New Pathophysiological Pathways and the Role and Relevance of Novel Diagnosis and Treatment Tools Targeting the Sympathetic Nervous System in Patients with Heart Failure

Dear Colleagues,

Cardiovascular diseases have been considered the most predominant cause of death and one of the most critical public health hitches worldwide. In the past two decades, cardiovascular mortality has declined in high-income countries owing to preventive measures, which have resulted in the reduced burden of coronary artery disease and heart failure. In spite of these promising results, cardiovascular diseases are responsible for ~17 million deaths per year globally, with ~25% of these attributable to sudden cardiac death. The prevalence of heart failure is ~1–2% of the adult population in developed countries, rising to ≥10% amongst people >70 years of age. Amongst the people >65 years of age that present to primary care with breathlessness upon exertion, one in six will have unrecognised heart failure. The heart failure lifetime risk at age 55 years is 33% for men and 28% for women.

Myocardial systolic dysfunction is correlated to neurohormonal overactivity as a compensatory mechanism for maintaining cardiac output in the face of declining cardiac function. Sympathetic nervous system overactivity is supported by increased plasma noradrenaline and adrenaline levels, raised central sympathetic outflow, and increased organ-specific spillover of noradrenaline into plasma. Cardiac noradrenaline spillover in untreated patients with heart failure can reach ~50-fold higher levels compared to those of healthy individuals under maximal exercise conditions. Increased sympathetic outflow to the renal vascular bed can contribute to the anomalies of renal function; these are often associated with heart failure and feed into a vicious cycle of elevated blood pressure, the progression of renal disease, and worsening heart failure. Increased sympathetic activity, amongst other factors, contributes to the progress of cardiac arrhythmias, which can lead to sudden cardiac death due to sustained ventricular tachycardia.

Analogues of noradrenaline have been well described and studied for assessing cardiac sympathetic function using single-photon emission tomography (SPECT). Many autonomic nervous system radiotracers have also been created for use in positron emission tomography (PET) cardiac imaging, and cumulative data have shown the usefulness of PET-scanning in critical clinical conditions, such as for predicting lethal arrhythmias and sudden cardiac death in patients with heart failure presenting reduced ejection fraction. Currently, therapies to avoid arrhythmic consequences of heart failure are antiarrhythmic drugs, endocardial catheter ablation, and the use of implantable electronic cardiac devices. Recently, novel treatment options targeting new pathways have emerged for subjects with heart failure, such as sacubitril/valsartan through the inhibition of the angiotensin receptor and neprilysin, reducing sudden cardiac death events ~20%, as well as a catheter-based renal denervation approach.

Within this research topic, we envisage submissions on new pathophysiological pathways, and the role and relevance of novel diagnosing and treatment tools targeting the sympathetic nervous system, aiming to manage patients with heart failure and its associated consequences.

Dr. Márcio Galindo Kiuchi
Guest Editor

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• atrial fibrillation
• heart failure
• hypertension
• positron emission tomography
• renal denervation
• sudden cardiac death
• sympathetic nervous system
• ventricular arrhythmias