The acute haemodynamic effects of quinapril, a new non-sulfhydryl angiotensin converting enzyme inhibitor, in patients with severe congestive cardiac failure

Holt, P.; Najm, J.; Sowton, Edgar

doi:10.1007/bf00870978

Cited by 21 publications

(7 citation statements)

References 18 publications

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“…Our observations record a significant blood pressure fall up to 10 h post-dose with the maximum fall at 5 h. This contrasts with the earlier times to maximal blood pressure response of 2-2.5 h reported in CHF with 5 mg orally by Holt et al [13] and with 2.5-10 mg orally by Nieminen & Kupari [17]. These uncontrolled studies reported a shorter duration of effect on blood pressure.…”

Section: Discussioncontrasting

confidence: 96%

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Haemodynamic response and pharmacokinetics after the first dose of quinapril in patients with congestive heart failure.

Squire

Lees

et al. 1994

Brit J Clinical Pharma

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1. Twenty‐four elderly patients with stable, chronic congestive heart failure, NYHA II‐IV, requiring addition of an ACE inhibitor to their existing therapy were randomised to receive double‐blind a single dose of quinapril 2.5 mg p.o. or matching placebo after 24‐48 h supervised diuretic withdrawal. 2. The effect of treatment on resting supine blood pressure, heart rate, plasma angiotensin converting enzyme (ACE) and circulating plasma renin activity was compared between groups over the first 24 h after dosing. The pharmacokinetic profiles of quinapril and the active metabolite quinaprilat were determined. 3. Compared with placebo, quinapril caused a statistically significant but modest fall in blood pressure from 3 to 10 h post dose. The maximum fall of 12 mm Hg (95% C.I. 5.4‐18.5) was seen at approximately 5 h. Circulating ACE activity was 40% inhibited within 1 h. Maximum ACE inhibition (83.6%, 95% C.I. 76.7‐90.5) was observed at 3 h. ACE remained 60% inhibited at 24 h post dose. tmax for quinapril was seen at 2.6 +/‐ 1.2 h. while tmax for quinaprilat was at 3.6, +/‐ 0.8 h. 4. Treatment with quinapril was associated with a significant rise in plasma renin activity (PRA) of 8.83 ng AI ml‐1 h‐1 (95% C.I. 0.30‐17.96) compared with placebo. 5. Compared with placebo, quinapril 2.5 mg inhibits plasma ACE by over 60% for 24 h and reduces blood pressure for at least 10 h in patients with stable, chronic congestive heart failure. The blood pressure fall, although moderate and well tolerated, is more sustained than previously described for quinapril in heart failure.

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Section: Discussioncontrasting

confidence: 96%

“…Previous studies with quinapril in heart failure have shown beneficial haemodynamic changes both acutely [13] and with chronic therapy [14]. While the currently recommended starting dose of quinapril in CCF is 2.5 mg, the timing and extent of the haemodynamic response to this dose are unknown.…”

Section: Introductionmentioning

confidence: 99%

Haemodynamic response and pharmacokinetics after the first dose of quinapril in patients with congestive heart failure.

Squire

Lees

et al. 1994

Brit J Clinical Pharma

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“…The haemodynamic effects of quinapril have been assessed in patients with congestive heart failure [15][16][17] and those with hypertension. [18] However, the effects of this drug on cardiac morphology, which are associated with its beneficial haemodynamic effects, require further investigation.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin Converting Enzyme Inhibition with Quinapril and Left Ventricular Mass in the Hypertensive Patient

Lavezzaro¹,

Raule²,

Toppi³

et al. 1994

Drug Invest

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The effects of quinapril (an angiotensin converting enzyme inhibitor) on cardiac hypertrophy were evaluated in a noncomparative study of 98 patients with mild to moderate hypertension over 4 months. Left ventricular hypertrophy (LVH) was diagnosed using echocardiography in 60% of patients at baseline. Combination therapy with hydrochlorothiazide (HCTZ) was initiated after I month in patients with inadequate blood pressure control to achieve a target diastolic pressure reduction from baseline (~ 10mm Hg) and/or reduction to < 90mm Hg. Left ventricular mass index (LVMI) was significantly reduced for patients of either sex with a baseline diagnosis of LVH, but not for those in whom LVH was not detected at enrolment. Systolic and diastolic blood pressures were also significantly reduced. The response rate was 83%, while 28% of patients required combination therapy with HCTZ. There was no correlation between the hypotensive effects of quinapril and change in LVMI. Furthermore, the addition of a diuretic did not appear to affect the LVMI response. Thus, the amelioration of LVH noted in this investigation appears to be attributable to quinapril.Electrocardiographically detected left ventricular hypertrophy (LVH) has been recognised as an independent risk factor for increased cardiovascular morbidity and mortality for many years. [1,2] However, diagnostic ECG signs of LVH are relatively infrequent among patients with hypertension; their prevalence ranged from 3 to 5% in adults recruited to the Framingham study[l] and the Hypertension Detection and Follow-up Program. [3] The introduction of the echocardiographic technique as a much more sensitive and accurate method for LVH detection [4,5] has significantly increased the estimated prevalence of LVH, which is currently thought to range between 25 and 30% in

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“…Three acute and two long-term hemodynamic studies have been completed, [10][11][12] and shown quinapril to demonstrate sustained hemodynamic benefit. A placebo-controlled dose- a, study utilizing 4-wk titration; 0 study utilizing I-wk titration.…”

Section: Quinapril In the Treatment Of Congestive Heart Failurementioning

confidence: 99%

Overview of the clinical development of quinapril

Frank¹

2009

Clin Cardiol

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Summary:Quinapril hydrochloride is the newest member of a family of angiotensin-converting enzyme (ACE) inhibitors. On completion of laboratory and animal studies, a clinical program was initiated to evaluate the antihypertensive and other properties of the drug in human subjects. The initial phase of clinical development was concerned with the pharmacokinetics and pharmacology of quinapril. The latter studies established a dose range for the drug and explored its effect on human hernodynamics and blood pressure. Safety and interactions with other drugs were also examined. Subsequent studies explored the safety and efficacy of quinapril in patients with mild to moderate hypertension and, later, in patients with more severe hypertension. Results of these studies supported the recommendation of a once daily dosage of quinapril, 10-40 mg, as first-line therapy in the management of hypertension, with diuretics as concomitant therapy as required in patients with severe hypertension. Quinapril has also been found to be the most potent of all available ACE inhibitors in binding to tissue ACE, which may contribute to its potent and sustained duration of action. Clinical evaluation of quinapril has also been undertaken in patients with congestive heart failure. Initial findings indicate that doses of 10-20 mg/day, given twice daily, are therapeutic when administered with diuretic or digitalis. Safety of the drug has been established in 2700 patients.

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The acute haemodynamic effects of quinapril, a new non-sulfhydryl angiotensin converting enzyme inhibitor, in patients with severe congestive cardiac failure

Cited by 21 publications

References 18 publications

Haemodynamic response and pharmacokinetics after the first dose of quinapril in patients with congestive heart failure.

Haemodynamic response and pharmacokinetics after the first dose of quinapril in patients with congestive heart failure.

Angiotensin Converting Enzyme Inhibition with Quinapril and Left Ventricular Mass in the Hypertensive Patient

Overview of the clinical development of quinapril

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