Medical & Clinical Research

Author(s): Prof. Dasaad Mulijono

For fifty years, cardiology has followed a stenosis-centric dogma—mistaking a narrowed lumen for a lethal plaque and assuming ischemia inevitably dictates a patient’s fate. Yet the global convergence of multimodality imaging, pathology, and contemporary trials now reveals a striking contradiction: the plaques that kill are not the tight, ischemia-producing stenoses targeted by guidelines, but the biologically unstable, angiographically “mild,” FFR-negative lesions that silently rupture or erode. In this perspective— anchored in PROSPECT, PROSPECT ABSORB, PREVENT, DEBuT-LRP, CLIMA, LRP, emerging AI-based risk models, and a unique pandemic cohort—we argue that MI is fundamentally a disease of plaque vulnerability rather than stenosis severity. The COVID-19 era provided the ultimate real-world stress test: a global inflammatory surge that amplified plaque instability and exposed the fatal limitations of ischemia-driven decision-making. During this period, Bethsaida Hospital, led by Prof. Dasaad Mulijono, implemented an unprecedented vulnerability-guided strategy combining routine CTCA, selective preventive PCI for VPs, ultra-low LDL targets, metabolic optimization, and WFPBD therapy. Among 3,500 COVID-positive or exposed patients, this
approach achieved zero mortality, demonstrating that treating biological risk—not luminal narrowing—can alter the natural history of coronary disease, even before modern vulnerability-guided trials were published.

This manuscript advances a disruptive thesis: treating stenosis relieves angina, but treating vulnerability prevents MI and death. We show why ischemia testing fails, why FFR cannot identify high-risk lesions, how AI reveals the dominance of morphobiological risk over luminal risk, and why the next generation of trials must randomize patients based on plaque biology rather than percent stenosis. A new era of coronary care is emerging—one in which OCT, IVUS, NIRS, CTCA, and computational shear-stress mapping form the backbone of risk assessment; preventive PCI, especially with DCB therapy, is directed at rupture-, erosion-, and calcium-driven substrates; WFPBD restores endothelial health and reduces pan-coronary vulnerability; and AI enables precision prevention. The stenosis paradigm has reached its scientific end. A vulnerability-centred framework offers a more mechanistically coherent, ethically defensible, and clinically transformative path toward making MI a preventable event rather than an unpredictable catastrophe.