A Look at the Effect of Sleep Patterns on Cardiovascular Health
Studies have increasingly shown that short and excessively long sleep durations are linked to worse cardiovascular outcomes,1 and accumulating research has begun to shed light on the deleterious effects of other components of poor sleep patterns, such as nighttime waking and increased sleep latency. In light of these findings, the American Heart Association (AHA) has made sleep health 1 of the “Essential 8” factors in reducing cardiovascular disease (CVD) risk, in an update to the previous “Essential 7” list.2
“Poor sleep quality or decreased amounts of sleep can elevate insulin resistance, trigger inflammation, throw off circadian rhythms, and elevate sympathetic nervous system activity,” explained Dr Tamara Horwich, MD, MS, attending cardiologist, clinical professor of medicine at the David Geffen School of Medicine at the University of California, Los Angeles, and medical director of UCLA’s Cardiac Rehabilitation Program.
In a study published in August 2022 in the Journal of the American Heart Association (JAHA), Wang et al examined associations between sleep patterns and CVD risk in 12,268 individuals (mean age, 70.3 years) in the Swedish Twin Registry who were free of CVD at baseline.3 In a follow-up period of up to 18 years, hazard ratios (HRs) for CVDs were 1.14 for less than 7 hours of sleep per night (95% CI, 1.01-1.28) and 1.10 for 10 or more hours per night (95% CI, 1.00-1.21) compared to 7 to 9 hours per night.
Another 2022 study investigated the CVD-sleep connection based on data from 7,850 US adults in the National Health and Nutrition Examination Survey (NHANES).4 According to the results, sleep problems (defined as frequent trouble falling or staying asleep) were associated with an increase in CVD risk (OR, 1.75; 95% CI, 1.41-2.16) after adjustment for confounding variables, with a stronger association noted for individuals younger than 60 years (P =.019).
Chronically sleep-deprived people who regularly sleep less than 6 hours face a greater risk of hypertension, heart attack, arrhythmias, congestive heart failure, stroke, and death.
Prolonged sleep-onset latency was associated with increased risk for CVD (OR, 1.59; 95% CI, 1.17-2.15), congestive heart failure (OR, 2.08; 95% CI, 1.33-3.23), and myocardial infarction (OR, 1.76; 95% CI, 1.29-2.41), while short sleep-onset latency was linked to a reduction in the risk for stroke (OR, 0.64; 95% CI, 0.45-0.90).4
Compared to sufficient sleep, inadequate sleep was associated with greater odds of CVD (OR, 1.42; 95% CI, 1.13-1.78) and myocardial infarction (OR, 1.59; 95% CI, 1.19-2.13).4
In a 2021 cross-sectional study of 521,364 adults, poor self-reported sleep was associated with higher odds of having each CVD risk factor, especially physical inactivity.5 Compared to participants reporting difficulty falling asleep, unrestful sleep, and sleep duration of less than 6 hours per night, those with no difficulty falling asleep, restful sleep, and sleep duration of 6 to 9 hours per night showed a lower CVD risk score (all P < .001).
Findings published in 2020 suggest that irregular sleep schedules may increase CVD risk independently of sleep quality and or duration or traditional CVD risk factors.6 The odds of CVD were as much as roughly 2-fold higher among participants with high variability in the duration or timing of sleep compared with those with less variability. Similar results were found after shift workers were excluded from the analyses.
A 2021 study of 873 patients in China demonstrated that going to bed at 12:00AM or later (OR, 4.005; P <.001), waking at 7:00AM or later (OR, 2.544; P =.011), and sleeping less than 6 hours per night (OR, 2.968; P <.001), were associated with an elevated risk for acute myocardial infarction.7 Additionally, frequent nighttime waking was associated with greater acute myocardial infarction risk among participants older than 65 years.
