Decreased exercise capacity in mild essential hypertension: non-invasive indicators of limiting factors.

Available data suggest that exercise capacity is limited in hypertension. The mechanism of this reduced maximal exercise capacity has not been fully elucidated. In this study 22 patients with mild essential hypertension (162 +/- 22 mmHg systolic and 95 +/- 8 mmHg diastolic) and 36 normotensive control subjects (128 +/- 13 mmHg systolic and 80 +/- 7 mmHg diastolic) (P less than 0.01) performed an ergometer test till exhaustion. Body mass index in the two groups did not differ. The maximal oxygen consumption VO2 was lower in the hypertensive group (18 +/- 7 versus 23 +/- 8 ml/kg/min; P less than 0.02) as was the maximal workload (141 +/- 52 vs. 185 +/- 70 Watt; P less than 0.01). Rate pressure product rose only 2.7 fold in hypertensive patients versus 3.5 fold in the control group (P less than 0.001). In hypertensive patients maximal workload decreased with increasing resting systolic blood pressure (P less than 0.05) while in the normotensive subjects maximal workload rose with increasing resting systolic blood pressure (P less than 0.05). In conclusion both high and low blood pressure was associated with a decreased maximal voluntary exercise capacity. Even mild hypertension was accompanied by lower maximal exercise capacity. Hypertensive patients also had a lower maximal VO2 and lower maximal rate pressure product than did normotensive subjects.     

Altered hemodynamics during exercise in older essential hypertensive subjects

This study was designed to compare the resting and exercise hemodynamics of older adults with moderate hypertension with those of age-matched normotensive controls. Thirty-one hypertensive (20 men, 11 women; mean age, 63.9 +/- 2.8 years) and 28 normotensive subjects (15 men, 13 women; mean age, 62.6 +/- 2.4 years) were studied. There were no differences between the groups in terms of body weight, body composition, and maximal O2 consumption (VO2). At rest, there were no differences in VO2, cardiac output, stroke volume, or heart rate between the two groups, although systolic (158 +/- 13 vs 121 +/- 12 mm Hg) and diastolic blood pressures (94 +/- 7 vs 79 +/- 8 mm Hg) were higher in the hypertensive subjects. The hypertensive subjects' elevated blood pressure at rest was the result of a higher total peripheral resistance. During exercise, the hypertensive subjects had a lower cardiac output and stroke volume, no difference in heart rate and VO2, higher systolic, diastolic, and mean blood pressures, and a higher total peripheral resistance compared with their normotensive peers. The results indicate that older hypertensive persons have an altered cardiovascular response to exercise as compared with age-matched normotensive subjects. The responses also indicate that older essential hypertensive persons do not undergo excessive myocardial demands during exercise of the intensity usually prescribed in rehabilitation programs.     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Exercise performance in patients with uncomplicated essential hypertension. Effects of nifedipine-induced acute blood pressure reduction.

In untreated patients with uncomplicated essential hypertension, exercise induces an abnormal increase in blood pressure; the influences of this increase on exercise were evaluated by a cardiopulmonary exercise test (CPX) performed in control conditions (step 1) and during acute blood pressure reduction (step 2). Patients were classified as (1) normotensive (resting diastolic blood pressure [BPd] less than 90 mm Hg; n = 14), (2) mildly hypertensive (BPd of 90 to 104 mm Hg; n = 9), and (3) moderately to severely hypertensive (BPd greater than or equal to 105 mm Hg; n = 16). For the three groups, peak mean blood pressure during exercise was 125 +/- 5 mm Hg (mean +/- SEM), 144 +/- 3 mm Hg (p less than 0.01 vs normotensive), and 161 +/- 4 mm Hg (p less than 0.01 vs normotensive and p less than 0.01 vs mild hypertension), respectively. Oxygen consumption (VO2) at peak exercise and at ventilatory anaerobic threshold was 26.1 +/- 1.1 and 17.2 +/- 0.5 ml/min/kg, 25.4 +/- 1.1 and 16.9 +/- 0.8 ml/min/kg, and 26.4 +/- 1.3 and 17.5 +/- 1.2 ml/min/kg in normotensive subjects, those with mild hypertension, and those with moderate to severe hypertension, respectively. Fourteen normotensive subjects, six with mild hypertension, and nine with moderate to severe hypertension participated to step 2 (nifedipine vs placebo, double-blind crossover). Nifedipine reduced blood pressure at rest and at peak exercise in those with hypertension. Peak exercise VO2 was unaffected by nifedipine in both normotensive subjects and those with hypertension. With nifedipine, ventilatory anaerobic threshold occurred earlier and at a lower VO2 in mild and in moderate to severe hypertension (delta VO2 = -1.9 and -2.4 ml/min/kg, respectively). These findings might be due to nifedipine-induced redistribution of blood flow during exercise and might be the reason for the complaint of weakness after blood pressure reduction in hypertensive subjects.     

