Peripheral and central ventilatory responses in central sleep apnea with and without congestive heart failure

Given that the apnea-ventilation cycle length during central sleep apnea (CSA) with congestive heart failure (CHF) is approximately 70 s, we hypothesized that rapidly responsive peripheral CO(2) ventilatory responses would be raised in CHF-CSA and would correlate with the severity of CSA. Sleep studies and single breath and rebreathe hypercapnic ventilatory responses (HCVR) were measured as markers of peripheral and central CO(2) ventilatory responses, respectively, in 51 subjects: 12 CHF with no apnea (CHF-N), 8 CHF with obstructive sleep apnea (CHF-OSA), 12 CHF-CSA, 11 CSA without CHF ("idiopathic" CSA; ICSA), and 8 normal subjects. Single breath HCVR was equally elevated in CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (0.58 +/- 0.09 [mean +/- SE] and 0. 58 +/- 0.07 versus 0.23 +/- 0.06, 0.25 +/- 0.04, and 0.27 +/- 0.02 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Similarly, rebreathe HCVR was elevated in both CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (5.80 +/- 1.12 and 3.53 +/- 0. 29 versus 2.00 +/- 0.25, 1.44 +/- 0.16, and 2.14 +/- 0.22 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Furthermore, in the entire CHF group, single breath HCVR correlated with central apnea-hypopnea index (AHI) (r = 0.63, p < 0.001) and percentage central/total apneas (r = 0.52, p = 0.022). Rebreathe HCVR correlated with awake Pa(CO(2)) (r = -0.61, p < 0.001), but not with central AHI or percentage central/total apneas independent of its relationship with single breath HCVR. In conclusion, in subjects with CHF, raised central CO(2) ventilatory response predisposes to CSA promoting background hypocapnia and exposing the apnea threshold to fluctuations in ventilation, whereas raised and faster-acting peripheral CO(2) ventilatory response determines the periodicity and severity of CSA.     

Left Ventricular Dysfunction, Pulmonary Hypertension, Obesity, and Sleep Apnea

The purpose of this study was to determine the frequency of central and obstructive sleep apnea in adult patients who have echocardiographic evidence of left ventricular dysfunction and pulmonary hypertension. Subjects with left ventricular dysfunction, pulmonary hypertension (pulmonary artery systolic pressure >30 mm Hg) and no lung disease were evaluated for risk factors associated with pulmonary hypertension. Of eight eligible adults, six completed the study. Subjects were from suburban and inner city family practices. Spirometric assessment, pulse oximetry on room air, rheumatologic evaluation, polysomnography, and additional history were taken. All six subjects had sleep apnea (apnea-plus-hypopnea index, or AHI, 20): obstructive, central, or mixed. All were obese, and almost all the subjects had a restrictive pattern on spirometry, which is consistent with obesity. All had a pulmonary artery systolic blood pressure of 35 mm Hg or greater. None had daytime hypoxemia or collagen vascular disease, and none had ever used appetite suppressants. This study found a strong association between pulmonary hypertension and obstructive or central sleep apnea in obese patients with congestive heart failure (CHF). We propose that a pulmonary artery systolic pressure of 35 mm Hg or greater in ambulatory patients with CHF may signify an increased risk of sleep apnea.     

Tissue Doppler imaging evaluation of cardiac adaptation to severe pulmonary hypertension

Tissue Doppler imaging (TDI) was used to obtain additional insight into the cardiac adaptation to severe pulmonary arterial hypertension. Pulmonary hemodynamics and right and left ventricular function were investigated in 18 untreated patients, 12 with pulmonary arterial hypertension and 6 with chronic thromboembolic pulmonary hypertension. Fourteen age-matched healthy subjects served as controls for TDI measurements. Pulsed TDI was determined using atrioventricular planes and strain and strain rate along the right ventricular free wall, ventricular septum, and left ventricular lateral wall from 4-chamber apical views. Patients had early diastolic dysfunction, with decreased E-wave peak velocity and increased isovolumic relaxation time, both more important in the right than left ventricle. Compared with controls, strain and strain rate decreased along the right ventricular free wall with a midapical predominance (midbasal strain rate 1.7 +/- 0.6 vs 2.2 +/- 0.5; p = 0.02; midapical strain rate 0.9 +/- 0.9 vs 2.3 +/- 0.7; p <0.001), but were preserved along the left ventricular lateral wall. Tricuspid E-wave and isovolumic relaxation time (R = 0.62, p = 0.006), as well as midapical (r = 0.65, p = 0.004), but not midbasal, right ventricular strain and strain rate correlated with mean pulmonary artery pressures. In conclusion, cardiac function was abnormal in patients with severe pulmonary hypertension because of a combination of alterations in both diastolic and systolic right ventricular function and left ventricular diastolic function. Only right ventricular dysfunction correlated with pulmonary artery pressures.     

