Drugs targeting the renin-angiotensin-aldosterone system show promising results in preventing secondary cardiovascular events in heart failure and lowering the risk of certain cancers.
This review highlights the pathophysiological overlap between ischemic heart failure and cancer, emphasizing the potential of RAAS inhibitors to improve outcomes in both diseases.
The current global prevalence of heart failure is estimated at 64.34 million cases, and it is expected to increase in the coming years, especially in countries with a medium-low sociodemographic index where the prevalence of risk factors is increasing alarmingly. Heart failure is associated with many comorbidities and among them, cancer has stood out as a contributor of death in these patients. This connection points out new challenges both in the context of the pathophysiological mechanisms involved, as well as in the quality of life of affected individuals. A hallmark of heart failure is chronic activation of the renin-angiotensin-aldosterone system, especially marked by a systemic increase in levels of angiotensin-II, a peptide with pleiotropic activities. Drugs that target the renin-angiotensin-aldosterone system have shown promising results both in the prevention of secondary cardiovascular events in myocardial infarction and heart failure, including a lower risk of certain cancers in these patients, as well as in current cancer therapies; therefore, understanding the mechanisms involved in this complex relationship will provide tools for a better diagnosis and treatment and to improve the prognosis and quality of life of people suffering from these two deadly diseases.
Garcia-Garduño et al. (Thu,) conducted a review in Ischemic Heart Failure and Cancer. Drugs targeting the renin-angiotensin-aldosterone system was evaluated. Drugs targeting the renin-angiotensin-aldosterone system show promising results in preventing secondary cardiovascular events in heart failure and lowering the risk of certain cancers.