Research Article, J Sleep Disor Treat Care Vol: 5 Issue: 2
Positive Airway Pressure Therapy for Sleep Disordered Breathing in Congestive Heart Failure is Associated with Reduction in Pulmonary Artery Systolic Pressure
| Tan M1, Tavela R1, Lee K1, Willes L2, Mather P1 and Sharma S1* | |
| 1Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, USA | |
| 2Willes Consulting group Inc, California, USA | |
| Corresponding author :Sharma S, MD FAASM, Associate Professor of Medicine, Director, Pulmonary Sleep Medicine, Associate Director, Jefferson Sleep Disorders Center, Thomas Jefferson University and Hospitals, 211 South Ninth Street, Suite 500, Philadelphia, PA 19107 USA Tel: 215 955 8285 Fax: 215 955 9783 Email: Sunil.Sharma@jefferson.edu |
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| Received: April 13, 2016 Accepted: May 19, 2016 Published: May 24, 2016 | |
| Citation: Tan M, Tavela R, Lee K, Willes L, Mather P, et al. (2016) Positive Airway Pressure Therapy for Sleep Disordered Breathing in Congestive Heart Failure is Associated with Reduction in Pulmonary Artery Systolic Pressure. J Sleep Disor: Treat Care 5:2. doi:10.4172/2325-9639.1000170 |
Abstract
Background: Sleep disordered breathing and pulmonary hypertension are both highly prevalent in patients with congestive heart failure (CHF). Since (SDB) has been shown to increase pulmonary pressures, we hypothesized that initiation of positive airway pressure (PAP) may reduce pulmonary artery systolic pressure (PASP) in compliant patients.
Methods: A total of 125 consecutive CHF patients admitted for decompensation were screened. Of these patients, 18 met inclusion criteria for the study which included a PASP ≥ 36 and polysomnogram-proven SDB. A repeat echocardiogram performed at mean 8 weeks post intervention was reviewed to compare PASP.
Results: There was no statistically significant difference in mean age, BMI, AHI, baseline PASP, and ejection fraction between the PAP-compliant group and PAP non-compliant group. A statistically significant mean reduction in PASP of 13.8 ± 7.0 mmHg (range: -25, -1) was observed in CHF patients with SDB who were compliant with PAP therapy, versus a mean increase of 0.9 ± 8.7 mmHg (range: -8, 15) in heart failure patients with SDB who were noncompliant with PAP therapy.
Conclusions: The findings suggest that PAP therapy is associated with improvement in pulmonary hypertension with congestive heart failure and sleep disordered breathing.
Keywords: Sleep disordered breathing; Congestive heart failure; Pulmonary hypertension; Echocardiogram; Positive airway pressure therapy
Keywords |
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| Sleep disordered breathing; Congestive heart failure; Pulmonary hypertension; Echocardiogram; Positive airway pressure therapy | |
Introduction |
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| Sleep-disordered breathing (SDB) is highly prevalent in patients with congestive heart failure (CHF) and confers an increased mortality risk in this set of patients [1]. Pulmonary hypertension (PH) is also a known risk factor for increased morbidity and hospitalizations in patients with CHF [1,2]. SDB can increase pulmonary pressures by various mechanisms including: constriction of pulmonary arterioles (due to nocturnal desaturation and hypercapnia), intermittent hypoxia, intrathoracic pressure swings, and by indirect contribution to systemic hypertension [3]. | |
| Positive airway pressure (PAP) therapy has been shown to improve hypopnea, apnea, cardiac function, and hemodynamic status in patients with SDB [4-7]. Based on the association between SDB and PH, we hypothesized that PAP therapy would have a salutary effect on pulmonary pressures in patients with SDB, CHF, and PH. | |
Methods |
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| This was a retrospective analysis of patients admitted to an academic tertiary care hospital from March 2013 to February 2014. The Thomas Jefferson University Institutional Review Board approved of prospective data collection. Subjects were consecutive patients admitted to the cardiology, internal medicine, and family practice services for decompensated CHF and found to have pulmonary artery systolic pressures (PASP) Equal to or > 36 mmHg by echocardiogram. This cohort was then screened for risk of SDB based on clinical analysis. Clinical assessment included the screening of patients using the STOP-BANG questionnaire (Appendix 1) and subsequent high resolution pulse-oximetry on patients with positive STOP-BANG (positive on 3 or more questions). This protocol has been validated for detecting obstructive sleep apnea (OSA) in hospitalized CHF patients in our prior publication. The STOPBANG questionnaire evaluates the risk factors for OSA and serves as a validated screening tool for OSA in preoperative clinics [8] and non-surgical populations [9]. Inclusion criteria for our study were polysomnogram (PSG)-proven SDB, PAP therapy with compliance data, and both pre- and post- intervention echocardiogram. | |
