During early vertebrate heart development, the heart transitions from a linear tube to a complex asymmetric structure. This process includes looping of the tube and ballooning of the emerging cardiac chambers, which occur simultaneously with growth of the heart. A key driver of cardiac growth is deployment of cells from the Second Heart Field (SHF) into both poles of the heart, and cardiac morphogenesis and growth are intimately linked in heart development. Laminin is a core component of extracellular matrix (ECM) basement membranes. While mutations in specific laminin subunits are linked with a variety of cardiac abnormalities, including congenital heart disease and dilated cardiomyopathy, no role for laminin has been identified in early vertebrate heart morphogenesis. We identified dynamic, tissue-specific expression of laminin subunit genes in the developing zebrafish heart, supporting a role for laminins in heart morphogenesis. lamb1a mutants exhibit cardiomegaly from 2dpf onwards, with subsequent progressive defects in cardiac morphogenesis characterised by a failure of the chambers to compact around the developing atrioventricular canal. We show that loss of lamb1a results in excess addition of SHF cells to the atrium, revealing that Lamb1a functions to limit heart size during cardiac development by restricting SHF addition to the venous pole. While heart rate is unaffected, lamb1a mutants exhibit hallmarks of altered cardiac function or haemodynamics. Specifically blocking cardiac contractility in lamb1a mutants rescues heart size and atrial SHF addition. Furthermore, loss of contractility results in altered balance of FGF and RA signalling in both sibling and lamb1a mutants, suggesting that interactions between SHF deployment, heart biomechanics, and biochemical signalling are regulated by laminins during heart development. Together, this describes the first requirement for laminins in early vertebrate heart morphogenesis, reinforcing the importance of specialised ECM composition in cardiac development.