Mechanosensory Silence During Cardiac Stress

Despite being one of the most densely innervated organs in the thorax, the human heart exhibits a relative insensitivity to chronic visceral pain. Unlike other viscera or enlarging visceral masses of comparable size, progressive mechanical or volumetric stress typically fails to elicit persistent nociception; pain arises predominantly during acute events. Clinical and epidemiological observations show that many individuals with hypertrophied hearts can remain asymptomatic for decades, highlighting a paradox of silent cardiac enlargement. This suggests that cardiac sensory processing is not merely deficient but subject to selective gating. Integrating insights from cardiac mechanobiology, neurophysiology, and myocardial energetics, we propose the Cardiac Mechanoafferent Silencing Model (CMSM) as a conceptual gating framework, consistent with selective attenuation of chronic visceral nociceptive signaling while preserving sensitivity to acute ischemic and inflammatory threats. Furthermore, we outline anatomically and physiologically constrained buffering processes that may limit the emergence of other types of cardiac pain under physiological conditions. CMSM offers a testable conceptual framework to reconcile the dissociation between structural stress and perception, and to prioritize future experimental and translational investigations.