Decrease in blood pressure and increase in total peripheral vascular resistance in supine resting subjects with normotension or essential hypertension

Hemodynamic changes in the supine resting position were investigated in 70 male subjects, consisting of 15 healthy volunteers with normotension (blood pressure of 113 +/- 7/70 +/- 5 mmHg, M +/- SD), 25 patients with borderline essential hypertension (143 +/- 12/90 +/- 6 mmHg) and 30 patients with established essential hypertension (166 +/- 13/108 +/- 6 mmHg). The supine position reduced blood pressure, heart rate, stroke volume and cardiac output (p less than 0.001), but increased total peripheral vascular resistance (p less than 0.001). The decrease in systolic blood pressure (p less than 0.01), stroke volume (p less than 0.05) and cardiac output (p less than 0.05), and the increase in total peripheral vascular resistance (p less than 0.01) were significantly greater in the borderline and established essential hypertensive groups than in the normotensive group. The results demonstrated that the decrease in blood pressure was due to a reduction in both heart rate and stroke volume, and that the decrease in stroke volume and increase in total peripheral vascular resistance seen in the supine position were greater in the hypertensive groups than in the normotensive group. These hyperresponses may contribute to the development and persistence of high blood pressure in patients with essential hypertension.     

Absence of post exercise hypotension and sympathoinhibition in normal subjects: additional evidence for increased sympathetic outflow in borderline hypertension

OBJECTIVE: In young men (mean age 25 years) with borderline hypertension the authors have documented a reduction in systolic blood pressure and muscle sympathetic nerve activity 60 mins after 45 mins of submaximal treadmill exercise. The aim of this study was to determine if post exercise hypotension occurs in normotensive young men, and if so, if it is accompanied by a decrease in sympathetic nerve activity. DESIGN: Replicating a previous protocol, the authors recorded blood pressure, heart rate, plasma noradrenaline and muscle sympathetic nerve activity (microneurography; peroneal nerve) before and 60 mins after submaximal treadmill exercise. SUBJECTS: Ten healthy male volunteers (mean age 28 +/- 5 years). INTERVENTION: Forty-five minutes of treadmill exercise at 70% of resting heart rate reserve. MAIN RESULTS: In contrast to borderline hypertensive subjects, prior exercise had no effect on either systolic or diastolic blood pressure or muscle sympathetic nerve activity in healthy volunteers. Plasma noradrenaline concentrations were similar before and after exercise. Resting heart rate (56 +/- 3 versus 70 +/- 3 beats/min; P less than 0.002), and sympathetic burst frequency (10 +/- 4 versus 20 +/- 2 bursts/min; P = 0.026) were lower in normal than in borderline hypertensive men. CONCLUSIONS: At rest, discharge to muscle sympathetic nerves is increased in young borderline hypertensive men; and blood pressure and sympathetic nerve activity are decreased after exercise in borderline hypertensive but not normotensive men. These observations suggest that the depressor response to prolonged rhythmic exercise in young men with borderline hypertension may be due in part to transient suppression of augmented central sympathetic outflow.     

Effects of S-596, a new beta-adrenoceptor blocking agent on the left ventricular performance of normal subjects during exercise

