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Effects of ACE Inhibitors on Coronary Haemodynamics and Angina Pectoris

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Effects of ACE Inhibitors on Coronary Haemodynamics and Angina Pectoris S 52 Br Heart JT (Supplement) 1994; 72: 52-56 CORONARY ARTERY DISEASE Br Heart J: first published as 10.1136/hrt.72.3_Suppl.S52 on 1 September 1994. Downloaded from Effects of ACE inhibitors on coronary haemodynamics and angina pectoris M K Davies Angiotensin II is a potent vasoconstrictor of in incidence of sudden death observed after both coronary and peripheral vasculature; it ACE inhibitors in heart failure may be due in increases myocardial contractility, promotes part therefore to a beneficial effect on the myocardial hypertrophy, and possibly con- coronary circulation, atherogenesis, or the tributes to the process of atherosclerosis. In thrombotic process.20 Both the recent SOLVD addition, the renin-angiotensin system and treatment'3 and SAVE2' studies have shown a the sympathetic nervous system are inter- reduction in the rate of recurrent infarction in dependent, each stimulating the activity of patients with heart failure or with impaired the other. Angiotensin II enhances the activity left ventricular function after myocardial of the sympathetic nervous system by infarction who have been treated with ACE facilitating the release of noradrenalinelA and inhibitors. Thus, indirect data are available to by interfering with its neuronal reuptake.5 6 suggest that ACE inhibitors have anti- Angiotensin II has important central and ischaemic effrects that could account for some peripheral vagolytic effects.7-'0 Vasodilatation of their beneficial therapeutic and prognostic and decreased fluid retention reduce preload, effects. afterload, heart size, and left ventricular wall stress, thereby reducing myocardial oxygen demand. Similarly, reductions in the left Effects of ACE inhibitors in patients with ventricular hypertrophy associated with hyper- stable angina tension and heart failure and reductions in the The effects of ACE inhibitors on coronary positive inotropic effects of angiotensin II vascular tone was studied by Karsch et al in could contribute to reduced myocardial 12 patients with coronary heart disease and oxygen demand. A reduction in sympathetic exertional angina.22 Central haemodynamic and increase in parasympathetic tone at rest measurement and coronary angiography and on exercise, due to inhibition in activity of were carried out during control pacing and atrial pacing both the renin-angiotensin system and the during angina induced by rapid http://heart.bmj.com/ sympathetic nervous system by angiotensin before and after ACE inhibition with intra- converting enzyme (ACE) inhibitors, will venous captopril. At rest and during ischaemia reduce heart rate, or the reflex tachycardia captopril resulted in coronary vasodilatation at usually associated with peripheral vaso- the site of coronary atherosclerotic narrowing, dilatation, and thereby reduce the rate- increasing coronary artery diameter by 0 1 mm pressure (double) product. A concurrent at rest and by 0-2 mm during ischaemia. reduction in vasoconstriction mediated by These changes were associated with a fall angiotensin II at the coronary vascular bed in left ventricular end diastolic pressure on September 27, 2021 by guest. Protected copyright. should result in coronary vasodilatation and an and peripheral vasodilatation. Despite these improvement in myocardial oxygen supply. favourable haemodynamic changes, however, Despite these diverse potential mechanisms only one patient experienced a significant affecting both myocardial oxygen demand and reduction in angina, captopril having no supply beneficially, a consistent and clinically significant effect on coronary artery diameter significant anti-ischaemic effect of ACE in the non-diseased segments. Ikram et al also inhibition has been difficult to show. used intravenous captopril and atrial pacing to ACE inhibitors improve prognosis in all examine the effects on angina threshold and grades of symptomatic heart failure, reducing systemic and coronary haemodynamics in 12 mortality from progressive heart failure and patients with documented coronary artery sudden death.1 1-14 Sudden death is often disease.23 Captopril resulted in an increased presumed to be arrhythmic in origin, but time to angina and increased paced heart rate most patients with heart failure have com- for the development of angina, with a trend plex ventricular ectopic activity on Holter towards increased coronary blood flow (229 to monitoring.'5 Although the presence of these 296 ml/min, P = 0-1 1) and decreased coronary Department of arrhythmias is related to prognosis in some vascular resistance (53 to 47 dyn s cm-5/1000, Cardiology, studies, their predictive accuracy is generally P=0-11). Selly Oak Hospital, weak.'2 16-19 There