RAMIPRIL

The concept for the first angiotensin converting enzyme inhibitor (ACEI) was derived from snake venom in the 1950s. An orally active version was eventually found, and captopril was licensed in 1981 for hypertension and heart failure #prescribing

Improved me-too ACEI versions followed, such as #ramipril, which was approved in the UK in 1989. Captopril is now out-moded, but is still used in paediatrics #prescribing

Long-acting, high affinity ACEIs, such as #ramipril, are highly successful in cardiovascular and renal medicine for hypertension, heart failure, post-MI prophylaxis and nephropathy. #ramipril is one of the most prescribed ACEI in the UK: In January 2019, 2.5 million items were prescribed at the cost of over £3 million #prescribing

Mechanism of action (MOA): #ramipril inhibits the conversion of angiotensin I to the active ATII. Less ATII means less SNS stimulation, less aldosterone output (<circulating volume) and less peripheral vasoconstriction, so <pre-load and afterload #prescribing

ATII (and aldosterone) drives remodelling (fibrosis etc) in the myocardium, ultimately leading to heart failure decompensation. Less ATII/aldosterone levels restrain progress of heart failure. Effects on nephropathy are unclear, but may be by reducing intra-glomerular pressure, there is less basement membrane damage, which slows diabetic nephropathic damage #prescribing