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Global Translational Medicine Inflammation in CVD: Mechanisms and markers

1. Introduction retinopathy, nephropathy, myocardial infarction, and
stroke
1.1. The prevalence of cardiovascular disease viii. Blood pressure: Managing systolic and diastolic blood
Globally, cardiovascular disease (CVD) remains the pressure prevents strokes, heart failure, and renal
leading cause of mortality and morbidity, accounting for damage, reducing the overall CVD burden.
over 20.6 million deaths and approximately 393 million Studies indicate that achieving high scores across
disability-adjusted life years annually. While high-income these domains reduces CVD risk by up to 80% and could
1,2
countries have achieved a 34.9% decline in CVD mortality prevent an estimated 2 million CVD events annually in the
from 1990 to 2022, reflecting the impact of preventive United States (U.S.) alone. A recent analysis highlighted
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measures and advancements in treatment, low- and the significant impact of adhering to the updated Life’s
middle-income countries are experiencing a rising burden. Essential 8 framework in improving CVH and reducing
These alarming statistics underscore the urgent need for mortality, demonstrating a linear association between
comprehensive strategies that combine population-level CVH scores and reductions in all-cause and CVD-specific
prevention, risk factor management, and equitable access mortality. Among a cohort of nearly 20,000 U.S. adults,
to healthcare to mitigate the profound impact of CVD on those achieving high CVH scores (≥75) experienced
global health systems. a 58% reduced risk of all-cause mortality and a 64%

1.2. Reduction in cardiovascular disease reduced risk of CVD-specific mortality compared to
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inflammation through risk factor control those with low scores. Physical activity emerged as the
most significant contributor, with improvements linked
Reducing the global burden of CVD requires prioritizing to a 17.8% reduction in CVD-specific mortality. Similarly,
the control of modifiable risk factors to decrease disease optimal control of blood pressure and glucose were
prevalence, mortality, and healthcare costs. The American critical, accounting for 12.5% and 10.3% of preventable
Heart Association’s Life’s Essential 8 framework provides deaths, respectively.
a comprehensive roadmap for achieving and maintaining
cardiovascular health (CVH) across diverse populations 2. Inflammation in atherosclerotic
(Figure 1). The framework is as follows: cardiovascular disease (ASCVD)

i. Diet: Adherence to dietary patterns such as the 2.1. The inflammatory mechanisms underlying
Dietary Approaches to Stop Hypertension or the ASCVD pathogenesis
Mediterranean diet lowers hypertension, atherogenic
lipids, and ischemic risk by emphasizing whole foods, Inflammation is now recognized as a key driver of ASCVD,
healthy fats, and low sodium redefining it from a passive lipid accumulation process to
ii. Physical activity: Regular exercise boosts endurance, a dynamic interplay of immune activation and vascular
lowers blood pressure, enhances insulin sensitivity, injury. Biomarkers such as high-sensitivity C-reactive
and reduces inflammation, reducing the risk of protein (hs-CRP) highlight the residual inflammatory
myocardial infarction and heart failure risk, even in patients with optimal low-density lipoprotein
iii. Nicotine exposure: Avoiding smoking and (LDL) levels on statins.
secondhand smoke prevents endothelial dysfunction
and atherogenesis, lowering the risk of peripheral 2.2. Plaque formation
arterial disease and coronary events The formation of atherosclerotic plaques is initiated by
iv. Sleep health: Adequate sleep (7 – 9 h) supports CVH endothelial injury (Figure 2). Endothelial dysfunction
by regulating metabolism, reducing sympathetic promotes the retention of apolipoprotein B-containing
overactivity, and mitigating hypertension and obesity lipoproteins, such as LDL, within the subendothelial
v. Body mass index (BMI): Maintaining a healthy BMI space. These lipoproteins undergo oxidative modification,
lowers the prevalence of metabolic syndrome and triggering the expression of adhesion molecules, such
reduces the risk of coronary artery disease and non- as vascular cell adhesion molecule 1 and intercellular
ischemic cardiomyopathy adhesion molecule 1, which facilitate the recruitment
5,6
vi. Blood lipids: Controlling non-high-density of circulating monocytes. On transmigration into the
lipoprotein (HDL) cholesterol slows atherosclerosis intima, monocytes differentiate into macrophages and
progression and stabilizes plaques, especially in high- engulf oxidized LDL, forming foam cells. Concurrently,
risk individuals smooth muscle cells migrate from the media to the intima
vii. Blood glucose: Optimized glucose control prevents and synthesize extracellular matrix components, such as
diabetes-related vascular complications, including collagen, which stabilize the nascent plaque. However,

Volume 4 Issue 3 (2025) 2 doi: 10.36922/GTM025100023