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Congestive heart failure (HF) is a major focus of medical research. Its incidence has greatly increased in recent decades because of an aging population base and the increasingly successful treatment of other forms of chronic cardiac disease. Relevant large animal models of HF should reflect the complex interactions of cardiac dysfunction, neurohumoral dynamics and peripheral vascular abnormalities found in human HF. A number of large animal models have been developed, especially in dogs, sheep and swine, using naturally occurring HF, or single or combinations of interventions, as instruments to trigger the development of HF. Naturally occurring HF models are not commonly used because of ethical or perceived ethical grounds, however, King Charles Cavalier Spaniel and Yucatan Mini Pig models have been described. Tachycardia induced HF is the most commonly used HF model. Ventricular pacing at 220-240 bpm results in profound low output, biventricular, oedematous failure in two to three weeks. Lower pacing rates result in a more stable, sustainable, lesser degree of failure. Positive features of this model include 'acceptance', aetiological relevance to patient tachycardia induced HF, neurohumoral and functional profile similar to most human HF, relatively low cost simple preparation, ability to manipulate the degree of failure with pacing rate, reversibility, reliability and a large amount of published multi species data. Limitations to the use of the model are the rapid onset, the fact that reversibility is only relevant to the tachycardia induced patient HF, the absence of hypertrophy in failure, the diminished plasma atrial natriuretic peptide (ANP) levels, absence of ANP of ventricular origin, and the interference between rapid pacing and therapeutic interventions. Myocardial damage models of HF include those models induced by ischaemia, eg due to coronary occlusion (ligation or aneroid) or intracoronary microembolism, transmyocardial DC shock, toxic cardiomyopathy from adriamycin, doxorubicin or catecholamines. Overload models of HF may be induced by high pressure from aortic constriction, aortic regurgitation, renal artery constriction, pulmonary stenosis or aortocaval shunts, or by induction of mitral regurgitation from chordae or leaflet damage. No single, all-encompassing, large animal model of HF exists to date. Selection of the type of model to be used should be based primarily on the hypotheses to be tested and secondarily on the available resources and facilities.

Extrapolation of clinical trial results to clinical practice requires consideration of whether the trial patients were representative of clinical practice, whether the trial therapy studied was optimal, whether the sample size was adequate, and the impact of adjunctive treatments. In thrombolytic trials in particular, regional variations in attitudes to coronary angiography may have affected outcomes. Clinical trial results need to be interpreted in the light of the cost effectiveness of the application. The assessment of clinical outcomes depends on interplay between the structure and process of care, patient factors and chance. Large standardised databases are necessary to assess clinical practice and outcomes.

Background: Dobutamine stress echocardiography (DSE) is a new non-invasive imaging modality which combines two-dimensional echocardiography with cardiovascular stress induced by dobutamine infusion. Its use in patients with suspected or documented coronary artery disease (CAD) is currently under extensive investigation., Aims: To illustrate the clinical utility, safety and diagnostic value of DSE., Methods: One hundred and thirty-seven consecutive patients referred for DSE were studied. Eighty-four patients also underwent coronary angiography., Results: Eleven patients (8%) did not undergo DSE because of poor image quality. Of the remaining 126 patients, 110 (87%) achieved their target heart rate or reached a pre-determined end point during DSE. Eight patients (6%) developed non-cardiac side effects during DSE, none of which required premature termination of the procedure. Cardiac arrhythmias were documented in 15 patients (12%) but only one required intervention. In 84 patients who underwent coronary angiography, DSE showed a sensitivity and specificity of 88% and 83%, respectively, in detecting the presence of, and 75% and 75%, respectively, in localising significant CAD. In 35 patients who underwent DSE after uncomplicated myocardial infarction, the positive and negative predictive values for cardiac events following infarction in a six-month followup period were 74% and 62%, respectively., Conclusions: DSE is a well tolerated, safe and useful test in detecting and localising significant CAD. It can also provide useful post-infarctional prognostic information.

