Angiotensin converting enzyme inhibition in chronic stable angina: effects on myocardial ischaemia and comparison with nifedipine.

Ikram, Hamid; Low, Clive J.S.; Shirlaw, Teresa; Foy, S. G.; Crozier, Ian; Richards, A. Mark; Khurmi, Nardev S.; Horsburgh, R.J.

doi:10.1136/hrt.71.1.30

Cited by 20 publications

(7 citation statements)

References 27 publications

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“…Other antianginal agents like molsidomine, and nicorandil with pharmacologic properties similar to nitrates may be effective in the treatment of stable angina pectoris but their role in vasospastic angina is unknown [14][15][16]. ACE inhibitors efficacy has not been established for treatment of either stable or variant angina [17]. Before the negative results of Heart and Estrogen/Progestin Replacement Study-II (HERS-II), estrogen therapy has been recommended in postmenopausal women with variant angina because of its beneficial effects on endothelial function [18].…”

Section: Discussionmentioning

confidence: 99%

Refractory case of coronary artery spasm with interesting findings: A case report

et al. 2011

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This is a case of refractory vasospastic angina with unusual electrocardiographic findings and rare coronary angiographic documentation of diffuse spasm of the left coronary system with a baseline of near normal coronary arteries. A 66-year-old man presented with severe vasospastic angina that eventually progressed to non-ST elevation myocardial infarction (NSTEMI). During the episodes of chest pain, the electrocardiogram revealed ST segment depression rather than elevation. Coronary angiography revealed near normal coronary arteries with initial diffuse spasm of the left coronary system. The patient continues to be symptomatic despite treatment with different forms and doses of nitrates and calcium channel blockers.

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Section: Discussionmentioning

confidence: 99%

Refractory case of coronary artery spasm with interesting findings: A case report

et al. 2011

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“…Benazepril has been compared with metoprolol [18] and nifedipine [19], In both studies, ben azepril was shown to reduce the severity and number of ischemic episodes and the duration of S-T depression during ambulatory monitoring. However, in contrast to metoprolol and nifedipine, benazepril did not produce any clinical benefit in terms of exercise test variables.…”

Section: Discussionmentioning

confidence: 99%

Short-Term Effects of Captopril on Exercise Tolerance in Patients with Chronic Stable Angina pectoris and Normal Left Ventricular Function

Steffensen¹,

Grande²,

Madsen³

et al. 1995

Cardiology

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A double-blind, placebo-controlled, crossover study was carried out to evaluate the short-term effects of captopril on exercise tolerance in 18 normotensive patients with chronic stable angina pectoris and normal left ventricular function. Captopril 25 mg (or placebo) was given twice, i.e. in the evening (10 p.m.) and the following morning (8 a.m.), prior to a maximal symptom-limited bicycle exercise test (11 a.m.). Captopril reduced the systolic and dia-stolic blood pressures at rest (p < 0.01) without causing any reflex tachycardia. The time to onset of S-T depression was prolonged (p < 0.05), and the maximal S-T depression was reduced (p < 0.02). No differences were found between captopril and placebo in total exercise duration or time to onset of angina. The effects of captopril on exercise-induced ischemia were demonstrated most clearly in patients who responded with a greater than 10 mm Hg fall in the resting systolic blood pressure. In conclusion, this study suggests that captopril has anti-ischemic properties, which may be of importance in the treatment of patients with chronic stable angina and normal left ventricular function. These beneficial effects probably relate to a reduction in afterload and myocardial wall stress and therefore a reduction in myocardial oxygen demand.

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“…Exercise testing has produced variable results but ambulatory electrocardiographic assessment of ischaemia has generally shown that ACE inhibitors have worthwhile antiischaemic effects.75 77 80 There is a dichotomy in anti-ischaemic effects as assessed by maximal exercise testing and the total 24 hour ischaemic burden by ambulatory electrocardiography, which is seen in the case of nitrates and nifedipine. 8' In general, most of the double blind investigations into the anti-anginal effects of ACE inhibition have used near maximal exercise stress testing in order to induce myocardial ischaemia.…”

Section: Chronic Stable Anginamentioning

confidence: 99%

The renin-angiotensin-aldosterone system and cardiac ischaemia

Ikram¹

1996

Heart

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The renin-angiotensin-aldosterone system is a remarkably complex homoeostatic neuroendocrine entity. It is an endocrine system regulating vascular tone and salt and water balance. It is a tissue based system with paracrine and autocrine effects, and also a neuromodulator. These attributes result in an extensive range of actions on the heart, many of which play an important role in cardiac ischaemia and hence are of immense interest to clinicians and basic scientists.There are several theoretical reasons why the renin-angiotensin system should play a pivotal role in cardiac ischaemia. Angiotensin II is a potent coronary and systemic vasoconstrictor and a positive inotropic and chronotropic agent. These attributes of angiotensin II promote ischaemia in vulnerable areas of the myocardium. Initial attempts to block these pro-ischaemic effects by angiotensin converting enzyme (ACE) inhibitors produced equivocal results, due largely to inadequacies of experimental design, are were themselves the victims of inadequate knowledge. More recently, with better understanding of the fundamental biophysiology of the renin-angiotensin system and better drugs, blockade of the system in patients after acute myocardial infarction has yielded promising results, especially in patients with impaired systolic left ventricular function. Research has now focused on ways and means of using these newly discovered anti-ischaemic properties of ACE inhibitors as agents for secondary and perhaps also for primary prevention of acute and chronic coronary events. Research into this aspect of the renin-angiotensin system appears set for spectacular growth as knowl- In this article I shall endeavour to review the basic physiological action of angiotensin II on the coronary vasculature and the myocardium as well as the therapeutic use of angiotensin blocking agents in the management of acute and chronic ischaemic conditions. Actions on myocardial oxygen supply: demand ratio Experimental and clinical data indicate that angiotensin II has a modest action on the heart in normal subjects when the renin-angiotensin system is not activated.1 2 However, if the system is stimulated by sodium deprivation,' diuretic therapy,3 acute cardiac ischaemia,4 8 or renovascular hypertension,9 then the cardiovascular effects are intensified.The earliest view of the effects of angiotensin II effects on the heart was that it had four major actions. First, it had a direct positive inotropic action on the ventricular myocardium.'0 " Second, there was a further inotropic effect resulting from its neuromodulator role of augmenting sympathetic tone.'2 Third, angiotensin II increased heart rate directly and through augmentation of sympathetic activity.'3 14 Fourth, there was tonic modulation of sympathetic coronary vasoconstriction. I5Left ventricular hypertrophy is a common consequence of systemic hypertension and has been shown to be associated with a considerably enhanced risk of cardiovascular morbid events, including myocardial infarction.'618' A consequence of left vent...

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Angiotensin converting enzyme inhibition in chronic stable angina: effects on myocardial ischaemia and comparison with nifedipine.

Cited by 20 publications

References 27 publications

Refractory case of coronary artery spasm with interesting findings: A case report

Refractory case of coronary artery spasm with interesting findings: A case report

Short-Term Effects of Captopril on Exercise Tolerance in Patients with Chronic Stable Angina pectoris and Normal Left Ventricular Function

The renin-angiotensin-aldosterone system and cardiac ischaemia

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