Ageing does not influence the sleep-related decrease in the hypercapnic ventilatory response.

In young people, a sleep-related reduction in the gain of the ventilatory chemoreflex feedback loop occurs; in the elderly, it has been reported that no sleep-related reduction occurs. A relatively high loop gain could contribute to periodic breathing and central sleep apnoea in the elderly. This study tested the hypothesis that ageing is associated with a reduction in the magnitude of the sleep-related decrease in the hypercapnic ventilatory response (HCVR). The HCVR was measured using a steady state method, awake and asleep, in groups (n = 10) of elderly (66-81 yrs) and young (23-35 yrs) nonapnoeics. Upper airway resistance was maintained close to wakefulness levels using continuous positive airway pressure (mean sleep-related increase in resistance: elderly 1.6 +/- 1.2 cmH2O L x s(-1), young 1.2 +/- 0.8 cmH2O x L x s(-1)). The sleep-related decrease in the HCVR was similar in the elderly and young groups (elderly: wake 0.14 +/- 0.06 and sleep 0.06 +/- 0.02 L min(-1) x kPa and young, wake 0.19 +/- 0.07 and sleep 0.10 +/- 0.04 L x min(-1) x kPa). Ageing per se was shown not to change the magnitude of the sleep-related decrease in hypercapnic ventilatory response. The authors speculate that age-related changes in the hypercapnic ventilatory response are unlikely to contribute to the increased prevalence of central sleep apnoea in the elderly.     

Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study.

AIMS: We tested the hypothesis that: (i) obstructive sleep apnoea (OSA) by itself originates pulmonary hypertension (PH); and (ii) the application of continuous positive airway pressure (CPAP) can reduce pulmonary pressure. METHODS AND RESULTS: In this randomized and cross-over trial, 23 middle-aged OSA (apnoea-hypopnoea index, 44.1 +/- 29.3 h(-1)) and otherwise healthy patients and 10 control subjects were included. OSA patients randomly received either sham or effective CPAP for 12 weeks. Echocardiographic parameters, blood pressure recordings, and urinary catecholamine levels were obtained at baseline and after both treatment modalities. At baseline, OSA patients had higher pulmonary artery systolic pressure than control subjects (29.8 +/- 8.8 vs. 23.4 +/- 4.1 mmHg, respectively, P = 0.036). Ten out of 23 patients [43%, (95% CI: 23-64%)] and none of the control subjects had PH at baseline (P = 0.012). Two patients were removed from the study because of inadequate CPAP compliance. Effective CPAP induced a significant reduction in the values for pulmonary systolic pressure (from 28.9 +/- 8.6 to 24.0 +/- 5.8 mmHg, P < 0.0001). The reduction was greatest in patients with either PH or left ventricular diastolic dysfunction at baseline. CONCLUSION: Severe OSA is independently associated with PH in direct relationship with disease severity and presence of diastolic dysfunction. Application of CPAP reduces pulmonary systolic pressure levels.     

Echocardiographic estimation of pulmonary artery pressure in transposition of the great arteries

To determine their usefulness in estimating pulmonary artery pressure, left ventricular systolic time intervals (STI) were determined by echocardiography in 65 patients with dextro-transposition of the great arteries (TGA). The STI were measured from recordings of pulmonary valve motion at 100 mm/sec paper speed. The pre-ejection period (PEP) and the ratio of PEP to left ventricular ejection time (PEP/LVET) were directly related to pulmonary artery pressure. The strongest correlations were that between PEP/LVET and pulmonary artery diastolic pressure (r = 0.70) and that between PEP/LVET and the ratio of mean pulmonary pressure to mean systemic pressure (r = 0.71). A value of PEP/LVET of less than 0.26 was consistently associated with pulmonary artery diastolic pressures of less than 20 mm Hg and, in 28 of 31 patients, pulmonary artery pressure less than one-third of mean systemic arterial pressure. Pulmonary hypertension was present in 18 of 22 patients with PEP/LVET of 0.30 or greater; elevated PEP/LVET was also present in four patients with abnormalities of cardiac rhythm or conduction, two of whom also had angiographic evidence of myocardial dysfunction.     

