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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is a major potential problem among the increasing number of older persons in the population, threatening their health and shortening their life expectancy due particularly to stroke and congestive heart failure (CHF). Controlled studies have shown that antihypertensive drug therapy reduces the incidence of severe CHF, stroke and cardiovascular mortality in the elderly. Special consideration should be given to altered drug metabolism, altered responses to drugs, and concomitant medications when pharmacotherapy is instituted in the elderly. Angiotensin-converting enzyme (ACE) inhibitors are acceptable in the hypertensive older patient as first-line therapy for all grades of hypertension and as second-line therapy for the patient with CHF. Use of ACE inhibitors avoids many of the symptoms and metabolic disturbances associated with beta-blockers and diuretics. Quinapril is a new non-sulphydryl ACE inhibitor whose active metabolite, quinaprilat, has a relatively short accumulation half-life compared with enalapril and lisinopril but has an enhanced affinity for the converting enzyme, allowing rapid excretion of the drug while retaining a 24-hour antihypertensive effect with once-daily dosing. Quinapril is a valuable addition to the ACE inhibitor class, with demonstrated efficacy and safety in the older patient.
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PMID:ACE inhibitors in the treatment of hypertension in the older patient. 219 9

This study investigates the acute haemodynamic effects of Quinapril (CI-906) a new non-sulphydryl angiotensin converting enzyme inhibitor in 15 patients with refractory congestive cardiac failure. There were 14 males and 1 female mean age 59.5 years. After administration of Quinapril there was a significant reduction in mean arterial pressure (MAP) from 93.1 to 79 mmHg, systemic vascular resistance (SVR) from 1887 to 1349 dyn s cm-5 and PCW from 27.3 to 15.3 mmHg. This was accompanied by an increase in CO from 3.7 to 4.71/min, cardiac index (CI) from 1.97 to 2.51/min/m2 and Stroke volume index from 21.1 to 28.7 ml/m2. There was no significant change in heart rate (HR), right atrial pressure (RAP), or pulmonary vascular resistance. The peak effect on pulmonary capillary wedge pressure (PCW) and cardiac output (CO) occurred at 75-120 min after Quinapril administration. The maximum effect on mean arterial pressure (MAP) occurred slightly later at 120-150 min. SVR and CI exhibited 2 periods of peak effects, at 90 and 180 min. This time course is very similar to that observed in studies on the acute effects of Captopril. The significant improvement in haemodynamic measurements acutely, following administration of Quinapril 5 mg orally, suggests that this drug is worthy of further study in the management of patients with refractory congestive cardiac failure, in particular its long term effects.
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PMID:The acute haemodynamic effects of quinapril, a new non-sulfhydryl angiotensin converting enzyme inhibitor, in patients with severe congestive cardiac failure. 302

The effects of long-term oral administration of quinapril on the occurrence of stroke and on mortality were investigated in young salt-loaded stroke-prone spontaneously hypertensive rats (SHR-SPs) during the treatment period (8th-34th week of age) and up to 6 weeks thereafter. Simultaneously, blood pressure, saline intake, diuresis, and proteinuria were investigated at regular intervals, and cerebrovascular, renal, and cardiac lesions were assessed after death. Untreated SHR-SPs served as controls. Quinapril completely suppressed stroke and mortality, afforded only limited protection v blood pressure rise, and prevented any increase in saline intake, diuresis, and proteinuria both during and after the treatment period. Quinapril long-lastingly prevented vascular fibrinoid necrosis development at the cerebral, but also at the renal and cardiac levels. In the kidneys, vascular intimal and medial hyperplasia were strongly reduced, as were the glomerular and tubulo-interstitial lesions. At the cardiac level, intimal and medial hyperplasia were slightly reduced but infarction and fibrosis were hardly affected. As the renin-angiotensin system is highly stimulated in SHR-SPs and as angiotensin II (AII) is responsible for fibrinoid necrosis formation, vessel obstruction, and stroke in these animals, we conclude that the long-lasting protection afforded by quinapril v stroke and mortality in SHR-SPs both during and after the treatment period is mostly due to the drug-induced interruption of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quinapril prevents stroke both during and after the treatment period in stroke-prone spontaneously hypertensive rats. 830 70

Twenty horses with mitral valve insufficiency, but without signs of congestive heart failure, and five horses without signs of heart disease were examined before and after medication with an angiotensin-converting enzyme (ACE) inhibitor. The examination included echocardiography assessment as well as heart catheterization. The echocardiographic examination included B-mode, M-mode, conventional and colour Doppler techniques. For 8 weeks, all horses were treated with Accupro 20 (active substance: Quinapril) at an oral dose rate of 120 mg/horse/day. A follow-up of the horses with mitral valve insufficiency after 8 weeks revealed a statistically significant increase in the stroke volume and the cardiac output as well as a decrease in regurgitation velocity time integral (VTI). The regurgitation blood velocity remained the same. The severity of mitral valve insufficiencies revealed a moderate improvement in five horses, from moderate to mild, after therapy. Significant changes of cardiac dimension (B-mode) and shortening fraction (M-mode) before and after treatment could not be observed. The owners' judgement of the horses' performance was that of a minor improvement. In the horses without clinical findings the results of examination before and after treatment remained the same.
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PMID:Effects of the ACE inhibitor quinapril on echocardiographic variables in horses with mitral valve insufficiency. 1510 41