Use of Angiotensin‐Converting Enzyme Inhibitors as Monotherapy and in Combination with Diuretics and Calcium Channel Blockers

Cheng, Angela; Frishman, William H.

doi:10.1002/j.1552-4604.1998.tb05784.x

Cited by 9 publications

(2 citation statements)

References 98 publications

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“…Thirdly, systemic vasodilation induced by CCBs (especially dihydropyridines) signals a reflex increase in sympathetic nervous activity, which thereby increases heart rate and enhances renal renin excretion,111 reducing the hypotensive properties of the drug; these effects may be counterbalanced by RAS blockade. Fourthly, vasodilatory edema that may occur with CCBs is often diminished when an ACE inhibitor is added to the antihypertensive regimen 112.…”

Section: Ace Inhibitor Plus Ccbmentioning

confidence: 99%

Choice of ACE inhibitor combinations in hypertensive patients with type 2 diabetes: update after recent clinical trials

Reboldi¹,

Gentile²,

Angeli³

et al. 2009

VHRM

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The diabetes epidemic continues to grow unabated, with a staggering toll in micro- and macrovascular complications, disability, and death. Diabetes causes a two- to fourfold increase in the risk of cardiovascular disease, and represents the first cause of dialysis treatment both in the UK and the US. Concomitant hypertension doubles total mortality and stroke risk, triples the risk of coronary heart disease and significantly hastens the progression of microvascular complications, including diabetic nephropathy. Therefore, blood pressure reduction is of particular importance in preventing cardiovascular and renal outcomes. Successful antihypertensive treatment will often require a combination therapy, either with separate drugs or with fixed-dose combinations. Angiotensin converting enzyme (ACE) inhibitor plus diuretic combination therapy improves blood pressure control, counterbalances renin-angiotensin system activation due to diuretic therapy and reduces the risk of electrolyte alterations, obtaining at the same time synergistic antiproteinuric effects. ACE inhibitor plus calcium channel blocker provides a significant additive effect on blood pressure reduction, may have favorable metabolic effects and synergistically reduce proteinuria and the rate of decline in glomerular filtration rate, as evidenced by the GUARD trial. Finally, the recently published ACCOMPLISH trial showed that an ACE inhibitor/calcium channel blocker combination may be particularly useful in reducing cardiovascular outcomes in high-risk patients. The present review will focus on different ACE inhibitor combinations in the treatment of patients with type 2 diabetes mellitus and hypertension, in the light of recent clinical trials, including GUARD and ACCOMPLISH.

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Section: Ace Inhibitor Plus Ccbmentioning

confidence: 99%

Choice of ACE inhibitor combinations in hypertensive patients with type 2 diabetes: update after recent clinical trials

Reboldi¹,

Gentile²,

Angeli³

et al. 2009

VHRM

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“…ACE inhibitors are widely used as standard treatment for hypertension and congestive heart failure [3,25]. After the first report of hepatotoxicity following treatment with captopril [27] there have been several additional reports with captopril [1,6,10,18,19,21,24,28] as well as with enalapril [12,15,17,20,26] and other ACE inhibitors [4,13].…”

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

Acute Liver Failure due to Enalapril

Jeserich

Ihling²,

Allgaier³

et al. 2000

Herz

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This report presents a 46-year-old man who was treated for hypertension with the angiotensin-converting-enzyme (ACE) inhibitor enalapril. After 3 years of continuous treatment he presented with jaundice and progressive liver failure that continued despite withdrawal of the medication. The patient was taking no other medication. All known causes of acute liver failure could be excluded indicating a drug-induced liver damage after long-term treatment with enalapril. Analysis of liver biopsies revealed a pathomorphological pattern comparable to than observed in severe halothane hepatitis. Serological studies including T-cell stimulation with enalapril and a broad spectrum of tests for autoimmunity including autoantibodies against calreticulin, the major Ca2+ and Zn2+ binding protein of the endoplasmic reticulum and suggested to be involved in the pathogenesis of halothane hepatitis were negative. Thus, the mechanism of enalapril-induced liver injury remains obscure. Liver failure progressed and finally led to orthotopic liver transplantation. To our knowledge, this is the longest duration of chronic treatment with an ACE inhibitor before liver failure occurred. In addition, liver failure progressed despite withdrawal of the medication. It is concluded that even after long-term treatment with an ACE inhibitor liver failure may be induced. Therefore, regular monitoring of liver enzymes should be considered.

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