Background: Conventional methods of quantifying heart rate variability using summary statistics have shown that decreased variability is associated with increased mortality in heart failure. However, many patients with heart failure have arrhythmias which make the 'raw' heart rate variability data less suitable for the use of summary statistical measures., Aims: To examine the clinical potential of a new measure of heart rate variability data, presented by the Poincaré plot pattern, as an adjunct to the summary statistical measures of R-R interval variability., Methods: We used the Poincaré plot pattern to display beat-to-beat heart rate variability data from a group of 23 patients with heart failure and compared them with data collected from 20 healthy age-matched control subjects. The data, which consists of 2000 consecutive R-R intervals, were gathered over 20-40 minutes while the subjects rested supine in a quiet darkened room., Results: The morphological classification scheme proposed reflected the functional status of patients in heart failure. There was a significant difference (chi-square = 27.5, p < 0.0001) in the different pattern types between patients with NYHA Class I and II compared to patients with NYHA Class II and IV. All healthy subjects displayed a 'cluster' type of pattern characterised by normally distributed data. Sixteen of the 23 patients in heart failure also produced data which were normally distributed but the remaining seven produced data which required careful filtering to make them suitable for analysis using summary statistics, but which could be analysed by the Poincaré plot., Conclusions: The Poincaré plot pattern is a semi-quantitative tool which can be applied to the analysis of R-R interval data. It has potential advantages in that it allows assessment of data which are grossly non-Gaussian in distribution, and is a simple and easily implemented method which can be used in a clinical setting to augment the standard electrocardiogram to provide 'real time' visualisation of data.

Background: Mitral valve repair is the procedure of choice in the surgical management of mitral regurgitation. Intraoperative confirmation of successful repair is essential to the effectiveness of this procedure., Aims: The aims of this study were: (a) to compare intraoperative transoesophageal echocardiography (TOE) with the surgeon's assessment of valve competence; (b) to assess the impact of routine intraoperative imaging on the hospital echocardiography laboratory., Methods: Eighty-six consecutive patients undergoing mitral valve repair formed the study population. Valve competence following repair was assessed intraoperatively by: TOE; saline insufflation of the flaccid left ventricle; and evaluation of the pulmonary capillary wedge pressure for the presence of a significant V wave., Results: TOE demonstrated successful valve repair (< or = 1 + residual regurgitation) in 75 patients (87%) and detected significant residual regurgitation (> or = 3+) in seven (8.2%). The mechanism of regurgitation was also clearly shown. Of these seven patients, four underwent immediate valve replacement, two had successful revision of the initial repair and one required valve replacement one week later. In all seven patients the valve repair had been assessed as successful by saline testing and only one had a post-repair V wave 10 mmHg above the mean pulmonary capillary wedge pressure. In 30 non-selected patients the imaging equipment was required in theatre for 43 +/- 18 minutes., Conclusions: TOE is currently the most sensitive method for detection and quantitation of residual mitral regurgitation following valve repair. Evaluation can be performed within a similar time to that required for one complete transthoracic study and can usually be performed with minimal disruption to the hospital echocardiography laboratory.

Background: The importance of cardiogenic embolism as a cause of cerebral ischaemic events may be underestimated if potential cardiac sources of embolism remain undetected. Transoesophageal echocardiography (TOE) is more sensitive in detecting such abnormalities than earlier methods and may result in more frequent recognition of cardiogenic embolism., Aims: To establish in an unselected stroke population the prevalence of potential cardiac sources of embolism detectable on TOE and their relationship to atrial fibrillation and carotid stenosis., Methods: One hundred and thirty-five consecutive patients with cerebral ischaemic events were studied using transthoracic and monoplane transoesophageal contrast echocardiography and carotid Duplex imaging or cerebral angiography., Results: Thirty patients (22%) had atrial fibrillation. In 43 patients (32%), no cardiac source of embolism was identified; in eight echocardiography was normal. At least one potential cardiac source of embolism was identified in 92 patients (68%) with multiple findings in 41; these patients were older (70 +/- 9 years vs 61 +/- 14 years; p = 0.0001), more frequently in atrial fibrillation (28/92 vs 2/43; p = 0.0017) and more frequently had cortical or large subcortical stroke (71/92 vs 23/43; p = 0.005). Carotid stenoses were detected in 55% of patients, not significantly different in those with and without cardiac abnormalities., Conclusion: When bias in selection of patients is avoided, TOE detects a potential cardiac source of embolism in most patients with cerebral ischaemia, particularly those older and in atrial fibrillation. Multiple cardiac abnormalities and coexistent carotid disease are common. The implication of these findings for prevention of stroke awaits age-matched controlled studies.

