion of the fiducial timing point optimizing routine in the signal averaging program was examined in 21 patients. Exclusion of the optimizing routine effectively reduced the high frequency response of the system at the -3dB point from 350 Hz to about 60 Hz. The QRS complex was prolonged, and attenuation and spreading of signals in the ST segment occurred so that some delayed potentials merged with background noise and were no longer visible. We conclude that the system has several theoretical and practical advantages when compared with other techniques. A major benefit is the inclusion of a routine to optimize the QRS fiducial timing point. This minimizes distortion and attenuation of signals in the ST segment, thereby enhancing the probability of detecting the signals.

Halothane anesthesia reduces inducibility of ventricular tachyarrhythmias in chronic canine myocardial infarction.

SummaryThis study examined the effects of 2% halothane general anesthesia on ventricular electrophysiological properties and inducibility of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF). Dogs with chronic anterior infarction and control dogs (no infarction) were studied before and after anesthesia using chronically implanted ventricular epicardial electrodes. PQ interval was increased by 15% with halothane, but QRS duration, QT interval, QTc, and sinus rhythm cycle length were unaffected by anesthesia. Diastolic threshold was unchanged by halothane. Halothane caused significant increases of 10–30% in ventricular effective refractory period (ERP) both in control and in infarct animals. VT and VF were not inducible in any of the nine control animals either before or after anesthesia. In infarct animals 34 of 75 (45%) had inducible VT or VF prior to halothane, but the incidence of inducible arrhythmias was significantly lower at 29% (22 of 75 animals) after halothane (p<0.01). In 75% of animals in which halothane suppressed inducibility of tachyarrhythmias, halothane-induced increases in ERP prevented achievement of the short extrastimulus coupling intervals at which the arrhythmias were induced before anesthesia. In conclusion: halothane anesthesia reduces the incidence of inducible sustained ventricular tachyarrhythmias in chronic canine myocardial infarction.

The action of physalaemin on electrolyte excretion by the mandibular and sublingual salivary glands of the rat.

The effect of physalaemin, an undecapeptide belonging to a family known collectively as the tachykinins, on water and electrolyte excretion of the mandibular and sublingual salivary glands of the rat has been investigated and compared to that of acetylcholine. Drugs were administered intravenously or by close-arterial infusion. Physalaemin is a powerful stimulant of fluid secretion by both glands although less potent than acetylcholine. The Na and K excretion patterns in physalaemin-evoked saliva resembled, but were by no means identical to those evoked by acetylcholine and other parasympathomimetic drugs: saliva evoked by physalaemin was considerably poorer in Na and K at all secretory rates. The HCO3 excretion curves, on the other hand, seemed to be identical to those evoked by parasympathomimetic drugs. From an analysis of the Na and K excretion patterns, it can be concluded, both for the mandibular and the sublingual glands, that physalaemin stimulates Na reabsorption and K secretion across the gland duct epithelium, whereas acetylcholine has the opposite effect. These findings agree nicely with what has previously been demonstrated in vitro in the isolated perfused main excretory duct of the rat mandibular gland.

Rapid‐access cardiology services: can these reduce the burden of acute chest pain on Australian and New Zealand health services?

Chest pain is common and places a significant burden on hospital resources. Many patients with undifferentiated low‐ to intermediate‐risk chest pain are admitted to hospital. Rapid‐access cardiology (RAC) services are hospital co‐located, cardiologist‐led outpatient clinics that provide rapid assessment and immediate management but not long‐term management. This service model is described as part of chest pain management and the National Service Framework for coronary heart disease in the United Kingdom (UK). We review the evidence on the effectiveness, safety and acceptability of RAC services. Our review finds that early assessment in RAC outpatient services of patients with suspected angina, without high‐risk features suspicious of an acute coronary syndrome, is safe, can reduce hospitalisations, is cost effective and has good medical practitioner and patient acceptability. However, the literature is limited in that the evaluation of this model of care has been only in the UK. It is potentially suited to other settings and needs further evaluation in other settings to assess its utility.

Early and long-term outcomes after manual and remote magnetic navigation-guided catheter ablation for ventricular tachycardia

Aims Remote magnetic navigation (RMN) is a safe and effective means of performing ventricular tachycardia (VT) ablation. It may have advantages over manual catheter ablation due to ease of manoeuvrability and catheter stability. We sought to compare the safety and efficacy of RMN vs. manual VT ablation. Methods and results Retrospective study of procedural outcomes of 139 consecutive VT ablation procedures (69 RMN, 70 manual ablation) in 113 patients between 2009 and 2015 was performed. Remote magnetic navigation was associated with overall higher acute procedural success (80% vs. 60%, P = 0.01), with a trend to fewer major complications (3% vs. 9% P = 0.09). Seventy-nine patients were followed up for a median of 17.0 [interquartile range (IQR) 3.0-41.0] months for the RMN group and 15.5 (IQR 6.5-30.0) months for manual ablation group. In the ischaemic cardiomyopathy subgroup, RMN was associated with longer survival from the composite endpoint of VT recurrence leading to defibrillator shock, re-hospitalization or repeat catheter ablation and all-cause mortality; single-procedure adjusted hazard ratio (HR) 0.240 (95% CI 0.070-0.821) P = 0.023, multi-procedure HR 0.170 (95% CI 0.046-0.632) P = 0.002. In patients with implanted defibrillators, multi-procedure VT-free survival was superior with RMN, HR 0.199 (95% CI 0.060-0.657) P = 0.003. Conclusion Remote magnetic navigation may improve clinical outcomes after catheter ablation of VT in patients with ischaemic cardiomyopathy. Further prospective clinical studies are required to confirm these findings.