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Pulmonary arteriovenous malformations: effect of embolization on right-to-left shunt, hypoxemia, and exercise tolerance in 66 patients.

OBJECTIVE: This study assessed the effect and safety of percutaneous transcatheter coil embolization of pulmonary arteriovenous malformations. MATERIALS AND METHODS: In 58 (88%) of 66 patients, all malformations with feeding vessels greater than or equal to 3 mm in diameter were embolized with steel coils. Arterial oxygen saturation at rest and exercise, intrapulmonary right-to-left anatomic shunt fraction ((99m)Tc-macroaggregate injection), maximum exercise capacity (incremental work rate test), and pulmonary function were measured before and after embolization. Complications were analyzed. RESULTS: Three categories of patients were identified. Patients in group 1 (27%) had complete occlusion of all angiographically visible pulmonary arteriovenous malformations; patients in group 2 (61%) had complete occlusion of all malformations with feeding vessels greater than or equal to 3 mm in diameter, but with smaller lesions persisting; and patients in group 3 (12%) had incomplete embolization, with feeding vessels greater than or equal to 3 mm in diameter remaining. The mean right-to-left shunt after embolization was least in group 1 (7%), intermediate in group 2 (10%), and greatest in group 3 (19%). Arterial oxygen saturation and right-to-left shunt fraction returned to normal levels (>96% and <3.5%, respectively) in 33% of patients. A significant improvement occurred after embolization in carbon monoxide diffusing capacity per unit of alveolar volume and in exercise capacity in 16 and 10 patients, respectively. In 93 procedures, 12 complications (13%) occurred. CONCLUSION: Coil embolization of pulmonary arteriovenous malformations is effective in reducing right-to-left anatomic shunt fraction and in improving arterial oxygenation. Coil embolization of pulmonary arteriovenous malformations is well tolerated and has a low complication rate.

Adolescent↗

Reduced exercise tolerance in chronic heart failure and its relationship to neurohumoral factors.

There is some evidence that exercise intolerance in chronic heart failure is linked to the activity of compensatory mechanisms, including neurohumoral factors. However, there is a lack of correlation between exercise capacity and the degree of LV-dysfunction in this setting. Impaired skeletal muscle perfusion during exercise appears to be involved in reduced exercise capacity in patients with heart failure. The peripheral vasoconstriction mediated by increased sympathetic tone and activated plasma renin-angiotensin-aldosterone system (RAAS) may act primarily for short-term control and its short-term inhibition does not restore exercise capacity. The effects of the vascular RAS, impaired flow-dependent endothelium-mediated dilation (e.g. due to chronically reduced flow) and structural alterations of the vessel wall only slowly emerge over time. In addition, fluid retention may contribute to increased vascular stiffness in chronic heart failure. Improved cardiac output with acute administration of vasodilators and inotropes is not immediately translated into increased flow to skeletal muscle, because (1) the reversal of the above delineated peripheral alterations develops slowly over time; such agents given acutely may cause redistribution of blood flow in skeletal muscle without improving oxygen availability, (2) intrinsic abnormalities of skeletal muscle exist in chronic heart failure; e.g. due to chronic deconditioning, resulting in reduced oxidative capacity of skeletal muscle, as suggested by ultrastructural analysis and NMR-spectroscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise↗

Influence of thyroid hormones on exercise tolerance and lactate threshold in rats.

Effects of thyroid hormone deficit, and triiodothyronine (T3) treatment on exercise performance, blood lactate (LA) concentrations and LA threshold (TLA) were studied in trained and untrained rats. Fourteen rats were thyroidectomized and then treated with propylthiouracil for 30 days (THY + PTU group). Fourteen sham operated rats served as controls. In each group there were 7 sedentary and 7 endurance-trained animals. Six weeks after thyroidectomy or sham operation the rats were subjected to a multistage running test with speed increasing from 13 m/min at 10 degrees treadmill inclination till maximum. Blood samples for LA were taken from the rats' tail after each 3-min exercise stage. During 3 days following this test rats from all groups were injected (i.p.) with 75 micrograms/100 g of triiodothyronine (T3), and 24 hrs afterwards the second exercise test was performed. In THY + PTU rats maximal running speed (RSmax) and the speed at which TLA occurred were markedly decreased in comparison with control group. The level of LA at the maximal speed (LAmax) and that corresponding to TLA were higher in THY + PTU rats than in controls. T3 injection to control animals diminished their RSmax and TLA, whereas in THY + PTU rats it increased RSmax and shifted TLA to a higher speed. Both in THY + PTU and control animals T3 elevated LAmax and the threshold LA concentration. Endurance training in control and THY + PTU animals markedly enhanced RSmax and TLA. This was accompanied by increases in LAmax and concentration of LA at TLA only in control group. After T3 injection to control trained rats RSmax and TLA were diminished, whereas in THY + PTU trained group RSmax was unchanged and TLA was elevated. Maximal blood LA increased only in THY + PTU trained rats whilst the threshold blood LA was elevated in both groups. It is concluded, that both the T3 deficiency and its excess reduce maximal exercise performance and shift TLA to lower workloads. Enduarance training or administration of T3 to hypothyroid rats markedly improve their exercise performance and elevate TLA, however, T3 treatment markedly increases maximal and submaximal LA levels.

Animals↗

The effect of caffeine on exercise tolerance and left ventricular function in patients with coronary artery disease.