| Transthoracic echocardiography (TTE) was performed on all patients admitted for decompensated CHF using Phillips IE33 Ultrasound Systems (Andover, MA). Standard parasternal longand short-axis, apical 4- and 2-chamber, and sub-costal 4-chamber views were used. PASP is determined by estimating the trans-valvular pressure gradient between the RV and RA using the peak tricuspid regurgitatant velocity and adding an estimate of the RA pressure by evaluating the inferior vena cava [10]. PH is defined as dopplerestimated PASP of ≥ 36 mmHg [11]. | |
| SDB was defined as apnea-hypopnea index (AHI) of ≥ 5. AHI was calculated as the number of apneas plus hypopneas per hour of total sleep time, with hypopneas defined using a desaturation criterion of 4% [12]. A single, board-certified sleep physician interpreted the polysomnograms PSGs. | |
| PSG evaluations were conducted at the Jefferson Sleep Disorder Center, an AASM accredited facility, and included an electrocardiograph, electroencephalograph, continuous oronasal airflow recording (with a thermistor and a pressure transducer), chest wall and abdomen movement recording (using respiratory inductive plethysmography belts), trans-cutaneous oximetry, and chin electromyography (Comet AS 40 PSG, Grass Technologies; Warwick, RI, USA). Sleep was staged manually according to AASM scoring guidelines by a registered PSG technologist [13]. All patients had in-laboratory polysomnography and objective compliance data. | |
| Patients who met the criteria were educated on the use of PAP therapy and advised to use the device every night during sleep. All patients were on CPAP device with fixed pressures as titrated during the split-night protocol. | |
| Compliance with PAP intervention was defined as > 4 hours per night for 70% of the nights during a consecutive 30 day period during the initial 3 months of usage. Pre-intervention and post- PAP intervention PASP was measured by echocardiogram. PASP measurements were compared in both PAP-compliant and PAP non-compliant patients. The average time to the post-intervention echocardiogram was 35 weeks for the PAP-compliant and PAP noncompliant groups. | |
| Baseline characteristics were obtained for the compliant and non-compliant groups descriptively and with the sample size, mean, standard deviation and range where applicable. Baseline characteristics were compared between the groups using a two-sided t-test and Wilcoxon rank-sum test, as appropriate. Pre-therapy comorbid conditions were compared between the groups using a chisquare test or Fisher’s exact test, as appropriate. The change in PASP from pre- therapy to post-therapy was calculated and compared between PAP-compliant and PAP non-compliant groups using a two-sided t-test. An alpha of 0.05 was used for all comparative tests of statistical significance. | |
Results |
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| A total of 125 consecutive patients were admitted to the cardiology, internal medicine, and family practice service for decompensated CHF and found to have PASP ≥ 36 mmHg by echocardiogram. Of these 125 patients, 71% (89) were deemed to have potential risk of SDB based on clinical analysis. Of these remaining 89 patients, 34 did not keep their outpatient follow-up appointment, 22 refused further evaluation, 10 were discharged to rehabilitation, and 5 wanted to be evaluated at a sleep center closer to their home. Ultimately, 18 patients met inclusion criteria of polysomnogram PSG-proven SDB, PAP therapy with compliance data, and both pre- and post- intervention echocardiogram (Figure 1). | |
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Figure 1: Flow chart of consecutive patients admitted with decompensated CHF |
| The mean (range) age, BMI, AHI, and baseline PASP in the compliant group was 67 ± 11 years (50-81), 33 ± 7 kg/m2 (23-45), 28 ± 25 e/hr (5-78) and 60 ± 13 mmHG (48-90) versus 64 ± 12 years (42- 76), 36 ± 8 kg/m2 (26-46), 16 ± 17 e/hr (5-54), and 50 ± 12 mmHG (35-70) in the non-compliant group (Table 1). Severe valvular disease was not present in the PAP-compliant and PAP non-compliant groups. | |
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Table 1: Baseline characteristics of PAP therapy compliant and non-compliant patients. |
| There was no statistically significant difference in mean age, BMI, AHI, baseline PASP, and ejection fraction between the PAPcompliant group and PAP non-compliant group. Comorbid conditions including hypertension, type 2 diabetes, coronary artery disease, chronic obstructive lung disease, and chronic kidney disease were also similar in these cohorts. All patients were on optimal heart failure medication regimens and medical records indicated that they were compliant with their medications. | |