Background: The recent advent of radiofrequency (RF) catheter ablation as a curative therapy for supraventricular tachyarrhythmias has challenged the role of long term drug treatment, which is essentially a palliative therapy. To date, however, no data have been published on the cost-effectiveness of RF ablation as compared with drug treatment in the Australian setting., Aims: The study aimed to compare actual and projected costs of these two treatment options in a consecutive group of patients having RF ablation as treatment for symptomatic tachyarrhythmias., Methods: The cost effectiveness of RF catheter ablation was assessed in 26 patients having RF ablation, using a hypothetical model of continued drug therapy in the same group of patients. A 'cost saving' criterion was used for cost effectiveness. Actual costs for the RF ablation and for continued drug therapy were based on data from medical records and from the answers to a detailed patient questionnaire. Analysis included costs of prior diagnostic electrophysiology (EP) study (17/26 patients), general anaesthesia (GA: 20/26 patients), post-ablation echocardiography (10/26 patients), and late follow-up EP study (7/26 patients). The in-hospital stay for the RF ablation was two days in all cases, and no patient required implantation of a permanent pacemaker. The RF ablation procedure was successful in 23/26 patients (88.5%) with late recurrence of tachycardia in one patient. After a median follow-up of nine months, 22/26 patients no longer require antiarrhythmic drug therapy., Results: The mean per patient cost of RF ablation was $4067 in the study group. This reduces to $2546 if prior EP study and GA are excluded. The mean per patient cost of continued medical therapy was $700 per year. Extrapolating over 20 years and allowing for an annual 5% inflation factor, RF ablation becomes cost saving in 5.5 years (3.8 years if prior EP and GA are excluded). Over 20 years, continued drug therapy would be four to five times more expensive than RF ablation in the patient study group. We consider RF ablation to be a cost-effective alternative to long term drug therapy in patients with supraventricular tachyarrhythmias.

Sudden cardiac death (SCD) is usually due to monomorphic ventricular tachycardia and/or ventricular fibrillation. However, in the vast majority of patients these arrhythmias are associated with advanced structural disease. In our society, this is usually due to coronary artery disease (CAD). The implantable cardioverter--defibrillator is the logical approach to management in survivors of SCD. Its rational use must be guided by electrophysiology study. However, a realistic and cost-effective approach to the prevention of a first cardiac arrest must be multifaceted and take cognisance of other aspects including primary prevention. Limitation of the size of myocardial infarction (MI) is vital. Trials already suggests that effective thrombolysis may impinge long-term on arrhythmic end-points. Following infarction, ventricular arrhythmias and sudden death may also be decreased by aspirin, beta-blockers, and possibly angiotensin converting enzyme inhibitors and amiodarone. Many post-infarction studies employ a combined end-point of death and clinical arrhythmias. However, death is usually confined to those with an ejection fraction < 35%. In them, treatment of associated heart failure is often a consideration and if the ejection fraction < 15-20%, depending on donor availability, transplantation may even be the preferred therapeutic option to the cardioverter-defibrillator.

Permanent pacing has usually been indicated for the treatment of organic disease of the sinus node or specific cardiac conducting tissue. We report three patients in whom profound syncope was apparently related to intense, transient autonomic dysfunction. Although ventricular standstill was documented in all three, detailed electrophysiology study, responses to graded Valsalva manoeuvres and carotid sinus massage, and repeated observations after cardiac autonomic blockade by IV atropine (0.03 mg/Kg) and propranolol (0.15 mg/Kg) were essentially normal. Permanent ventricular (VVI) pacing has controlled symptoms in all three, over follow-up period of 20 to 26 months. These observations suggest that transient autonomic imbalance may be a cause of undiagnosed cardiac syncope. This is neither excluded by normal electrophysiology study nor by normal responses to usual provocative autonomic interventions.

The periodicity of symptoms in patients who present with syncope restricts the diagnostic value of prolonged electrocardiographic monitoring and furthermore, demonstration of arrhythmias in the absence of symptoms may not enable a firm diagnosis. Because of this, electrophysiology study is often necessary. A series of 89 consecutive patients with syncope of unknown origin is reported, highlighting the value and limitations of this technique. A diagnostic yield of 35% was found, with the majority having abnormalities of atrioventricular conduction. The presence of organic heart disease, 12-lead electrocardiographic abnormalities and a number of syncopal episodes did not influence the diagnostic utility of electrophysiology study. Patient follow-up suggested that therapeutic decisions based on the findings of electrophysiology study provide satisfactory symptomatic relief in a high percentage of cases, with a recurrence rate of 25% at mean follow-up of 14 months.