Short sleep duration was also associated with a higher risk for coronary artery disease as indicated by a high Gensini score (OR, 2.374; P <.001).7
Daytime napping was linked to lower acute myocardial infarction risk (OR, 0.645; P =.046) in participants 65 years or younger, suggesting that regular naps may represent a protective CVD factor in young and middle-aged individuals.7 However, in the 2022 JAHA study, napping 1 to 30 minutes (HR, 1.11; 95% CI, 1.03-1.18) and longer than 30 minutes (HR, 1.23; 95% CI, 1.14-1.33) were associated with an increased risk of CVD compared to no napping.3
In research published in 2021 in Circulation, a lower risk for heart failure was associated with healthy sleep patterns, including early chronotype, sleeping 7 to 8 hours per night, and no frequent insomnia or daytime sleepiness (8%, 12%, 17%, and 34% lower for each component, respectively) in more than 400,000 patients in the UK Blood Biobank.8
In 2 studies drawing from the same cohort, a similar healthy sleep pattern was linked to reduced risk for atrial fibrillation/flutter (HR comparing extreme categories, 0.71; 95% CI, 0.64-0.80) and bradyarrhythmia (HR, 0.65; 95% CI, 0.54-0.77), as well as lower risk of all-cause mortality (HR, 0.94; 95% CI, 0.92–0.96), CVD-related mortality (HR, 0.89; 95% CI, 0.83–0.95), and cancer-related mortality (HR, 0.96; 95% CI, 0.93–0.99).9,10
In other recent research aiming to further elucidate the sleep-CVD connection, lower physical activity was associated with more pronounced associations between poor sleep and all-cause mortality as well as CVD-related and cancer-related mortality.11 In the 2021 cross-sectional study described above, poor sleep was linked to higher odds (approximately 3-fold) of physical inactivity compared to normal sleep.5
In addition, a laboratory study of 20 healthy adults found that moderate light exposure (100 lx) during sleep increased nighttime heart rate, sympathovagal balance (as indicated by decreased heart rate variability), and next-morning insulin resistance compared to dim light exposure (<3 lx) during sleep.12 In the 2021 study linking sleep patterns to increased acute myocardial infarction risk, lower nighttime light exposure was associated with reduced acute myocardial infarction risk (OR, 0.243; P =.009).7
Dr Horwich emphasizes the need to educate patients on ways to improve sleep quality and quantity, especially those at risk of CVD. “We can advise patients to prioritize sleep, keep consistent sleep hours, avoid smartphones and other light before bedtime,” she said. “Sleep consultation and sleep studies are important next steps when sleep disorders are suspected.”
To glean further insights regarding sleep patterns and CVD risk, we interviewed Bishnu Subedi, MD, FACC, board-certified cardiologist at the University of Pittsburgh Medical College Heart and Vascular Institute and director of cardiac imaging at UPMC Carlisle, and Steven Holfinger, MD, sleep medicine physician and clinical assistant professor of internal medicine The Ohio State University Wexner Medical Center in Columbus.
What does the current evidence suggest about associations between sleep patterns and CV risk?
Dr Subedi: Chronically sleep-deprived people who regularly sleep less than 6 hours face a greater risk of hypertension, heart attack, arrhythmias, congestive heart failure, stroke, and death. Various sleep patterns like chronotype, sleep duration, insomnia, snoring, and daytime sleepiness are important indicators for future outcomes.
Dr Holfinger: The lowest CV risk is at 7 hours sleep duration, with both decreased and increased sleep need increasing risk.13
Healthy sleep patterns have a nocturnal dip in blood pressure, while those without dipping will have higher CV risk and risk for obstructive sleep apnea (OSA).
CVDs including arrhythmias and MI incidence are linked to circadian rhythms. For example, 20% of MI occur between 12:00AM and 6:00AM.14
Patients with CVD are both more likely to have sleep disorders and may have worsening of their CVD by the untreated sleep disorder.
When patients have sleep disorders that cause circadian misalignment – such as shift work, jet lag, or shifts in daylight savings time – there is a higher risk of CVD.
What are some of the proposed mechanisms underlying this connection?
Dr Subedi: Sleep disorders can cause repeated episodes of nocturnal hypoxemia, oxidative stress, sympathetic nervous system activation, cortical arousal, and endothelial dysfunction, all of which are mediators of CVD.
