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REFLECTIONS
                                                                                                                   Dyslipidaemia
     Dyslipidaemia Global Newsletter #11 2026


     The analysis captured 601,025 CVD events in the KNHIS cohort and 1188 events in the MESA cohort. The findings revealed that prior
     exposure to at least one non-optimal risk factor was nearly universal, exceeding 99% across all studied CVD event subtypes. When
     considered by individual risk factor, prior exposure to non-optimal BP ranged from 95.6% to 96.1% in KNHIS and 93.0% to 96.8% in
                                                                                                                   Dyslipidaemia
     MESA; non-optimal cholesterol, 75.8% to 84.7% in KNHIS and 70.7% to 77.8% in MESA; non-optimal glucose, 72.8% to 77.7% in
     KNHIS and 53.8% to 60.3% in MESA; and past or current smoking, 47.9% to 68.1% in KNHIS and 54.1% to 63.3% in MESA. While
     most risk factors were similar, the KNHIS group showed a significantly higher frequency of non-optimal glucose levels compared to the
     MESA group. Furthermore, exposure to two or more non-optimal risk factors was also extremely common, ranging from 93.2% to 97.2%
     of individuals prior to their first CVD event.


     Even when the researchers applied the higher cut-points for the
     clinically elevated risk factors, antecedent exposure remained the
     rule, presenting in roughly 90% to 95% of CVD cases. Clinically
     elevated BP and cholesterol were the two most common
     antecedent risk factor exposures. The small percentage of events
     that occurred without clinically elevated risk factors usually
     involved multiple risk factors at non-optimal levels.

     This binational, population-based cohort study strongly
     challenges recent claims that CV events frequently occur without
     antecedent major risk factors. The authors conclude that primary    CLICK HERE
     CV events, including CHD, MI, HF, and stroke, rarely ever           READ COMMENTARY BY THE
     manifest in the true absence of non-optimal traditional risk factors.   AMERICAN COLLEGE OF CARDIOLOGY
     These findings underscore the continuous, dose-dependent,           ON THIS PUBLICATION.
     and cumulative effect that even subclinical risk factor levels have
     on CVD risk. The near-universal presence of these non-optimal
     factors, especially high blood pressure and dyslipidaemia, even
     with widely accessible medicines and decades of experience,
     highlights the critical importance of early diagnosis, primordial   CLICK HERE
     prevention efforts, and the promotion of ideal CV health to reduce   FOR THE LINK TO FULL ARTICLE
     the global burden of CVD.



     TREATMENTS AND THERAPEUTICS

     The evolving therapeutic landscape of PCSK9 inhibition.

     Mansfield BS, et al. Atherosclerosis. 2026 Feb 9;414 :120670.

     CVD remains the leading cause of global mortality, with LDL-C acting as a primary, modifiable causal risk factor. Genetic studies
     have revealed the critical role of PCSK9, a liver-produced protein that degrades the receptors responsible for clearing LDL particles
     from the bloodstream. Researchers discovered that individuals with naturally occurring loss-of-function variants in the PCSK9 gene
     exhibit lifelong lower LDL-C levels and a substantially reduced risk of ASCVD, validating PCSK9 as a prime therapeutic target.

     This review investigates the clinical evidence supporting currently approved PCSK9 inhibitors (PCSK9i) while exploring novel
     therapeutic advancements and expanding indications for their use. The authors synthesized data from various major CV outcome
     trials and clinical studies (such as the FOURIER, ODYSSEY, and CORALreef trials) to evaluate the efficacy and safety of different
     therapeutic modalities, including monoclonal antibodies, small interfering RNA (siRNA), novel oral agents, and cutting-edge gene
     editing technologies.








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