脉压指数与原发性高血压左心室功能的相关性研究

目的探讨脉压指数（PPI）与原发性高血压患者左心室功能损害程度的关系。方法178例经外周肱动脉压力测定收缩压（sBP）、舒张压（DBP）,以PPI〉0．40、PPI≤0．40分组,两组进行分析。比较两组左心形态、左心室收缩功能和舒张功能情况。结果PPI〉0．40组左心房内径明显增大[PPI〉0．40、PPI≤0．40的LAD分别为（35．02±3．15）mm、（28．05±2．01）mm,P〈0．05];左心室内径无明显改变（P〉0．05）;室间隔、左心室后壁明显增厚,E／A值降低（P〈0．05）,而左心室射血分数差异无统计学意义（P〉0．05）。结论原发性高血压患者左心室舒张功能异常出现早于左心室收缩功能异常,PPI〉0．40提示高血压患者早期合并有舒张功能异常。     

Right ventricular diastolic pressure in coronary artery disease

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P < 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P < 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P < 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.     

脉压指数与原发性高血压左心室舒张功能相关性研究

目的探讨脉压指数(PPI)与原发性高血压患者左心室舒张功能损害程度的关系。方法162例经外周肱动脉压力测定收缩压(SBP)、舒张压(DBP)以PPI≤0.40、>0.40分组,2组进行分析。比较2组左心形态、左心室收缩功能和舒张功能情况。结果PPI>0.40组左心房内径明显增大(P<0.000 5);左心室内径无明显改变(P>0.05);室间隔、左心室后壁明显增厚,E/A值降低(P<0.0005),而左心室射血分数差异无显著性(P>0.05)。结论对于原发性高血压患者左心室舒张功能异常出现早于左心室收缩功能异常,PPI>0.400提示高血压患者早期合并有舒张功能异常。     

Hemodynamic characterization of patients with severe emphysema

In 120 patients with severe emphysema evaluated for participation in the National Emphysema Treatment Trial, pulmonary hemodynamics and ventricular function were assessed. Pulmonary function tests were (%predicted): FEV(1) = 27%; residual volume = 224.6%; diffusion capacity = 26.7%. In 90.8% of patients, end-expiratory pulmonary artery mean pressure was > 20 mm Hg; in 61.4%, end-expiratory wedge pressure was > 12 mm Hg. Cardiac index was normal. Mean pulmonary artery pressure correlated inversely with arterial PO(2), and severity of emphysema, and directly with wedge pressure. Multiple stepwise regression revealed that arterial PO(2) was not an independent predictor of mean pulmonary artery pressure. No correlation was found between indices of emphysema severity and PA pressures. Diastolic ventricular pressures were increased without evidence of systolic dysfunction. We conclude that (1) elevations of pulmonary vascular pressures are common, (2) pulmonary hypertension may be related to factors other than hypoxia, (3) pulmonary hypertension does not impair resting systemic O(2) delivery, and (4) elevated cardiac diastolic pressures do not represent systolic dysfunction.     

A case of left main systolic compression caused by a dilated pulmonary artery in a patient with congenital pulmonic stenosis

Dynamic compression of the left main coronary artery during systole is extremely rare. We report a case of a 29-year old female who presented with shortness of breath and chest pain with exertion. She had a history of congenital pulmonic stenosis and had a pulmonary valve resection at age 2. She subsequently developed chronic pulmonic insufficiency. She had normal left ventricular systolic function and a dilated right ventricle with pressure and volume overload diagnosed by echocardiography. She had pulmonary artery hypertension with pulmonary artery pressures noted to be systolic of 62mmHg, diastolic of 10 mmHg, mean of 29 mmHg on right heart catheterization. Her echocardiogram also showed an elevated mean pulmonary artery pressure of 25 mmHg, which was thought to be due to increased flow. On left heart catheterization, she was found to have dynamic systolic compression of the left main coronary artery by a dilated pulmonary artery. This is the first case report of a patient with congenital pulmonic stenosis with a dilated pulmonary trunk causing systolic compression of the left main coronary artery. Dynamic systolic compression of the left main coronary artery is a rare cause of angina, is rarely reported, and requires a high level of suspicion and careful investigation for accurate diagnosis.     

Isolated aortic stenosis with severe pulmonary hypertension

Severe pulmonary hypertension is rare in patients with aortic stenosis. When present, it usually implies either associated mitral valve disease, poor left ventricular function, or pulmonary disease. In this case report, severe pulmonary hypertension was present in a patient with isolated aortic stenosis and normal left ventricular systolic function. Pulmonary hypertension was probably related to left ventricular diastolic dysfunction. Following successful aortic valve replacement, pulmonary pressures declined but symptoms of shortness of breath persisted and the patient still required daily diuretics.     

