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The formation of bi-directional block in atrial flutter can be adversely affected by problems with the delivery of effective energy related to isthmus anatomy and contact. Higher energies can produce larger and more effective lesions. The optimum setting for power delivery using temperature controlled ablation has not been established, with the maximum reported being 100 W. This is a retrospective review of the first 50 new cases assessing the efficacy and safety of using temperature controlled (60–65 °C) flutter ablation with an 8 mm tip electrode catheter and up to 150 W. All cases had either typical flutter alone (34%) or predominant flutter as the indication, no combined procedures were included. Acute procedural success was 94% and long-term success of 88%. Median number of ablations required was 11 (interquartile range 10–19), median procedure time 120 min (IQR 102–164), fluoroscopy time 22 min (IQR 17–36), radiation dose 17 Gy cm2 (IQR 10–27), median number of lines 1 (IQR 1–2). Six patients achieved 150 W, but 42 achieved >100 W (median watts 142 W, IQR 104–147). Patients (12%) experienced an uncomplicated pop during the procedure. None experienced a significant complication. There were three late relapses. The setting of 150 W maximum delivered energy in temperature regulated ablation allowed higher energies (>100 W) to be delivered in most patients. This resulted in acute and long-term success rates that compare well with the literature but is associated with a 12% rate of pop. Subsequent to this series our 54th patient sustained a pop due to high energy ablation that resulted in perforation and tamponade, from which there was survival. [ABSTRACT FROM PUBLISHER]

The aim of this multicenter study was to investigate the performance of a new cardiac pacemaker lead with a titanium nitride cathode coated with a copolymer membrane. In particular, the electrophysiological effect of steroid dissolved in this ion-exchange membrane was evaluated by randomized comparison. Ninety-five patients were randomized either to the 1450 T (n = 51) or the 1451 T ventricular lead (n = 45) and received telemeteral VVI(R) pacemakers with identical diagnostic features. Both leads were bipolar, were passively affixed, and had a porous titanium nitride tip with a surface area of 3.5 mm². The only difference between the two electrodes was 13 µg of dexamethasone added to the 1450 Ts membrane coating. Voltage thresholds (VTH) at pulse durations of 0.25, 0.37, and 0.5 ms, lead impedance, and sensing thresholds were measured at discharge, 2 weeks, 1 month, 3 months, and 6 months after implantation. Mean amplitude and the slew rate from three telemetered intracardiac electrograms, chronaxie-rheobase product, and minimum energy consumption were calculated. After a 6-month follow-up, mean voltage thresholds of 0.65 ± 0.20 V and 0.63 ± 0.34 were achieved for the 1450 T lead and 1451 T lead, respectively. As a result, a VTH < 1.0 V was obtained in all patients with 1450 T electrodes and in 97.7% of patients with 1451 T leads after 6 months follow-up. In both electrodes, stable VTH was reached 2 weeks after implantation, and no transient rise in threshold was observed. No differences were observed between the steroid and the nonsteroid group in respect to VTH. chronaxie-rheobase product, minimum energy consumption, and potential amplitude and slew rate. In conclusion, safe and efficient pacing at low pulse amplitudes were achieved with both leads. The tip design, independently of... [ABSTRACT FROM AUTHOR]

OBJECTIVES--To determine the anti-ischaemic effects of a new angiotensin converting enzyme inhibitor, benazepril, compared with nifedipine, alone and in combination, in chronic stable angina caused by coronary artery disease. DESIGN--Placebo controlled, double blind, latin square design. SETTING--Regional cardiology service for a mixed urban and rural population. SUBJECTS--40 patients with stable exertional angina producing at least 1 mm ST segment depression on exercise test with the Bruce protocol. 34 patients completed all four phases of the trial. INTERVENTIONS--Each patient was treated with placebo, benazepril (10 mg twice daily), nifedipine retard (20 mg twice daily), and a combination of benazepril and nifedipine in the same doses, in random order for periods of two weeks. MAIN OUTCOME MEASURES AND RESULTS--Total duration of exercise was not increased by any treatment. Exercise time to the development of 1 mm ST segment depression was not significantly changed with benazepril alone or in combination with nifedipine but was increased with nifedipine from 4.18 (1.8) min to 4.99 (1.6) min (95% confidence interval (95% CI) 0.28 to 1.34; p < 0.05). There was a significant relation between increase in duration of exercise and resting renin concentration (r = 0.498; p < 0.01). Myocardial ischaemia during daily activity, as assessed by ambulatory electrocardiographic monitoring, was reduced by benazepril and by the benazepril and nifedipine combination. This was significant for total ischaemic burden (451(628) min v 231(408) min; 95% CI -398 to -41 min; p < 0.05) and maximal depth of ST segment depression (-2.47(1.2) mm v -2.16 mm; 95% CI 0.04 to 0.57; p < 0.05) for the combination and for maximal ST segment depth for benazepril monotherapy (-2.47 (1.2) mm v -1.96(1.2) mm; 95% CI 0.18 to 0.91; p < 0.05). Benazepril significantly altered the circadian rhythm of cardiac ischaemia, abolishing the peak ischaemic periods at 0700 to 1200 and 1700 to 2300 (p < 0.05). CONCLUSIONS--Benazepril, an angiotensin converting enzyme inhibitor, had a modest anti-ischaemic effect in effort angina, but this effect was not as pronounced as with nifedipine. The anti-ischaemic action was more noticeable in asymptomatic ischaemia during daily activity, whereas nifedipine had little effect on this aspect of myocardial ischaemia. The combination of benazepril and nifedipine reduced ischaemia of daily activity. [ABSTRACT FROM PUBLISHER]

