Background: Previous studies have yielded disparate results regarding the effect of obstructive sleep apnoea (OSA) syndrome on left ventricular (LV) function. Objectives: In order to clarify this, we performed a prospective study investigating OSA patients with no history of systemic hypertension, coronary artery disease, myocardial, pericardial or valvular problems, asthma or chronic obstructive pulmonary disease before and after treatment with nasal continuous positive airway pressure (nCPAP). Methods: Fifteen patients (3 women, 12 men) with an apnoea/hypopnoea index >15 (mean ± SD = 52 ± 21) were studied with complete polysomnography, ambulatory blood pressure monitoring, M-mode two-dimensional echocardiography and pulsed Doppler echocardiography in two phases, i.e. before and after 12–14 weeks of nCPAP therapy. We measured systolic and diastolic blood pressure (BP) separately in the daytime and night-time, isovolumic relaxation time (IVRT), the ratio of peak early filling velocity (E) to peak late velocity (A) diastolic transmitral flow (E/A), posterior wall thickness (PWT) and septal thickness (IVST). The shortening fraction (SF) was also calculated. Eleven overweight non-apnoeic normal subjects matched for age were used as the control group. Results: Our results showed that the patient group exhibited, before treatment, LV diastolic, but not systolic, dysfunction compared with the normal group (IVRT = 94.3 ± 11.6 ms, p < 0.05; E/A = 0.94 ± 0.26, p < 0.02; SF = 39.9 ± 4.1%, not significant (NS); IVST = 9.9 ± 1.2 mm, NS; PWT = 8.3 ± 1.2 mm, NS). Moreover, the patient group developed diastolic hypertension both in the daytime and night-time (BP/diastolic/daytime = 93.3 ± 9.2 mm Hg, BP/diastolic/night-time = 90.3 ± 10.7 mm Hg). After 12–14 weeks of nCPAP treatment (no change in body mass index), significant improvement in LV diastolic function and a drop in blood pressure were noticed (IVRT = 85.6 ± 8.8 ms, p < 0.05; E/A = 1.07 ± 0.3, p < 0.05; BP/diastolic/daytime = 86.3 ± 5.5 mm Hg, p < 0.02; BP/diastolic/night-time = 83.9 ± 8.6 mm Hg, p < 0.05) in our patient group. Conclusions: We conclude that repetitive apnoeas/hypopnoeas are very important factors in the development of both LV diastolic dysfunction and diastolic systemic hypertension in patients with OSA syndrome. Treatment with nCPAP leads to significant improvement in both ventricular function and systemic hypertension.

Keywords:
Ventricular function, Obstructive sleep apnoea, Nasal CPAP
1.
Karam M, Wise RA, Natarajan TK, Permutt S, Wagner HN: Mechanism of decreased left ventricular stroke volume during inspiration in man. Circulation 1984;69:866–873.
2.
Laks L, Lehrhaft B, Grunstein RR, Sullivan CE: Pulmonary hypertension in obstructive sleep apnoea. Eur Respir J 1995;8:537–541.
3.
Millman RP, Redline S, Carliste CC, Assaf AR, Levinson PD: Daytime hypertension in obstructive sleep apnea. Prevalence and contributing risk factors. Chest 1991;99:861–866.
4.
Hedner J, Ejnell H, Caidahl K: Left ventricular hypertrophy independent of hypertension in patients with obstructive sleep apnoea. J Hypertens 1990;8:941–946.
5.
Krieger J, Laks L, Wilcox I, Grunstein RR, Costas LJ, McDougall JG, Sullivan CE: Atrial natriuretic peptide release during sleep in patients with obstructive sleep apnoea before and during treatment with nasal continuous positive airway pressure. Clin Sci (Colch) 1989;77:407–411.
6.
Quidry GG, Anderson W McD, Chesson AL Jr, Goel YS, Reed MD, Bairnsfather L, et al: Myocardial performance at rest and during exercise in patients with obstructive sleep apnea. Am Rev Respir Dis 1990;141:A373.
