Introduction

Sleep Breathing Disorders (SBD) include Central Sleep Apnea Syndrome (CSA), Cheyne-Stokes respiration (CSR) and Obstructive Sleep Apnoea Syndrome (OSAS) and are alterations of normal breathing occuring during sleep. The association between SBD and Heart Failure (HF) is widely reported in literature [1], with a prevalence reaching 75% in Heart Failure with Reduced Ejection Fraction (HFrEF). In particular, CSA prevalence ranges between 25% and 40% in HFrEF and it’s related to increased mortality and adverse prognosis through different mechanisms still not well understood [2]. First of all, contrasting apnoic and hypopnoic events generates an inspiratory effort, which modifies intrathoracic pressure and haemodynamics, resulting in an augmented myocardial oxygen request, alterations of cardiac chambers volumes and a reduced cardiac output. Concurrently intermittent hypoxia combined with repeated arousals, causes sympathetic nervous system hyperactivation, further worsening haemodynamics. Even without sufficient evidencies on prevalence and association of SBD with HF and valvulopathies, data about the impact of surgical correction of mitral valve disease on SBD, in particular on CSA are encouraging [3] and corroborating our suggestion to screen SBD patients with HF and valvulopathies.

Case Report

We present the case of a 75 years-old man who was admittesd to our department complaing of ingravescent dyspnea (NYHA II-III). He had an history of dilated cardiomyopathy (DCM), pacemaker-implantable cardioverter-defibrillator (PM-ICD) implanted after an acute myocardial infarction (AMI) (treated with PTCA and stents on anterior interventricular artery and left coronary), chronic obstructive pulmonary disease (COPD), nocturnal respiratory failure secondary to OSAS on CPAP and O₂ therapy at 2 L/min. Our first approach evaluating the patient involved: chest X-Rays (negative), EGA (normal blood gas values) and ecocardiography. Ecocardiography highligted a reduction of EF from 42% to 33% Simpson, worsened mitral valve insufficiency (from moderate to severe), left atrial enlargement and increased PAPS (from 40 to 55 mmHg), when compared to the last one (Figures 1A-1C). So we decided to optimize medical treatments for HFrEF and record a new cardiorespiratory polygraphy exam (PG) in basal condition. Nocturnal respiratory failure was confirmed: TC90 60,1%; ODI >3% 88/h; average SpO₂ 89% (Figure 2). Severe CSA with CSR was diagnosed with an number of apnoic/hypopnoic events (AHI) of 87,8/h. According to AASM guidelines, ventilation mode has been changed to BILEVEL PSV (IPAP min-max 13-18 cmH₂O, EPAP 7 cmH₂O) keeping O₂ therapy at 2L/min. Ater one week there was a reduction in AHI (AHI 12/h) and resolution of nocturnal respiratory failure (TC90 4.5%). Due to functional mechanism of mitral insufficiency, we requested a cardiological consult to evaluate the need of a percutaneous treatment of the underlying mitral insufficiency (MitraClip^®). After one month, the patient underwent MitraClip®, with notable reduction of symptoms (NYHA I-II). Three months later even echocardiographic parameters improved  (Figures 3A and 3B). One year later, the patient was hospitalized for COPD exacerbation and treated with antibiotic therapy. After the resolution of the acute state, we recorded a nocturnal oximetry on NIV and O₂ therapy at 2L/min, to test the efficacy of past prescribed therapy demonstrating not only the persistance but a further improvement of previously achieved benefits (TC90 from 60.1% to 1.4%, ODI> 3% from 88/h to 18.6/h, SpO2 average from 89% to 94%). After three months, the patient (as his symptoms further regressed) autonomously chose to lower O₂ therapy to 1,5 L/min and to interrupt NIV. A new PG in O₂ therapy at 1.5 L/ min was recorded, showing a reduction in AHI 9.2/h, stable valuse for TC90, ODI> 3 and average SpO2 % (Figure 4). EGA in O₂ therapy at 1,5 L/min: pH 7.42, PCO2 38 mmHg, PO2 81.5 mmHg, SpO2 97%. The clinical and instrumental evolution led us to descharge the patient prescribing only O₂ therapy at 1,5 L/min, deeming NIV no longer necessary.

Discussion

CSA can develop through two different mechanisms: an increased sensitivity of the chemoreceptor centers (controller gain), showing an hyperventilatory response even for modest increases in nocturnal PaCO₂, with subsequent hypocapnia and ventilatory drive suppression leading to apnea/hypopnea events; an increased circulatory time (feedback delay) in which apnea-induced-hypercapnia stimulates central chemoreceptors at a slower rate, delaying ventilation resumption. This situation can also be exacerbated by overload volume, as in the case of our patient [4].These two phenomena can occur in HF, stroke, opiates use and brainstem diseases. Finally, in HF and valvulopathies, lung vascular congestion triggers the juxtacapillary receptors (J receptors), increasing hyperventilation and worsening apneas. Therefore, to reduce apnoic/hypopnoic episodes, it is crucial to normalize the circulatory time by improving cardiac output and reducing volume overload, through medical and when feasible, percutaneous or surgical therapy. Oxygen therapy, in conditions of normal circulatory time, can contribute to reduce central apneas by decreasing chemoreceptor centers sensitivity.

This clinical case documents the need of a multidisciplinary approach to patients with HF and respiratory diseases and highlights the usefulness of PG in patients with mitral insufficiency elegible for MitraClip^®. The presence of CSR and the severity of CSA could suggest the need for early treatment of even moderate and/or paucisymptomatic mitral insufficiency.

Figures

References

1. Paulino A, Damy T, Margarit L, Stoïca M, Deswarte G, et al. (2009) Prevalence of sleep-disordered breathing in a 316-patient French cohort of stable congestive heart failure. Archives of Cardiovasc Diseases 102: 169-175.
2. Cowie MR, Woehrle H, Wegscheider K, Angermann C, d'Ortho M, et al. (2015) Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure. N Eng J Med 373: 1095-1105.
3. Abe H, Takahashi M, Yaegashi H, Eda S, Kitahara H, et al. (2009) Valve repair improves central sleep apnea in heart failure patients with valvular heart diseases. Circul Journal. 73: 2148-2153.
4. Berssenbrugge A, Dempsey J, Iber C, Skatrud J, Wilson P (1983) Mechanisms of hypoxia-induced periodic breathing during sleep in humans. J Physiol 343: 507-524.