Right ventricular failure in patients with preserved ejection fraction and diastolic dysfunction: an underrecognized clinical entity

It is well recognized that patients with severe left ventricular (LV) systolic dysfunction develop pulmonary venous hypertension or postcapillary pulmonary hypertension, which leads to an increase in pulmonary vascular resistance (PVR) and right ventricular (RV) systolic failure. It is often underrecognized, however, that patients with heart failure with preserved LV ejection fraction and diastolic dysfunction may also develop postcapillary pulmonary hypertension with elevated PVR leading to RV systolic failure. This form of biventricular failure is a result of diastolic failure on the left in patients with preserved LV ejection fraction and systolic failure on the right. At this time, there are no randomized trials or guidelines addressing the management of patients with diastolic heart failure with and without resultant RV failure. The authors review the pathophysiology, clinical presentation, and suggested treatment of this underrecognized clinical entity.     

Heart failure with normal ejection fraction

Opinion statement Heart failure with normal ejection fraction, also known as diastolic heart failure, is a major problem for patients and health-care providers and is a substantial expense to society. The main pathophysiologic processes involved are increased left ventricular stiffness and abnormal relaxation, with resulting impaired left ventricular filling. These processes typically displace the pressure-volume relationship in an upward direction, resulting in increased left ventricular end-diastolic, left atrial, and pulmonary capillary wedge pressures, leading to symptoms of pulmonary congestion. The most common clinical disorders leading to diastolic heart failure are 1) hypertension with concentric left ventricular hypertrophy, 2) coronary artery disease with decreased left ventricular compliance, 3) hypertrophic cardiomyopathy, and 4) aortic stenosis with concentric left ventricular hypertrophy. Echocardiography and cardiac catheterization with magnetic resonance imaging hold promise as future diagnostic tools. The approach to the treatment of diastolic heart failure is focused on four treatment goals: 1) persistent control of elevated blood pressure, with regression of left ventricular hypertrophy, 2) careful reduction of central blood volume (diuretics), 3) maintenance of atrial contraction and control of heart rate (beta-blockers, digoxin, atrioventricular pacing); and 4) improvement of left ventricular relaxation. There is currently no drug treatment specific for abnormal relaxation, although efforts are being made to develop such compounds. A promising future therapy includes agents that lyse advanced glycation end-products as an approach to relieving increased ventricular stiffness. In addition to pharmacotherapy, maintaining ideal body weight and a regular exercise program are also helpful in the treatment of diastolic heart failure. Although the overall prognosis of patients with diastolic dysfunction is more favorable than that of patients with systolic dysfunction, the frequency of treatment failure and recurrent symptoms underscores the need for further improvement in treatment of this condition.     

Left ventricular function in persistent pulmonary hypertension of the newborn. Computer analysis of the echocardiogram.

Regional and global left ventricular function was assessed in 23 neonates with persistent pulmonary hypertension using computer assisted analysis of their left ventricular echocardiograms and compared with that in 50 healthy neonates. End diastolic left ventricular dimension was normal and end systolic dimension increased while percentage left ventricular shortening and peak velocity of circumferential fibre shortening decreased indicating impaired systolic performance. The peak rate of increase in left ventricular diameter in early diastole was significantly decreased and the durations of the rapid filling and isovolumic relaxation periods were prolonged suggesting resistance to left ventricular filling due to changes in diastolic myocardial properties. This abnormal left ventricular cavity function may have been due to a combination of increased diastolic wall thickness, reduced percentage systolic wall thickening, increased relative wall thickness, and pronounced reduction in peak rates of systolic wall thickening and diastolic wall thinning Seven neonates with persistent pulmonary hypertension died, and of the three examined at necropsy all had left ventricular hypertrophy and two extensive subendocardial haemorrhage and infarction affecting the right and left ventricular papillary muscles. Thus left ventricular dysfunction appears to be a common feature in neonates with this disorder and may be readily detected using computer analysis of left ventricular echocardiograms. Unfortunately, no single echo measurement was useful prognostically. Left ventricular dysfunction in persistent pulmonary hypertension probably results from a combination of hypoxaemia, acidaemia, and pulmonary hypertension, and although it may contribute to the high mortality in this syndrome, a correlation between the severity of left ventricular dysfunction and clinical outcome could not be shown.     