7.
Hanly P, Sasson Z, Zuberi N, Aldersson M: Ventricular function in snorers and patients with obstructive sleep apnea. Chest 1992;102:100–105.
8.
Nahmias J, Lao R, Karetzky M: Right ventricular dysfunction in obstructive sleep apnoea: Reversal with nasal continuous positive airway pressure. Eur Respir J 1996;9:945–951.
9.
Rechtschaffen A, Kales A: A Manual of Standardised Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects. Washington, National Institutes of Health, Publication No 204, 1968.
10.
Rokey R, Kuo LC, Zoghbi WA, Limacher MC, Quinones MA: Determination of parameters of left ventricular diastolic filling with pulsed Doppler echocardiography: Comparison with cineangiography. Circulation 1985;71:543–550.
11.
O’Brien E, Atkins N, O’Malley K: Defining normal ambulatory blood pressure. Am J Hypertens 1993;6:201S–206S.
12.
Lindberg E, Janson C, Svärdsudd K, Gislason T, Hetta J, Boman G: Increased mortality among sleepy snorers: A prospective population based study. Thorax 1998;53:631–637.
13.
Malone S, Liu P, Holloway R: Obstructive sleep apnoea in patients with dilated cardiomyopathy: Effects of continuous positive airway pressure. Lancet 1991;338:1480–1484.
14.
Gardin JM, Drayer JI, Rohan MK, et al: Doppler evaluation of left ventricular filling in mild and severe hypertension. J Am Coll Cardiol 1986;7:185–192.
15.
Pearson AC, Labovitz AJ, Mrosek D, Williams GA, Kennedy HL: Assessment of diastolic function in normal and hypertrophied hearts: Comparison of Doppler echocardiography and M-mode echocardiography. Am Heart J 1987;113:1417–1425.
16.
Buda AJ, Li Y, Brant D, Krause LC, Julius S: Changes in left ventricular diastolic filling during the development of left ventricular hypertrophy: Observations using Doppler echocardiography in a unique canine model. Am Heart J 1991;121:1759–1767.
17.
Inouye IK, Massie BM, Loge D, Simpson P, Tubau JF: Failure of hypertensive therapy with diuretic, beta-blocking and calcium channel-blocking drugs to consistently reverse left ventricular diastolic filling abnormalities. Am J Cardiol 1984;53:1583–1587.
18.
Mureddu GF, de Simone G, Greco R, Rosato GF, Contaldo F: Left ventricular filling pattern in uncomplicated obesity. Am J Cardiol 1996;77:509–514.
19.
Alpert MA, Terry BE, Mulekar M, Cohen MV, Massey CV, Fan TM, Panayiotou H, Mukerji V: Cardiac morphology and left ventricular function in normotensive morbidly obese patients with and without congestive heart failure, and effect of weight loss. Am J Cardiol 1997;80:736–740.
20.
Yu CM, Sanderson JE: Right and left ventricular diastolic function in patients with and without heart failure: Effect of age, sex, heart rate, and respiration on Doppler-derived measurements. Am Heart J 1997;134:426–434.
21.
Konermann M, Sanner B, Klewer J, Kreuzer I, Laschewski F, Burmann-Urbanek M: Modification of cardiopulmonary performance parameters in patients with obstructive sleep apnea treated with nCPAP therapy (in German). Wien Med Wochenschr 1996;146:340–343.
22.
Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA: Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model. J Clin Invest 1997;99:106–109.
23.
Lies A, Nabe B, Pankow W, Kohl FV, Lohmann FW: Hypertension and obstructive sleep apnea. Ambulatory blood pressure monitoring before and with nCPAP therapy. Z Kardiol 1996;85(suppl 3):140–142.
24.
Davies RJO, Vardi-Visy K, Clarke M, Stradling JR: Night-time blood pressure in obstructive sleep apnoea, snoring and normal sleep (abstract). Thorax 1992;47:216–217.
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2000
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