Several factors influence cardiac function in this context: (1) myocardial hypertrophy and fibrosis driven by neurohumoral activation; (2) impaired β-adrenergic receptor signaling due to prolonged sympathetic nervous system (SNS) stimulation; and (3) the suppressive effects of circulating cytokines—such as tumor necrosis factor-α (TNF-α) and nitric oxide (NO)—on ventricular performance [113,114]. Here, TNF is linked to cardiac hypertrophy.