The effects of d1-2-(3'-t-butylamino-2'-hydroxypropylthio)-4-(5'-carbamoyl-2'-thi enyl) thiazole hydrochloride (S-596) were evaluated in 9 normal volunteers. Exercise echocardiography was performed in the semi-supine position before and 2, 4 and 24 hours after the oral administration of 15 mg of S-596. Two hours after administration, resting heart rate was unchanged, compared with control, but systolic blood pressure at rest was slightly decreased (114 +/- 6 vs 106 +/- 10 mmHg, p less than 0.05). Left ventricular dimensions were unchanged, but shortening fraction was increased in the resting state (30.3 +/- 4.6 vs 33.1 +/- 4.8%, p less than 0.05). During exercise on oral S-596, heart rate and systolic blood pressure responses were reduced (127 +/- 11 in control vs 108 +/- 6 beats/min on S-596, 198 +/- 25 vs 168 +/- 23 mmHg, p less than 0.001 and 0.05, respectively). Left ventricular end-diastolic dimension was not significantly altered by S-596 compared with the preceding control exercise test; however, end-systolic dimension was significantly larger after beta blockade with S-596 (2.6 +/- 0.4 vs 3.0 +/- 0.4 cm, p less than 0.05). Shortening fraction and cardiac output decreased significantly (43.7 +/- 3.7 vs 40.0 +/- 5.7%, 9.5 +/- 1.4 vs 8.4 +/- 1.3 L/min, p less than 0.05 and 0.01, respectively). These effects of S-596 were maximal at 2 hours after oral administration with reduced response of heart rate to exercise lasting for 24 hours. Compared with the effects of propranolol (30 mg, given orally) in the same subjects, beta-adrenergic blockade during exercise with S-596 was equivalent to or greater than that of propranolol. Thus, S-596 has little, if any, effect on resting left ventricular performance, but demonstrates potent negative chronotropic and inotropic effects during exercise in normal human subjects. Its beta-adrenergic blocking action also has long acting properties, especially its chronotropic effect.     

Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure. Muscle blood flow is reduced with maintenance of arterial perfusion pressure

We studied the central hemodynamic, leg blood flow, and metabolic responses to maximal upright bicycle exercise in 30 patients with chronic heart failure attributable to severe left ventricular dysfunction (ejection fraction, 24 +/- 8%) and in 12 normal subjects. At peak exercise, patients demonstrated reduced oxygen consumption (15.1 +/- 4.8 vs. 32.1 +/- 9.9 ml/kg/min, p less than 0.001), cardiac output (8.7 +/- 3.2 vs. 18.6 +/- 4.4 l/min, p less than 0.001), and mean systemic arterial blood pressure (116 +/- 15 vs. 135 +/- 13 mm Hg, p less than 0.01) compared with normal subjects. Leg blood flow was decreased in patients versus normal subjects at rest and matched submaximal work rates and maximal exercise (2.1 +/- 1.9 vs. 6.4 +/- 1.4 l/min, all p less than 0.01). Mean systemic arterial blood pressure was no different in the two groups at rest or at matched submaximal work rates, whereas leg vascular resistance was higher in patients compared with normal subjects at rest, submaximal, and maximal exercise (all p less than 0.01). Although nonleg blood flow was decreased at rest in patients, it did not decrease significantly during exercise in either group. Peak exercise leg blood flow was related to peak exercise cardiac output in patients (r = 0.66, p less than 0.01) and normal subjects (r = 0.67, p less than 0.01). In patients, leg vascular resistance was not related to mean arterial blood pressure, pulmonary capillary wedge pressure, arterial catecholamines, arterial lactate, or femoral venous pH at rest or during exercise. Compared with normal subjects during submaximal exercise, patients demonstrated increased leg oxygen extraction and lactate production accompanied by decreased leg oxygen consumption. Thus, in patients with chronic heart failure compared with normal subjects, skeletal muscle perfusion is decreased at rest and during submaximal and maximal exercise, and local vascular resistance is increased. Our data indicate that nonleg blood flow and arterial blood pressure were preferentially maintained during exercise at the expense of leg hypoperfusion in our patients. This was associated with decreased leg oxygen utilization and increased leg oxygen extraction when compared to normal subjects, providing further evidence that reduced perfusion of skeletal muscle is important in causing early anaerobic skeletal muscle metabolism during exercise in subjects with this disorder.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of nisoldipine on systemic and leg blood flow, oxygen transport and metabolism, and hemodynamics during exercise in effort angina pectoris

