Heart attacks often occur when atherosclerotic plaques rupture by blocking blood flow to the heart muscle. Inflammation has emerged as a critical factor in heart attacks, challenging the traditional view in the coronary arteries built up as a primary cause. The body’s natural response to injury and infection when it is excessive form the inflammation by exacerbating heart disease. However, in cardiovascular disease, molecule infiltrates of arterial plaques and inflammatory cells destabilize them by making it more prone to rupture and cause bleeding risk. This process significantly raised likelihood of blood clot formation. However, the chemical mediators play an intermediate role in pathological mechanism that leads to heart attack which influence coagulation, inflammation, and vascular dysfunction. Inflammatory mediators like cytokines and chemokines initiate inflammation sustainability whereas interleukin-1 (I-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) act as pivotal role in progression of coronary artery disease (CAD) which chronically facilitates the weakening and formation of atherosclerosis. The interplay between thrombosis and inflammation is now understood as a multifactorial process that highlight hypertension, diabetes, and genetics as the main contributors. The modern understanding of heart attack pathologically integrates lipid-based mechanism in newer insights, offering comprehensive strategies for treatment. Furthermore, based on the present evidence in the effectiveness and consideration of medications, that is, ACE inhibitors and antiplatelet concise a better option to expectedly treat cardiac inflammation. In addition, the new therapeutic approaches literally emphasize the actual targeted inflammatory causes that adversely reduce vascular resistance in a stressed condition in terms of preventive measure.