Non-invasive assessment of left ventricular function in coronary artery disease by Doppler stress testing.

Left ventricular (LV) function in 62 patients presenting with chest pain typical of angina was studied non-invasively at rest and at maximum-tolerated supine exercise using the continuous-wave Doppler technique of transcutaneous aorto-velography (TAV). The signals were analysed to derive peak velocity (Vp), systolic velocity integral [an index of stroke volume or stroke distance (Sd)], and minute distance (Md; index of cardiac output = Sd X heart rate). Comparison was made with results obtained from 66 normal volunteers. The percentage change in stroke distance with exercise (% delta Sd) was significantly related to the resting ejection fraction (EF) calculated from left ventriculography (r = 0.84), and was below 6% (lowest value observed in normal volunteers) in all of the 23 patients with coronary artery disease (CAD) whose EF was below 60%. No significant difference was observed in the % delta Sd between normal individuals and the 12 patients presenting with chest pain but who had normal coronary arteriograms. However, the % delta Vp, delta % Sd and % delta Md in the 50 patients with CAD were significantly lower than the normal individuals and the 12 patients with normal coronary arteriograms. Lower TAV measurements were observed with exercise, rather than at rest, with increasing number of coronary arteries with significant stenoses and the presence of history of myocardial infarction (linear trend p less than 0.003). These results suggest that Doppler recording of aortic blood velocity with exercise is a clinically useful non-invasive technique for studying LV performance in patients with CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiological actions of somatostatin on the atrioventricular junction in sinus rhythm and reentry tachycardia.

Because somatostatin, a neuroregulatory peptide, is found in abundance in the atria and atrioventricular node, its electrophysiological and antiarrhythmic properties were compared with those of verapamil in ten patients with paroxysmal atrioventricular tachycardia. During sinus rhythm, intravenous somatostatin slowed the heart rate whereas verapamil increased it. Though both agents prolonged atrioventricular conduction time and refractoriness, verapamil was more potent. They were equally effective at terminating reentry atrioventricular tachycardia, restoring sinus rhythm in six of seven patients. Whereas verapamil consistently blocked conduction in the atrioventricular node, somatostatin usually induced ventricular extrasystoles at the time of conversion. Somatostatin may have physiological importance in the neurohumoral control of cardiac impulse formation and conduction.

Atrial demand pacing to protect against vagal overactivity in sympathetic autonomic neuropathy.

The clinical features, investigation and management of a patient with a subacute autonomic neuropathy are described. A series of physiological and biochemical studies indicated severe but selective sympathetic cardiovascular dysfunction, associated with bradycardia. The bradycardia was enhanced by raising blood pressure but there was no other evidence either of cardiac vagal impairment or hyperreactivity. Oral atropine prevented the bradycardia but had to be withdrawn because of intolerable side effects. An atrial demand pacemaker was implanted to elevate basal heart rate and prevent bradycardia. The pacemaker alone did not improve postural hypotension but it enabled the blood pressure to be readily and safely controlled by a combination of drugs.

The value of exercise-induced U-wave inversion on ECG chest wall mapping in the identification of individual coronary arterial lesions.

Exercise-induced U-wave inversion on chest wall mapping was compared with coronary arteriographic findings in 160 consecutive patients who presented with chest pain suggestive of ischaemic heart disease. ECG recordings were made from 16 points on the chest wall before, during and after exercise. None of the 27 patients with normal coronary arteriograms developed U-wave inversion during or after exercise (specificity = 100%). In 21 (all males) of the 133 patients (15.8%) with significant coronary arterial lesions, U-wave inversion on exercise was noticed on different coronary artery territories on the chest wall map, and its localization was correlated with angiographic evidence of individual coronary arterial lesions (100% projection rate). In 9 patients (6.8%) this sign was observed in the absence of any ST segment changes or Q waves. Exercise-induced U-wave inversion was the sole ECG criterion reflecting a lesion of the left anterior descending artery in 12 cases (9%), of the circumflex in 6 cases (4.5%), and in only one case of right coronary artery disease. This sign was not detectable in the conventional V5 site in 9 cases (7.1%) with significant disease of the left anterior descending coronary artery. These nine patients showed U-wave inversion on other areas of the left anterior descending coronary artery territory on exercise. Exercise-induced U-wave inversion disappeared in all the ten patients who underwent coronary artery bypass graft surgery. It is suggested that exercise-induced U-wave inversion shown on chest wall mapping is a reliable indicator of coronary artery disease, which disappears after myocardial revascularization, and in addition, aids identification of individual coronary arterial lesions.

