Unlocking the Puzzle: Unraveling the Relationship Between Sleep Apnea, Breathing Quality, and Cardiovascular Decline

Unlocking the Puzzle: Unraveling the Relationship Between Sleep Apnea, Breathing Quality, and Cardiovascular Decline

Patient uses Wesper to identify poor breathing quality as a probable cause for ongoing cardiovascular issues


I present a 61-year-old woman with a BMI of 24.7 and a long history of cardiovascular problems. She reported hypertension and high cholesterol since her teens, and is currently working with her primary care physician and endocrinologist. Her cardiovascular issues have not improved with treatment, including bariatric surgery leading to significant weight loss, increased exercise and improved diet, and medications for her cholesterol and hypertension.

The patient also complained that she hasn’t had deep, refreshing sleep in over a year. A sleep study was previously considered before her bariatric surgery but hasn’t been recommended by her healthcare team since, and she has not been referred to a sleep specialist. Her healthcare team has not discussed sleep apnea as a possible risk factor for her cardiovascular issues.

The patient noted that her father died early of cardiovascular disease and her goal is to live a normal, healthy life. She purchased Wesper to identify sleep problems as a part of her health improvement journey.

Explanation of metrics:

  1. Apnea/Hypopnea Index (AHI) - the combined average number of apneas and hypopneas that occur per hour of sleep
  2. Oxygen Desaturation Index (ODI) - the number of times per hour of sleep that the blood oxygen level drops by ≥ 4% from baseline
  3. T88 - the time in minutes the patient had an SPO2 at or below 88%
  4. Mean SPO2: The average blood oxygen saturation score 
  5. Minimum SPO2: The lowest blood oxygen saturation score
  6. Sleep efficiency: The total percentage of time spent asleep vs. the total time spent trying to sleep. 
  7. Total sleep time: The amount of actual sleep time achieved


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The patient completed 7 tests over a one month period with the Wesper 3-component system, which includes two abdominal biosensor patches and a pulse oximeter. Her average AHI across all 7 tests was 26 (min/max: 18/34), with several of her tests qualifying as severe (AHI >30). Her average ODI was 29.5 (min/max: 23.3/37.4). Her average T88, or time spent below an SPO2 of 88% was 33.5 minutes (min/max: 21/44). Her average mean SPO2 was 91.2% (min/max: 91/92) and her average lowest SPO2 was 76.2% (min/max: 70/80). The above findings placed her at very high risk for moderate-severe sleep apnea.

Interestingly, the patient’s sleep quality metrics were consistently normal despite reporting low quality sleep. She had an average sleep efficiency of 94% (min/max 88/98) and her average total sleep time was 7.6 hours (min/max: 6.75/8.5), which is considered healthy for an adult. It is therefore likely, that her poor breathing quality is responsible for her light, unrefreshing sleep.

Wesper generated sleep report illustrates the initial findings with the patient

Wesper generated sleep report illustrates the initial findings with the patient.


All 7 tests completed tests showed consistently poor breathing quality and placed the patient at a very high risk for severe sleep apnea. There was no indication that her respiration improved while sleeping on her side.

On meeting with the Wesper Sleep Expert, it was explained to the patient how sleep disordered breathing affects the cardiovascular system and is a major risk factor for cardiovascular disease. Due to her continuing decline in cardiovascular health and poor sleep quality, it was highly recommended that the patient see a sleep specialist as soon as possible. The patient noted that she works for a hospital system and wanted to take her Wesper results to her primary care physician to get a referral to a sleep specialist in her hospital network.

This study demonstrated the dangers of long-term, uncontrolled sleep apnea. Despite the patient having normal appearing sleep quality (normal sleep time and sleep efficiency), her severe respiratory irregularities reduce overall sleep quality and likely contribute to poor cardiovascular health.

Individuals with sleep apnea have frequent, long pauses in their breathing that cause a drop in their blood oxygen levels, called intermittent hypoxia (IH). IH can trigger a “cortical arousal”, in which the brain shifts from deep sleep to light sleep or from sleep to wakefulness [1]. Thus, SA is highly disruptive and leads to chronically poor sleep quality. This very likely explains why the patient described her sleep as poor and lacking in “deep sleep”, despite having normal sleep efficiency and sleep time.

IH also results in hypercapnia (increase in blood carbon dioxide), which places a large strain on the brain and body, especially the cardiovascular system [2]. Sleep apnea also cause frequent increases in intrathoracic (chest) pressure, which places a direct strain on the heart [3]. Sleep apnea has also been shown to increase systemic (body-wide) oxidative stress, which is harmful to DNA, cells, and tissues [4]. The above factors are likely playing a large role in the patient’s continued cardiovascular decline.

Due to the patient’s family history of cardiovascular disease, including her father, it is very possible that her breathing irregularities were inherited. Studies have shown that your risk for developing sleep apnea is 50% when you have a first degree relative (a parent, sibling, or child) with the sleep disorder.

Wesper allowed the above individual to identify poor breathing quality as a likely factor for her worsening cardiovascular problems. Affordable, accessible, easy sleep testing with Wesper will also continue to help people identify their sleep issues before it leads to chronic, deadly, health conditions. 

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  1. American Academy of Sleep Medicine. International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine, 2014.
  2. Bonsignore, M.R., Baiamonte, P., Mazzuca, E. et al. Obstructive sleep apnea and comorbidities: a dangerous liaison. Multidiscip Respir Med 14, 8 (2019). https://doi.org/10.1186/s40248-019-0172-9
  3. Kasai T, Bradley TD. Obstructive sleep apnea and heart failure: pathophysiologic and therapeutic implications. J Am Coll Cardiol. 2011 Jan 11;57(2):119-27. doi: 10.1016/j.jacc.2010.08.627. PMID: 21211682.
  4. Eisele HJ, Markart P, Schulz R. Obstructive Sleep Apnea, Oxidative Stress, and Cardiovascular Disease: Evidence from Human Studies. Oxid Med Cell Longev. 2015;2015:608438. doi: 10.1155/2015/608438. Epub 2015 Jun 8. PMID: 26167241; PMCID: PMC4475750.

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