| A statistically significant mean reduction in PASP of 13.8 ± 7.0 mmHg (range: -25, -1) was observed in CHF patients with SDB who were compliant with PAP therapy, versus a mean increase of 0.9 ± 8.7 mmHg (range: -8, 15) in heart failure patients with SDB who were non-compliant with PAP therapy (p=0.001) (Figure 2). | |
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Figure 2: PASP in PAP therapy compliant and PAP therapy non-compliant patients. |
Discussion |
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| Our pilot study found an association between PAP compliance and reduced PASP (mean reduction of 13.8 mmHG) in patients with CHF, PH, and SDB. Our findings are consistent with prior reports on improvement of pulmonary pressures with PAP therapy [14]; however, no study in the past has specifically looked at PH in CHF. Our novel findings suggest that PAP may improve pulmonary hypertension in patients with CHF and SDB. | |
| Finding an effective treatment for PH in CHF is important since PH occurs commonly in patients with CHF and worsens overall prognosis [15-17]. While the prevalence of PH in CHF is not well documented, recent data demonstrates that up to 79% of patients with systolic CHF and 63% in diastolic CHF have PH, defined as mean pulmonary artery pressures of > 25 mmHG. The vast majority of the PH is of “passive type” from the passive increase in left-sided filling pressures; a minority (12%) may have “out- of proportion” PH, defined as diastolic pulmonary vascular gradient of > 7 mmHG [18]. Overall, PH in CHF portends poor prognosis and higher mortality. It is also a risk factor for increased mortality in CHF patients undergoing heart transplant [19,20]. | |
| Pathophysiologically, PH in CHF appears to present as passive congestion of the vasculature due to left heart dysfunction and elevated left ventricular filling pressures. Over time, chronic remodeling of the vascular and endothelial damage leads to irreversible changes in some susceptible patients. Medial hypertrophy of the muscular pulmonary vasculature has been observed in vascular lesions on autopsy [21]. Risk factors for the development of PH in patients with CHF appear to include the presence of mitral regurgitation and disease duration > 3 years [22]. Interestingly, low ejection fraction has not been found to be a risk factor [23]. | |
| Treatment of PH in patients with CHF has been elusive. An initial single-center study on the treatment of PH with pulmonary vasodilators showed a benefit for sildenafil in these patients, however, two subsequent randomized controlled trials found no significant impact of the pulmonary vasodilators on hemodynamics or symptoms [24,25]. | |
| OSA is a common disorder [26] and is known to be associated with both CHF [27] and PH [28]. OSA with PH has also been shown to have higher morbidity and mortality [29]. Treatment of OSA with continuous positive airway pressure therapy has been shown to improve pulmonary hemodynamics [30,31]. This improvement is noted most in patients with underlying diastolic dysfunction [31-33]. | |
| As discussed above, OSA may have significant hemodynamic consequences and play a causal role in pulmonary hypertension. The two conditions, PH and SDB are not only highly prevalent, but also most likely to negatively impact heart failure. Based on the hemodynamic influence of apneic events on pulmonary vascular hemodynamics, SDB treatment may have salutatory effects on PH in CHF. Our findings in CHF are consistent with prior data in non-CHF patients. Considering that almost 50% of the heart failure may be due to diastolic dysfunction with no effective therapy, these findings may signal new therapeutic options for PH in heart failure with preserved ejection fraction (HFpEF). | |
Limitations |
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| Our current study has some limitations. First, we used TTE to assess pressures, whereas right heart catheterization may be more accurate to assess right heart pressures. The TTE was used because it is a less invasive method and we were consistent with TTE use to record PASP pressures. Secondly, our study is limited as a retrospective analysis with a small sample size which may have led to selection bias and potential misclassification. Since the criteria for inclusion required both polysomnography testing and echocardiogram before and after the initiation of PAP therapy, a significant number of patients had to be excluded. | |
| However, considering the high prevalence of SDB in patients with CHF and PH, the impact on even a sub-segment of patients would still be clinically relevant | |
Conclusion |
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| The findings of our retrospective observational pilot study suggest that positive airway pressure therapy is associated with improvement in pulmonary hypertension with congestive heart failure and sleep disordered breathing. Larger, prospective studies to confirm this important clinical signal is recommended. | |
References |
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