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Background: The exact mechanism that explains the phenomenon of cold intolerance in patients with angina remains controversial. Although the response to the effects of a cold environment has been examined in these patients, their response to cold air inhalation has produced conflicting results. In addition, the possible role of vasoactive peptides in the pathophysiology has not been explored., Objectives: The aims of this study were to examine the response of patients with stable angina to the effects of cold air inhalation during exercise testing, and to investigate the possible role played by the vasoconstrictor peptides endothelin-1 (ET-1) and angiotensin-II (AT-II) in the pathophysiology., Methods: In a randomised order, 12 men with stable angina, whose medication had been stopped, underwent two separate symptom limited treadmill exercise tests. At one visit the patients exercised while breathing room air and at the other visit they exercised while breathing cold air from a specially adapted freezer. Serial peripheral venous blood samples were taken for ET-1 and AT-II estimations during each visit., Results: Cold air inhalation resulted in a significant reduction in the mean time to angina (232.7 (20.4) s v 274.1 (26.9) s, P = 0.04) and the mean total exercise time (299.5 (27.0) s v 350.3 (23.9) s, P = 0.008), but no significant change in the time to 1 mm ST depression (223.3 (29.0) s v 241.3 (29.2) s, P = 0.25). There was no significant difference between the rate-pressure products at the onset of angina (P = 0.13) and the time to 1 mm ST depression (P = 0.85), but at peak exercise the rate-pressure product was significantly lower in patients breathing cold air as opposed to room air (P = 0.049). There was an equivalent significant decrease in ET-1 concentrations at peak exercise compared with that at rest at both visits (room air 5.0 (0.7) pmol/l v 4.3 (0.7) pmol/l, P = 0.03; cold air 4.4 (0.6) pmol/l v 3.8 (0.5) pmol/l, P = 0.02). There was a significant increase in AT-II concentrations 10 min after peak exercise in patients breathing room air (39.2 (6.1) pmol/l v 32.1 (4.8) pmol/l, P = 0.01) which was not repeated during cold air inhalation (36.6 (3.4) pmol/l v 28.3 (3.4) pmol/l, P = 0.07)., Conclusions: Cold air inhalation in patients with stable angina results in an earlier onset of angina and a reduction in exercise capacity. Both peripheral and central reflex mechanisms appear to contribute to the phenomenon of cold intolerance. Peripheral ET-1 and AT-II do not appear to play a significant role in the pathophysiology.

A 45 year old farmer was kicked in the chest by a horse. In the days following the injury episodic breathlessness developed and he was admitted to hospital with right ventricular failure and pulmonary emboli. Echocardiography showed global right ventricular dysfunction but a right ventricular mural thrombus, the likely source of the pulmonary emboli, was not seen. He gradually recovered after treatment with anticoagulant. One month later he presented with a further complication--complete atrioventricular dissociation--that required a dual chamber pacemaker implantation. This patient had few initial manifestations of right ventricular myocardial contusion and this case illustrates that such patients should be closely monitored for delayed complications.

Objective: To assess the sensitivities of Doppler indices to changes in global cardiac function during and after controlled myocardial ischaemia induced by coronary angioplasty., Design: Continuous wave Doppler signals of aortic flow were recorded during coronary angioplasty. The following Doppler indices of cardiac function were measured before, during, and after balloon inflation: V (peak velocity), MA (mean acceleration), V2/T (T = time from onset to peak ejection), and MD (minute distance corrected for baseline heart rate)., Setting: A tertiary care cardiological unit in a university hospital., Patients: Sixteen patients undergoing coronary angioplasty of the left anterior descending coronary artery. Eight patients had multivessel disease., Main Outcome Measures: The primary outcome measures were planned before data collection began., Results: 12 patients showed a significant fall of three or more Doppler indices from their baseline values during balloon inflation. This occurred in all patients with multivessel disease. The Doppler indices V2 T, MD, V, and MA fell by 43.7%, 37.7%, 27.4%, and 23% respectively from their baseline values (p less than 0.0001). The relative sensitivities of the Doppler indices to ischaemia were V2/T greater than MD (p less than 0.02), MD greater than (p less than 0.001), and V greater than MA (p less than 0.01). The impairment of global left ventricular function resulting from brief balloon inflation during single vessel angioplasty was reversible in all the patients., Conclusions: The Doppler indices V2/T, MD, V, and MA are all sensitive, in order of magnitude, to falls in global cardiac function resulting from ischaemia. They may prove useful for assessing cardiac function during ischaemia in the clinical setting.

