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Obstructive sleep apnea (OSA) is an independent risk factor for hypertension and cardiovascular disease. OSA is the frequent underlying disease of secondary hypertension and resistant hypertension. In 2003, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure recognized sleep apnea as a common and identifiable cause of hypertension and suggested blood pressure screening among patients with OSA. OSA increases both daytime and nocturnal ambulatory blood pressures through the activation of various neurohumoral factors including the sympathetic nervous system and the renin-angiotensin-aldosterone system. Randomized, controlled trials have evaluated the use of continuous positive airway pressure (CPAP) to reduce BP among persons with OSA. The benefits of OSA treatment are related to implications for hypertension management.

Obstructive sleep apnea (OSA) is strongly associated with hypertension. The seventh report of the joint national committee (JNC-VII) guidelines have placed OSA at the top of the list to induce secondary hypertension. Severe OSA patients revealed the high prevalence of hypertension. Compared with normal subjects, patients with OSA had a higher 24-hour blood pressure, especially nighttime blood pressure. More recently, prospective data showed that sleep apnea syndrome was an independent risk for onset of hypertension. There is a lot of evidence that demonstrates that treating OSA using continuous positive airway pressure (CPAP) is an effective for management of OSA.

Objectives: To develop a measure for disease-specific health-related quality of life in patients with heart failure and examine its reliability and validity., Methods: One hundred and four patients with stable chronic heart failure (74 males, 30 females, mean age 64.2 +/- 10.0 years) with left ventricular ejection fractions of less than 40% were enrolled in this study. Each patient responded to the Medical Outcomes Study Short Form 36 (SF-36) and a disease specific questionnaire comprising four categories (dyspnea, sleep, appetite and fatigue), each consisting of five to six questions. A stepwise exploratory factor analysis was applied to the disease-specific measure to consider categorical fitness. In 25 of the 104 patients, the data in the questionnaire were compared with peak oxygen uptake, anaerobic threshold, slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO2 slope) and peak work rate. Correlations between the questionnaire and eight components of SF-36 were evaluated., Results: The appetite category proved unreliable and was excluded from consideration, so 12 questions were adopted from the other three categories. Cronbach's a values ranged from 0.68 to 0.89 and the coefficients of test-retest were from 0.84 to 0.94, so both internal consistency and reproducibility of these questions were considered excellent. The scores of three categories well reflected the severity of heart failure based in New York Heart Association functional class. The anaerobic threshold (r = 0.53), peak oxygen uptake (r = 0.66), VE/VCO2 slope (r = -0.48) and peak work rate (r = 0.41) correlated with the total score of the 12 questions. The total scores were closely correlated with the eight components of SF-36., Conclusions: This study suggests that the disease-specific questionnaire is applicable to evaluation of the health-related quality of life in patients with heart failure.

Objectives: Physical training in cardiac patients can increase exercise capacity and reduce plasma brain natriuretic peptide(BNP) concentration, but these effects may depend on the etiology of cardiac disease. The change in exercise capacity and BNP during the training period were investigated in patients with different cardiac diseases., Methods: Ninety-one patients after coronary artery bypass grafting(CABG) and 78 patients after valve replacement (VR) underwent a symptom-limited incremental cardiopulmonary exercise test before (1 month) and 6 months after physical training. Anaerobic threshold and peak oxygen uptake(peak-Vo2) were measured during the cardiopulmonary exercise test. Before each cardiopulmonary exercise test, a blood sample was obtained in the resting condition for measuring BNP., Results: Anaerobic threshold and peak-Vo2 were increased significantly from 1 month to 6 months in both groups. BNP in the CABG group indicated a tendency to decrease (194.6 +/- 155.3-->144.2 +/- 232.2 pg/ml, p < 0.1) from 1 month to 6 months. BNP in VR group was significantly decreased (159. 9 +/- 115.5-->112.8 +/- 131.7 pg/ml, p < 0.05) during the training period. The CABG group showed a significant negative correlation between peak-Vo2 and BNP at 1 month(r = -0.28, p < 0.01) and at 6 months(r = -0.39, p = 0.001). The VR group showed a significant negative correlation between peak-Vo2 and BNP at 6 months(r = -0.32, p < 0.01), but not at 1 month., Conclusions: Six months of physical training in patients after cardiac surgery may improve exercise capacity and reduce BNP. BNP concentration in the VR group before physical training did not reflect functional capacity.