are few large postmortem The clinical effects of ACE inhibitors in Birmingham M K Davies studies in heart failure, but the data available angina pectoris were investigated by Gibbs the associated with et al in 12 patients with chronic stable Correspondence to: suggest that arrhythmias Dr M K Davies, sudden death in these patients are often the angina.24 In a two week double blind placebo Department of Cardiology, or controlled the effects of oral on Selly Oak Hospital, manifestation of some intercurrent coronary study enalapril Birmingham B29 6JD. pulmonary thrombotic event.19 The reduction angina frequency and treadmill exercise Effects ofACE inhibitors on coronary haemodynamics and angina pectoris S 53 testing were determined. Enalapril reduced cantly fewer patients developed chest pain resting and exercise double product (each by during exercise: 74 given placebo v 42 given Br Heart J: first published as 10.1136/hrt.72.3_Suppl.S52 on 1 September 1994. Downloaded from about 10%) by reducing systolic blood cilazapril, P = 0-03). In another study of 12 pressure at rest and on exercise without an patients cilazapril did not improve exercise effect on heart rate. In the group as a whole, time to angina. 29 Similarly, enalapril did not however, the frequency of angina and improve exercise time to development of consumption of glyceryl trinitrate was not angina in a group of 12 patients with stable improved with enalapril. On formal exercise angina after one week's treatment.30 testing enalapril increased exercise duration by Thus in chronic stable angina several 43 s (from 466 s to 509 s) and exercise studies, each of small numbers of patients, duration to ST segment depression (0 1 mV) have failed to show a convincing anti- by 42 s (from 345 s to 387 s). However, ischaemic effect with ACE inhibitors whether interpatient variability was considerable, with this is assessed by symptoms, exercise testing, four patients showing an increase in total or ambulatory ST segment monitoring. exercise time of more than 20% with enalapril Although beneficial systemic and coronary and two patients showing a marked reduction haemodynamic effects can occur, which might in exercise capacity and an increase in angina be expected to improve myocardial ischaemia, frequency. Thus, although ACE inhibitors individual patient responses are unpredictable seemed to reduce myocardial ischaemia in and the use of ACE inhibitors may cause a some patients, deterioration was evident in a deterioration in angina in some patients. large proportion. The effects of ACE inhibition on myo- cardial ischaemic episodes has also been Effects of ACE inhibitors on unstable examined using ambulatory ST segment angina monitoring over 24 hours. In a study of 11 In patients with unstable angina cardiac normotensive patients with angiographically sympathetic activity is significantly increased proved coronary artery disease Thurmann et al compared with that in patients with stable showed that the number of angina attacks and angina. Tritiated noradrenaline infusions in ischaemic episodes was not significantly patients undergoing coronary angiography reduced after treatment with the ACE show that cardiac noradrenaline spillover and inhibitor benazepril.25 On formal exercise coronary sinus noradrenaline concentration testing these patients' exercise double product are increased in patients who have had and maximal exercise induced ST segment unstable angina within the preceding three depression were not improved. Interpatient months compared with those with stable variability was again considerable, with six angina.3' This suggests that the increase in patients improving (as assessed by maximal sympathetic activity may be sustained and ST segment depression) and three patients persist for several months after a period of manifesting worsening of ischaemia. In a unstable angina. A similar increase in cardiac similar study by Klein et al in 29 patients with sympathetic overactivity has been shown in chronic stable angina benazepril did not alter another study of unstable angina, but http://heart.bmj.com/ exercise time or improve exercise induced persistent abnormalities were not found as ischaemia.26 Although the number of episodes patients with inactive unstable angina (unstable of ST segment depression on ambulatory angina occurring 8-12 weeks previously but monitoring and the total ischaemic burden no angina for at least four weeks) had no was reduced from 1549 minutes in the placebo change in cardiac noradrenaline spillover group to 879 minutes in the benazepril group, compared with controls.32 In this study a these changes were not significant. Benazepril correlation was found between the number of on September 27, 2021 by guest. Protected copyright. did not reduce angina frequency or con- silent ischaemic episodes or the overall sumption of glyceryl trinitrate.
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