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

This paper is a post-hoc analysis of a previous study performed to investigate the relationship between computerized tomography (CT) and lung function in 51 outpatients with mild-to-moderate COPD. We studied whether changes in lung function and radiographic patterns may help to explain dyspnea, the most disturbing symptom in patients with COPD. The Medical Research Council (MRC) dyspnea scale shows, by univariate analysis, a similar strength of association to CT expiratory lung density and to DL(CO), a functional index of lung parenchymal loss. The MRC dyspnea scale shows a somewhat less strength of association with a small vertical heart on plain chest films. In multivariate analysis, the model with the strongest association to the MRC dyspnea scale (r = 0.76, p < 0.0001) contains 4 explanatory variables (DL(CO), FRC, PaCO(2), and radiographic pattern of pulmonary hypertension). We suggest that diffusing capacity reflects the emphysematous component of hyperinflation, associated by definition with destruction of terminal airspace walls, as distinct from the air trapping component, which is ascribed to airway obstruction and associated with FRC. PaCO(2) mainly reflects the ventilatory components, i.e., ventilatory drive and ventilatory constraints, of pulmonary gas exchange in COPD, while radiographic pattern of pulmonary hypertension likely reflects hypoxic vascular changes, which depend mainly on ventilation/perfusion mismatch and give rise to pulmonary arterial hypertension that may contribute per se to dyspnea. In conclusion, our analysis points out that chronic effort dyspnea variance may account for up to 58% (r(2) = 0.58) by lung function tests and radiographic patterns. Thus, about 42% of the MRC dyspnea variance remains unexplained by this model. On the other hand, dyspnea ascertainment is dependent on subjective behavior and evaluation and in tests is influenced by individual performance and perception. For example in the 6-minute walk test, a similar or higher proportion (60%) of the overall variance is unexplained.
COPD 2007 Sep
PMID:Chronic effort dyspnea explained by lung function tests and by HRCT and CRX radiographic patterns in COPD: a post-hoc analysis in 51 patients. 1772 59

Pulmonary artery hypertension secondary to chronic lung diseases is a clinical entity with no specific symptoms that can develop as a result of parenchymal lung disorders (COPD-emphysema, sleep apnea syndrome, diffuse parenchymal lung diseases, etc.) and pulmonary vascular disorders (vasculitis, sarcoidosis, etc.). In the clinical history of these chronic and invalidating diseases, pulmonary vasculature goes through various degenerative and/or proliferative changes, responsible of the pulmonary arterial hypertension appearance. The rise in pulmonary artery pressure can be subtle and the progression from an asymptomatic disease to a more severe syndrome is often common in all forms of secondary pulmonary arterial hypertension. Etiopathology of pulmonary artery hypertension secondary to chronic lung diseases is based on one or more of the following mechanisms: hypoxic vasoconstriction, decreased area of pulmonary vascular bed, volume/pressure overload. In these forms, the above three mechanisms show common mediators, all responsible of disease progression but singularly potential reversible. Therapies for secondary pulmonary artery hypertension consist primarily on the treatment of the underlying disease. Therapy is most effective when initiated prior to the onset of irreversible pulmonary vascular damage. In the last two decades, new medical treatments (prostacyclins, endothelin receptor antagonists, phosphodiesterase inhibitors) for pulmonary arterial hypertension have been available for the sporadic and the secondary to systemic sclerosis forms. The role of these drugs in the other forms of pulmonary arterial hypertension has not been well studied yet. This review will go through the pathogenesis and the several therapeutic approaches for pulmonary artery hypertension secondary to chronic pulmonary diseases or pulmonary vasculature disorders.
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PMID:Pulmonary arterial hypertension secondary to chronic lung diseases: pathogenesis and medical treatment. 1803 16

