Academic literature on the topic 'Neurohumoral activation'

The pathophysiological hallmarks of the syndrome of heart failure with reduced ejection fraction (HFrEF) are the activation of the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system. Much of the success in reducing morbidity and mortality from HFrEF has resulted from pharmacological counteraction of the RAAS and the sympathetic nervous system using angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, and beta blockers. Despite these advances, the prognosis of HFrEF remains poor, and novel ways of improving outcomes are necessary. Augmenting alternative endogenous protective neurohumoral pathways, promoting vasodilatation and sodium excretion, as well as inhibiting pathological growth (hypertrophy and fibrosis), by means of neprilysin inhibition, is such a novel approach.

The two main forms of sleep apnoea are obstructive (OSA) and central (CSA) sleep apnoea. In the presence of cardiovascular disease, CSA can manifest as Cheyne–Stokes respiration. OSA and CSA both can cause substantial oxygen desaturations, alterations in sympathovagal balance, neurohumoral activation, and endothelial dysfunction; OSA also causes marked negative intrathoracic pressure swings, which have a number of undesirable cardiovascular consequences (e.g. increased cardiac transmural pressure gradients, sympathetic activation). OSA is the most common type of sleep apnoea in the general population, but rates are higher in cardiovascular disease. CSA is particularly prevalent in patients with underlying cardiac, neurological, or renal disease. Typical OSA risk factors include obesity, male gender, smoking, and age, while the severity of heart failure is predictive of the prevalence and severity of CSA. Recognition and diagnosis of sleep apnoea can be difficult because patients often do not present with typical symptoms. Sleep apnoea is an important co-morbidity in cardiovascular disease because of links with a number of conditions. OSA is an independent risk factor for the development of hypertension and heart failure, and has a negative impact on the effectiveness of treatments for atrial fibrillation. OSA has also been linked with the development of coronary artery disease, worse outcomes after acute myocardial infarction, and higher event rates in patients with coronary artery disease. CSA with Cheyne–Stokes respiration has important links with heart failure and is a risk factor for poor outcome even when other therapies are optimized. Cheyne–Stokes respiration has also been documented in stroke patients, increasing stroke severity and worsening prognosis.