Why the Left Internal Mammary Artery (LIMA) Resists Atherosclerosis
The LIMA's remarkable resistance to atherosclerosis stems from two primary structural and biochemical mechanisms: a nearly continuous internal elastic lamina that prevents smooth muscle cell migration, and abundant endothelial release of prostacyclin and nitric oxide, which are potent vasodilators and platelet function inhibitors. 1
Structural Protection Against Atherosclerosis
The LIMA possesses unique anatomical features that create a physical barrier to atherosclerotic disease development:
The nearly continuous internal elastic lamina acts as a mechanical barrier preventing smooth muscle cells from migrating into the intimal layer, thereby blocking a critical early step in atherosclerotic plaque formation 1
The endothelial layer demonstrates fewer fenestrations and lower intercellular junction permeability compared to other vessels, which reduces the transfer of lipoproteins responsible for atherosclerosis development 2
This structural integrity maintains endothelial barrier function and prevents the lipid infiltration that initiates atherogenesis 2
Biochemical and Molecular Resistance
The LIMA's endothelium produces protective molecules that actively prevent atherosclerotic processes:
Prostacyclin and nitric oxide production by the IMA endothelium provides dual protection through vasodilation and platelet aggregation inhibition 1
Enhanced nitric oxide synthase expression leads to accentuated nitric oxide release, which maintains vascular homeostasis and prevents inflammatory cell adhesion 3
Greater concentrations of anti-thrombotic molecules including heparin sulfate and tissue plasminogen activator further protect against thrombosis and early atherosclerotic changes 2
The vascular smooth muscle cells exhibit reduced tissue factor expression, high tissue-type plasminogen activator production, and blunted migration and proliferation, collectively mitigating intimal thickening 3
Clinical Impact of Atherosclerosis Resistance
This biological resistance translates directly into superior clinical outcomes:
Only 4% of IMAs develop atherosclerosis, and merely 1% develop atherosclerotic stenoses of hemodynamic significance 1
10-year patency exceeds 90% for LIMA grafts, dramatically superior to saphenous vein grafts where only 50-60% remain patent at 10 years 1
This exceptional patency directly correlates with reduced mortality, decreased recurrent myocardial infarction, lower rehospitalization rates, and fewer repeat revascularizations compared to venous conduits 1
Comparison to Other Conduits
The contrast with saphenous vein grafts highlights the LIMA's unique properties:
Saphenous vein grafts suffer endothelial damage during harvesting and initial exposure to arterial pressure, leading to platelet aggregation and graft thrombosis 1
Platelet adherence to damaged venous endothelium initiates intimal hyperplasia that progresses to SVG atherosclerosis, a process the LIMA inherently resists 1
At 10 years post-CABG, only half of patent SVGs have no angiographic evidence of atherosclerosis, whereas the LIMA maintains its structural and functional integrity 1
Common Pitfalls
Despite the LIMA's inherent resistance, certain technical factors can compromise outcomes:
Poor surgical technique represents the primary cause of early LIMA failure rather than thrombosis or atherosclerosis 2
Significant proximal left subclavian stenosis is a contraindication to LIMA use as it compromises graft flow 4
Unligated LIMA side branches can create coronary steal phenomena causing LAD ischemia despite patent grafts 5