Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone antagonists and angiotensin receptor blockers in heart failure: Putting guidelines into practice

2005 ◽  
Vol 7 (5) ◽  
pp. 710-721 ◽  
Author(s):  
John McMurray ◽  
Alain Cohen-Solal ◽  
Rainer Dietz ◽  
Eric Eichhorn ◽  
Leif Erhardt ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ace Inhibitors ◽  
Beta Blockers ◽  
Angiotensin Receptor Blockers ◽  
Angiotensin Receptor ◽  
Aldosterone Antagonists ◽  
Receptor Blockers ◽  
Practical Recommendations

scholarly journals The Management of Heart Failure with Preserved Ejection Fraction

2015 ◽  
Vol 1 (1) ◽  
pp. 11 ◽  
Author(s):  
Andrew JS Coats ◽  
Louise G Shewan ◽  
◽  
◽  
◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Beta Blockers ◽  
Angiotensin Receptor Blockers ◽  
Left Ventricular ◽  
Clinical Syndrome ◽  
Aldosterone Antagonists ◽  
Sharp Separation ◽  
Clinical Trial Evidence ◽  
Receptor Blockers

Heart failure is defined as a clinical syndrome and is known to present with a number of different pathophysiological patterns. There is a remarkable degree of variation in measures of left ventricular systolic emptying and this has been used to categorise heart failure into two separate types: low ejection fraction (EF) heart failure or HF-REF and high EF heart failure or HF-PEF. Here we review the pathophysiology, epidemiology and management of HF-PEF and argue that sharp separation of heart failure into two forms is misguided and illogical, and the present scarcity of clinical trial evidence for effective treatment for HF-PEF is a problem of our own making; we should never have excluded patients from major trials on the basis of EF in the first place. Whilst as many heart failure patients have preserved EFs as reduced we have dramatically under-represented HF-PEF patients in trials. Only four trials have been performed in HF-PEF specifically, and another two trials that recruited both HF-PEF and HF-REF can be considered. When we consider the similarity in outcomes and neurohormonal activation between HF-REF and HF-REF, the vast corpus of trial data that we have to attest to the efficacy of various treatment (angiotensinconverting-enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], beta-blockers and aldosterone antagonists) in HF-REF, and the much more limited number of trials of similar agents showing near statistically significant benefits in HF-PEF the time has come rethink our management of HF-PEF, and in particular our selection of patients for trials.

scholarly journals Stroke Prevention: Not all Antihypertensive Drugs are Created Equal

2005 ◽  
Vol 6 (1_suppl) ◽  
pp. S4-S7 ◽  
Author(s):  
Franz H Messerli ◽  
Simbo M Chiadika
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Ace Inhibitors ◽  
Beta Blockers ◽  
Angiotensin Receptor Blockers ◽  
Antihypertensive Agents ◽  
Channel Blockers ◽  
At2 Receptor ◽  
Angiotensin Receptor ◽  
Receptor Blockers

Reductions in blood pressure (BP) through intervention can significantly reduce the risk of cardiovascular events in hypertensive patients. However, a number of trials indicate that beta-blockers, despite lowering BP, do not reduce the risk of stroke. A recent meta-analysis suggested that, over and beyond BP reduction, angiotensin-converting enzyme (ACE) inhibitors appear superior to calcium channel blockers for prevention of coronary heart disease whereas calcium channel blockers appear superior to ACE inhibitors for prevention of stroke. Indeed, in the Syst-EUR study a 42% reduction in strokes was achieved in the calcium antagonist arm when compared to the placebo arm.It is hypothesised that antihypertensive agents that stimulate the AT2-receptor (thiazide diuretics, dihydropyridine calcium antagonists and angiotensin receptor blockers) are more cerebroprotective than drug classes that do not stimulate the AT2-receptor (beta-blockers and ACE inhibitors).The angiotensin receptor blockers are the only drug class that have a dual mechanism of action that could be helpful in preventing strokes in that they not only inhibit the AT1-receptor but also allow stimulation of the AT2-receptor. Not surprisingly therefore, in trials such as LIFE, VALUE and MOSES, angiotensin receptor blockers showed excellent cerebroprotection.

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