Menopause Heart Risk: Why Your LE8 Trend Matters

Your cardiovascular health during menopause is not a fixed score. In a prospective U.S. study, women whose American Heart Association Life's Essential 8 (LE8) scores improved over the menopausal transition had lower subsequent risks of vascular disease markers, cardiovascular events, and death; women's starting scores also mattered. The useful question is therefore not only, "What is my score today?" It is, "Is it moving in the right direction?"

The finding comes from the 2025 SWAN analysis, which followed 2,924 multiethnic U.S. women, average age 46, through the menopausal transition. Investigators recorded 213 cardiovascular disease events and 161 deaths. Higher LE8 scores at baseline and larger improvements from baseline each independently predicted better outcomes. The study also tracked carotid intima-media thickness, pulse-wave velocity, and carotid plaque—measures of arterial aging and atherosclerosis rather than heart attacks themselves.

Only 21% of participants maintained an ideal LE8 score of at least 80 at every follow-up visit. That does not mean the other 79% were destined for disease. It means a one-time score misses much of the practical story.

A scorecard that changes with the transition

LE8 combines diet, physical activity, nicotine exposure, sleep health, body mass index, blood lipids, blood glucose, and blood pressure. It is a broad cardiovascular-health framework, not a menopause-specific diagnostic test. SWAN's contribution was to examine both the initial level of that score and its change over time in women moving through natural menopause.

That design matters. Menopause is not simply a birthday followed by lower estrogen. Menstrual-cycle patterns during the transition have been prospectively associated with subclinical atherosclerosis measured after menopause in another SWAN study, reported in 2022. Separately, research on oxylipins—lipid mediators involved in vascular tone—found that menopause-related changes in these compounds were associated with adverse vascular-health patterns independent of traditional cardiovascular risk factors.

These studies cannot prove that menopause itself caused every change in LE8 or every vascular outcome. Aging, medication use, social conditions, and health behaviors travel alongside the transition. Still, the prospective SWAN findings make the transition a sensible period to monitor trends rather than wait for a risk calculator to deliver a gloomy postcard years later.

Blood pressure, glucose, and nicotine led the risk signal

In SWAN, glucose, blood pressure, and nicotine exposure showed the strongest and most consistent associations with the three vascular measures, cardiovascular events, and all-cause mortality. Both their baseline levels and their changes over time mattered. This is an association hierarchy within one cohort, not proof that the remaining LE8 components are minor.

Blood pressure deserves particular attention because trouble can appear before a conventional hypertension diagnosis. In an observational study of normotensive perimenopausal women, Wali and colleagues linked non-dipping nighttime blood pressure and higher maximum blood pressure with arterial stiffness. A normal clinic reading can therefore coexist with a less favorable 24-hour pattern. That does not make ambulatory monitoring necessary for everyone, but it explains why an upward blood-pressure trend warrants action and clinical discussion.

Nicotine avoidance is simpler to state than to achieve, but the evidence gives it no loophole. Nicotine exposure was among the components most consistently associated with worse outcomes in SWAN. If someone uses combustible tobacco or nicotine products, quitting support belongs in a cardiovascular plan, not in the optional-wellness drawer.

Glucose is also worth tracking as a trend. SWAN identified it as a high-priority LE8 component, but the paper's abstract does not provide a per-10-point LE8 hazard ratio or a numerical risk reduction for an individual glucose or LE8 improvement. No responsible article should fill that blank with motivational arithmetic.

Sleep had an independent association with cardiovascular events

Sleep was more than background scenery in the SWAN analysis. Favorable sleep scores at baseline and/or improvements in sleep quality were independently associated with lower cardiovascular-event risk after adjustment for the other LE8 components. That makes sleep a distinct risk marker in this population, though it does not prove that improving sleep prevents heart attacks.

Several lines of evidence make the association biologically plausible. In postmenopausal SWAN participants, Everson-Rose et al. found that leptin-related proinflammatory adipokine pathways were independently associated with subclinical cardiovascular disease measures after cardiovascular risk-factor adjustment. A separate prospective UK Biobank study found that evening chronotype adversely interacted with LE8 score in relation to cardiovascular disease risk. Circadian timing, sympathetic activity, metabolic disruption, and inflammation are plausible intermediates, but these studies do not establish one completed causal chain from poor sleep to vascular disease.

The practical implication is modest but useful: treat persistent insomnia, fragmented sleep, or a severely delayed schedule as health issues worth addressing. The available evidence does not include a randomized trial showing that a sleep intervention reduces cardiovascular events or vascular biomarkers specifically in perimenopausal women.

Do not misread the weaker diet and exercise signals

Diet and physical activity showed weaker associations than glucose, blood pressure, and nicotine in the SWAN analysis. That finding does not mean a brisk walk or a better diet has become decorative during menopause. Cohort measures of diet often rely on 24-hour recalls, and activity measures may rely on self-report or limited accelerometer data. Both can blur real exposure differences and weaken observed associations.

Randomized and intervention evidence points in a different direction. A 2024 systematic review found that exercise programs improved cardiorespiratory fitness and reduced arterial stiffness in postmenopausal women. In a randomized trial of sedentary postmenopausal women, interval exercise training improved vascular-health outcomes. A broader meta-analysis found that both high-intensity interval exercise and moderate-intensity continuous training improved cardiometabolic risk factors.

Those trials tested interventions and mostly vascular or cardiometabolic surrogate outcomes, not the same long-term cardiovascular-event endpoint as SWAN. They therefore cannot be pasted together into one exact risk estimate. They do show that exercise has measurable vascular effects even when an observational component score looks less predictive.

Diet can also target blood pressure directly. A GRADE-assessed meta-analysis of randomized trials found dose-dependent blood-pressure reductions with dietary nitrate. That supports a food-based route to improving one high-priority LE8 metric. It does not establish that nitrate-rich foods reproduce the full LE8 association or prevent events in menopausal women.

What a 12-month audit can do

Use LE8 as a dashboard, not a grade on your character. Review blood pressure, glucose, nicotine exposure, sleep, activity, diet, weight, and lipids with a clinician when appropriate; then compare results over months, using consistent measurements. For many women, the first actionable priorities will be blood-pressure control, glucose management, nicotine cessation, and sleep assessment. Keep exercise and diet in the plan even if SWAN ranked their observational signals lower.

• Measure blood pressure correctly and look for a sustained rise, not one stressful Tuesday reading.
• Discuss abnormal glucose results and medication decisions with a clinician rather than treating a consumer score as a diagnosis.
• Seek evidence-based cessation support for nicotine use.
• Address chronic sleep problems, especially when hot flashes, mood symptoms, or obstructive sleep apnea may contribute.
• Choose an activity pattern you can repeat; interval and moderate continuous exercise both have trial support for cardiometabolic outcomes.

The limits of the headline

SWAN is the central prospective evidence here, but it is still one cohort study. Its abstract reports the direction of the associations, not the specific per-10-point hazard ratios for LE8 change. It also does not establish whether LE8 predicts risk better than the Framingham score or ASCVD Pooled Cohort Equations in women aged 40 to 60.

The results apply most directly to women traversing natural menopause. Surgical menopause causes abrupt estrogen withdrawal and may produce a different vascular trajectory. Supporting links between LE8 and metabolic syndrome or serum klotho come from cross-sectional analyses, including a 2024 NHANES study of klotho; they show correlation, not that raising an LE8 score raises klotho or slows biological aging.

The evidence supports a grounded conclusion: cardiovascular health can worsen through menopause, but its direction remains modifiable. Track the trend, act on the measurable risks, and do not let a single score impersonate a prognosis.