Asthma control is a key point in patient management. GINA's most recent report emphasises the need to investigate uncontrolled asthma, of which non-compliance with treatment, COPD, smoking, chronic sinusitis, gastroesophageal reflux disease and obesity are the usual causes. The aim of this work is to evaluate the role of pulmonary thromboembolism (PTE) in cases of difficult- -to-treat asthma. We reviewed the case reports of patients with severe persistent asthma followed in our Asthma Outpatients Clinic between 2004 and 2006. We selected the ones that maintained uncontrolled disease despite an optimal therapeutical approach and investigated the causes. In this group (n=254), 28 (11%) had severe persistent asthma and their mean age was 44 +/- SD18 years old. 86% were females. Of these, 57% (n=16) had uncontrolled disease: 35% (n=6) due to non-compliance with treatment; 29% (n=5) pulmonary thrombombolism (scintigraphic confirmation); 12% (n=2) severe rhinosinusitis; 6% (n=1) hypereosinophilic syndrome; 6% (n=1) persistent allergen exposure and 6% (n=1) are still being investigated. Patients with TPE (mean age 56 +/- SD9 years old; 80% females; 80% Caucasians) were diagnosed with asthma as adults (mean age 37 +/- SD14 years old). The mean time until the diagnosis of TPE was 18 +/- SD12 years. Predisposing factors for TPE were venous insufficiency (40%), hypertension (40%) and deficit of functional protein C and S (20%). All these patients received anticoagulant therapy (80% are still medicated). It should be noted that after the beginning of anticoagulants, 40% of the patients achieved control of their asthma and 40% have partially controlled disease. There were no hospital admissions for asthma exacerbations after the beginning of anticoagulation in this group. This study supports the inclusion of TPE in the group of comorbidities to consider while investigating uncontrolled asthma.
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PMID:[Pulmonary embolism and difficult-to-treat asthma]. 1818 29

Homeless veterans have numerous medical and behavioral health problems. Grouping homeless people based on comorbidity patterns may assist in determining severity of illness and triaging health care more effectively. We sought to determine if a finite number of profiles could be identified related to demographic characteristics, living situation, length of homelessness, and referral areas using interview data from 2,733 veterans who were presently or recently homeless. We considered 12 disorders: eye problems, hypertension, cardiovascular problems, COPD/emphysema, tuberculosis, gastrointestinal problems, hepatic disease, neurologic disorders, orthopedic problems, skin problems, and trauma. Ratings were evaluated using cluster analysis. Comparison statistics were used to compare intercluster differences in demographics, homeless situation, and referral recommendations. A four-cluster solution is proposed: generalized illness, hepatic disease, lung disease, and neurologic disorder. Medical health problems are common and heterogeneous in homeless individuals. Classifications of these problems may be useful in planning treatment and predicting outcome.
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PMID:A Taxonomy of medical comorbidity for veterans who are homeless. 1867 85

In 2007 we provided an overview of clinical advances in the nursing home based on a series of presentations at the American Medical Directors Association. This will now be a regular yearly series. Topics covered this year are nutrition, exercise, diabetes mellitus, lipids, hypertension, pressure ulcers, COPD, and osteoporosis.
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PMID:Clinical update on nursing home medicine: 2008. 1875 19

Metoprolol is a widely used cardioselective beta-blocker. However, like all other beta-blockers it is also a racemic mixture of R- and S- isomers. The beta 1 blocking activity (cardioselectivity) of metoprolol resides in S-isomer while R-isomer exhibits beta 2 blocking activity. As both these isomers have different pharmacological properties, racemic metoprolol can be considered a combination of two different drugs in a fixed 1:1 ratio. The needless administration of the non beta-blocking R-enantiomer that makes up 50% of racemate actually puts the patient at an increased risk of side-effects, drug interactions and loss of cardioselectivity with up-titration of dosing. Clinical experience with chirally pure S-metoprolol at half the dose of racemate has shown it to be as effective as racemate in the treatment of patients with hypertension and angina. S-metoprolol has been shown to be effective and well-tolerated in patients with coexisting diabetes, COPD, and hyperlipidaemia. This confirms higher cardioselectivity of S-metoprolol in clinical settings. Less interaction potential of S-metoprolol compared to R-isomer further makes it a sensible choice in patients taking CYP2D6 inhibitors or in patients with heart failure or hepatic insufficiency. This article reviews differing properties of two isomers of metoprolol with focus on clinical experience with S-metoprolol.
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PMID:S-metoprolol: the 2008 clinical review. 1882 49

