Two Pulses Per Beat: Parallel Energetics of Myocardium and Coronary Wall

Each heartbeat is initiated by a sinoatrial node action potential that propagates through the myocardial syncytium, triggering sequential contraction of the four chambers and propelling blood through the coronary, pulmonary, and systemic circulations. This mechanical event is fueled by two coupled energetic pulses: one in the working myocardium, where ATP is consumed by Ca²⁺ cycling, cross-bridge cycling and ion pumping, and a second in the coronary vascular wall, where smooth muscle cells (SMCs), endothelial cells, and pericytes expend ATP to maintain tone, manage Ca²⁺, and coordinate perfusion against systolic compression that arrests their blood supply. Cardiac myocytes and coronary SMCs share the same actomyosin machinery but are activated differently. In myocytes, beat-to-beat Ca²⁺ transients drive Ca²⁺ binding to troponin C to permit synchronous contraction; in coronary SMCs, Ca²⁺/calmodulin activates myosin light-chain kinase (MLCK), which phosphorylates myosin to sustain tone. In both cell types, ATP availability sets the ceiling on excitability: when the energetic budget is met, ion pumps, SERCA, and ATP-sensitive channels operate within range and electrical behavior is stable; when it is not, excitability fails. Biosensor measurements reveal beat-to-beat ATP gains and dips in sinoatrial node and ventricular myocytes across systole and diastole. The vascular wall undergoes its own synchronous cycle: systolic compression arrests perfusion while MLCK, SERCA, and Kir2.1-mediated retrograde signaling compete for a diastolic replenishment window that narrows with each heart-rate increment. We propose that cardiac energetics must treat these pulses as co-equal, reframing heart failure as a vascular and computational disease of the coronary wall.