Pattern formation is fundamental to embryonic morphogenesis. In the zebrafish heart, spatially 20 confined single-cell delamination in the ventricle outer curvature initiates trabeculation, a 21 conserved morphogenetic process critical for heart function and embryonic life. Yet, what 22 confines delamination in the ventricle outer curvature remains ill-understood. Contrary to the 23 prevailing notion of patterning through biochemical signals, we now show that mechanical 24 fracturing of the cardiac extracellular matrix (cECM) patterns delamination in the outer 25 curvature. cECM fractures emerge preferentially in the outer curvature, cells delaminate into 26 these fractures and experimental blocking of fractures blocks delamination. These fractures 27 display characteristic signature of mechanical defects and myocardial tissue contractility is 28 sufficient to fracture the cECM, independent of molecular signals, enzymatic activity, or 29 delamination events. Notably, the anisotropic geometry of myocardial tissue generates higher 30 mechanical strain in the outer curvature, thereby locally patterning cECM fractures and 31 delamination. Consequently, cECM fractures evolve in response to dynamic changes in tissue 32 geometry, and experimental manipulation of tissue geometry is sufficient to alter the fracture 33 pattern. Together, our findings underscore mechanical fractures as a morphogenetic strategy, 34 and more generally, corroborate the long-standing but understudied paradigm that tissue 35 form-function can feed back to steer its own patterning.