Pulmonary hypertension is an important complication of COPD. A small subset of patients with COPD have severe pulmonary hypertension (PH) that is out of proportion to the mild increase in pulmonary arterial pressure observed commonly. Severe PH associated with COPD is associated with increased morbidity and mortality. Treatment options in this group of patients are limited with no conclusive evidence of benefit when drugs approved for treatment of pulmonary arterial hypertension are used. We describe a patient with severe PH associated with COPD who improved clinically and hemodynamically when treated with inhaled iloprost. The improvement was sustained for 2 years. Severe PH in patients with COPD needs to be recognized and novel treatment approaches considered.
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PMID:Sustained improvement with iloprost in a COPD patient with severe pulmonary hypertension. 1920 16

Respiratory problems are common in patients with chronic liver diseases. The most common causes are disorders that are not related to liver diseases such as asthma and COPD. In addition certain liver diseases that are associated with specific pulmonary abnormalities, and conditions associated with end stage liver disease like tense ascites and intercostal muscular wasting are considered. Finally two unique disorders characterizing by vascular abnormalities independent of cardiorespiratory disorder-the hepatopulmonary syndrome (HPS) and portopulmonary hypertension (POPH) are observed. These disorders have different pathogenesis, different clinical pictures, treatment and prognosis. This article reviews the epidemiology, pathophysiology, clinical features, evaluation and current therapy of these two disorders.
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PMID:Pulmonary manifestations of liver diseases. 1933 39

This work had the aim to study effect of systemic inflammation in patients with COPD and COPD with arterial hypertension (AH) based on the state of endothelium and the degree of atherosclerosis of common carotid arteries. The study included 51 men (mean age 50.9 +/- 3 yr) 20 of whom (mean age 54.5 +/- 13.2 yr) had grade I-II COPD (GOLD, 2006) and 1-2 grade AH (WHO, 1999). The patients were allocated to 2 groups, one comprising 11 subjects with isolated AH (mean age 47.5 +/- 8.4 yr) the other 10 men with isolated COPD (mean age 51.8 +/- 4.6 yr). The control group included 10 men (mean age 49.6 +/- 5.3 yr). IMT, C-reactive protein, and blood lipid spectrum were determined in all the patients. Patients with COPD with and without AH developed atherosclerosis of common carotid arteries caused by persistent systemic inflammation. Increased serum C-reactive protein and IMT in patients of the two groups contributed to the initiation and progress of atherosclerosis of common carotid arteries.
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PMID:[Systemic inflammation and atherosclerosis of common carotid arteries in patients with chronic obstructive pulmonary disease]. 1934 94

In order to calculate the cardiovascular risk in patients with chronic renal failure (CRF), we retrospectively analyzed 1482 acute myocardial infarctions (AMIs) treated in the ICU at C. Poma General Hospital, Mantua, Italy, from 1 December 2004 to 31 July 2007. Of these patients, 133 suffered from CRF at hospital admission (eGFR <40 mL/min/1.73 m2 body surface and/or serum creatinine >2 mg/dL). During hospitalization for AMI, the CRF-affected patients showed a 2.7 times higher relative risk of mortality than patients without CRF (Yates chi square 14.46; p = 0.0001432). The evaluated comorbidities (hypertension, type 2 diabetes, supra-aortic vascular stenosis >70%, previous PTCA, COPD, previous AMI, previous coronary artery bypass and chronic obliterative peripheral arteriopathy) increased the relative risk of death 1.2- to 3.76-fold in those affected. In accord with recent evidence in the international literature, our results point to the importance of early assessment of CRF for the prognosis of patients with AMI.
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PMID:[Mortality triplicates in acute myocardial infarction patients affected by chronic renal failure]. 1938 88


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