STUDY OBJECTIVE: To determine whether acute oral caffeine ingestion by patients with coronary artery disease results in decreased treadmill exercise performance or deterioration of echocardiographic measures of systolic or diastolic left ventricular function. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Referral-based cardiovascular exercise laboratory at an urban teaching hospital. PATIENTS: Thirteen volunteers with clinically stable coronary artery disease who had exercise tests after a 2-week caffeine-free washout period. Patients continued treatment with standard antianginal medications during the study period. INTERVENTIONS: Maximal exercise treadmill testing and exercise echocardiography were done at baseline, after acute ingestion of a placebo beverage (97% caffeine-free coffee), or after drinking an identical beverage containing 250 mg of caffeine sodium benzoate. MEASUREMENTS AND MAIN RESULTS: Acute ingestion of caffeine produced a serum level of 4.50 +/- 0.16 micrograms/mL, but had no effect on resting supine heart rate, blood pressure, left ventricular fractional shortening, posterior left ventricular wall thinning or peak rates of increase in left ventricular diastolic dimension. Despite a small increase in peak systolic blood pressure during exercise (baseline, 153 +/- 8; placebo, 154 +/- 8; caffeine, 161 +/- 7 mm Hg; P less than 0.05), exercise duration, time to onset of angina, and time to 0.1 mV ST depression did not differ after ingestion of placebo or caffeine. Rate-pressure product at onset of angina and onset of 0.1 mV of ST depression were also unchanged. In response to exercise, echocardiographic measures of left ventricular systolic and diastolic function were unchanged after caffeine compared with placebo ingestion. CONCLUSIONS: These data suggest that patients with exercise-induced ischemia who are receiving appropriate antianginal therapy tolerate the caffeine-equivalent of three cups of coffee without detrimental effect on intensity of ischemia, myocardial function, or exercise duration.

Adult↗

Low intensity peripheral muscle conditioning improves exercise tolerance and breathlessness in COPD.

This randomized, controlled study investigated the physiological effects of a specially designed 12 week programme of isolated conditioning of peripheral skeletal muscle groups. The programme required minimal infrastructure in order to allow continued rehabilitation at home after familiarization within hospital. Forty eight patients, aged 40-72 yrs with chronic obstructive pulmonary disease (COPD) (mean (SD) forced expiratory volume in one second (FEV1) 61 (27)% of predicted normal) were randomly allocated into training (n = 32) and control (n = 16) groups. Physiological assessments were performed before and after the 12 week study period, and included peripheral muscle endurance and strength, whole body endurance, maximal exercise capacity (maximum oxygen consumption (V'O2,max)) and lung function. The training group showed significant improvement in a variety of measures of upper and lower peripheral muscle performance, with no additional breathlessness. Whole body endurance measured by free arm treadmill walking increased by 6,372 (3,932-8,812) 3 (p < 0.001). Symptom-limited maximal V'O2 was unchanged. However, the training group showed a reduction in ventilatory equivalents for oxygen and carbon dioxide, both at peak exercise and at equivalent work rate (Wmax). In summary, low intensity isolated peripheral muscle conditioning is well-tolerated, simple and easy to perform at home. The various physiological benefits should enable patients across the range of severity of chronic obstructive pulmonary disease to improve daily functioning.

Exercise↗

Exercise tolerance with nebivolol and atenolol.

Patients treated with beta-blocking agents often complain of fatigue during exercise. Exercise capacity is decreased under this condition. Nebivolol is a new beta 1-adrenoceptor antagonist with a particular hemodynamic profile, which might be due to an ancillary property. Five milligrams once daily seems the optimal dose for antihypertensive treatment. In a double-blind, placebo-controlled crossover study, the effects of nebivolol on maximal and endurance exercise capacity are compared with those of atenolol in healthy volunteers. The hemodynamic and metabolic effects during exercise are also studied. Nebivolol 5 mg once daily and atenolol 100 mg once daily decrease blood pressure at rest similarly. At these dosages nebivolol shows a smaller decrease in heart rate than atenolol. During exercise, the rise in systolic blood pressure and heart rate is less depressed with nebivolol than with atenolol. In contrast to atenolol, nebivolol does not decrease maximal and endurance exercise capacity, and does not increase perceived exertion significantly. Changes in hemodynamics influence maximal exercise capacity. Since nebivolol has less effect on exercise hemodynamics than atenolol, this might explain why maximal work capacity is not changed during nebivolol. During endurance exercise metabolic effects are thought to be more important. Under nebivolol glycerol and NEFA production is less depressed during exercise and might explain the preserved endurance capacity. These data suggest less beta blockade during nebivolol than during atenolol at the dosages used in this study. In conclusion, at a dose known to be antihypertensive, nebivolol does not alter exercise capacity significantly in healthy volunteers.

Adrenergic beta-Antagonists↗

Exercise tolerance test. Single-sample screening technique to rule out growth-hormone deficiency.

Parent-directed vigorous exercise was evaluated as a screening test for adequacy of pituitary growth-hormone release in 57 short-statured children. This method obviated the need for pharmacologic provocative testing in all but the four children with growth-hormone deficiency. In 92% of the euendocrine children, the immediate postexercise venous sample demonstrated an adequate growth-hormone level. Vigorous physical exercise after an 8- to 12- hour fast with a single postexercise serum growth-hormone sample is a reliable, safe, and cost-effective screening test for growth-hormone deficiency.

Adolescent↗