The utility of transesophageal electrocardiography using a bipolar 'pill electrode' was assessed in 17 consecutive patients with tachycardia presenting to our casualty department. Standard 12-lead electrocardiography showed regular narrow QRS tachycardia in 12 patients, and five patients had wide QRS tachycardia. Esophageal atrial electrogram recordings were obtained in 14 patients (82%), and these were helpful in determining the mechanism of tachycardia in 11 patients (78%). Of these 11, seven patients fulfilled criteria for atrioventricular junctional (AVJ) tachycardia based on measurement of the minimum interval between the onset of ventricular depolarisation and earliest atrial (esophageal) activity. One of these patients had presented with a wide QRS tachycardia. The other four patients were diagnosed as having ventricular tachycardia (VT) following diagnosis of AV dissociation. Atrial overdrive pacing, via the pill electrode, successfully reverted four of the nine patients (44%) with narrow QRS tachycardia but no patient with VT. Esophageal recording during tachycardia is a simple, relatively non-invasive technique which is helpful in suggesting the mechanism of tachycardia both in patients with narrow and wide QRS tachycardia, and may have a therapeutic role in patients with AVJ tachycardia.

A 38-year-old woman presented with syncopal attacks for 27 years. The electrophysiology techniques which enabled the diagnosis of both sinus node dysfunction (sick sinus syndrome) and presence of an atrionodal bypass tract (Lown-Ganong-Levine syndrome) are illustrated.

The diagnostic and potential therapeutic value of rapid right atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction, was examined. The effect of right atrial pacing at incremental rates beginning 10 bpm above the rate of the tachycardia was studied in five patients with ventricular tachycardia, and in four patients with supraventricular tachycardia with rate-related bundle branch block aberration, the mechanism of tachycardia having been demonstrated at electrophysiology study. Atrial pacing resulted in persistent (four) or occasional (one) normalisation of the QRS complexes to that seen in sinus rhythm in those five patients with ventricular tachycardia. The intraventricular conduction pattern persisted with atrial pacing in those patients with supraventricular tachycardia and aberrant intraventricular conduction. This confirms that atrial pacing is a useful and simple diagnostic test in wide QRS tachycardia, which does not require sophisticated electrophysiological facilities. In three of the patients with ventricular tachycardia, atrial pacing terminated the arrhythmia, suggesting potential therapeutic use of rapid atrial pacing in such patients.

Electrophysiology study was performed in 93 patients with bifascicular block and unexplained syncope. Clinical evidence of organic heart disease was present in 33 (35%). Electrophysiological abnormalities were detected in 45 patients (48%). Of these, 36 had distal conduction disease, including 28 with an HV interval greater than 55 ms (mean 76.4 ms), and eight who developed infraHisian block following either intravenous procainamide (four) or atrial pacing (four). Sick sinus syndrome was evident in six patients and a further two had carotid sinus hypersensitivity. Sustained monomorphic ventricular tachycardia (VT) was induced in only three patients, two of whom also had prolonged HV interval. Among the 93 patients, 45 had therapy which was guided by positive findings at electrophysiology study (Group 1). Of these, 42 received permanent pacemakers, two were treated with combined permanent pacing and antiarrhythmic drug therapy, and one was treated with antiarrhythmic drug alone. In addition, eight patients without electrophysiologic abnormalities were treated empirically by pacing (Group 2). Finally, 40 patients without electrophysiologic abnormalities received no specific therapy (group 3). At a mean follow-up of 39 months (range two-125 months), recurrence of syncope had occurred in 4% of Group 1 patients, and 25% of Group 3 patients (p less than 0.05). No patient in Group 2 had had recurrence. Total mortality was 40%, including 47% of patients in Group 1, 25% of Group 2, and 35% of Group 3. Death was sudden in seven patients. We concluded that among patients with bifascicular block and syncope, therapy directed by findings at electrophysiology study was associated with symptomatic improvement, but mortality was not significantly influenced.(ABSTRACT TRUNCATED AT 250 WORDS)

