Background. Professor Franz Halberg contributed greatly to our understanding of the importance of chronobiology in prevention, intervention, and treatment of CVD: hence this article of remembrance. Clinical and biochemical manifestations of chronic heart failure (HF) may be due to interactions of the brain and the heart. Circadian rhythms may be lost via neuro-humoral adaptations, such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems in the brain, heart, and peripheral vessels in a milieu of melatonin deficiency. Methods. Internet and database searches and discussion with colleagues. Results. Experimental and clinical evidence indicates that chronic HF may be associated with autonomic imbalance with increased sympathetic nerve activity and a withdrawal of parasympathetic activity, with the target of involvement being the heart. Brain-heart interactions may result from an increased systemic and cerebral angiotensin II signaling since plasma angiotensin II is increased in humans and animals with chronic HF. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites causing increased contractility of the heart, as an adaptation, during chronic HF. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus (PVN), rostral ventrolateral medulla (RVLM) and area postrema (AP) via neuregulin-brain natriuretic peptide release from these sites which influences the function of cardiomyocytes and the heart. We propose that blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the PVN. Experimental studies indicate that administration of an angiotensin receptor blocker by injection into the AP activates the sympatho-inhibitory baroreflex indicating that receptor blockers act by increasing parasympathetic activity which has a beneficial effect on cardiomyocyte function. Angiotensin II also elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings in chronic HF resulting in an increase in sympathetic nerve activity. A rise in circulating angiotensin II during chronic HF may increase the sympatho-excitatory chemoreflex and inhibit the sympatho-inhibitory baroreflex resulting in cardiomyocyte dysfunction and worsening of HF. Conclusion. Brain-heart interactions and damage to the circadian system with increased circulating angiotensin II signaling may directly act on the brain via the subfornical organ and the AP to increase sympathetic outflow and worsening of neurohumoral adaptations leading to chronic HF. © 2016 Nova Science Publishers, Inc.