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Water Pipe (Hookah) Smoking and Cardiovascular Disease Risk: A Scientific Statement From the American Heart Association
Tobacco smoking with a water pipe or hookah is increasing globally. There are millions of water pipe tobacco smokers worldwide, and in the United States, water pipe use is more common among youth and young adults than among adults. The spread of water pipe tobacco smoking has been abetted by the marketing of flavored tobacco, a social media environment that promotes water pipe smoking, and misperceptions about the addictive potential and potential adverse health effects of this form of tobacco use. There is growing evidence that water pipe tobacco smoking affects heart rate, blood pressure regulation, baroreflex sensitivity, tissue oxygenation, and vascular function over the short term. Long-term water pipe use is associated with increased risk of coronary artery disease. Several harmful or potentially harmful substances present in cigarette smoke are also present in water pipe smoke, often at levels exceeding those found in cigarette smoke. Water pipe tobacco smokers have a higher risk of initiation of cigarette smoking than never smokers. Future studies that focus on the long-term adverse health effects of intermittent water pipe tobacco use are critical to strengthen the evidence base and to inform the regulation of water pipe products and use. The objectives of this statement are to describe the design and operation of water pipes and their use patterns, to identify harmful and potentially harmful constituents in water pipe smoke, to document the cardiovascular risks of water pipe use, to review current approaches to water pipe smoking cessation, and to offer guidance to healthcare providers for the identification and treatment of individuals who smoke
Compared with obstructive sleep apnea (OSA), the prevalence of central sleep apnea (CSA) is low in the general population. However, in adults, CSA may be highly prevalent in certain conditions, most commonly among those with left ventricular systolic dysfunction, left ventricular diastolic dysfunction, atrial fibrillation, stroke, and opioid users (Javaheri S, et al. J Am Coll Cardiol. 2017; 69:841). CSA may also be found in patients with carotid artery stenosis, cervical neck injury, and renal dysfunction. CSA can occur when OSA is treated (treatment-emergent central sleep apnea, or TECA), notably, and most frequently, with continuous positive airway pressure (CPAP) devices. Though in many individuals, this frequently resolves with continued use of the device.
PAP may reduce mortality in patients with obesity and severe OSA
The prescription of positive airway pressure is associated with reduced all-cause mortality, according to the results of a cohort study published in JAMA Otolaryngology–Head & Neck Surgery.
The association becomes evident several years after positive airway pressure (PAP) initiation, according to the researchers. Obstructive sleep apnea (OSA) is among the top 10 modifiable cardiovascular risk factors, and is associated with increased risks of coronary artery disease, stroke, and death. PAP is the most effective treatment for OSA, but this treatment’s effect on all-cause and cardiovascular mortality is uncertain. Randomized trials have yielded inconclusive answers to this question, and evidence from observational studies has been weak.
To investigate the association between PAP prescription and mortality in patients with obesity and severe OSA, Quentin Lisan, MD, of the Paris Cardiovascular Research Center and his colleagues conducted a multicenter, population-based cohort study. The researchers examined data for 392 participants in the Sleep Heart Health Study, in which adult men and women age 40 years or older were recruited from nine population-based studies between 1995 and 1998 and followed for a mean of 11.1 years. With each participant who had been prescribed PAP, the investigators matched as many as four participants who had not been prescribed PAP, on the basis of age, sex, and apnea-hypopnea index. Of this sample, 81 patients were prescribed PAP, and 311 were not.
All participants had a clinic visit and underwent overnight polysomnography at baseline. At 2-3 years, participants had a follow-up visit or phone call, during which they were asked whether their physicians had prescribed PAP. Participants were monitored for cardiovascular and all-cause mortality.
In all, 319 of the 392 participants were men; the population’s mean age was 63 years. Patients who had received a PAP prescription had a higher body mass index and more education, compared with patients who had not received a prescription. Mean follow-up duration was 11.6 years in the PAP-prescribed group and 10.9 years in the nonprescribed group.
