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

100% oxygen breathing during submaximal exercise in patients with diffuse interstitial lung disease diminishes cardiac output and pulmonary artery hypertension. The pressure drop in the pulmonary artery is most marked in patients with concomitant bronchial obstruction. At rest hyperoxia produced only minimal cardiopulmonary changes. The ventilatory and hemodynamic responses are discussed to find out if differences in these variables during oxygen breathing could be a reliable index for functional classification.
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PMID:Oxygen breathing during exercise in patients with diffuse interstitial fibrosis. 88 Apr

Polymyositis-dermatomyositis (PM-DM) is an inflammatory disease of muscle and skin mediated by autoimmune and cellular events. Most typically, muscle weakness is the usual presentation. This review emphasizes that often the systemic components of this disease may mask the usual presentation and actually may be the presenting and only manifestations; more often than not they are the causes of increased morbidity and mortality. In particular, the cardiopulmonary manifestations may dominate the disease course. Cardiac complications include congestive heart failure resulting from a primary cardiomyopathy, disrhythmias and atrioventricular conduction disturbances, sick sinus syndrome, and cor pulmonale either secondary to interstitial lung disease (ILD) or primary pulmonary artery hypertension. Recurrent aspiration pneumonia results from pharyngeal muscle involvement by the myositic process. Several histologic patterns of ILD can emerge with varying outcomes and responses to immunosuppresive therapy. Involvement of the muscles of respiration can lead to hypercapnic respiratory failure, diaphragmatic dysfunction, hypostatic pneumonia, and restrictive lung disease.
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PMID:Pulmonary and cardiac manifestations of polymyositis-dermatomyositis. 157 25

A prospective study was performed in our center on 60% (n = 36) of patients with systemic lupus erythematosus (SLE) to determine the prevalence and severity of pulmonary hypertension. Twenty-six healthy subjects of similar age and sex served as controls. Pulmonary artery systolic pressure was calculated from the sum of the peak tricuspid insufficiency Doppler pressure gradient and an estimate of right atrial pressure based on inferior vena cava size and its degree of inspiratory collapse. Five patients with SLE (14%) had pulmonary hypertension, defined as pulmonary artery systolic pressure greater than 30 mm Hg. Cardiac indices determined by planimetry of biplane apical 2-dimensional echocardiographic images were low or normal in the patients with pulmonary hypertension implying increased pulmonary vascular resistance as the etiology for elevated pulmonary artery pressure. The mean pulmonary artery systolic pressure in patients with SLE was 25 +/- 10 mm Hg vs 20 +/- 2 in controls (p = 0.002). No control had a pulmonary artery systolic pressure greater than 23 mm Hg. Patients with pulmonary hypertension had a shorter duration of SLE and steroid therapy and a higher prevalence of cytotoxic treatment and Raynaud's phenomenon in comparison to those with normal pulmonary artery pressures. The prevalence of systemic hypertension, interstitial lung disease, pleurisy, pericarditis, cutaneous manifestations, arthritis, renal disease, central nervous system involvement, and hematologic abnormalities was similar in patients with SLE with normal and elevated pulmonary artery pressure. Our study suggests that pulmonary hypertension in SLE is common but usually mild.
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PMID:Pulmonary hypertension in systemic lupus erythematosus. 233 68