Objectives: This study investigated whether myocardial infarction patients with diabetes mellitus had lower heart rate reserve to exercise by measuring the increment in heart rate (HR) divided by the increment of norepinephrine (NE) concentration from rest to peak exercise (delta HR/log delta NE). The difference in exercise training effects was also investigated., Methods: The 148 patients after myocardial infarction were divided into two groups, the DM group (n = 34) and the non-DM group (n = 114). Cardiopulmonary exercise testing was performed in each subject at 1 and 3 months after the onset. Blood samples were taken at rest and immediately after peak exercise, rest brain natriuretic peptide, rest and peak norepinephrine were analyzed. Exercise training was performed from 1 to 3 months after the onset., Results: Resting heart rates were significantly higher in the DM group than in the non-DM group both at 1 and 3 months although peak heart rates were not significantly different. Peak oxygen uptake were lower in the DM group both at 1 and 3 months after onset of myocardial infarction compared to the non-DM group. End-tidal carbon dioxide pressure was lower and the rate of increase of minute ventilation to carbon dioxide output was higher in the DM group. Plasma brain natriuretic peptide was higher in the DM group. delta HR/log delta NE was 19.4 +/- 4.0 in the DM group and 22.2 +/- 5.6 in the non-DM group (p < 0.01), and increased in only the non-DM group. delta HR/log delta NE was more closely correlated with peak oxygen uptake in the DM group than in the non-DM group., Conclusions: Impaired response to exercise training may be caused, in part, by impaired heart rate reserve to exercise in patients with diabetes mellitus.

Objectives: Sympathetic heart rate response decreases in patients with left ventricular dysfunction. Angiotensin converting enzyme (ACE) inhibitors effectively prevent heart failure after myocardial infarction. However, the effect of ACE inhibitors on heart rate response is not well known. The present study investigated the effect of ACE inhibitors on sympathetic heart rate response in the early phase of acute myocardial infarction., Methods: Sixty-five patients with acute myocardial infarction receiving no beta-blocking agents participated in the study. The subjects consisted of 25 patients (mean age 60.2 +/- 10.7 years) treated with ACE inhibitor lisinopril from the initial stage and 40 control subjects (mean age 57.7 +/- 7.6 years). Cardiopulmonary exercise testing with a treadmill was performed using the ramp protocol in the first month and the third month after the onset of the disease. Heart rate (HR) was measured in the resting state (rest) and immediately after peak exercise (peak). At the same time, blood samples were obtained to investigate the changes in the plasma level of norepinephrine (NE). The degree of sympathetic heart rate response was evaluated as follows: (peak HR - rest HR)/¿(peak NE - rest NE)/rest NE¿ x 100., Results: There were no significant differences between the 2 groups in the first month in anaerobic threshold, peak oxygen uptake and plasma brain natriuretic peptide concentration. Though the change of heart rate was not significant, the change in the plasma level of norepinephrine was significantly lower in the lisinopril group (9.3 +/- 4.4 vs 5.7 +/- 2.8, p < 0.01). In the first month, the heart rate response in the control group was markedly lower than that in the lisinopril group (8.7 +/- 3.5 vs 15.2 +/- 8.5 beats/min/%, p < 0.01). In the third month, the significant difference between the 2 groups disappeared (10.7 +/- 7.9 vs 14.0 +/- 9.7 beats/min/%, NS) due to the increase of the value in the control subjects., Conclusions: From these results, we conclude that ACE inhibitors are effective to improve sympathetic heart rate response during exercise in the early phase of myocardial infarction.

Cardiac index is widely used as a parameter of cardiac function for cardiovascular patients, but its value is limited when measured in the resting supine position, because it never demonstrates the maximal cardiac index performance. The incremental increase in cardiac index (delta CI) was evaluated during incremental exercise (delta work rate: delta WR), delta CI/delta WR, in patients with chronic congestive heart failure, and compared to brain natriuretic peptide (BNP), which is known to be increased in patients with chronic left ventricular dysfunction. The subjects were 18 heart failure patients (16 males and 2 females, mean age [+/-SD] 63.8 +/- 8.9 years). Symptom-limited cardiopulmonary exercise test using cycle ergometer was performed. Cardiac index was calculated with the Benchmark Exercise Test device using oxygen uptake, carbon dioxide output and respired flow. Blood samples were taken in the resting state before the exercise test. A positive correlation was obtained between delta CI/delta WR and peak oxygen uptake (peak VO2) (r = 0.71, p < 0.01), and delta CI/delta WR and peak oxygen pulse (r = 0.66, p < 0.01). A negative correlation was obtained between delta CI/delta WR and BNP (r = 0.45) in the resting state. Peak VO2 (20.9 +/- 7.5 vs 13.9 +/- 2.7 ml/min/kg, p < 0.05), peak cardiac index (7.2 +/- 1.7 vs 5.5 +/- 0.9 l/min/m2, p < 0.05), and delta CI/delta WR (20.1 +/- 8.1 vs 12.4 +/- 2.5 ml/m2/W, p < 0.05) were significantly higher in the group with normal BNP (mean [+/-SD] 11.0 +/- 3.2 pg/ml) than in the group with high BNP (40.7 +/- 22.7 pg/ml). Delta CI/delta WR reflects the grade of exercise tolerance and may be useful for evaluating exercise capacity in patients with congestive heart failure.