A total of 96 deaths occurred during follow-up: 12 in the PAP-prescribed group and 84 in the nonprescribed PAP group. The crude incidence rate of mortality was 24.7 deaths per 1,000 person-years in the nonprescribed group and 12.8 deaths per 1,000 person-years in the PAP-prescribed group. The difference in survival between the prescribed and nonprescribed groups was evident in survival curves after 6-7 years of follow-up. After adjustments for prevalent cardiovascular disease, hypertension, diabetes, body mass index, education level, smoking status, and alcohol consumption, the hazard ratio of all-cause mortality for the prescribed group was 0.38, compared with the nonprescribed group.
Dr. Lisan and his colleagues identified 27 deaths of cardiovascular origin, one of which occurred in the prescribed group. After adjusting for prevalent cardiovascular disease, the hazard ratio of cardiovascular mortality for the prescribed group was 0.06, compared with the nonprescribed group.
One reason that the reduction in mortality associated with PAP was not found in previous randomized, controlled trials could be that their mean length of follow-up was not long enough, the researchers wrote. For example, the mean length of follow-up in the SAVE trial was 3.7 years, but the survival benefit was not apparent in the present analysis until 6-7 years after treatment initiation.
These results are exploratory and require confirmation in future research, Dr. Lisan and his colleagues wrote. No information on adherence to PAP was available, and the researchers could not account for initiation and interruption of PAP therapy. Nevertheless, “prescribing PAP in patients with OSA should be pursued and encouraged, given its potential major public health implication,” they concluded.
The Sleep Heart Health Study was supported by grants from the National Institutes of Health.
Author: Erik Greb
Obstructive sleep apnea (OSA) is common in morbidly obese patients, with a reported prevalence as high as 45% in obese subjects.1 In fact, according to one study presented at the American Society of Metabolic and Bariatric Surgery, of 359 patients who had preoperative polysomnography, 86% had positive tests, which showed severe OSA in half of the cases.2
Obesity predisposes to and potentiates OSA, which demonstrates the need to diagnose OSA through polysomnography testing as part of the preoperative evaluation for bariatric surgery. Preoperative diagnosis of OSA is important for both perioperative airway management and the prevention of postoperative pulmonary complications.3
Assessment of OSA
Polysomnography remains the gold standard for diagnosis and assessment of OSA. Assessing a patient’s BMI is not a fully diagnostic indicator for OSA. In one study, 40 patients being evaluated for bariatric surgery underwent a polysomnography regardless of symptoms. OSA was present in 71% of patients. The majority of the patients were women whose patient characteristics failed to predict the severity of OSA. For that reason, providers should have a low threshold for ordering a polysomnography as part of the preoperative evaluation for bariatric surgery.4
Preoperative Treatment for OSA
CPAP is the mainstay treatment for moderate to severe OSA and has been shown to improve objective and subjective measures of OSA. Appropriate therapy with CPAP perioperatively would theoretically prevent hypoxic complications associated with OSA.5
CPAP has been shown to be a highly effective treatment if appropriately used. Medical literature demonstrates that CPAP can also lead to an improvement in hypertension, especially for patients with moderate to severe OSA.4
Postoperative Treatment for OSA
Data in the literature demonstrates subjective improvement in symptoms of OSA after bariatric surgery, including improvement in self-reported postoperative sleep quality and the reduction in daytime sleepiness. Improvement in validated quality of life scores was shown after bariatric surgery.7
Continuous pulse oximetry (in a critical care or step-down unit or by a dedicated, appropriately trained professional observer in the patient’s room) is felt to reduce the likelihood of complications among patients with OSA.8
Another report recommends continuous monitoring should be maintained for as long as patients remain at increased risk and for at least 3 hours beyond the standard observation time of their non-OSA counterparts.9
Postoperative use of CPAP should not be viewed as potentially adverse to outcomes following bariatric surgery due to any such concerns, and its use should be employed by bariatric surgeons based on the patient’s pulmonary status postoperatively. The risk of anastomotic complications is not increased by CPAP use in the immediate postoperative period following routine gastric bypass based on the existing literature.10 In fact, the risk for prolonged or repeat hospital stays is reduced with CPAP treatment.
