The hidden fuel of accelerated atherogenesis. Beyond LDL.

Abstract

Introduction: Cardiovascular diseases are the main cause of mortality globally. Atherosclerosis, characterized by the formation of plaques in the arteries, is at the heart of this problem. Lipoproteins and their protein components, Apo A and Apo B, are indisputable protagonists in the mechanisms underlying this disease.

Case: A 45-year-old woman with a history of hypertension (HTN) who presents persistent angina and dyspnea on minimal exertion for 3 months. The stress test was positive and the coronary angiography revealed a multivessel coronary lesion with complex anatomy for interventionism. High levels of Lp(a) and Apo B, and low levels of Apo A were detected, which unmasked genetic dyslipidemia and the factor responsible for accelerated atherogenesis. Multivessel coronary artery disease in a patient younger than 50 years is unusual (<5% of cases), suggesting unconventional risk factors.

Intervention: Myocardial revascularization surgery (3 bridges) was planned and successfully performed. Postoperative treatment was emphasized on aggressive lipid-lowering therapy due to the high residual risk.

Discussion: The synergy between elevated Lp(a) and Apo B multiplies the risk of infarction by 4-5 times and accelerates the formation of complex and unstable plaques. Apo B reflects the total number of atherogenic lipoprotein particles, and levels greater than 130 mg/dL are associated with a high cardiovascular risk. Lp(a) and Apo B are not only lipid markers, but also central drivers of accelerated atherogenesis.

Conclusion: Elevated Lp(a) is an independent and heritable risk factor whose early diagnosis can save lives through personalized strategies. Without treatment, 10-year mortality in these patients can exceed 50%.