We studied the effect of hydralazine (HDL) on peripheral oxygen transport (TO2) in 8 patients with chronic obstructive lung disease (EPOC, group I) and 11 patients with chronic interstitial lung disease (NI, group II) and pulmonary arterial hypertension (HAP). Mean pulmonary artery pressure (Pp) at basal conditions were 31 +/- 3 mmHg for the EPOC group and 26 +/- 9 mmHg for NI patients. After HDL, pulmonary vascular resistance (Rp) decreased significantly only in NI patients (Rp basal = 7.1 +/- 4, Rp post HDL = 5.9 +/- 3u m2). In EPOC patients Pp increased after HDL (Pp basal = 31 +/- 3, Pp post HDL = 36 +/- 4 mmHg, p less than 0.05). This was not the case for NI patients in whom Pp did not change. Both groups showed reduction in systemic vascular resistance after HDL. PaO2, PvO2, SaO2, CvO2 and TO2 were significantly increased in both groups after HDL. TO2 change was correlated with the increasing cardiac index in both diseases and with arterial oxygen content in group II only. Our study suggest that TO2 improves in EPOC and NI patients after HDL, however only in NI was associated with a reduction in pulmonary vascular resistance.
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PMID:[Hydralazine and oxygen transport in interstitial and chronic obstructive pneumopathies]. 296 46

Pulmonary blood volume (PBV) measurements have been reported in chronic lung disease that do not include diffuse interstitial lung disease (ILD) and cor pulmonale (CP). In this study, PBV was measured using the double injection single sampling method, at rest and at exercise in ten patients with ILD due to extrinsic allergic alveolitis (n = 6) or usual interstitial pneumonia (n = 4). Lung biopsies were obtained in 8 patients, and in none of them the stage of fibrosis was predominant over inflammation. The degree of vascular lesions was in four patients grade I and in four grade II (Heath-Edwards classification). At rest, most of the patients had elevated mean pulmonary artery pressure (PAP) and vascular resistance (PVR), (mean PAP 30 +/- 4 mmHg and 336 +/- 171 d.s. cm.-5, respectively), hypoxemia (paO2 = 48 +/- 2 mmHg) and a severely reduced PBV (53.6 +/- 11 ml.s.qm.). At exercise, pulmonary arterial hypertension worsened and, although PBV value increased significantly (rest = 53.6 +/- 11.6 ml.m2, s.qm. exercise 132 +/- 28 ml.s.qm.p less than 0.01) it remained abnormally low with respect to normal value. Comparison of the mean intravascular pressure-PBV measurements relationship in different lung diseases showed that ILD patients with CP have the greatest abnormality. Possible explanations for the severe reduction in PBV include restriction of extra-alveolar vessels as a consequence of lung volume loss, restriction of intra-alveolar vessels due to structural and functional changes imposed by the inflammation-fibrosis process and vascular restriction due to vasoactive factors (alveolar hipoxia).
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PMID:[Pulmonary blood volume in patients with interstitial pneumopathy and pulmonary heart disease. Its study at rest and during exercise]. 319 Mar 62

Hydralazine was administered short-term to 13 patients who had stable interstitial lung disease (ILD), pulmonary arterial hypertension (PAH); mean pulmonary arterial pressure ( [PAP]=26 +/- 9 mm Hg), and cor pulmonale (CP). All patients were studied at rest and during exercise. After intravenous hydralazine at rest, there were statistically significant increases in cardiac index (CI) (p less than 0.001), arterial oxygen saturation (SaO2) (p less than 0.01), and mixed venous saturation (S-vO2) (p less than 0.01). Pulmonary vascular resistance (Rp) (p less than 0.005) and systemic resistance (Rs) decreased (p less than 0.001), and PAP did not change. During exercise, PAP did not change; however, CI (p less than 0.01), PaO2 (p less than 0.001), and S-vO2 (p less than 0.01) increased further. The increase in Rp was significantly reduced (p less than 0.01). After continuation of oral hydralazine therapy in 12 patients for 7 days, PAP at rest was not statistically different from control; Rp and Rs remained decreased (p less than 0.001). The same results were found for CI, PaO2, S-vO2, and Rs during exercise. Although PAP did not change from control values, the drug significantly reduced the increase in Rp (p less than 0.005). Vasodilator therapy with hydralazine could be useful in patients with stable ILD who have inflammation with minimal to moderate fibrosis and PAH and might be used as an adjunct to conventional therapy for ILD and CP.
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PMID:Hemodynamic effect of hydralazine in interstitial lung disease patients with cor pulmonale. Immediate and short-term evaluation at rest and during exercise. 398 68

