Background: Coronary Artery Disease due to atherosclerosis is one of the major causes of mortality and morbidity. It occurs in a significantly large number of patients without any risk factors. Even in patients with known risk factors, the exact mechanism is not known. Hence, there has been a great interest in the infectious origin of the disease. Many studies have demonstrated Helicobacter pylori association with atherosclerotic plaques. However, exact mechanism is still not established. In our present study, we have tried to find association between HSP-70 and Cag-A gene for causing atherosclerosis in coronary arteries. Methods: Serum, LIMA and endarterectomy specimen of 45 patients undergoing CABG were collected. The serum was subjected to ELISA for HSP-70 Antibodies, LIMA for HSP-70- IHC and endarterectomy specimen for IHC and PCR for 16SrRNA and Cag-A gene. Results 45 samples were positive for HSP-70 Ab by ELISA. Of 45 endarterectomy plaques, 41 were positive by IHC for HSP70 and 4 were negative whereas, 2 of 45 LIMA samples were IHC positive and 43 were negative. 43 out of 45 samples were positive for 16SrRNA genes and 2 were negative. Out of 45 endarterectomy specimens, 38 were positive and 7 were negative for Cag-A gene as detected by PCR. Of 41 IHC positive samples, 38 were positive and 3 were negative for CagA gene. Of 4 negative samples, all 4 were negative for Cag-A. LIMA specimens were not subjected to PCR. Conclusion: In our present study, we have clearly demonstrated circulating antibodies in serum against HSP-70(45), presence of HSP-70 in plaques (41) along with Cag-A gene of H. pylori (38). Presence of Cag-A gene indicates infection by H. pylori. This chronic H. pylori infection induces overexpression of HSP70 in vascular wall of coronary arteries. Interaction between HSP-70 and HSP-70 antibodies initiates immune-mediated injury to vascular wall, leading to inflammation and atherogenesis