Abstract

<h3>Lead Author's Financial Disclosures</h3> Nothing to disclose. <h3>Study Funding</h3> None. <h3>Background/Synopsis</h3> We review a case of a 43-year-old male referred for optimal management of dyslipidemia and cardiovascular risk reduction. This is intended to highlight key features in diagnosis and management of atherogenic dyslipidemia in the setting of metabolic syndrome. <h3>Objective/Purpose</h3> To review a clinical scenario involving LDL discordance in a patient with atherogenic dyslipidemia and its impact on management. <h3>Methods</h3> Clinical management done at tertiary care lipid program. Advanced lipid testing including LDL particle number and size is ordered through Quest Diagnostics. <h3>Results</h3> A 43-year-old nonsmoker male with metabolic syndrome and recently diagnosed insulin dependent type 2 diabetes mellitus was referred to the lipid clinic for further evaluation. With subclinical atherosclerosis noted with calcium score of 6.6 at age 43 (50-75th percentile) and above-average carotid intimal medial thickness, he was treated with rosuvastatin 20 mg daily. Subsequently, he had a good response of ∼50% LDL reduction with LDL-c of 75 mg/dL. At this point, while most clinicians as well as guideline directed approach may suggest a sufficient management of his dyslipidemia, the advent of advanced lipid testing contrasts this dogma otherwise. LDL discordance noted based on higher-than-expected particle number strongly warrants further aggressive LDL lowering for optimal cardiovascular risk reduction in the setting of metabolic syndrome. <h3>Conclusions</h3> While calculated LDL cholesterol has been well established as a primary target of treatment to reduce cardiovascular risk, in patients with hypertriglyceridemia or metabolic syndrome, this may underestimate the true burden of atherogenic, cholesterol-carrying lipoproteins. Measurements of apoB or LDL particle number by NMR may more closely quantify the atherogenic lipoprotein load and thus prove to be better indices of cardiovascular disease risk than calculated LDL cholesterol or non-HDL cholesterol in such a population. In our clinical case, the patient may not be adequately treated based on a calculated LDL of 75 mg/dL on high intensity statin, however, an advanced lipid panel revealing LDL discordance suggests intensification and more aggressive LDL lowering for optimal cardiovascular risk reduction.

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