The acute effects of 10 mg of oral nisoldipine on hemodynamics, oxygen transport and metabolism, and distribution of cardiac output, at rest and during semiupright bicycle exercise, were evaluated in 10 men with effort angina receiving long-term beta 1 blockade. Cardiac output and leg blood flow were measured using the thermodilution technique. At rest, nisoldipine decreased systemic resistance from 18.9 +/- 1.0 to 15.9 +/- 1.2 dynes.s.cm-5.10(2) (p less than 0.05) and cardiac output increased from 4.8 +/- 0.2 to 5.3 +/- 0.3 liters/min (p less than 0.05) without changing leg blood flow. During maximal exercise with nisoldipine, systemic resistance was reduced (10.6 +/- 0.9 to 8.6 +/- 0.5 dynes.s.cm-5.10(2), p less than 0.05) and cardiac output increased 18% (10.3 +/- 0.7 to 12.2 +/- 0.6 liters/min, p less than 0.05) when compared with control values. Exercise heart rate was higher with nisoldipine (113 +/- 4 vs 106 +/- 4 beats/min, p less than 0.01), but the mean arterial pressure was not significantly changed, giving a higher rate-pressure product. The increase in mean pulmonary artery wedge pressure was attenuated (26 +/- 3 vs 30 +/- 3 mm Hg during control exercise, p less than 0.05), but ST depression was unaltered. Exercise leg flow was reduced by nisoldipine from 4.3 +/- 0.4 to 3.9 +/- 0.3 liters/min (p = 0.07) and the proportion of cardiac output distributed to the legs was reduced from 42 +/- 3 to 33 +/- 3% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Baroreflex function and pressor responsiveness in normotensive young subjects with a family history of hypertension

Baroreflex control of heart rate, pressor responses to alpha agonist (phenylephrine) and isometric exercise before and during salt loading were compared between 13 normotensive subjects with hypertensive relatives (group A) and 9 normotensive subjects with no family history of hypertension (group B). Baroreflex slope was significantly lower in group A than in group B (9.6 +/- 1.6 vs 17.6 +/- 1.9 msec/mmHg; p less than 0.01), although blood pressure, heart rate and aortic distensibility were not different between two groups. Pressor responses to phenylephrine and isometric exercise were identical for both groups. During salt loading, pressor responses to phenylephrine and isometric exercise were significantly greater in group A than in group B. Baroreflex slope was not affected by salt loading in the two groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated arterial pressure and decreased aortic distensibility. Pressor responses to alpha agonist and isometric exercise during high-sodium diet were augmented in subjects with a family history of hypertension.     

Exaggerated atrial natriuretic peptide release during acute exercise in essential hypertension

The effects of acute exercise on plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and plasma renin activity (PRA) were studied in 13 patients with previously untreated essential hypertension, and 8 matched normotensive control subjects. Resting levels of ANP and PRA were similar in the two groups, while resting AVP concentrations were 1.4 times higher in hypertensive subjects. Graded exercise was performed on a bicycle ergometer with workload increased each minute until exhaustion (Wmax). Wmax was higher in normal subjects than in hypertensive patients. Blood pressure and heart rate rose more steeply in hypertensive patients. Plasma ANP increased during acute exercise in both groups, but the average increase in hypertensives was substantially greater than in normal subjects (P less than 0.05). The increase in ANP during exercise was greater in hypertensives with left ventricular (LV) hypertrophy, and there was a positive correlation between LV mass and the percentage rise in ANP during exercise (r = 0.56, P less than 0.005). Plasma AVP did not alter during exercise. Plasma renin concentrations showed a small rise during exercise in both groups, which was 16% less in hypertensive subjects (P less than 0.05). The enhancement of ANP release during exercise in hypertensive subjects may reflect both cardiac structural changes and increased redistribution of blood to the cardiopulmonary compartment.     

Insulin, renin-aldosterone system and blood pressure in obese people.

OBJECTIVE: To evaluate the relationship between insulin, the renin-aldosterone system and blood pressure in obese subjects. DESIGN AND METHODS: A cross sectional study of a group of severely obese normotensive subjects who were surgical candidates (n=39; mean BMI: 47.8+/-1.4) and a group of hypertensive patients (n=57; mean BMI: 28.0+/-0.7) twenty-nine of whom had BMI>27. All subjects were studied after 15 days on a balanced diet. Insulin, plasma renin activity and aldosterone were measured. RESULTS: Fasting insulin, plasma renin activity and aldosterone were higher in severely obese normotensive subjects than in hypertensive subjects (respectively 32.3+/-3.0 vs 13.1+/-1.0 mU/l, P=0.0001; 1.34+/-0.22 vs 0.88+/-0.12 ng/ml/h, P=0.04; 137.2+/-16.2 vs 87.9+/-12.1 pg/ml, P=0.015). Insulin was related to BMI and to aldosterone both in normotensive and in hypertensive patients. CONCLUSION: Hyperinsulinemia itself does not determine hypertension; in some people it could play a vasodilator role in opposition to the renin-aldosterone system.     

