ACE Inhibition with Cilazapril Improves Myocardial Perfusion to the Ischemic Regions During Exercise

Gasić, S; Dudczak, Robert; Korn, A.; Kleinbloesem, C. H.

doi:10.1097/00005344-199002000-00008

Cited by 29 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3). These findings are in accordance with previous studies showing benefi cial effects on exercise-induced ischemia with captopril [8,9,14] and other ACE inhibitors [15][16][17] in patients with uncomplicated angina. We did not find any effects of captopril on exercise duration or time to onset of angina.…”

Section: Discussionsupporting

confidence: 93%

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 93%

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

View full text Add to dashboard Cite

show abstract

“…56 Global coronary blood flow to isolated rat hearts is unaltered in the chronic phase post- OP < 0 05, sham v sham and quinapril; +P < 0 05, MI v MI and quinapril. (Horn M, et al, 1996.58) Tc99mMIBIN to the cold spot in the scintigram.59 60 Thus, taken together, these results suggest that angiotensin II may control coronary blood flow under certain circumstances and in various models with myocardial ischaemia.…”

Section: Ischaemiamentioning

confidence: 89%

The renin-angiotensin system and coronary vasomotion

Ertl¹,

Hu²,

Bauer³

et al. 1996

Heart

View full text Add to dashboard Cite

Coronary vasomotion, which controls myocardial perfusion, is closely regulated by myocardial metabolic demand and has been assessed by changes of coronary vascular resistance. Only two decades ago evidence of neural and hormonal control overriding the metabolic control of coronary arterioles, which represent the "resistance vessels" was reported (fig 1). Numerous groups reported persistence of a coronary vasodilator reserve or progressive vasoconstriction despite ischaemia.1-11 Studies showed that a adrenergic receptor mediated coronary constriction may restrict metabolic dilatation to avoid wasting blood flow to the heart muscle. ' Springer Verlag, 1988:454-64.) culature for various mediators, and the physiological significance of such mediators remains obscure.Vasomotion of large conductance vessels does not normally contribute to regulation of coronary blood flow. However, in the presence of atherosclerotic lesions, coronary thrombosis, and spasm, large vessels limit myocardial perfusion and induce ischaemia, angina pectoris, and infarction. Abnormal vasomotion of large coronary vessels has been appreciated in the last decades, when coronary angiography became available during acute coronary syndromes. Atherosclerotic vessels seem to respond with vasoconstriction in situations where vasodilatation should be required. The endothelium and mediators released by the endothelium play a critical role in mediating vasomotion in normal and diseased large and small coronary vessels. However, multiple potential mediators confuse our understanding of coronary vasomotion.Previously, agonists and antagonists of various mediator systems have been used to identify a potential role for coronary vasomotion. Effects of agonists are dose dependent, and it remains unclear from most studies which concentrations of agonists may occur under physiological or pathophysiological conditions. The use of antagonists might increase our understanding, but the specificity of available inhibitors is limited. In addition, the effect of mediators is balanced by other mediators, and blockade of one may activate others. For the coronary circulation, the situation is even more complicated since coronary blood flow is under the influence of aortic pressure, compressive forces of the ventricle, and myocardial metabolic demand. Thus interventions in the coronary circulation with any agonist or antagonist result in complex changes which are difficult to analyse. Response to mediators may be different in various sections of coronary circulation,'9 and diseases which alter vasomotion may affect large and small vessels differently. Finally, acute effects of an agonist or antagonist may be different from chronic effects. Changes of coronary vascular muscle tone are responsible for acute coronary vasomotion, but coronary vasomotion may well be influenced by chronic morphological changes of the coronary vessel wall and perivascular tissue.

show abstract

“…8 Subsequent clinical studies have corroborated the capacity of ACE inhibition to enhance the coronary blood flow, especially in the absence of fixed anatomical obstruction, 9,10 and have demonstrated the anti-anginal effect of this treatment in patients with symptomatic coronary insufficiency. [11][12][13][14] Essentially, these data establish angiotensininduced vasoconstriction as an independent mechanism capable of inducing permanent myocardial injury in the absence of atherosclerotic or thrombotic coronary obstruction. The widespread necrotic lesions resulting from these prolonged vasospastic episodes can initiate the sequence of events leading eventually to heart failure and/or sudden death.…”

Section: Myocardial Ischaemiamentioning

confidence: 97%

Angiotensin II as a cardiovascular risk factor

Gavras

2002

J Hum Hypertens

View full text Add to dashboard Cite

A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Angiotensin acts both as a circulating hormone and as a locally acting paracrine/autocrine/intracrine factor. The adverse effects of angiotensin on the heart include the mechanical results of elevated resistance to the pumping function of the myocardium, as well as the effects of neurohumoral abnormalities on various cardiac structures. In addition, cardiac damage follows acute ischaemic injury or chronic energy starvation due to coronary artery disease, attributable to either mechanical obstruction Keywords: angiotensin II; renin-angiotensin system; cardiovascular disease; myocardial infarction Myocardial ischaemiaAngiotensin II (A II) is one of the major systemic pressor hormones (others include noradrenaline, vasopressin and endothelin). The idea that excessive levels of circulating A II can cause myocardial infarctions originated from an early experiment in which exogenous infusion of A II produced widespread areas of myocardial necrosis in rabbits. 1 Clinical observations in patients subjected to extreme stimulation of the renin-angiotensin system during haemodialysis revealed that these patients were prone to coronary death. This was attributed to intense coronary vasoconstriction, because focal myocardial necrosis was described in areas with no detectable coronary obstructive lesions. 2 These experiments were later replicated and amplified by other investigators. 3,4 It was found that an excess of endogenous or exogenous A II can damage the myocardium via several additional mechanisms, such as increased sarcolemmic permeability and death of cardiac myocytes, or increased permeability and destruction of coronary microvascular endothelial cells. All these eventually lead to the replacement of contractile myocardium by fibrotic tissue.Angiotensin II exerts a preferential pressor action on the coronary, renal, cerebral and adrenal vasculaCorrespondence: H Gavras, Department of Medicine, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. E-mail: hgavrasȰbu.edu (atherosclerotic and/or thrombotic) or functional stenosis (vasospasm). Activation of the renin-angiotensin system has several haemodynamic and humoral consequences, all of which may damage the myocardium. These include acute myocardial ischaemia, left-ventricular hypertrophy, arrhythmias, alterations in the coagulation-fibrinolysis equilibrium, increased oxidative stress, and pro-inflammatory activity. A brief review of some of the mechanisms by which activation of the renin-angiotensin system can inflict damage on the heart is presented.

show abstract

ACE Inhibition with Cilazapril Improves Myocardial Perfusion to the Ischemic Regions During Exercise

Cited by 29 publications

References 0 publications

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

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

The renin-angiotensin system and coronary vasomotion

Angiotensin II as a cardiovascular risk factor

Contact Info

Product

Resources

About