Hypertension fosinopril

Hyperkaiemia Elevated serum potassium (at least 0.5 mEq/L greater than the upper limit of normal) was observed in 0.4% of hypertensive patients given trandolapril, approximately 1% of hypertensive patients given benazepril, enalapril, ramipril, or moexipril approximately 2% of patients receiving quinapril or lisinopril, approximately 2.6% of hypertensive patients given fosinopril, and approximately 4.8% of CHF patients given lisinopril. Hyperkalemia also occurred with captopril. Vaivuiar stenosis Theoretically, patients with aortic stenosis might be at risk of decreased coronary perfusion when treated with vasodilators, because they do not develop as much afterload reduction as others. 

Enalapril is an oral prodrug that is converted by hydrolysis to a converting enzyme inhibitor, enalaprilat, with effects similar to those of captopril. Enalaprilat itself is available only for intravenous use, primarily for hypertensive emergencies. Lisinopril is a lysine derivative of enalaprilat. Benazepril, fosinopril, moexipril, perindopril, quinapril, ramipril, and trandolapril are other long-acting members of the class. All are prodrugs, like enalapril, and are converted to the active agents by hydrolysis, primarily in the liver. 

Reviews of clinical studies with fosinopril in the treatment of essential hypertension (151,152) and heart failure (153,154) are available. It is approved for both indications in the United States and is used in antihypertensive therapy at a recommended initial dose of 10 mg once per day, which may be increased to 80 mg once per day. For the treatment of heart failure, the initial dose is also 10 mg, which is often increased to a maintenance dose of 20-40 mg once per day. 

A 64-year-old woman with insulin-dependent diabetes mellitus and pemphigus vulgaris controlled by deflaza-cort 12 mg/day was given fosinopril 10 mg/day for hypertension. Within 1 month her skin lesions worsened and an indirect immunofluorescence test became positive. Fosinopril was withdrawn and her skin lesions improved without modification of her steroid regimen 10 months later the immunofluorescence test was negative. 

Non-steroidal anti-inflammatory drugs (NSAIDs) are often reported to interfere with the blood pressurelowering action of thiazide diuretics (SED-14, 667). In 17 women with arthritis and hypertension taking fosinopril and hydrochlorothiazide, ibuprofen, sulindac, and nabu-metone, each for 1 month, had no effect on mean arterial pressure (47). These results suggest that the ACE inhibitor fosinopril may neutralize the tendency of NSAIDs to increase blood pressure in thiazide-treated hypertensive patients. However, the design of this study precluded such a conclusion, since no evidence was provided that any of the NSAIDs increased blood pressure in the absence of fosinopril. Furthermore, the numbers were small and the precision of the comparison is likely to have been low. Careful monitoring of blood pressure is necessary when NSAIDs are introduced in thiazide-treated hypertensive patients, even when ACE inhibitors are co-prescribed. 

Pool, J.L., Cushman, W.C., Saini, R.K., Nwachuku, C.E., and Battikha, J.P. Use of the factorial design and quadratic response models to evaluate the fosinopril and hydrochlorothiazide combination in hypertension. American Journal of Hypertension 1997 10 117-123. 

Fosinopril, an ACE inhibitor with antihypertensive properties (10 mg p.o. daily), is used in the treatment of hypertension (see also Figure 24). 

In their paper, Tangen and Koch (2001) concentrate primarily on the analysis of contrasts of particular interest. The approach is thus in the spirit of that described as the disconnected treatment approach in Section 20.2.1. For an alternative regression approach, an extremely interesting paper is that of Pool et al. (1997). This reports and analyses a 4 x 4 factorial trial of hydrochlorothiazide and fosinopril in hypertension in 550 patients. They fit a quadratic surface model in both doses to the... 

Epoetin may cause hypertension and thereby reduce the effects of antihypertensive drugs. An additive hyperkalaemic effect is theoretically possible with ACE inhibitors or angiotensin II receptor antagonists and epoetin. It is not entirely clear whether captopril, enalapril, fosinopril or other ACE inhibitors affect the efficacy of epoetin or not, but any interaction may take many months to develop. 

In one study, sulindac 200 mg twice daily given to patients taking capto-pril 100 to 200 mg twice daily caused only a small rise in blood pressure (from 132/92 to 137/95 mmHg). Sulindac 150 mg twice daily did not attenuate the blood pressure response to captopril when it was substituted for ibuprofen in an elderly woman. Similarly, sulindac 200 mg twice daily did not blunt the antihypertensive effect of enalapril in 9 patients with hypertension. Two studies in black women also found that sulindac 200 mg twice daily for one month did not alter the antihypertensive effect of fosinopril 10 to 40 mg daily or lisinopril 10 to 40 mg daily (given with hydrochlorothiazide 25 mg daily). - ... 

---