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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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