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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current pharmacotherapy for chronic obstructive pulmonary disease (COPD) relieves symptoms and reduces exacerbation through improving airflow limitation. Such drugs do not effectively improve exercise tolerance due in part to pulmonary hypertension associated with severe COPD, nor impact on its increased morbidity and mortality. Exercise intolerance is often improved (temporarily) by lung volume reduction surgery and pulmonary rehabilitation. Ambulatory oxygen is the most effective treatment of exercise limitation. Chronic cigarette smoking is the principal cause of COPD. An early change in smokers' lungs is pulmonary artery intimal thickening and vessel narrowing, which, as COPD develops, is correlated with both the severity of emphysema and bronchiolitis. This may be the consequence of combined smoking-induced apoptosis, inflammation, and imperfect repair. End-stage bronchiolitis and emphysema are likely to limit the effectiveness of bronchodilators and corticosteroids. There are effective treatments for idiopathic and scleroderma pulmonary arterial hypertension, which increase exercise tolerance and improve survival. Because idiopathic and COPD pulmonary hypertension share a common vascular intimal thickening, excess endothelin receptor expression, and plasma endothelin-1, an important therapeutic question to address is whether an oral endothelin-1 antagonist can improve exercise tolerance in severe COPD.
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PMID:Pulmonary hypertension and chronic obstructive pulmonary disease: a case for treatment. 1611 63

Exercise intolerance and heart failure with preserved ejection fraction are common in females. Recently, arterial stiffness has been suggested to be a significant contributor in the development of heart failure. How gender difference affects arterial stiffening and its response to exercise is not well known. We hypothesized that arterial elastance index during exercise would be more abnormal in females with hypertension than males. Arterial elastance index was estimated as arterial end systolic pressure/stroke volume controlled for body surface area and was measured at rest and during graded supine bicycle exercise (25 watts, 3-minute increments) in 298 patients with hypertension (149 males; 149 females; mean age, 59). The subjects were divided into 2 groups by gender. Exercise duration was significantly shorter in females compared to males (692+/-222 versus 483+/-128 seconds, P<0.001). Although arterial elastance index at baseline was significantly higher in males, the magnitude of increase was steeper in females with the magnitude of change at 75 W of exercise being significantly higher in females compared to males (0.69+/-0.83 versus 0.43+/-0.69, P=0.018). Arterial elastance index at each stage of exercise up to 75 W was independently associated with decreased exercise duration. In conclusion, despite lower arterial elastance index at rest, the increase during exercise was steeper in women with hypertension, suggesting a gender-related difference in dynamic arterial stiffness. The arterial elastance index during exercise was significantly associated with exercise duration in patients with hypertension.
Hypertension 2008 Apr
PMID:Gender-related difference in arterial elastance during exercise in patients with hypertension. 1825 19

Hypertension, diabetes and obesity cause cardiac diastolic dysfunction (DD) which could reduce exercise capacity. Our aim was to determine if 10% weight loss by exercise at 60% VO(2max) five days/week (approximately -375 kcal/session) and caloric restriction (approximately -600 kcal/d) over 6 months improves exercise capacity and DD in Metabolic syndrome (MetS). Eighteen subjects (40 +/- 1y, women = 6, BMI = 33.5 +/- 1.0 kg/m(2)) successfully completed the study. Maximal treadmill stress echocardiography was performed at baseline and post weight loss to determine VO(2max), resting and stress DD as the ratio of peak early diastolic mitral inflow velocity (E) to tissue Doppler early diastolic annular decent (E'). After weight loss (mean = 9.5 +/- 0.2%), all metabolic parameters improved. Resting and stress E/E' values remained normal before and after weight loss. Exercise intolerance is likely due to general deconditioning and not cardiac dysfunction in early MetS as VO(2max) increases significantly with lifestyle while cardiac function remains unchanged.
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PMID:Exercise and weight loss improve exercise capacity independent of cardiac function in metabolic syndrome. 2011 6

Exercise intolerance is the main characteristic of pulmonary arterial hypertension (PAH). The six-minute walk test (6MWT) and cardiopulmonary exercise test are widely used in assessing exercise capacity of PAH patients. Six-minute walk distance (6MWD) has been specified as the main clinical outcome in PAH and has been used as the primary end-point in many studies conducted for new PAH treatments. Using 6MWD as the end-point in clinical studies has many advantages. 6MWT is an inexpensive, easily applicable, and repeatable standardized test that is well-tolerated by PAH patients. Moreover, it is a valid measure of symptomatic improvement. It is correlated with variables of maximal cardiopulmonary exercise test as a measure of submaximal exercise capacity and disease severity markers such as functional class and pulmonary hemodynamics. It is widely used in clinical practice together with other invasive and non-invasive disease markers in assessing disease progression and response to treatment. In addition, it has prognostic importance and is a good prognostic marker. On the other hand, there are limitations to the use of 6MWD as the primary end-point in PAH treatment. It has decreased sensitivity in individuals with less severe disease and high 6MWD at baseline and decreased adequacy in assessing the effects of treatment in patients who are still under PAH treatment. Despite the limitations, 6MWD plays a key role in the evaluation and management of PAH patients.
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PMID:Six-minute walk test in pulmonary arterial hypertension. 2588 Jan 78