Page 12 - reflections_newsletter

REFLECTIONS
Dyslipidaemia
Dyslipidaemia Global Newsletter #11 2026

Furthermore, intensive targeting proved to be highly safe.
There were no substantial between-group differences regarding Dyslipidaemia
adverse events like new-onset diabetes, worsening glycaemic
control, statin-associated muscle symptoms, or liver enzyme
elevations. Surprisingly, the intensive group experienced a
significantly lower incidence of creatinine elevation than the
conventional group (1.2% vs. 2.7%).

Among patients with ASCVD, this trial shows that targeting
an LDL-C level of less than 55 mg/dL was associated with
a significantly lower three-year risk of CV events than the
conventional 70 mg/dL target, firmly supporting the latest CLICK HERE
guideline recommendations. The present study supports WATCH DR. C. MICHAEL GIBSON
intensive LDL cholesterol-lowering therapy through an active INTERVIEW ONE OF THE AUTHORS
use of ezetimibe, and if necessary, other non-statin agents. DR. BYEONG-KEUK KIM ON THE
EZ-PAVE STUDY IN PATIENTS
WITH ATHEROSCLEROTIC
CLICK HERE CARDIOVASCULAR DISEASE IN
FOR THE LINK TO FULL ARTICLE SECONDARY PREVENTION (5:17 MIN)

HDL-C: Helpful, harmful, hopeful, or guilty by association.
McLean P, et al. J Clin Lipidol. 2025 Nov-Dec;19(6):1564-1574.

Atherosclerosis has been directly associated with LDL-C and indirectly associated with HDL-C. More recently, the nuances in the
relationship between HDL and ASCVD have been uncovered. Some of these nuances include HDL-C-raising medications not
reliably improving CV outcomes and a potentially harmful relationship found in observational studies between high levels of HDL-C
and ASCVD risk. Despite the mixed data around HDL-C impact on ASCVD risk, there is persistent evidence that elevated HDL-C
influences the prescription frequency of statins in adults with elevated ASCVD risk.

This review highlights the shift from HDL-C quantity to HDL particle functionality as the critical determinant of CV risk. The
authors synthesise evidence from a broad literature review encompassing epidemiological data, Mendelian randomisation
studies, and various genetic phenotypes. Furthermore, they analyze multiple pharmacologic trials that attempted to modify
HDL-C levels or functionality, evaluating the clinical outcomes to determine if HDL-C is truly a helpful therapeutic target, a
harmful risk factor at extreme levels, a hopeful avenue for future treatments, or simply a biomarker that is guilty by association
with other metabolic diseases.

Historically, HDL-C was deemed universally “helpful” due to its role in reverse cholesterol transport, as well as its secondary
antioxidant, anti-inflammatory, and antithrombotic properties. The strong inverse relationship between HDL-C and ASCVD led to its
inclusion in standard clinical risk assessment tools.

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