Untreated OSA is a comorbidity observed with high prevalence in the bariatric patient population that leads to increased mortality and increased medical disability from several cardiovascular diseases.
Polysomnography is recommended prior to bariatric surgery to determine the if OSA is present and manage symptoms prior to surgery.
Appropriate follow up with a sleep medicine physician is needed to ensure postoperative compliance with CPAP treatment. Management of OSA after bariatric surgery can help aid in postoperative weight loss in the long term.
Click here to download a PDF of this case study.
1Young T, Palta M, Dempsey J, Skatrud J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230–1235.
2Bangura AS, Gibbs KE. Is routine preoperative polysomnography necessary in patients having bariatric surgery. ASMBS 2011; Abstract P-77.
3O’Keeffe T, Patterson EJ. Evidence supporting routine polysomnography before bariatric surgery. Obes Surg. 2004 Jan;14(1):23-6.
4Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;18(4):CD005308.
5Frey WC, Pilcher J. Obstructive sleep-related breathing disorders in patients evaluated for bariatric surgery. Obes Surg. 2003 Oct;13(5):676-83.
6Lettieri CJ, Eliasson AH, Greenburg DL. Persistence of obstructive sleep apnea after surgical weight loss. J Clin Sleep Med. 2008;4(4):333-8.
7Dixon JB, Schachter LM, O’Brien PE. Polysomnography before and after weight loss in obese patients with severe sleep apnea. Int J Obes (Lond). 2005;29(9):1048-54.
8Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: A report by the american society of anesthesiologists task force on perioperative management of patients with obstructive sleep apnea. Anesthesiology. 2006;104(5):1081-93.
9Schumann R, Jones SB, Cooper B, Kelley SD, Bosch MV, Ortiz VE, et al. Update on best practice recommendations for anesthetic perioperative care and pain management in weight loss surgery, 2004-2007. Obesity (Silver Spring). 2009;17(5):889-94.
10Ramirez A, Lalor PF, Szomstein S, Rosenthal RJ. Continuous positive airway pressure in immediate postoperative period after laparoscopic roux-en Y gastric bypass: Is it safe? Surg Obes Relat Dis. 2009;5(5):544-6.
Obstructive Sleep Apnea and Cardiovascular Disease
Sleep-related breathing disorders are highly prevalent in patients with established cardiovascular disease. Obstructive sleep apnea (OSA) affects an estimated 22 million adult Americans1 and is present in a large proportion of patients with hypertension and in those with other cardiovascular disorders, including coronary artery disease, stroke, tachycardia, cardiac arrhythmias, congestive heart failure and atrial fibrillation.2
Quantity and quality of sleep show secular trends alongside changes in modern society, reducing the average duration of sleep across westernized populations with increased reporting of fatigue, tiredness, and excessive daytime sleepiness. Too little or too much sleep are associated with adverse health outcomes, including hypertension and other cardiovascular disorders.3
Obstructive Sleep Apnea (OSA) and Cardiovascular Disease Correlation
Obstructive sleep apnea (OSA) is characterized by repetitive interruption of ventilation during sleep caused by collapse of the pharyngeal airway. A diagnosis of OSA is accepted when a patient has an apnea-hypopnea index (AHI; number of apneas and hypopneas per hour of sleep) >5 and symptoms of excessive daytime sleepiness.
