The renin-angiotensin-aldosterone system: a crossroad from arterial hypertension to heart failure

Heart Fail Rev. 2020 Jan;25(1):31-42. doi: 10.1007/s10741-019-09855-5.

Abstract

The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in the regulation of blood pressure and volume homeostasis, promoting critical structural changes in every component of the cardiovascular system, including the heart and blood vessels. Consequently, the RAAS is a crucial therapeutic target for several chronic diseases of the cardiovascular system, spanning from arterial hypertension (AH) to heart failure (HF). AH represents a leading risk factor for the development of symptomatic HF, particularly with left ventricle (LV) preserved ejection fraction (HFpEF). LV diastolic dysfunction and cardiac remodelling are the first discernible manifestations of heart disease in patients with AH. Typically, AH develops many years before the diagnosis of overt HF, providing a therapeutic target for preventive strategies. Treatment of AH is based on different classes of antihypertensive drugs, which show differences in their capacity to prevent the evolution towards HF. The blockers of the RAAS are effective drugs to treat AH and prevent HF with reduced ejection fraction (HFrEF), but the evidence of the potential benefits in patients with HFpEF remains limited. In this review, the authors summarise data from several clinical trials of HFpEF and HFrEF, focusing on the mechanisms leading the transition from AH to HF and late complications.

Keywords: Arterial hypertension; Heart failure; Preserved ejection fraction; Renin-angiotensin-aldosterone system.

Publication types

  • Review

MeSH terms

  • Angiotensin Receptor Antagonists / therapeutic use
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Antihypertensive Agents / therapeutic use*
  • Blood Pressure / drug effects
  • Heart Failure / drug therapy*
  • Heart Failure / physiopathology
  • Heart Failure / prevention & control*
  • Humans
  • Hypertension / drug therapy*
  • Hypertension / physiopathology
  • Mineralocorticoid Receptor Antagonists / therapeutic use
  • Randomized Controlled Trials as Topic
  • Renin-Angiotensin System / drug effects*
  • Stroke Volume / drug effects

Substances

  • Angiotensin Receptor Antagonists
  • Angiotensin-Converting Enzyme Inhibitors
  • Antihypertensive Agents
  • Mineralocorticoid Receptor Antagonists