An echocardiographic M-mode study has been performed on 58 patients with pulmonary arterial hypertension at rest or on exercise, with chronic lung disease, either obstructive (41 cases of COLD) or restrictive (17 cases of interstitial lung disease, ILD) in nature. The average Ppa was practically the same (i.e. 27.3 +/- 11.7 mmHg and 26.0 +/- 8.0 mmHg respectively) in the two groups of patients, even though the COLD patients were older than the ILD patients (58.7 +/- 9.3 vs 38 +/- 11 years). The echo detection of the pulmonary valve was successful in only 35% of COLD patients and in 86% of ILD patients (p less than 0.01). A multiple regression analysis disclosed a rather weak, but nevertheless statistically significant, correlation (p less than 0.01) between 1) Ppa and the ratio of right ventricular to left ventricular end-diastolic volume, and 2) between right ventricular end-diastolic pressure and septal systolic displacement. The standard error of estimated versus actual Ppa taking into account the ventricular and septal echo variables was as high as +/- 7.63 mmHg, thus preventing a reliable prediction of Ppa in individual cases. An echocardiographic pattern of pansystolic mitral valve prolapse was observed in 29% of ILD patients, but never in cases with COLD.
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PMID:Echocardiographic aspects of pulmonary arterial hypertension in chronic lung disease. 674 67

Pulmonary hypertension is an uncommon complication of sarcoidosis and is usually related to the development of end-stage, interstitial fibrosis or honeycomb lung. We describe a patient with sarcoidosis who developed pulmonary hypertension in the absence of significant parenchymal fibrosis. The pulmonary hypertension in this case was caused by granulomatous destruction of arteries and veins, as documented by an open-lung biopsy and autopsy. Clinical features, including pulmonary function tests, are presented which suggested that end-stage interstitial lung disease was not causing the hypertension. Recognition of this complication of sarcoidosis is important if effective therapy is to be found.
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PMID:Vascular sarcoidosis: a rare cause of pulmonary hypertension. 682 15

A 58 year old woman developed systemic symptoms, interstitial lung disease, splenomegaly, leukopenia and anti-histone and anti-nuclear antibodies (ANA), while treated with hydralazine for hypertension. Five months after presentation she was admitted with high fever, skin rash and atypical lymphocytosis due to acute cytomegalovirus (CMV) infection. Worsening leukopenia and increased ANA were found, and high titres of anti-DNA antibodies, anti-cardiolipin antibodies and rheumatoid factors appeared. Hydralazine was stopped and the patient gradually became asymptomatic. All autoantibodies spontaneously disappeared (over 16 weeks), and the white cell count and spleen size became normal. The patient was found to be a slow acetylator and to have both HLA-DR4 and selective IgA deficiency. Thus, a multifactorial genetic susceptibility to develop drug-induced lupus was brought out in stages first by hydralazine and then by CMV, yet all manifestations and autoantibodies resolved spontaneously, demonstrating the complex interplay of varied environmental factors with a genetic predisposition in the pathogenesis of autoimmunity.
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PMID:Effect of acute cytomegalovirus infection on drug-induced SLE. 783 Nov 73

We report an 18 year old black woman who presented with nephrotic syndrome in whom the investigations led to the diagnosis of diffuse Takayasu's disease, renal amyloidosis of AA type and interstitial lung disease. Proteinuria in Takayasu's disease is usually ascribed to hypertension or more rarely to glomerulonephritis. This case suggests that amyloidosis should be considered also in the investigation of proteinuria in these patients in view of the serious prognostic implications. This case represents further evidence that Takayasu's disease can be the cause of systemic reactive amyloidosis which may also be the presenting feature.
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PMID:Takayasu's disease presenting as a nephrotic syndrome due to amyloidosis. 791 68


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