The short and long term effects of successful percutaneous transluminal coronary angioplasty on left ventricular function, at rest and on exercise were investigated in 49 patients. Thirty-four had had no previous infarction (group 1) and 15 had (group 2). Technetium-99m gated blood pool images were obtained at rest and during exercise before, six weeks after, and a mean of fifteen months after successful angioplasty. Before angioplasty the mean (SD) ejection fraction fell significantly on exercise in both groups from 58 (10)% to 53 (13)% in group 1 and from 48 (10)% to 40 (16)% in group 2. This change was paralleled by a worsening wall motion score (from 0.6 (0.4) to 1.6 (1.2) in group 1 and from 2.3 (1.9) to 3.3 (2.4) in group 2). Six weeks after the procedure there was little change in resting ejection fraction but it increased significantly on exercise (to 62 (11)% in group 1 and to 53 (13)% in group 2). There was a concomitant significant improvement in the exercise wall motion score (to 0.4 (0.6) in group 1 and to 1.8 (1.1) in group 2). This improvement in exercise ejection fraction and wall motion was maintained at later follow up with no significant deterioration in either variable and a clearly sustained improvement in ejection fraction (60 (10)% in group 1 and 51 (10)% in group 2) and wall motion score (0.2 (0.2) in group 1 and 1.3 (0.8) in group 2) compared with values before angioplasty. The initial improvement in left ventricular function on exercise after successful angioplasty was maintained for at least 9-24 months both in patients with previous myocardial infarction and in those without.

One hundred and five patients with unstable angina and 175 with chronic stable angina were treated by primary percutaneous transluminal coronary angioplasty. Patients with unstable angina had had symptoms for a shorter time and were more likely to have angiographically complex lesions and lesions less than 10 mm in length than patients with chronic stable angina. Other baseline variables were not significantly different in the two groups. The overall primary success rate was similar in both groups (87% v 86%). Nine of the 14 unsuccessful procedures in those with unstable angina and nine of the 24 unsuccessful procedures in those with stable angina were the result of acute occlusion. These results led to a 9% frequency of procedure related myocardial infarction in patients with unstable angina and a 5% rate in those with stable angina (NS). The procedure related infarct rate tended to be higher in patients with unstable angina who had coronary angioplasty soon after an episode of unstable angina (mean 10 days) than in those in whom it was delayed (mean 35 days) (12% v 3%) (NS). In patients with unstable angina who had had a previous myocardial infarction procedure related infarction was significantly more common (18%) than in patients with no previous myocardial infarction (3%). The difference between those with and without previous infarction was also significant in patients with stable angina (10% v 3%).

A 67 year old woman with a permanent pacemaker was admitted with pulmonary oedema and mitral valve incompetence two months after a myocardial infarction. Echocardiograms showed good left ventricular function and a large coil of apparent thrombus in the right atrium prolapsing into the right ventricle. Intermittent loss of pacemaker sensing and capture was noticed on admission and probably caused the supraventricular tachycardia and ventricular fibrillation that occurred before an exploratory bypass operation. At operation rupture of the papillary muscle was found and the mitral valve was replaced. A large piece of thrombus was retrieved from the right pulmonary artery. The right heart contained no clot and the pacemaker wire was not displaced. It is envisaged that the strand of venous thrombus was caught in the permanent pacing wire at the tricuspid valve level resulting in an unusual case of pacemaker malfunction. The eventual poor outcome was almost certainly influenced by the arrhythmias and pulmonary embolism caused by the clot and might have been avoided by early operation.