The relationship between ischemic ST depression and oxygen uptake kinetics was examined during cardiopulmonary exercise test using the ramp protocol in 22 patients (17 males and 5 females, mean age 61.4 +/- 8.1 years) with ischemic ST change (horizontal or down sloping ST depression over 1 mm) during a previous multi-stage exercise test (Bruce method). Patients were classified into three groups according to coronary angiographic findings: absence of significant stenosis group (control, n = 7), single-vessel disease group (n = 7) and multivessel disease (MVD) group (n = 8). Peak exercise time, peak heart rate, peak systolic blood pressure, anaerobic threshold, peak oxygen uptake (peak Vo2), exercise time, heart rate, systolic blood pressure, and oxygen uptake at appearance of ischemic ST change were measured. The ratio of oxygen uptake increase at appearance of ischemic ST change was calculated. Peak Vo2 was lower in the MVD group than in the control group (20.9 +/- 6.2 vs 27.3 +/- 3.3 ml/min/kg, p < 0.05), and exercise time from the beginning of ramp exercise to the appearance of ischemic ST depression was shorter in the MVD group than in the control group (5.2 +/- 2.1 vs 8.2 +/- 1.9 ml/min/kg, p < 0.05). The ratio of oxygen uptake increase was smaller in the MVD group than in the control group (0.7 +/- 0.3 vs 1.2 +/- 0.2, p < 0.01). These results could be caused by impaired increase of cardiac output due to myocardial ischemia occurring during exercise. In the clinical setting, these phenomena could be used as a parameter for differentiating ischemic from non-ischemic ST depression or evaluating the sensitivity of ischemic heart disease.

The effect of combined aerobic and weight training on indexes of muscle strength and exercise capacity was investigated in 59 patients after myocardial infarction. Subjects were randomly assigned into three groups: group I performing combined aerobic and weight training (n = 22), group II performing ordinary aerobic training alone (n = 19) and group III not performing physical training (n = 18). Before and after the training, isokinetic knee extension strength was measured and cardiopulmonary exercise testing was performed. Physical training was prescribed for 8 weeks. Weight training of knee extensors was performed at 60% of 1 repetition maximum and aerobic training was prescribed at the heart rate of anaerobic threshold (AT) level. After 8 weeks, the increase of isokinetic knee extension strength was significantly greater in group I (26 +/- 14%) than group II (6 +/- 8%) and III (4 +/- 8%). Increases in peak VO2, exercise time, AT and peak O2 pulse were greater in groups I and II than group III. Furthermore, increase of exercise time was greater in group I (25 +/- 14%) than group II (16 +/- 9%). The rating of perceived exertion in submaximal exercise decreased significantly only for group I. In patients with myocardial infarction, combined aerobic and weight training is a more effective method for increasing muscle strength and exercise capacity than only ordinary aerobic training.

Exercise training usually involves the sustained performance of exercise at a prescribed intensity. The effects of exercise performed at the anaerobic threshold (AT) have been widely studied. The effects of single-level exercise on catecholamines and cardiac function were assessed at the AT, and at 120% of the AT in eight healthy Japanese men (mean age 21.9 +/- 1.8 years). 1) Symptom-limited exercise testing utilized the ramp protocol with a bicycle ergometer (20 watts/min) for measuring AT and peak oxygen uptake (peak VO2). 2) Exercise testing was repeated on another day, following the same protocol, with blood sampled to measure norepinephrine (NE) and epinephrine (E) in the resting control state and at the AT and peak exercise. 3) Single-level exercise testing at the AT and at 120% of AT utilized the bicycle ergometer on yet another day. Blood for measurement of NE and E was drawn at 3 and 7 min after achieving a steady-state condition. In addition, the cardiac index (CI) and stroke index (SI) were measured by the CO2 rebreathing method. (1) Mean AT and peak VO2 were 18.3 +/- 1.3 and 40.2 +/- 3.0 ml/min/g, respectively. (2) NE and E measured during ramp exercise testing increased rapidly when the intensity of exercise exceeded the AT. NE measured after 3 and 7 min at the AT during single-level exercise equalled 94.7% and 94.5% of the NE value measured at the AT of ramp exercise, respectively. NE measured after 3 and 7 min at 120% of the AT during single-level exercise was 124.7% and 144.7% at the AT of ramp exercise, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)