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Home NEWS Science News Health

Heart Fat Linked to Nighttime Blood Pressure Swings in Healthy Young Adults

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October 29, 2026
in Health
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Heart Fat Linked to Nighttime Blood Pressure Swings in Healthy Young Adults

Heart Fat Linked to Nighttime Blood Pressure Swings in Healthy Young Adults

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A layer of fat wrapped around the heart may be quietly tracking how wildly blood pressure fluctuates at night — even in people who seem perfectly healthy. In a new cross-sectional study of 172 apparently healthy young adults aged 18 to 41, researchers report that epicardial fat thickness, a measure of the visceral fat surrounding the heart, was positively correlated with several measures of 24-hour blood pressure variability, with the strongest association seen for nighttime systolic blood pressure variability. The work, published in Artery Research, is among the first to examine this relationship in a population free of hypertension, diabetes, and other chronic disease.

Blood pressure variability, or BPV, refers to the fluctuations in blood pressure over time, which can be measured over short, medium, and long terms. Elevated BPV has been strongly associated with serious health outcomes including cardiovascular disease, stroke, kidney disease, dementia, and death — and, according to the study’s authors, these associations extend even to normotensive individuals. Epicardial adipose tissue, meanwhile, is a metabolically active visceral fat depot that surrounds the heart and releases proinflammatory cytokines and mediators, contributing to both local and systemic inflammation. Increased epicardial fat thickness has been linked to coronary artery and myocardial disease as well as systemic conditions such as metabolic syndrome, diabetes, and liver disease, making it a recognized biomarker of cardiometabolic risk.

Previous research had connected epicardial fat to blood pressure variability mainly in hypertensive or otherwise high-risk patients. The research team hypothesized that the same relationship might already exist in young adults with low baseline cardiovascular risk — a population that, to their knowledge, had not been specifically studied before. They recruited participants from a cardiology outpatient clinic where they had presented with atypical chest pain, defined as non-anginal, non-exertional chest discomfort without features suggestive of acute coronary syndrome. All volunteers had normal physical examinations, resting electrocardiograms, and routine laboratory results, and anyone with known chronic cardiovascular, metabolic, renal, hepatic, or inflammatory disease, regular medication use, active or recent infection, obesity, or laboratory evidence of systemic inflammation was excluded.

The study was prospective and cross-sectional, running between October and November 2025. Each participant underwent transthoracic echocardiography, during which epicardial fat thickness was measured in the parasternal long-axis view with an M-mode cursor positioned perpendicular to the aortic annulus along the free wall of the right ventricle at end-diastole, averaging three consecutive cardiac cycles. The authors note that echocardiography is a low-cost, radiation-free, and reproducible surrogate that correlates well with MRI- and CT-derived epicardial fat measurements, though it is more operator-dependent and less sensitive than three-dimensional imaging techniques.

To capture blood pressure variability, each participant wore a 24-hour ambulatory blood pressure monitoring device starting between 08:00 and 10:00 on a typical working day. The device recorded readings at 30-minute intervals during both daytime (07:00 to 23:00) and nighttime (23:00 to 07:00) hours, and recordings were considered valid only if at least 80 percent of scheduled readings were obtained, with at least 70 percent valid in both daytime and nighttime windows. Participants kept diaries of sleep and wake times and were instructed to continue their usual daily activities. Blood pressure dipping status was calculated as the percentage reduction in mean nighttime blood pressure relative to daytime levels, with declines of 10 percent or more classified as dipping.

The cohort had a mean age of 29.08 years, was 39 percent male, and had a mean body mass index of 23.36 kg/m². Mean epicardial fat thickness was 4.1 millimeters. Pearson correlation analysis showed significant positive associations between epicardial fat thickness and 24-hour systolic blood pressure variability (r = 0.171, p = 0.028), 24-hour diastolic variability (r = 0.173, p = 0.025), nighttime systolic variability (r = 0.193, p = 0.012), and nighttime diastolic variability (r = 0.183, p = 0.018). No significant correlations emerged with the ambulatory arterial stiffness index, the ambulatory blood pressure smoothing index, or dipping patterns. Epicardial fat was also significantly thicker in males than females, though none of the blood pressure variability measures differed significantly between the sexes.