Resting and maximal forearm skin blood flows are reduced in hypertension.

To find whether the vasodilator capacity of nonacral skin is reduced in hypertension, we measured forearm blood flow by venous occlusion plethysmography in 10 seated normotensive (mean +/- SD mean arterial pressure, 94 +/- 5 mm Hg) and 10 hypertensive (112 +/- 9 mm Hg) men at rest for 39 minutes while the forearm was heated with water at 42 degrees C, a maneuver known to selectively and maximally vasodilate skin. Blood pressure, measured every 5 minutes, did not change with heating. We found that in the normotensive group resting forearm blood flow was higher (3.64 +/- 1.12 versus 2.48 +/- 0.58 ml/100 ml tissue per minute, p less than 0.001; normotensive group versus hypertensive group) and resting forearm vascular resistance lower (30.17 +/- 10.99 versus 48.88 +/- 17.37 mm Hg.min.100 ml tissue per minute, p less than 0.05; normotensive group versus hypertensive group), and maximal forearm blood flow with local heating was higher (29.32 +/- 11.99 versus 18.19 +/- 4.50 ml/100 tissue per minute, p less than 0.018; normotensive group versus hypertensive group and vascular resistance lower (4.07 +/- 1.04 versus 6.54 +/- 1.17 mm Hg.min.100 ml tissue per minute, p less than 0.005; normotensive group versus hypertensive group). To find whether this degree and duration of local warming maximally vasodilated the skin in hypertensive subjects (as it does in normotensive subjects), we measured forearm skin blood flow before and during local heating plus 10 minutes of ischemia using a laser Doppler flowmeter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aftereffects of exercise on regional and systemic hemodynamics in hypertension.

Several studies have indicated that a single bout of physical exercise induced a significant antihypertensive effect during the hours after the activity. However, little information is presently available on the underlying hemodynamic changes. We examined 13 essential hypertensive patients and nine normotensive subjects in a randomized, crossover study design during 3 hours after a 30-minute period of upright leg cycling at 50% of peak aerobic capacity and during 3 hours after a 30-minute control period of rest. Blood pressure, heart rate, cardiac output, total peripheral resistance, and regional vascular resistance in the forearm as well as venous plasma catecholamine concentrations were measured repeatedly. After exercise, systolic (-11 +/- 2 mm Hg) and diastolic (-4 +/- 1 mm Hg) blood pressures, total peripheral resistance (-27 +/- 5%), forearm vascular resistance (-25 +/- 6%), and plasma norepinephrine levels (-21 +/- 7%) were significantly (p less than or equal to 0.05) decreased, and cardiac output was increased (+31 +1- 8%) compared with control in hypertensive subjects. In contrast, in normotensive subjects blood pressure, forearm vascular resistance, and plasma norepinephrine were unchanged, and systemic hemodynamics changed to a lesser extent than in hypertensive subjects after exercise. It is concluded that a decrease in regional vascular resistance in skeletal muscles and possibly in the skin in hypertensive patients may contribute importantly to the antihypertensive effect of prior exercise. A decreased sympathetic nervous activity, as seen from lower plasma norepinephrine levels, may be involved in this effect.     

Left ventricular structure and function in normotensive adolescents with a genetic predisposition to hypertension

It has been suggested that the heart plays an active role in the pathogenesis of arterial hypertension. If this is true, there must be early cardiac involvement in young normotensive subjects who develop hypertension later in life and differences in cardiac morphology or function may exist between young normotensive subjects with different risks of developing hypertension. M-mode echocardiography was performed in 51 normotensive male adolescents with at least one hypertensive parent (SHT). These subjects were compared with 55 normotensive sons of normotensive parents (SNT) and with 25 adolescents with borderline hypertension (BH). Control groups were matched for sex and age. The following morphologic parameters were significantly greater in the SHT group than in the SNT group: interventricular septum (0.54 +/- 0.08 vs 0.49 +/- 0.09 cm/m2; p less than 0.01) and posterior wall (0.54 +/- 0.11 vs 0.50 +/- 0.08 cm/m2; p less than 0.05) thickness, left ventricular mass (125.0 +/- 29.1 vs 109.2 +/- 25.4 gm/m2; p less than 0.005), and cross-sectional area (9.9 +/- 1.8 vs 8.9 +/- 1.6 cm2/m2; p less than 0.005). No significant differences between SHT and BH subjects were observed. Excursion of left ventricular posterior wall was significantly higher in the BH group. No differences were observed between SHT and SNT subjects. These data show that the same kinds of changes in cardiac morphology are present in normotensive subjects with a family history of hypertension and in subjects with borderline hypertension, suggesting that cardiac involvement may precede elevation of blood pressure.     

