Exercise tolerance improvement

The goals of therapy are to prevent disease progression, relieve symptoms, improve exercise tolerance, improve overall health status, prevent and treat exacerbations, prevent and treat complications, and reduce morbidity and mortality. 

Intravenous epoprostenol increases exercise tolerance, improves pulmonary hemodynamics, and improves survival in patients with primary pulmonary hypertension. However, there are limitations to intravenous administration, and a significant proportion of patients develop catheter-related problems, such as thrombosis, pump failure, and catheter-related sepsis. In an attempt to improve delivery, several trials of aerosolized prostacyclin have been undertaken, primarily in patients with primary pulmonary hypertension. 

Prevent disease progression Relieve symptoms Improve exercise tolerance Improve overall health status Prevent and treat exacerbations Prevent and treat complications Reduce morbidity and mortality... 

Propranolol. Propranolol (Table 1), a Class II antiarrhythmic agent, is usefiil in the management of hypertrophic subaortic stenosis, especially for the treatment of exertional or other stress-induced angina by improving blood flow. The dmg can increase exercise tolerance in patients suffering from angina. Propranolol has been shown to have cardioprotective action in post-MI patients (37—39,98,99,108). 

If diuretic therapy is warranted, monitor for therapeutic response by assessing weight loss and improvement of fluid retention, as well as exercise tolerance and presence of fatigue. 

Bronchodilators are the mainstay of treatment for symptomatic COPD. They reduce symptoms and improve exercise tolerance and quality of life. 

The medications available for COPD are effective for reducing or relieving symptoms, improving exercise tolerance, reducing the number and severity of exacerbations, and improving quality of life. No medications presently available have been shown to slow the rate of decline in lung function. 

Other outcomes include improvement in exercise tolerance and fatigue, decreased nocturia, and a decrease in heart rate. 

After initiation of antiinflammatory therapy or an increase in dosage, most patients should begin experiencing a decrease in symptoms within 1 to 2 weeks and achieve maximum symptomatic improvement within 4 to 8 weeks. Improvement in baseline FEVj or PEF should follow a similar time frame, but a decrease in BHR as measured by morning PEF, PEF variability, and exercise tolerance may take longer and improve over 1 to 3 months. 

Chronic theophylline use in COPD has been shown to produce improvements in lung function, including vital capacity and FEVj. Subjectively, theophylline has been shown to reduce dyspnea, increase exercise tolerance, and improve respiratory drive. Nonpulmonary effects that may contribute to better functional capacity include improved cardiac function and decreased pulmonary artery pressure. 

As with other bronchodilators in COPD, parameters other than objective measurements such as FEVj should be monitored to assess efficacy. Subjective parameters, such as perceived improvements in dyspnea and exercise tolerance, are important in assessing the acceptability of methylxanthines for COPD patients. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

Mechanism of Action AnACE inhibitor that suppresses the renin-angiotensin-aldos-terone system and prevents conversion of angiotensin I to angiotensin 11, a potent vasoconstrictor may also inhibit angiotensin II at local vascular and renal sites. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance, pulmonary capillary wedge pressure improves cardiac output and exercise tolerance. Pharmacokinetics ... 

Mecfianism of Action A prostaglandin that dilates systemic and pulmonary arterial vascular beds, alters pulmonary vascular resistance, and suppresses vascular smooth muscle proliferation. Therapeutic Effect Improves symptoms and exercise tolerance in patients with pulmonary hypertension delays deterioration of condition. Pharmacokinetics Protein binding 60%. Metabolized in liver. Primarily excreted in urine minimal elimination in feces. Half-life 20-30 min. 

The investigators found that 70% of the group had improvement in chnical status and that, in the group as a whole, there was a significant improvement in exercise tolerance time compared with baseline. Nine patients were entirely free of angina at the 12-week point. All adverse events were related to the administration procedure. The single death that occurred seemed unrelated to treatment. 

Other investigators reported the results of a phase II trial in which 337 patients were randomized to receive recombinant fibroblast growth factor-2 (FGF-2) or placebo during cardiac catheterization. Although the primary end point—a significant improvement in exercise tolerance... 

Casaburi R et al Improvement in exercise tolerance with the combination of tiotropium and pulmonary rehabilitation in patients with COPD. Chest 2005 127 809. [PMID 15764761]... 

The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theoretical basis for such benefit could be metabolic protection of the ischemic myocardium. Double-blind, placebo-controlled trials have demonstrated that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein a, high-density lipoprotein cholesterol, exercise tolerance, and time to development of ischemic changes on the electrocardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%). 

The precise testing required to diagnose GH deficiency is controversial. Treatment of GH-deficient adults can cause increased lean body mass and bone density, decreased fat mass, increased exercise tolerance, and an improved sense of well-being. Adverse effects often include arthralgias and fluid retention. 

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