Angiotensin Converting Enzyme Inhibitors and Cardiopulmonary Bypass: Is ACE Inhibitor Safe for Heart Surgery?

2005 ◽  
Vol 1 (3) ◽  
pp. 253-256
Author(s):  
Yasuyuki Shimada ◽  
Hideshi Itoh
1995 ◽  
Vol 80 (3) ◽  
pp. 473-479 ◽  
Author(s):  
Kenneth J. Tuman ◽  
Robert J. McCarthy ◽  
Christopher J. OʼConnor ◽  
Wendy E. Holm ◽  
Anthony D. Ivankovich

1995 ◽  
Vol 80 (3) ◽  
pp. 473-479 ◽  
Author(s):  
Kenneth J. Tuman ◽  
Robert J. McCarthy ◽  
Christopher J. OʼConnor ◽  
Wendy E. Holm ◽  
Anthony D. Ivankovich

1996 ◽  
Vol 30 (11) ◽  
pp. 1242-1245 ◽  
Author(s):  
Peter V Dicpinigaitis

OBJECTIVE: To determine whether baclofen can suppress the cough induced by angiotensin-converting enzyme (ACE) inhibitors. DESIGN: Prospective, open-label, clinical trial of a 4-week course of low-dose oral baclofen (5 mg tid days 1–7, 10 mg tid days 8–28). SUBJECTS: Seven patients with severe, persistent ACE inhibitor-induced cough. SETTING: University-affiliated teaching hospital. MAIN OUTCOME MEASURES: Study participants kept daily diaries monitoring the frequency of cough during and after completion of baclofen therapy. RESULTS: All subjects demonstrated diminution of cough after initiation of baclofen. Initial improvement was noted by a mean of 4.0 days (range 3–6), and maximal improvement during treatment was achieved by a mean of 10.7 days (range 5–15). In addition, all subjects demonstrated persistent suppression of cough (range 25–74 d) after discontinuation of the study drug. CONCLUSIONS: Low-dose oral baclofen therapy caused a prolonged antitussive effect in all subjects without inducing any adverse reactions. Baclofen may offer an alternative to the discontinuation of ACE inhibitor therapy in patients for whom these drugs are required.


2006 ◽  
Vol 84 (9) ◽  
pp. 1110-1113 ◽  
Author(s):  
Xiao-hua Cai ◽  
Bing Xie ◽  
Hui Guo

Methyl 2-methoxycarbonyl-3-phenylpropionate derivatives were prepared, and their inhibitory activities for angiotensin converting enzyme (ACE) were evaluated. Compounds 5b (IC50 = 0.0039 µmol/L), 5d (IC50 = 0.0027 µmol/L), 5e (IC50 = 0.0021 µmol/L), and5f (IC50 = 0.0052 µmol/L) exhibited more potent ACE inhibitiory activity than the control drug Captopril® (IC50 = 0.0075 µmol/L).Key words: hypertension, 2-methoxycarbonyl-3-phenyl propionate derivative, ACE inhibitor.


2016 ◽  
Vol 4 (16) ◽  
pp. 67
Author(s):  
Kenneth Iwuji ◽  
Hezekiah Sobamowo ◽  
James Tarbox ◽  
Rose Egbe

Angiotensin-converting enzyme (ACE) inhibitors are the leading cause of drug-induced angioedema in the United States because these drugs are widely prescribed for several common medical disorders. Angiotensin-converting enzyme inhibitors cause angioedema in 0.1 to 0.7 percent of recipients. When prescribing ACE-inhibitors to patients, angioedema should always be considered as a potential adverse reaction during treatment.


1993 ◽  
Vol 27 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Wayne R. Melchior ◽  
Vinita Bindlish ◽  
Linda A. Jaber

OBJECTIVE: Diabetic nephropathy (DN) is a leading cause of kidney disease in the US. At least four factors influence whether people with diabetes will develop DN: (1) hypertension, (2) hyperglycemia, (3) dietary protein intake, and (4) intrarenal hemodynamics. The angiotensin-converting enzyme (ACE) inhibitors are known to affect blood pressure (BP) and intrarenal hemodynamics; thus, they may prevent the onset of DN or slow the decline in renal function once DN has been diagnosed. DATA SOURCES: English-language, controlled, and crossover studies published between 1973 and 1991 and indexed in MEDLINE under the headings diabetic nephropathies and angiotensin-converting enzyme inhibitors. MAIN OUTCOME MEASURES: The primary outcome indicators of interest were the effects of the ACE inhibitors captopril, enalapril, and lisinopril on BP control and urinary albumin excretion rate. CONCLUSIONS: ACE inhibitors delay the onset and slow the progression of DN in people with diabetes independent of BP effects. They also slow the progression of DN in people with diabetes who have poorly controlled hyperglycemia. The proper dose and time at which to initiate ACE inhibitor therapy to prevent the appearance of DN is not known. It is also not known how long the beneficial effects of ACE-inhibitor therapy persists as only two studies have followed patients for more than one year. Finally, large, long-term, controlled clinical trials are needed before ACE inhibitors can be considered for prophylactic use to prevent the onset and/or progression of DN.


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