OBJECTIVE--To document regional plasma concentrations of brain natriuretic factor (BNF) and their relations to concurrent concentrations of atrial natriuretic factor, cyclic guanosine monophosphate, and haemodynamic state. DESIGN--Regional blood sampling from a systemic artery and vein, renal vein, and coronary sinus together with concurrent haemodynamic indices in patients coming forward for left and right cardiac catheterisation. SETTING--Tertiary referral centre. PATIENTS--22 consecutive unselected patients coming forward for left and right cardiac catheterisation or electrophysiological studies in the course of standard diagnosis for a range of cardiac disorders. MAIN OUTCOME MEASURES--Significant arteriovenous gradients for plasma BNF concentration were found across the lower limb, the kidney, and the heart. These were less than concurrent arteriovenous gradients in plasma atrial natriuretic factor (ANF). Arterial concentrations of plasma BNF were positively related to concurrent concentrations of ANF (r = 0.72, p < 0.01) and cyclic guanosine monophosphate (r = 0.52, p < 0.05). Arterial plasma concentrations of BNF showed a significant positive correlation with right atrial pressure and pulmonary artery wedge pressure and an inverse relation to cardiac output. CONCLUSIONS--Regional plasma concentrations of BNF indicate cardiac secretion of this peptide and clearance in a number of tissues. Renal clearance is proportionally greater than that found across the limb. Absolute and proportional arteriovenous gradients of this peptide are considerably less than for concomitant concentrations of ANF suggesting slower metabolic clearance of BNF. Plasma BNF concentrations rise with increasing cardiac impairment and are related to indices of cardiac function. These findings are consistent with a role for BNF in the neurohumoral response to cardiac impairment. [ABSTRACT FROM PUBLISHER]

The variability of pulmonary arterial pressure, the relation of pulmonary pressure to systemic pressure, pulmonary pressure responses to stimuli (exercise, hypoxia, smoking, free ambulation), and plasma catecholamine responses were assessed in five patients with primary pulmonary hypertension. Ambulatory monitoring techniques provided data for the computerised analysis of continuous, beat-to-beat, direct recordings of both pulmonary and systemic arterial pressures for 8 to 10 hours. The absolute variability of pulmonary arterial pressure and the magnitude of absolute changes in this variable in response to stimuli were increased in primary pulmonary hypertension. The variability of systemic pressure was similar to that in healthy volunteers. Basal and stimulated plasma catecholamine values were normal, suggesting preservation of normal sympathetic nervous system activity in primary pulmonary hypertension. [ABSTRACT FROM PUBLISHER]

Because anecdotal reports suggest that concentrations of atrial natriuretic peptide are raised during tachycardias, plasma immunoreactive atrial natriuretic peptide concentrations were measured in 34 consecutive patients when tachycardia was diagnosed and again five and 15 minutes after conversion to sinus rhythm. Plasma atrial natriuretic peptide concentrations were raised in all but four patients, and were higher in patients with known heart disease than in those without. The concentrations were higher with ventricular tachycardia than with atrial fibrillation or supraventricular tachycardia, and in acute versus chronic tachycardia. There was only a weak positive relation between ventricular rate and atrial natriuretic peptide (r = 0.31); but there was a closer inverse correlation between atrial natriuretic peptide and systolic arterial pressure (r = -0.60). Conversion to sinus rhythm was associated with a definite fall in plasma atrial natriuretic peptide concentrations. Despite very high baseline concentrations of atrial natriuretic peptide only two patients reported polyuria. It is likely that atrial pressure rather than ventricular rate determines atrial natriuretic peptide release during tachycardia. Despite the absence of polyuria in all but two patients in this study atrial peptides could still contribute to, or cause, the polyuria of tachycardias. [ABSTRACT FROM PUBLISHER]

The course of dilated cardiomyopathy in New Zealand was studied in 72 cases that were followed up for less than or equal to 10 years after cardiac catheterisation and coronary angiography. Eighty one per cent were male and 86% were white; the remainder were Maori. The mean age of patients at the time of investigation was 50 X 15 years. Most patients were unskilled labourers. The commonest presenting symptom was dyspnoea and the commonest physical sign was cardiomegaly. Mean survival time from first hospital presentation was 85 months; half the deaths were sudden. Factors predicting a poor survival included cardiomegaly, age, arrhythmias, cigarette smoking, and subclinical thiamine deficiency. The syndrome of dilated cardiomyopathy in New Zealand appears to be identical with that seen in other European populations. [ABSTRACT FROM PUBLISHER]

Preliminary reports are that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are higher in essential hypertensive patients than in normotensive controls, and that the urinary response to injected alpha human atrial natriuretic peptide (α-hANP) is augmented in essential hypertension. Further, there are reports of positive relationships between IR-ANP levels and arterial pressure. Confirmation is needed, however, with larger numbers of patients and with careful matching of diet electrolytes, age and sex, body posture, time of day, and other factors which may alter release or plasma clearance of atrial peptides. If indeed IR-ANP levels are raised in essential hypertension, it is possible that increased demands on the atria as a consequence of altered left ventricular structure and function lead to augmented secretion of atrial peptides. Whether the observed minor increases in plasma IR-ANP could have biologic effects to oppose pressor systems, to sustain glomerular filtration rate, and to suppress vasoactive hormone secretion, is unclear since the threshold level of IR-ANP which has biologic actions in man, is unknown. Plasma IR-ANP levels are raised in primary aldosteronism, and fall with treatment. These early reports suggest that atrial peptides might play a role in the pathophysiology of primary aldosteronism and perhaps essential hypertension, but much more information is needed. [ABSTRACT FROM PUBLISHER]