The normal period of depression of sinoatrial node automaticity (sinus node recovery time, SNRT) following one minute of overdrive right atrial pacing was evaluated in 34 subjects, aged 27--83 years. Specific attention was paid to the influence of the patient's heart rate, atrial pacing rate (100 and 130 bpm) and site, and of vagal and sympathetic effects, as assessed by observations following the administration of atropine, 0 . 03 mg/kg, and propranolol, 0 . 15 mg/kg. Normal SNRT was 1046 +/- 17 ms at 100 bpm and 980 +/- 19 ms at 130 bpm. Linear regression analysis showed that at pacing rates of both 100 and 130 bpm, both before and after autonomic block, a highly significant relation existed between SNRT and the stable P-P interval observed after cessation of pacing. These regression equations were used to develop a correction factor for cycle length in assessing SNRT (corrected SNRT = SNRT--0 . 86 X cycle length, where 0 . 86 was the slope of the regression equation). The mean corrected SNRT was 314 +/- 10 ms and 290 +/- 8 ms at 100 and 130 bpm, respectively. Vagal influences increased SNRT and were of greater magnitude than the decrease in SNRT due to sympathetic effects. Corrected SNRT was significantly longer following left atrial than following right atrial pacing, but in those eight patients studied, was not significantly different following right atrial or right ventricular stimulation.

A patient is described who developed a systolic murmur soon after she was administered intravenous thrombolytic therapy for acute myocardial infarction. She died and autopsy revealed extensive hemorrhagic myocardial infarction and a free-wall rupture. A review of the literature suggests that this may be an unusual complication of thrombolytic therapy.

The antiarrhythmic effect of intravenous disopyramide phosphate was assessed in a multicentre open study of 141 patients admitted to coronary care units. Disopyramide was administered in a bolus dose of 2 mg/kg over 10 min with an optional second bolus of 1 mg/kg and infusion of 0.4 mg/kg hour. Atrial fibrillation was terminated in 57% of 56 patients, supraventricular tachycardia in 82% of 11 patients, ventricular tachycardia in 88% of 17 patients and premature ventricular contractions were controlled in 85% of 55 patients. Atrial flutter was terminated in only 2 of 17 patients (12%). Side effects occurred in 38% of the patients, the most frequent being those relating to anticholinergic properties of the drug (15%) or systemic hypotension (13%). Occasionally worsening of the arrhythmia (4%), QRS widening (3) or apparent hypertension (2%) were noted. It was concluded that intravenous disopyramide is an effective antiarrhythmic agent in the coronary care unit setting, but that side effects require close monitoring of dosage.

Pre-excitation has been defined as "a condition in which all or some portion of the ventricular muscle is activated earlier in relation to atrial events, than would be expected had the impulse reached the ventricle by way of the normal atrioventricular conduction system". The susceptibility of patients with pre-excitation to paroxysmal tachycardias had been described many years previously. The Wolff-Parkinson-White syndrome was initially thought to have a relatively benign prognosis. Subsequently, it was recognised that some patients were prone to life-threatening arrhythmias and sudden death. This recognition has given impetus to sophisticated electrophysiological study of the pre-excitation syndromes by recently developed techniques of catheterisation, epicardial mapping and surgery. The purpose of this review is to highlight the recent advances in management of the Wolff-Parkinson-White syndrome which have been based upon these electrophysiological techniques.

Twelve patients with clinical features suggesting possible intermittent high degree atrioventricular block were studied. All 12 patients had basic 1:1 atrioventricular conduction but nine had an electrocardiographic pattern of bifascicular distal conduction disease (right bundle branch block with left anterior or posterior hemiblock, or left bundle branch block). Intracardiac conduction was assessed by recording of the His bundle electrocardiogram and atrial pacing techniques, before and 20 minutes after intravenous administration of procainamide, in a dose of up to 10 mg/kg. Before procainamide administration, seven of the 12 patients had a prolonged H-V interval (greater than 55 ms). Procainamide administration lengthened the H-V interval in all 12 patients by 5--40 ms. In five patients, procainamide induced second or third degree AV block below the level of the bundle of His. It was concluded that the administration of procainamide may be a useful provocative test of distal conduction in patients with possible intermittent AV block.