Preload, adrenergic activity, and aortic compliance in normal and hypertensive patients

Aortic compliance is a major determinant of systolic blood pressure and of impedance to left ventricular ejection. However, little is known about its regulating factors. To assess the effects of preload and adrenergic activity on aortic compliance, we studied 10 normal subjects and nine untreated hypertensive patients at rest and during lower body negative pressure. Aortic compliance was measured invasively from the diastolic decay of the aortic pressure tracing and systemic vascular resistance. Preload was decreased stepwise by lower body negative pressure (-5 to -40 mm Hg) while adrenergic activity was assessed by the change in plasma norepinephrine at a maximum level of negative pressure suction. At rest, aortic compliance was lower in hypertensive subjects compared with its value in normal individuals (0.048 +/- 0.012 [SD] versus 0.071 +/- 0.009 units, p less than 0.001) but correlated inversely with systolic blood pressure in both groups (r = -0.64 in normotensive individuals, r = -0.83 in hypertensive subjects, r = -0.88 for the whole group, p less than 0.001 for all). Whereas resting pulmonary wedge pressure was higher in hypertensive subjects compared with normal individuals (16 +/- 4 [SD] versus 11 +/- 3 mm Hg, p less than 0.05), resting plasma norepinephrine levels were not different between the two groups (261 +/- 139 versus 251 +/- 103 pg/ml). Neither of these two resting indices correlated with baseline aortic compliance in both normotensive individuals and hypertensive patients. During lower body negative pressure (LBNP), cardiac filling pressure (right atrial pressure and pulmonary wedge pressure) as well as cardiac output decreased in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of aerobic training on exercise tolerance and echocardiographic dimensions in untrained postmenopausal women

The cardiovascular effects of physical training were evaluated in a controlled trial involving 32 healthy, untrained, postmenopausal women. The subjects were randomly assigned to an aerobic exercise training program or a control group. The exercise group participated in at least three 40-minute supervised sessions per week for 8 months. Twenty-five subjects completed the study: eight in the control group and 17 in the training group. The training group had a significant increase over the training period in maximal oxygen consumption (27.3 +/- 4.6 ml/kg/min vs 30.8 +/- 5.4 ml/kg/min, p less than 0.05) and maximal treadmill exercise duration (9.8 +/- 2.6 minutes vs 11.3 +/- 2.2 minutes; p less than 0.05). The control group had no significant change in maximal treadmill exercise duration (9.0 +/- 1.2 minutes vs 9.2 +/- 1.4 minutes) but had a slight increase in maximal oxygen consumption (23.7 +/- 3.4 ml/kg/min vs 24.4 +/- 4.1 ml/kg/min, p less than 0.05). The training group had significant increases in M-mode echocardiographic left ventricular end-diastolic dimension (4.6 +/- 0.6 cm vs 4.8 +/- 0.4 cm, p less than 0.05) and calculated left ventricular ejection fraction (0.66 +/- 0.14 vs 0.74 +/- 0.12, p less than 0.05). M-mode echocardiograms demonstrated no significant change in left ventricular dimensions or wall thickness in the control group. In this group of untrained postmenopausal women, a training effect was associated with enhanced resting left ventricular ejection fraction and increased resting left ventricular end-diastolic dimension.     