A dose response study with oral prenalterol in patients with chronic congestive cardiac failure.

Prenalterol is an orally active cardioselective beta agonist, with a long half-life. Previous studies have confirmed its inotropic activity following intravenous infusion in patients with heart failure. It has little chronotropic activity and no significant arrhythmogenicity. We have studied the response to sustained-release oral prenalterol given over four weeks at doses of 20, 40, 100, and 200 mg daily in 10 patients with New York Heart Association class II and III heart failure due to ischemic heart disease. All were in sinus rhythm and already receiving diuretics and digoxin. The drug was well tolerated and without side effects. Nine patients showed a dose-related improvement in their exercise tolerance as measured on the treadmill, up to a dose of 100 mg daily, with a significant increase in estimated oxygen uptake. There was a dose-related reduction in maximum heart rate, systolic blood pressure, and rate-pressure product during exercise, which is suggestive of a reduction in myocardial oxygen consumption. We conclude that prenalterol improves exercise tolerance without any significant cardiovascular or other side effects, and produces a clinically relevant and sustained improvement in patients with chronic heart failure. M-mode echocardiographic measurements of left ventricular dimension and function at rest did not show any change during the study.

Electrocardiographic chest wall mapping in the diagnosis of coronary artery disease.

Chest wall mapping of ST segment changes, inverted U waves, and Q waves using 16 electrocardiographic electrodes was performed at rest and during and after bicycle ergometry in 150 patients presenting with chest pain suggestive of angina. All patients underwent coronary angiography. The presence or absence of appreciable coronary artery disease (greater than or equal to 50% stenosis) was detected with a sensitivity of 98% and a specificity of 88%. The identification of lesions in individual coronary arteries was also possible with a sensitivity and specificity of 87% and 85% respectively for the territory of the left anterior descending and diagonal artery, 71% and 85% respectively for the right coronary artery, and 85% and 80% respectively for the circumflex artery. This test appears to be a reliable non-invasive screening method for selecting patients for angiography.

Immediate and sustained haemodynamic effects of prazosin during upright exercise in man.

To ascertain the immediate pharmacodynamic and long-term haemodynamic effects of prazosin in chronic ambulant heart failure, measurements were made during sitting, standing, and walking in 12 patients with severe ischaemic left ventricular failure before and after their first dose of prazosin (2 mg) and in six of these patients after a further 12 weeks of sustained treatment (2 mg tds). When first added to treatment with digoxin and frusemide, prazosin was followed within an hour by substantial reductions in systemic arterial, pulmonary arterial, and pulmonary venous pressures in both postures at rest and also during walking. These changes were significantly attenuated after continued treatment. Cardiac output while sitting and standing at rest was reduced in both instances but the response to exercise was unchanged. The pharmacodynamic effects of prazosin in heart failure are explicable in terms of blockade of alpha1 adrenoceptors in arterial resistance and venous capacitance vessels augmented perhaps by lessening of reflex vasoconstriction secondary to the reduction in pulmonary venous pressure. The cause of the attenuation of the acute haemodynamic effects of the drug during sustained treatment is unknown.

Haemodynamic dose-response effects of i.v. metoprolol in coronary heart disease.

The haemodynamic effects of intravenous metoprolol, over the dose-range 2.5--20 mg, were studied in 12 patients with coronary heart disease. The pharmacodynamic activity of the drug was confirmed by the suppression of exercise systolic pressure and tachycardia. There were statistically significant dose-response reductions in systolic and diastolic pressures, heart rate and cardiac output together with a dose-related increase in pulmonary wedge pressure. In patients with coronary heart disease intravenous metoprolol should probably not exceed the doses used in this study and should be administered with caution in patients with impairment of pumping function.

Propranolol in hypertension: a dose-response study.

The effect of propranolol was studied in a double-blind crossover trial in 24 carefully selected hypertensive outpatients. Each patient received propranolol 60 mg/day, 120 mg/day, 240 mg/day, and placebo for four weeks each according to a randomised sequence. Propranolol 60 mg/day was no better than placebo in reducing blood pressure. The effects of propranolol 120 mg/day and 240 mg/day were not significantly different. Both doses reduced lying blood pressure by about 20/10 mm Hg from an initial level of 173/104 mm Hg. No difference was detected between the effects of the different doses of propranolol and placebo on weight or on the occurrence of adverse reactions.