Why both too little and too much sleep appear risky
Large observational studies often find a U-shaped pattern: people who sleep much less or much more than average tend to have more cardiovascular disease. A 2025 systematic review of 38 studies found that prolonged sleep was consistently associated with higher risks of coronary artery disease, stroke (both ischemic and hemorrhagic), hypertension, and myocardial infarction [2]. That review also noted that short sleep has long been linked to cardiovascular risk, so the two extremes can look similar in broad population data [2].
The key difference is what kind of evidence supports each link. Observational associations can arise because poor health changes sleep, not only because sleep changes health. Studies that use genetic variants as natural experiments try to reduce that problem, and their results point in a different direction for long versus short sleep [3].
Short sleep has stronger evidence for causing heart problems
A Mendelian randomization study of about 404,000 UK Biobank participants found that genetically predicted short sleep (6 hours or less) was associated with higher risks of arterial hypertension, coronary artery disease, myocardial infarction, chronic ischemic heart disease, and pulmonary embolism [3]. The same study found no association between genetically predicted long sleep (9 hours or more) and any of the 12 cardiovascular diseases examined [3]. This suggests short sleep may be a causal risk factor, while long sleep is unlikely to be a causal factor for most cardiovascular diseases [3].
A separate prospective cohort using accelerometer-measured sleep in about 89,600 UK Biobank participants found that short sleep, but not long sleep, was linked to a 33% higher risk of incident heart failure over seven years [1]. That study also found that people who both slept short and did not meet recommended moderate-to-vigorous physical activity had the highest heart failure risk, with a hazard ratio of 1.78 compared with normal sleepers who met activity recommendations [1]. The fact that physical activity could partly offset the short-sleep risk supports the idea that short sleep is acting on heart failure risk through a modifiable pathway [1].
Long sleep may be a warning sign more than a cause
The systematic review proposed that long sleep might act as a modifiable risk factor, and it pointed to elevated inflammatory markers such as C-reactive protein and interleukin-6 as possible mediators, alongside age, gender, and socioeconomic status [2]. That is a hypothesis about mechanism, not a demonstrated cause. The genetic study's finding that long sleep was not associated with cardiovascular disease argues against long sleep itself being a direct cause for most of these conditions [3].
One plausible reading is that long sleep often reflects existing illness, fatigue, or other risk factors rather than creating cardiovascular damage. The review itself notes that the adverse effects of long sleep remain underexplored compared with short sleep [2]. So when long sleep appears alongside hypertension, stroke, or heart failure in observational data, it may be a marker of poor health rather than the driver of it.
After a stroke, both extremes matter for recovery
The picture changes when sleep is studied after a cardiovascular event rather than before one. Among 1,450 patients who had an acute ischemic stroke or transient ischemic attack, those who kept sleeping either long or short over the following year had a higher risk of post-stroke depression and poorer quality of life than those who kept a normal 7-to-8-hour schedule [4]. Patients whose sleep newly became abnormal also had a higher risk of poor functional outcome [4].
That study grouped long and short sleepers together, so it does not show that long sleep is worse than short sleep after a stroke. It does show that persisting abnormal sleep duration in either direction is a useful warning sign for recovery. In heart failure patients, a separate study of 166 people identified a long-sleep/low-efficiency phenotype and a short-sleep/high-efficiency phenotype, and both had worse outcomes than a healthy-sleep group [5]. That study is small and describes patterns rather than causes, but it reinforces that long sleep in people who already have heart failure can signal trouble [5].
Sources used in this answer
Associations of objective sleep duration and physical activity with risk of heart failure: A prospective cohort study
In about 89,600 UK Biobank participants, accelerometer-measured short sleep but not long sleep was associated with a 33% higher risk of incident heart failure, and meeting recommended moderate-to-vigorous physical activity partly offset that risk.
Implications of Long Sleep Duration on Cardiovascular Health: A Systematic Review
A systematic review of 38 studies found prolonged sleep consistently associated with higher risks of coronary artery disease, stroke, hypertension, and myocardial infarction, with inflammation proposed as a possible mediator.
Causal associations of short and long sleep durations with 12 cardiovascular diseases: linear and nonlinear Mendelian randomization analyses in UK Biobank
Genetically predicted short sleep was associated with higher risks of several cardiovascular diseases including hypertension, while genetically predicted long sleep was not associated with any of the 12 cardiovascular diseases studied.
Persisting Short or Long Sleep Duration Predicts Post-Stroke Depression One year After Stroke and Transient Ischemic Attack
Among 1,450 patients after acute ischemic stroke or transient ischemic attack, persisting long or short sleep was associated with higher risk of post-stroke depression and poor quality of life at one year.
Abstract 13353: Sleep Health Phenotypes Predict Symptoms, Cognitive Function, and Adverse Events in Patients With Heart Failure
In 166 heart failure patients, a long-sleep/low-efficiency phenotype and a short-sleep/high-efficiency phenotype both had worse outcomes than a healthy-sleep phenotype.