Increased coronary vascular resistance cannot be reduced by inhibiting sympathetic overactivity in hypertension

The aim of this study was to test whether increased coronary vascular resistance in hypertensive subjects can be reduced by centrally inhibiting sympathetic overactivity with dexamethasone. Coronary vascular resistance was quantitated in 11 men with untreated mild essential hypertension (RR 149 +/- 13/98 +/- 10 mm Hg) and 23 healthy, normotensive, otherwise matched men using positron emission tomography and [(15)O]H(2)O. The measurements were performed at baseline and during adenosine stimulation. Each subject was studied twice, with and without previous dexamethasone treatment for two days (0.5 mg x 4 per day). Before dexamethasone treatment, cardiac index and plasma norepinephrine concentration (1.9 +/- 0.6 vs. 1.3 +/- 0.5 nmol/l, p < 0.01) were significantly higher in hypertensive than in normotensive subjects. Additionally, both baseline and hyperemic coronary vascular resistances were higher in hypertensive than normotensive subjects (147 +/- 31 vs. 113 +/- 24 and 36 +/- 9 vs. 25 +/- 10 mm Hg.min.g.ml(-1); p < 0.05). Dexamethasone treatment significantly decreased plasma norepinephrine concentrations in hypertensive subjects, leading to comparable plasma norepinephrine concentrations in hypertensive and normotensive subjects (1.4 +/- 0.5 vs. 1.2 +/- 0.4 nmol/l; NS). However, coronary vascular resistances remained increased in hypertensive subjects. In conclusion, hypertensive subjects are characterized by sympathetic overactivity, which can be normalized by dexamethasone. However, coronary vascular resistances remained increased in hypertensive subjects after dexamethasone treatment, suggesting that other mechanisms than sympathetic overactivity-induced vasoconstriction explain the increased coronary vascular resistance in hypertension.     

Isometric exercise in patients with chronic advanced heart failure: hemodynamic and neurohumoral evaluation

We evaluated the hemodynamic effects of isometric exercise in 53 patients with congestive heart failure (CHF) and compared them with those found in 10 normal subjects. In both groups, isometric exercise increased heart rate and blood pressure. Systemic resistance increased in patients with CHF (1862 +/- 520 vs 2126 +/- 642 dyne-sec-cm-5; p less than .001) but not in normal subjects (1359 +/- 268 vs 1380 +/- 252 dyne-sec-cm-5). Cardiac index and stroke volume index increased mildly but not significantly in the normal subjects (2.8 +/- 0.5 vs 3.1 +/- 0.7 liters/min/m2 and 46 +/- 8 vs 47 +/- 7 ml/m2) and showed a significant fall in the patients with CHF (2.1 +/- 0.6 to 1.9 +/- 0.6 liters/min/m2, p less than .01 and 23 +/- 7 vs 20 +/- 7 ml/m2, p less than .01). Mean pulmonary arterial wedge pressure increased in patients with CHF from 26 +/- 7 to 30 +/- 8 mm Hg (p less than .001). Although no significant change was found in mean value for stroke work index (21 +/- 9 vs 20 +/- 9 g-m/m2), the individual changes were variable, with marked decrease (greater than 15%) in 17 of the patients. This hemodynamic deterioration could not be predicted from resting hemodynamics, left ventricular ejection fraction, or functional classification. Isometric exercise resulted in no significant change in circulatory catecholamine levels or plasma renin concentration in our 10 normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular findings in quadriplegic and paraplegic patients and in normal subjects

Seven normal, 7 paraplegic and 7 quadriplegic patients underwent cross-sectional cardiovascular evaluation, including recording of sitting heart rate, blood pressure and echocardiography. Quadriplegic patients had a 26% lower left ventricular (LV) mass index (75 +/- 13 g/m2, p less than 0.01) compared with normal volunteers (102 +/- 16 g/m2) or paraplegic patients (110 +/- 26 g/m2). Six quadriplegic patients and 3 paraplegic patients had an unusual pattern of LV posterior wall asynergy, which was associated with a significant rightward shift of the frontal-plane QRS axis (92 +/- 22 degrees vs 42 +/- 41 degrees, p less than 0.005) and smaller left atrial dimensions (2.4 +/- 0.4 vs 3.0 +/- 0.3 cm, p less than 0.005). The quadriplegic group was characterized by a significantly reduced mean blood pressure (67 +/- 7 vs 88 +/- 8 mm Hg in normal subjects, p less than 0.002), high normal peripheral resistances (22 +/- 5 vs 17 +/- 5 units in normal subjects, difference not significant) and a markedly reduced calculated cardiac output (3.2 +/- 0.6 vs 5.4 +/- 1.4 liters/min in normal subjects, p less than 0.01). Hemodynamic data for the paraplegic patients were similar to those in the normal group. A decrease in LV wall stress, mediated primarily by a decrease in venous return, appeared to result in the "adaptive" cardiac atrophy seen in these quadriplegic patients. LV asynergy was common and also may be related to a decrease in cardiac filling.