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A Practice-Changing Presentation on MI, ASCVD, and LDL at AHA

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As a second-year internal medicine resident, I found the presentations on Real-World Evidence in Understanding Current Lipid Management in Patients with ASCVD: A Focus on MI and ASCVD High risk Assessment, Evaluation, and Management most enlightening. Many patients who present to my outpatient continuity clinic have several risk factors for atherosclerotic disease, and unfortunately, many have already experienced their first myocardial infarction (MI). Of the patients I inherited during my intern year, I noticed that many were not optimized on current statin therapy, either the statin was low-intensity or moderate-high intensity with an LDL>70. Though I have become more aggressive in identifying at-risk patients, I have not achieved my goal of adequate LDL-C lowering with statin therapy. The AHA conference this year was a good review of AHA/ACC guidelines for ASCVD risk and current available therapies. 

In the presentation by Dr. Desai, I realized that I am not the only clinician who has not achieved goal LDL-C in post-MI patients. He initially presented the gradual accumulation of CV events after the first year following a MI is highest among CABG/PCI patients compared to MI and ischemic stroke patients. Then, despite intense medical management post-MI, the risk of recurrent CV events remains elevated. At this point in his presentation, I began to look at my own efforts at lowering ASCVD risk as futile. However, shortly thereafter, he presented real-world clinical practice data on lipid-lowering therapy. In summary, approximately <40% of patients reach a goal LDL-C based ESC/EAS and AHA/ACC guidelines. Per the DA VINCI study, 39% of patients reached the 2016 ESC/EAS goal LDL <70mg/dL and 18% reached the 2019 ESC/EAS goal LDL < 55mg/dL. Surprisingly, in a Medicare study investigating the achievement of LDL-C in the first year post-MI, <25% of patients reached LDL-C levels <50mg/dL; <30% of patients achieved levels 51-69mg/dL; and >40% of patients remained >70mg/dL. Finally, he presented that even patients on maximum statin therapy with the addition of ezetimibe still do not achieve goal LDL-C. He concluded his presentation that PCSK9 inhibitors are showing promising data in effectively lowering LDL-C, in addition to statin and ezetimibe therapy. By this time, I began to feel there was some hope for my patients. 

Many of my patients have type 2 diabetes mellitus (T2DM), so lowering their ASCVD risk is more challenging, especially prior to the first event. So, I watched Dr. Mintz’s presentation on ASCVD risk in type 2 diabetics. He highlighted that many opportunities are missed in prevention and treatment of CVD, such as modifiable risk factors, follow-up, diagnosis, and use of non-statin therapies. Then, he proceeded to discuss the role of LDL in ASCVD risk. In one of his slides, he presented cardiometabolic risk, which includes CVD risk plus risk factors associated with diabetes, prediabetes, and metabolic syndrome. Furthermore, he stated that clinicians need to be more cognizant of the “metabolic patient” or patients at-risk of metabolic syndrome, especially those with an atherogenic lipid profile. In the presentation, he cited the trialist collaboration, which essentially showed that statin therapy was better than standard therapy. He also showed that the relation between atherosclerotic risk reduction and LDL-C reduction is linear, thus citing the Robust trial, which revealed that lower LDL-C results in lower atheroma/plaque volume. Like Dr. Desi, he discussed that U.S. patients are not achieving the guideline-recommended LDL-C on statin-alone therapy. However, he noted that patients between ages 16-64, females and African American patients were LESS LIKELY to achieve LDL-C = 70mg/dl while on statin therapy. Finally, he stated that one-third of patients at risk or with ASCVD were treated in clinical practice WITHOUT prior knowledge of LDL-C levels within the previous two years. This is an eye-opener! He concluded by stating that LDL-C reduction has proven to show benefit in ASCVD risk reduction and adding a non-statin to high-intensity statin therapy improves CV outcomes. 

From the two presentations, I realized that, like me, many physicians are struggling to optimize their patients. Since my patient population is predominantly African American men and women in their 50s and 60s, it is an unfortunate realization that many of them possibly would not reach the AHA LDL-C goal on standard statin therapy. However, what I learned was that I should start using more non-statin therapies in my patients, such as ezetimibe and PCSK9 inhibitors (if possible), and be more vigilant for “metabolic patients.” From the presentation, I am very hopeful for my patients and the emerging therapies.

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