Health service costs of coronary angioplasty and coronary artery bypass surgery: the Randomised Intervention Treatment of Angina (RITA) trial.

For some patients with coronary artery disease, percutaneous transluminal coronary angioplasty (PTCA) is an alternative to coronary artery bypass grafting (CABG). We report comparative health service costs of these interventions within the Randomised Intervention Treatment of Angina (RITA) trial. Medications were costed at published UK prices; other resource use was costed with a set of unit costs estimated at two recruiting centres to the RITA trial, one in London and one outside. Over 2-year follow-up of 1011 patients, the estimated mean additional cost for those randomised to CABG compared with PTCA was 1050 pounds (95% CI 621 pounds-1479 pounds), with unit costs from the non-London centre, and 1823 pounds (1202 pounds-2444 pounds), with unit costs from the London centre. The initial average cost of treating a patient randomised to PTCA is about 52% of that of CABG, but after 2 years this increased to about 80% because of the greater need for subsequent interventions. The balance of advantage between PTCA and CABG may change after several years: funding has been obtained to continue RITA follow-up for 10 years. However, on the basis of patients' status at 2 years, the cost advantages of PTCA cannot be ignored. Further research is necessary to assess whether the advantage of PTCA in terms of cost is translated into one of cost-effectiveness.

Inappropriate discharges by the implantable cardioverter defibrillator during postoperative testing: implications for intraoperative assessment.

Inappropriate shocks were delivered to a patient while in sinus rhythm by an implantable cardioverter defibrillator (ICD) during routine prehospital discharge testing. This was induced by the standard programmer when the "read" telemetry sequence was initiated. The ICD was removed and found to suffer from electrical artifact that was sensed as ventricular tachycardia during telemetry. To avoid inadvertent telemetry-induced shocks during routine testing, all ICDs should be interrogated, using a standard programmer, intraoperatively, with the unit in "defibrillation on" mode.

Normal and stenotic human aortic valve opening: in vitro assessment of orifice area changes with flow.

The ability to measure aortic valve area clinically has emphasized the need to understand the changes in aortic valve orifice area during flow. To compare the performance of normal and stenotic human aortic valves we used a pulsatile flow model that simulated in vivo flow conditions. Five normal autopsy specimens and 15 stenotic valves removed at operation were mounted into the model. Valve function was assessed by analysis of video recordings of valve leaflet motion during flow. Over the flow rates tested normal valves demonstrated a linear increase in orifice area. There was no resistance to leaflet opening and valve closure was rapid. The majority of stenotic valves demonstrated an increase in orifice area at low flow rates. No valve showed any increase in maximal area beyond flow rates of 3 l min-1. Increased leaflet resistance of these abnormal valves resulted in notably slower opening and closing rates. In patients with a high cardiac output and severe stenosis, overestimation of the anatomic orifice area derived by the Gorlin equation can result. This is not related to variability in maximal orifice area.

Balloon dilatation of the aortic valve in a pulsatile flow model: assessment of the mechanisms and the magnitude and duration of changes in valve area and gradient.

Eighteen stenotic aortic valves (17 removed at operation) mounted in a pulsatile flow duplicator were dilated with a balloon catheter. Sequential measurements showed that the valve area initially increased from a mean (SD) of 0.52 (0.16) to 0.78 (0.17) cm2. It was 0.73 (0.16) cm2 five minutes after dilatation and this was little changed at four weeks (0.70 (0.15) cm2). Initially the mean transvalvar gradient fell significantly from 54 (27) to 32 (8) mm Hg but increased to 35 (10) mm Hg at five minutes and to 40 (11) mm Hg at four weeks. In six valves stretching of the orifice was the only mechanism responsible for the changes while in the remainder there was tearing through commissures with a greater initial increase in area (0.31 v 0.18 cm2) and a smaller decrease in area at five minutes (0.03 v 0.08 cm2). Fractures of calcific deposits in non-commissural positions were seen in one valve only. This laboratory study of isolated aortic valves showed a significant but small increase in valve area after balloon dilatation, which was greater when commissural tearing had occurred. Recoil of the stretched orifice was complete at five minutes and there was little further change over the next four weeks.

Assessment of chest pain in hypertrophic cardiomyopathy using exercise thallium-201 myocardial scintigraphy.

Exercise thallium-201 myocardial scintigraphy was performed in 23 patients with hypertrophic cardiomyopathy. Eighteen patients presented with chest pain which was a persistent symptom in 11. Selective coronary arteriography was performed in 16 patients and showed normal coronary arteries in 15 and insignificant luminal irregularities in one patient. Eighteen patients had abnormal scintigrams. Three had an abnormal distribution of tracer entirely attributable to asymmetric septal hypertrophy, whereas 15 had discrete tracer uptake defects which could not be explained solely by myocardial hypertrophy. In this latter group of patients three scintigraphic patterns were identified: (1) in 10 patients defects were seen in scintigrams immediately after exercise but not in delayed images obtained four to six hours later. Eight of these patients had chest pain. (2) Four patients had uptake defects seen in both initial and delayed images. One patient had chest pain. (3) In three patients, one of whom had chest pain, tracer defects were seen only in delayed images and were not apparent in the initial scintigrams. Chest pain occurred in eight out of 10 patients with scintigraphic evidence of myocardial ischaemia but was present in only three out of 13 patients with non-ischaemic scintigrams. The value of exercise thallium-201 myocardial imaging as a diagnostic technique in hypertrophic cardiomyopathy appears limited. Scintigraphic evidence of regional myocardial ischaemia in the absence of significant coronary artery disease, however, contributes to an understanding of the mechanism of angina production in patients with hypertrophic cardiomyopathy.

