Elsevier

Sleep Medicine

Volume 8, Issue 1, January 2007, Pages 51-59
Sleep Medicine

Original article
Effects of CPAP on left ventricular structure and myocardial performance index in male patients with obstructive sleep apnoea

https://doi.org/10.1016/j.sleep.2006.04.007Get rights and content

Abstract

Background

Obstructive sleep apnoea (OSA) has the potential to cause heart failure. We aimed to determine the effects of nasal continuous positive airway pressure (CPAP) therapy on left ventricular structure and myocardial performance index (MPI) in severe OSA patients.

Methods

Sixty-seven subjects without any cardiac or pulmonary disease had overnight polysomnography and echocardiography. In 33 males with severe OSA, thickness of interventricular septum (IVS) and posterior wall (LVPW) were measured by M-mode. Left ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/aortic ejection time by Doppler.

Results

Eight males were non-compliant with CPAP. Mean age was 47.9±8.2 years, and 20 of 25 patients (80.0%) were hypertensive. Patients had high body mass index (BMI: 31.0±3.9 kg/m2), but there was no change in BMI from baseline after 6 months. Thickness of IVS (11.0±1.1 mm) and LVPW (11.0±1.0 mm) at baseline were significantly decreased after 6 months of CPAP therapy (10.5±0.9 mm, P < 0.001 and 10.4±0.7 mm, P < 0.0001, respectively). Left ventricular MPI (60.1±13.8%) significantly decreased (53.0±10.7%, P < 0.0001) after CPAP usage.

Conclusions

In male patients with severe OSA, CPAP therapy significantly decreases left ventricular wall thickness and improves global function even with 6 months of usage.

Introduction

Obstructive sleep apnoea (OSA) might lead to cardiovascular complications such as heart failure (HF), myocardial infarction, arrhythmias, stroke and hypertension, all which increase morbidity and mortality [1], [2], [3], [4], [5], [6], [7]. Sleep apnoea is now recognized as an independent risk factor for hypertension [8]. Furthermore, OSA is closely associated with obesity [9] and aging [10].

Obstructive sleep apnoea contributes to the development of left ventricular hypertrophy (LVH), which is a major independent risk factor for morbidity and mortality from cardiovascular disease [11], [12]. The proposed causes include associated changes in left ventricular afterload, intermittent hypoxemia and recurrent arousals during sleep. It was shown that many subjects with LVH have normal blood pressure (BP), suggesting that factors other than hemodynamic overload may contribute to the hypertrophy [13]. Regression of LVH has favorable prognostic implications for reduction of cardiovascular events [14].

Diastolic dysfunction precedes left ventricular systolic impairment and accounts alone for about 30–40% of patients with left ventricular failure [15], [16]. Early recognition and appropriate therapy of left ventricular diastolic dysfunction is advisable to prevent further progression to HF and death [15], [16]. Since systolic and diastolic dysfunction frequently coexist, it was shown that a combined measure of left ventricular performance might be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone [17], [18]. The left ventricular myocardial performance index (MPI) reflects left ventricular systolic and diastolic functions (global function). In the presence of global dysfunction of the left ventricle, MPI increases in contrast to left ventricular ejection fraction (LVEF). MPI has previously been shown to be a sensitive indicator for symptomatic HF in a cross-sectional study [19]. In a recent study, it was shown that MPI provided important prognostic information for the risk of future congestive HF, beyond other measurements of cardiac function and traditional HF risk factors in elderly men [20]. MPI is a reproducible, widely applicable and simple non-invasive method for the estimation of left ventricular global function in patients.

Treatment of OSA by nasal continuous positive airway pressure (CPAP) has been shown to reduce BP [21], [22], and in patients with normal ventricular function it has been shown to prevent apnoea-related surges in muscle sympathetic activity and BP during sleep [23]. In contrast, we showed that CPAP therapy in patients with OSA and hypertension did not decrease systolic and diastolic BPs and heart rates (HR) acutely; however, it might reduce the variability of these parameters during sleep, though not during the day [24]. In patients with HF, the treatment of co-existing OSA reduces both nocturnal BP and HR [25]. Furthermore, randomised trials involving patients with HF have shown that treatment of co-existing OSA by CPAP improves daytime LVEF [26], [27].

In our previous study, we showed that increased apnoea–hypopnoea index (AHI) in the patients with OSA could result in left ventricular dysfunction [28]. In that study, a significant positive correlation was shown between MPI and severity of OSA. Since diastolic dysfunction might coexist with systolic dysfunction, especially severe OSA patients with diastolic dysfunction might have an increased risk of HF. It would also be important to resolve whether left ventricular dysfunction could be corrected by CPAP treatment aimed at reducing upper airway obstruction in patients with OSA.

In the present study, we aimed to determine the effects of nasal CPAP after 6 months of therapy on left ventricular structure and function (MPI) in male patients with severe OSA.

Section snippets

Study population

To be eligible all of the 92 subjects admitted to sleep clinic with symptoms of nocturnal snoring and/or excessive daytime sleepiness had to fulfill the following criteria: absence of (1) any known cardiac (except hypertension) and lung disease, (2) diabetes mellitus (DM), (3) angina pectoris, (4) atrial fibrillation or any arrhythmias, (5) chronic renal and hepatic diseases, and (6) serum electrolytes imbalances. A detailed sleep and cardiovascular history of the patients was recorded. Sleep

Results

The mean age of 25 compliant male patients was 47.9±8.2 years. None were using alcohol, and 72% were smoking cigarettes. Baseline characteristics of males with severe OSA are shown in Table 1. Study patients had high BMI (mean 31.0±3.9 kg/m2), and 20 of them (80.0%) were hypertensive. Antihypertensive therapy was re-arranged in 8 of 20 patients (40%) who had uncontrolled BP at baseline, but there were not any changes during the study. All hypertensive OSA patients (n = 20) had diastolic

Discussion

Patients with severe OSA often have coexisting disorders, which has been associated with increased LVM and diastolic dysfunction such as obesity [35], hypertension [36], and DM [37]. Arterial hypertension, evidence of LVH, high BMI, DM, and coronary artery disease (CAD) are independent predictors of left ventricular diastolic dysfunction. Especially severe OSA patients having diastolic dysfunction might have an increased risk of HF, since diastolic dysfunction might coexist with systolic

Conclusions

Sleep apnoea is usually associated with hypertension and obesity, which might cause LVH and left ventricular diastolic and systolic dysfunctions, so OSA patients are at increased risk for heart failure. Since the systolic and diastolic dysfunction frequently coexist, it was shown that a combined measure of left ventricular performance with the calculation of MPI might be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone. In severe OSA patients, CPAP

Study limitations

The small number of patients in our study population is an important limitation to determine the effects of CPAP on left ventricular structure and functions; also, our sleep clinic population may not reflect the findings in the general community. A larger population of study subjects would be helpful to determine the relative importance of such factors as BP, obesity, age, AHI, degree of hypoxemia, and presence or absence of 24-h hypertension in relationship to the presence of LVH and MPI.

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