To test whether the epicardial fat association held up under adjustment, the researchers built a multiple linear regression model for nighttime systolic blood pressure variability that included clinically relevant variables and those significant in univariate analyses. The model was statistically significant, accounting for 11.0 percent of the variance (R² = 0.110, adjusted R² = 0.084), with an effect size of Cohen’s f² = 0.124, described as small to medium. Within that model, epicardial fat thickness, smoking, and the platelet-to-basophil ratio were each independently associated with nighttime systolic variability, while age and thyroid-stimulating hormone were not. The authors emphasize that regression models of this kind are correlational and exploratory: they show that the variables are interrelated after adjustment, but cannot establish whether epicardial fat mechanistically drives blood pressure variability or the reverse.

Why nighttime systolic variability in particular? The authors draw on prior literature to propose — explicitly, as hypotheses rather than findings — that epicardial adipose tissue may influence cardiac autonomic function and vascular reactivity through pro-inflammatory and pro-atherogenic mediators, and that nighttime hours, when sympathovagal balance shifts and environmental and behavioral influences such as physical activity, stress, and nutrition recede, may be when autonomic and hormonal effects on blood pressure are most visible. Systolic pressure is also more sensitive than diastolic pressure to arterial wall elasticity, sympathetic activity, and cardiac output, whereas diastolic pressure in healthy young people depends more on peripheral vascular resistance and arterial relaxation, which tend to be stable. The study did not directly measure autonomic activity, inflammation, or vascular function, so these mechanistic explanations remain speculative.

The authors are careful to spell out the study’s limitations. The cross-sectional design cannot determine temporal direction or causality, and the associations should not be read as evidence of a direct causal effect. The sample was limited to healthy young adults with low cardiovascular risk, restricting generalization to older people or those with hypertension or metabolic syndrome. Because participants were recruited from a cardiology clinic for atypical chest pain, a degree of selection bias cannot be ruled out, and the population may not fully represent asymptomatic young adults in the general community. The regression model’s modest explanatory power may reflect limited variability in both fat thickness and blood pressure variability among healthy young people, and the absence of genetic, dietary, lifestyle, sleep, and stress data. Standardized resting office blood pressure measurements were also not available, so the analysis could not determine whether the association is independent of resting blood pressure levels.

If future longitudinal cohort studies confirm the findings, the authors suggest that epicardial fat measurement and ambulatory blood pressure variability monitoring could eventually be investigated as components of cardiovascular risk screening in young adults, and that ambulatory monitoring may be useful for further evaluating variability patterns in young people with increased epicardial fat. For now, the takeaway is more measured: the relationship between the fat surrounding the heart and the night-to-night swings of systolic pressure appears to be present before overt cardiovascular disease develops, but longitudinal and mechanistic studies are needed to clarify whether changes in one accompany changes in the other — and which, if either, drives the association.

Subject of Research: The association between epicardial fat thickness and ambulatory blood pressure variability in healthy young adults.

Article Title: Epicardial Fat Thickness and Nighttime Systolic Blood Pressure Variability in Healthy Young Adults

Article References: Sarıoğlu, G., & Yiğit, Y. (2026). Epicardial Fat Thickness and Nighttime Systolic Blood Pressure Variability in Healthy Young Adults. Artery Research, 32(1), Article 28. https://doi.org/10.1007/s44200-026-00126-x

Image Credits: AI Generated

DOI: 10.1007/s44200-026-00126-x

Keywords: epicardial fat thickness, blood pressure variability, ambulatory blood pressure monitoring, young adults, cardiometabolic risk, echocardiography, nighttime systolic BPV, cross-sectional study, visceral fat, cardiovascular risk screening, Epicardial, Thickness

News Source: Ophelia Keating. (October 29, 2026). Heart Fat Linked to Nighttime Blood Pressure Swings in Healthy Young Adults. Scienmag.

Tags: ambulatory blood pressure monitoringblood pressure variabilitycardiometabolic riskcardiovascular risk screeningCross-sectional Studyechocardiographyepicardialepicardial fat thicknessnighttime systolic BPVthicknessvisceral fatyoung adults
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