Left ventricular function in persistent pulmonary hypertension of the newborn. Computer analysis of the echocardiogram

Regional and global left ventricular function was assessed in 23 neonates with persistent pulmonary hypertension using computer assisted analysis of their left ventricular echocardiograms and compared with that in 50 healthy neonates. End diastolic left ventricular dimension was normal and end systolic dimension increased while percentage left ventricular shortening and peak velocity of circumferential fibre shortening decreased indicating impaired systolic performance. The peak rate of increase in left ventricular diameter in early diastole was significantly decreased and the durations of the rapid filling and isovolumic relaxation periods were prolonged suggesting resistance to left ventricular filling due to changes in diastolic myocardial properties. This abnormal left ventricular cavity function may have been due to a combination of increased diastolic wall thickness, reduced percentage systolic wall thickening, increased relative wall thickness, and pronounced reduction in peak rates of systolic wall thickening and diastolic wall thinning Seven neonates with persistent pulmonary hypertension died, and of the three examined at necropsy all had left ventricular hypertrophy and two extensive subendocardial haemorrhage and infarction affecting the right and left ventricular papillary muscles. Thus left ventricular dysfunction appears to be a common feature in neonates with this disorder and may be readily detected using computer analysis of left ventricular echocardiograms. Unfortunately, no single echo measurement was useful prognostically. Left ventricular dysfunction in persistent pulmonary hypertension probably results from a combination of hypoxaemia, acidaemia, and pulmonary hypertension, and although it may contribute to the high mortality in this syndrome, a correlation between the severity of left ventricular dysfunction and clinical outcome could not be shown.     

Left ventricular diastolic dysfunction in patients with COPD in the presence and absence of elevated pulmonary arterial pressure

BACKGROUND: Increased right ventricular afterload leads to left ventricular diastolic dysfunction due to ventricular interdependence. Increased right ventricular afterload is frequently present in patients with COPD. The purpose of this study was to determine whether left ventricular diastolic dysfunction could be detected in COPD patients with normal or elevated pulmonary artery pressure (PAP). METHODS: Twenty-two patients with COPD and 22 matched control subjects underwent pulsed Doppler echocardiography. Left ventricular systolic dysfunction and other causes of left ventricular diastolic dysfunction (eg, coronary artery disease) were excluded in all patients and control subjects. PAP was measured invasively in 13 patients with COPD. RESULTS: The maximal atrial filling velocity was increased and the early filling velocity was decreased in patients with COPD compared to control subjects. The early flow velocity peak/late flow velocity peak (E/A) ratio was markedly decreased in patients with COPD compared to control subjects (0.79 +/- 0.035 vs 1.38 +/- 0.069, respectively; p < 0.0001), indicating the presence of left ventricular diastolic dysfunction. The atrial contribution to total left diastolic filling was increased in patients with COPD. This was also observed in COPD patients with normal PAP, as ascertained using a right heart catheter. The atrial contribution to total left diastolic filling was further increased in COPD patients with PAP. PAP correlated with the E/A ratio (r = -0.85; p < 0.0001). CONCLUSIONS: Left ventricular diastolic dysfunction is present in COPD patients with normal PAP and increases with right ventricular afterload.     

Cardiovascular diseases in obstructive sleep apnea

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.     

Left ventricular diastolic function in systemic sclerosis

OBJECTIVE: To assess left ventricular diastolic function in patients with systemic sclerosis (SSc) and to verify if a "primary" diastolic dysfunction might exist. METHODS: In total 124 patients and 41 healthy subjects underwent complete echocardiographic examination. The following pulsed wave Doppler variables were evaluated: peak velocity during early filling (E), peak velocity during late atrial filling (A), E/A ratio, and early filling deceleration time. RESULTS: Seventy-seven patients (62.1%) had conditions potentially affecting left ventricular diastolic function (Group A) and 47 patients (37.9%) formed a homogeneous group without cardiac involvement or other causes of abnormal diastolic function (i.e., systemic and/or pulmonary hypertension, ventricular hypertrophy, pericardial disease, systolic dysfunction, valvular heart disease, coronary artery disease) (Group B). The entire SSc population and Group A showed significant differences in the Doppler variables of diastolic function compared to the control group. No significant differences were found between Group B and controls. CONCLUSION: In patients with SSc, left ventricular diastolic dysfunction was found only in patients with conditions potentially affecting left ventricular diastolic function. In patients without conditions potentially affecting left ventricular diastolic function no differences were seen in comparison with controls. SSc does not seem to cause "primary" diastolic abnormalities.     

Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index

BACKGROUND: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. OBJECTIVES: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. METHODS: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5-14, n = 11), and group 3: moderate-severe OSA (AHI > or = 15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. RESULTS: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 +/- 0.9, 6.9 +/- 1.0, 7.1 +/- 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 +/- 0.18) than in group 2 patients (0.50 +/- 0.10), and group 1 patients (0.48 +/- 0.08, p < 0.001). CONCLUSIONS: It was suggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.