Available data indicate that OSA prevalence is 2 to 3 times higher in patients with cardiovascular disease.4 Obstructive apneas may induce severe intermittent hypoxemia and CO2 retention during sleep, with oxygen saturation sometimes dropping to ≤60%, disrupting the normal structured autonomic and hemodynamic responses to sleep.5
The relationship between duration of sleep and vascular events is U-shaped, suggesting that different mechanisms may operate at either end of the distribution of sleep duration.6
In a systematic review of prospective population-based studies from 1966–2009, one study aimed to assess the relationship between duration of sleep and morbidity and mortality from coronary heart disease (CHD), stroke, and total cardiovascular disease (CVD).
This study showed an increased risk of developing or dying from CHD and stroke on either end of the distribution of sleep duration. Pooled analyses indicate that short sleepers have a greater risk of CHD and stroke than those sleeping 7–8 hours per night. Furthermore, long sleepers also show an increased risk for these events, confirming the presence of a U-shape association, with some heterogeneity among studies for CHD and CVD outcomes, no presence of publication bias, high statistical power, no difference between men and women, or by the duration of follow-up.7
Another respective study explored the incidence of CVD in a consecutive sleep clinic cohort of 182 middle-aged men (mean age, 46.8 ± 9.3; range, 30–69 years in 1991) with or without obstructive sleep apnea (OSA) throughout a period of seven years. The study concluded that the risk of developing CVD is increased in middle-aged OSA subjects independently of other risk factors like age, BMI, and smoking. Furthermore, the study concluded that efficient treatment of OSA reduces the excess CVD risk and may be considered also in relatively mild OSA without regard to daytime sleepiness.8
A systematic review of literature published in the Annals of Thoracic Medicine aimed to summarize a broad array of the pathophysiological mechanisms underlying the relationship between OSA and cardiac arrhythmias to assess the effects of OSA treatment on the presence of cardiac arrhythmias. The association between OSA and arrhythmias was first documented over 30 years ago. Since then, the literature has concluded that individuals with severe OSA were found to have two-to-fourfold higher odds of complex arrhythmias than those without OSA.9
Special emphasis should be given to recognizing the patient with cardiovascular disease who has coexisting sleep apnea to identifying strategies for co-management to best serve the patients needs. A board certified sleep medicine physician is best suited to work with you and your patients to determine an appropriate treatment plan.
SOMNAS and Allergy Sleep & Lung Care are dedicated to improving and maintaining the health status of our patients by providing compassionate, top-quality care. A patient’s special needs, concerns, and lifestyle, and those of their family, will guide our treatment planning. The care our patients receive with us will be on par with the highest national standards.
SOMNAS Sleep and wake disorders center offers state-of-the-art diagnostic options to identify specific sleep disorders and manage them using the latest treatments and therapies in an individualized treatment plan. Our office will work with your patients, communicating every step of the way for the overall health and wellbeing of your patients.
Click here to download a PDF of this case study.
1American Sleep Apnea Association.
2Caples S.M., Garcia-Touchard A., Somers V.K. (2007) Sleep-disordered breathing and cardiovascular risk. Sleep 30:291–303.
3Gangwisch JE, Heymsfield SB, Boden-Albala B, et al. Short sleep duration as a risk factor for hypertension: analyses of the first National Health and Nutrition Examination Survey. Hypertension 2006;47:833-839.
4Wolk R., Kara T., Somers V.K. (2003) Sleep-disordered breathing and cardiovascular disease. Circulation 108:9–12.
5Somers V.K., Dyken M.E., Mark A.L., Abboud F.M. (1993) Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med 328:303–307.
6Knutson KL, Turek FW. The U-shaped association between sleep and health: the 2 peaks do not mean the same thing. Sleep 2006;29:878-879.
7Francesco CP, Daniel C, Lanfranco D, et al. Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies. European Heart Journal 2001;1484-1492.
8Peker Y, Hedner J, Norum, J, et al. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med 2002;166:159–165.
9Ahmad Salah Hersi. Obstructive sleep apnea and cardiac arrhythmias. Ann Thorac Med. 2010 Jan-Mar; 5(1): 10–17.