Cardiac tumours: non-invasive detection and assessment by gated cardiac blood pool radionuclide imaging.

Four patients with cardiac tumours were investigated by gated cardiac blood pool radionuclide imaging and echocardiography. Contrast angiocardiography was performed in three of the cases. Two left atrial tumours were detected by all three techniques. In one of these cases echocardiography alone showed additional mitral valve stenosis, but isotope imaging indicated tumour size more accurately. A large septal mass was detected by all three methods. In this patient echocardiography showed evidence of left ventricular outflow obstruction, confirmed at cardiac catheterisation, but gated isotope imaging provided a more detailed assessment of the abnormal cardiac anatomy. In the fourth case gated isotope imaging detected a large right ventricular tumour which had not been identified by echocardiography. Gated cardiac blood pool isotope imaging is a complementary technique to echocardiography for the non-invasive detection and assessment of cardiac tumours.

Assessment of ventricular elements of mitral valve by left ventriculography.

In the left ventriculogram in the right anterior oblique projection the plane of the mitral valve is seen in profile and the papillary muscle shadows are outlined. The distance from the middle of the papillary muscles to the plane of the mitral valve during systole was used to assess the average length of the chordae tendineae, and the area of the papillary muscle shadows was measured as an index of hypertrophy in a series of hearts with mitral valve disease. Valvar mitral stenosis is characterised by slight reduction in the length of chordae tendineae and more hypertrophy of the papillary muscles, while in subvalvar mitral stenosis there is more shortening of the chordae tendineae and less papillary muscle hypertrophy. Valvotomy may lengthen the chordae tendineae in subvalvar mitral stenosis. In rheumatic mitral regurgitation length of chordae tendineae and papillary muscle size were normal. The measurements were not useful in assessing non-rheumatic mitral regurgitation.

Use of cardiac pacemakers in Britain.

In Britain during 1975 cardiac pacemakers were implanted at the rate of 56 new patients per million population. This is about one-third the rate for other Western countries but still represents an increase of 150% since 1972. Six-thousand generators were used, and apparatus worth about 2m pounds was implanted. Over 90% of the initial implantations were by the transvenous route, and the mortality from this operation was only 0-3%. Electrode repositioning was needed in 10% of cases. The average age of patients at the time of first implantation was 70. Most patients with pacemakers were able to obtain driving licenses and insurance; only 10% had to pay an additional premium. There is no evidence from insurance comparnies that such patients have an increased risk of accidents. Patients who wished to undertake paid employment almost always did so, often in their previous job. About 80% of the patients were able to increase or maintain their leisure activities at the same level of effort as before pacing became necessary. The number of implantations may be expected to increase by about three times over the next five years.

Assessment of metoprolol, a cardioselective beta-blocking agent, during chronic therapy in patients with angina pectoris.

Ten patients with typical angina pectoris and without hypertension, congestive heart failure or other disease were treated with alternating four-week courses of metoprolol (alpha beta1 cardioselective beta-blocking agent), propranolol and placebo. Midway through each four-week period, drug dosage was doubled; thus, regimes were metoprolol, 150 and 300 mg/day, propranolol, 120 and 240 mg per day and placebo, 3 and 6 tablets per day. Serum concentrations of metoprolol increased with increasing dosage in a proportion very similar to that seen with propranolol. Statistically significant reductions in angina frequency/nitroglycerin consumption, and statistically significant increases in total work performed on a bicycle ergometer, were found with both active compounds when compared with placebo. No significant differences were noted between the two active compounds. Though most patients showed greatest improvement on the higher of the two drug dosages, three patients with metoprolol and two with propranolol responded best on the lower dose regime. Both compounds reduced heart rate at rest and during exercise. Neither reduced arterial pressure at rest, but both reduced arterial pressure during exercise. It is concluded that metoprolol is as effective as propranolol in the reduction of angina attacks and improvement in exercise tolerance during chronic therapy in patients with uncomplicated angina pectoris. It is now appropriate to study the effects of metoprolol in patients with coronary artery disease in whom the harmful effects of non-selective beta-blockade heretofore have precluded optimal therapy with beta-blocking drugs.

Problems concerning assessment of anatomical site of accessory pathway in Wolff-Parkinson-White syndrome.

Twp patients with type B WPW syndrome and reciprocal tachycardias have been studied using intracardiac electrograms and programmed electrical stimulation of the heart. One patient, who had a right-sided accessory pathway giving the surface electrocardiographic appearances of type B WPW syndrome, was shown to have an additional left-sided accessory pathway as occurs in type A WPW syndrome. This concealed left-sided atrioventricular connexion formed the retrograde pathway during reciprocal tachycardia. In the second patient the appearances of type B WPW syndrome were shown to be caused by an accessory pathway between the atrial septum and the right side of the interventricular septum rather than an accessory pathway in the right atrioventricular groove. The significance of these findings when considering surgical interruption of an accessory atrioventricular conduction pathway is discussed.