Lower sleep times and fragmented sleep are independently associated with subclinical atherosclerosis, as determined by vascular ultrasonography and calcium scoring, and higher atherosclerotic biomarkers like high-sensitivity C-reactive protein.
Poor sleep can, independent of primary sleep disorders, contribute to several molecular, immune, and neural changes that play a role in disease development.
Dr Holfinger: For healthy people, during non-REM sleep, parasympathetic activity predominates with reduction in arrhythmias, and this is generally thought to be a restorative state for the heart and body. During REM sleep, CV risk is elevated due to relatively extreme swings in sympathetic and parasympathetic tone compared to wakefulness.
The overall circadian rhythmicity of CVDs is likely related to swings in sympathetic activity, but also related to variations in the peripheral circadian clocks, as peripheral clocks have been linked with platelet aggregation changes and ventricular repolarization abnormalities in animal models.15
A well-studied link is between OSA and systemic hypertension.16 This is likely due to a combination of mechanisms related to the repetitive intrathoracic pressure swings and intermittent hypoxia, with the largest factor being the effect of increased sympathetic activity on hypertension. This is primarily mediated by the peripheral chemoreceptors at the carotid body leading to the increase in sympathetic activity.
What are recommendations for clinicians in terms of advising patients on these issues and screening for sleep problems?
Dr Subedi: Patients with or at risk of sleep problems should be advised to engage in at least moderate exercise, quit smoking, avoid alcohol and stimulant or sedative medications before bedtime, and to optimize their sleep habits.
The AHA’s checklist to measure CV health has added healthy sleep as essential for optimal CV health.2 The new sleep metric suggests 7-9 hours of sleep daily for optimal CV health for adults, and more for children depending on age.
Patients at higher risk for OSA should undergo polysomnography to test for sleep apnea to see if they may benefit from positive airway pressure (PAP) therapy.
Dr Holfinger: The most pressing issue would be that in patients with CVD the prevalence of sleep apnea is high, and it is underrecognized both in the general population and in those with CVD. This may be in part because there are many ways sleep apnea can present, and those with CVD tend to report less sleepiness than other groups with sleep apnea.
Clinicians should keep an eye out for other clues that the patient may have sleep apnea, such as snoring, witnessed apneas, fragmented sleep, morning headaches, or nocturia. If sleep apnea is suspected, they should either be referred for a sleep study or to a sleep specialist for evaluation.
If patients have reasons for circadian misalignment, they should be addressed if possible. For example, ICU settings should strive to mimic circadian signaling by limiting light and disruptions at night, limiting 24-hour parenteral feeding, and increasing daytime light and activity levels.
For healthy patients, the recommendation should be to allow adequate sleep time to not force sleep restriction, in addition to maintaining a regular sleep schedule. Avoidance of bright light for the couple of hours when winding down before bed is also beneficial.
What should be the focus of future research pertaining to this topic?
Dr Subedi: Although sleep disorders have been linked to CVDs, the association between sleep characteristics – such as REM vs non-REM – and CVDs remains inconclusive.
Experts are proposing that a transdisciplinary research framework that integrates knowledge, methods, and measures from the fields of psychology and sleep research may be used to catalyze advances in the prevention and treatment of CVD.
Dr Holfinger: The impact on CV outcomes related to treating OSA using continuous PAP (CPAP) have been negative in large randomized studies, with most positive effects on CVD being reported in observational studies. Many sleep researchers cite methodological flaws in these RCTs – for example, low adherence to CPAP and exclusion of high-risk groups.
The evidence currently shows that use of CPAP can lead to a modest (2 mm Hg) reduction in systemic hypertension. And instead of CV risk, the aggregate evidence from the RCTs would suggest that CPAP reduces cerebrovascular risk.17
Specific strategies to reduce the effects of circadian misalignment are lacking in long-term studies evaluating the impact on CVD.
This article originally appeared on The Cardiology Advisor