In a study of the concept of pacemaker dependence, 86 patients who had permanent ventricular demand (VVI) pacemakers implanted for more than six months and were in predominantly paced rhythm underwent repeated interruption of pacing both abruptly and after gradual reduction of paced rate. Non-invasive pace slowing was accomplished by timed inhibiting pulses applied to the chest wall. The results identified a small group (A) of patients, 8% of those tested, who consistently failed to develop an adequate escape rhythm and may thus be considered highly pacing dependent. A second group B, 26%, developed an adequate intrinsic rhythm with serial decremental rate inhibition (SDRI) but suffered symptoms with abrupt complete inhibition (ACI). The remaining 66%, group C, developed no symptoms in any test. Analysis of clinical pre-test data showed that syncope, atrioventricular block and a low rate prior to implant, and a long duration of pacing were associated with a higher degree of pacing dependence, but were not reliably predictive. The clinical significance and value of the results are discussed. We conclude that SDRI is a reliable test for the high degree of pacemaker dependence and can be helpful especially in planning a procedure which may involve interruption of pacing.

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Balloon inflation during percutaneous transluminal coronary angioplasty is a useful human model of acute coronary occlusion and regional myocardial ischaemia. We assessed the prevalence and duration of ischaemia during successive sixty-second balloon inflations in sixteen patients undergoing routine single vessel angioplasty by continuous six lead electrocardiography and cross-sectional echocardiography. The influence of rate-pressure product on the evolution of ischaemia was also evaluated. ST segment elevation developed in fourteen of the patients within 19 +/- 12 seconds and returned to baseline within 20 +/- 9 seconds of deflation. Reciprocal ST segment depression occurred in four patients, only one of whom had multivessel disease. Wall motion abnormalities on echocardiography occurred in all sixteen patients and were seen significantly earlier than electrocardiographic changes. Thus, dyskinesis developed 15 +/- 5 seconds after balloon inflation and disappeared 13 +/- 3 seconds following balloon deflation. Time to onset of ischaemia by both methods remained constant during successive balloon inflations. Rate pressure product prior to balloon inflation correlated inversely with time to onset of ischaemia detected by either technique: r = -0.73, P less than 0.05 (ECG), r = -0.65, P less than 0.05 (echocardiography). Nevertheless, evidence of ischaemia developed within 30 seconds in all patients regardless of rate-pressure product. This investigation indicates that electrocardiography and cross-sectional echocardiography have similar sensitivity for the detection of acute ischaemia during coronary angioplasty although echocardiographic change is seen significantly earlier. Resting myocardial oxygen consumption, as reflected by rate-pressure product, is an important determinant of time to onset of ischaemia following balloon inflation.

SUMMARY The effects of early spontaneous coronary patency on the evolution of myocardial infarction were evaluated in 41 patients. They had coronary arteriography (mean (SEM)) 3-1 (02) hours after the onset of chest pain with repeat studies 90 minutes and three days later. In 12 (29%) patients the infarct related coronary artery was patent at the first arteriogram (group 1). A further 10 patients, nine of whom received thrombolytic treatment, showed early recanalisation of the infarct related coronary artery within 90 minutes of treatment (group 2). In the remainder the infarct related coronary artery was persistently occluded (group 3). Baseline values for infarct location, the sum of ST elevation in all leads, QRS scores, and serum creatine kinase activity did not permit discrimination between the groups. Nevertheless, patterns of ST segment change and enzyme release in group 1 were closely similar to those that occurred in response to thrombolysis in group 2. Thus compared with group 3, groups 1 and 2 showed earlier 50% reduction in the sum of peak ST elevation in all leads and earlier peaking of serum creatine kinase activity. Importantly, creatine kinase release was significantly attenuated in group 1, rising to a peak serum activity (mean (SEM)) of only 1242 (415) IU/1. Analysis of angiographic left ventricular ejection fractions at three days indicated limitation of infarct size in groups 1 and 2 compared with group 3. Mean (SEM) ejection fraction, however, was best preserved in group 1 (62 (6)%) and in this group the frequency of non-Q wave infarction was higher than in groups 2 and 3.Thus in patients who present with a patent infarct related coronary artery early during infarction: (a) there is a reduction in the pattern of infarct size as reflected by attenuation of release of creatine kinase, preservation of left ventricular ejection fraction, and a relatively high frequency of non-Q wave infarction; (b) patterns of ST segment change and creatine kinase release resemble those that occur after successful thrombolytic treatment, suggesting that early coronary patency is the result of spontaneous recanalisation of a previously occluded artery.The full transmural extent of myocardial infarction effects of thrombolytic treatment on infarct size5 6 may not be established for six hours or more after and hospital survival7-9 in patients treated early thrombotic coronary artery occlusion.' Thus early after the onset of symptoms.

Thirty patients undergoing cardiac catheterisation for coronary artery disease received parenteral ajmaline (15 patients) or prajmaline (15 patients). There were no statistically significant induced changes in left ventricular systolic or end diastolic pressures, indirect left atrial pressure, pulmonary artery mean pressure, cardiac output or left ventricular ejection fraction compared to control values. Intravenous prajmaline bitartrate in 15 patients with angina did not significantly alter work capacity, maximum exercise heart rate or systolic blood pressure compared to control values. Five patients developed transient minor conduction defects ( 2LBBB , 1 RBBB, 2 prolonged PR interval): all five were also receiving long-term treatment with beta blockers and nifedipine.