Table 1. Potential mechanisms underlying CAD in cancer patients.

Etiology	Mechanisms	Results
Cancer itself	Inflammatory cascade involving TNF-α, IL-1β, and IL-6	Microvascular endothelial dysfunction
	Oxidative stress	Neuron/axonal damage Demyelination
	ROS or RNS accumulation Mitochondrial dysfunction	Apoptosis
	RAAS activation: ATR1 and angiotensin 2; Sympathetic nerve activation: β-adrenergic receptor	Cardiac remodeling, cardiac hypertrophy, fibrosis, cardiac dysfunction
	Direct invasion, compression of autonomic nervous system	Cardiovascular autonomic neuropathy
Chemotherapy	Microtubule injury, mitochondrial dysfunction, ion-channel dysfunction, inflammatory cascade, ROS accumulation, autoimmunity	Neuronal apoptosis, axonal dysregulation (similar to CIPN) attributed to thinly myelinated or unmyelinated nerve fibers
Radiation therapy	Direct injury to vagus nerve, carotid sinus, baroreflex	Cardiovascular autonomic neuropathy
Lifestyle factors	Decreased physical activity, sleep disturbances, anxiety, emotional stress, weight gain, weakness	CAD
Coexisting disease	Diabetes mellitus, amyloidosis, heart disease	CAD

ATR1, angiotensin 1 receptor; CAD, cardiovascular autonomic dysfunction; CIPN, chemotherapy-induced peripheral neuropathy; IL, interleukin; RAAS, renin-angiotensin-aldosterone system; RNS, reactive nitrogen species; ROS, reactive oxygen species; TNF, tumor necrosis factor.