Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autopsy observations suggested that lesions of hypertensive pulmonary vascular disease (HPVD) due to elevated venous pressure differ from those with arterial hypertension only. Clinical and pathologic features were reviewed in patients from the Hopkins autopsy files with proved pulmonary hypertension; 50 had venous HPVD due to left-sided congestive heart failure, 50 had arterial HPVD due to congenital malformations, and 15 had idiopathic pulmonary hypertension (IPH). The two forms of HPVD have consistent distinctive histologic changes. In venous HPVD intimal fibroelastosis (IFE) develops in veins and arteries with retention of normal lumen diameters. Intensity of IFE correlates with severity and duration of venous hypertension. Arterial HPVD has IFE in conducting arteries, but the characteristic lesion is cellular intimal proliferation in regulatory arterioles, producing progresssive irreversible lumenal narrowing. Glomoid and angiomatoid lesions appear with prolonged severe arterial hypertension. They do not occur in venous HPVD. Hypertensive arteritis may develop with either form of HPVD. IPH has arterial-type HPVD. IFE of venous HPVD appears to be a response to increased mural tension. Arteriolar intimal cellular proliferations seen in arterial HPVD may be produced by blood flow boundary layer separations. IPH may be explainable as protracted inappropriate pulmonary arteriolar constriction.
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PMID:The pathogenesis of the two forms of hypertensive pulmonary vascular disease. 99 86

The presence of left ventricular hypertrophy (LVH) in either hypertensives -H- or in normotensives -N-, suggests that not only blood pressure is determining this anatomic change, but various factors, as neural or endocrine ones, could be involved in its genesis. In order to evaluate the role of sympathetic dys-reactivity on LVH, we studied three groups of subjects: a) 12 -H- (SBP 159+/-9; DBP 99.6+/-7; FC 80+/-7) with LVH, diagnosed by echocardiogram. b) 12 -N- (SBP 138.2+/-8; DBP 83+/-2; FC 75.6+/-4) with LVH. c) 12 -N- (SBP 136.6+/-11; DBP 81.8+/-5; FC 76.3+/-5) without LVH. Using computer interfaced equipment, we measured beat to beat, hemodynamic and extra-cardiovascular autonomic functions, during a session of stressors (Mental Arithmetic, Color Word Stroop, Cold Pressure and Handgrip Tests), preceded and followed by 10' of observation. Among the various considered indexes, we evaluated the Percentual Total Activity Index (PTAI), as percentual total activity change + percentual total recovery change. Our findings point out that the PTAI of N with LVH is significantly higher for SCL, PHT, HR, SV, CO, TPR than either in H with LVH or N without LVH. These data seem to demonstrate a prolonged reactivity in N without LVH and are according to the hypothesis that LVH could also be supported by a hyper-adrenergic state with sympathetic dys-reactivity, independently from high blood pressure values.
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PMID:[Left ventricular hypertrophy: physiopathological signs using a hemodynamic and cardio-autonomic approach]. 146 95

We studied sera of 371 consecutive new patients with systemic sclerosis (SSc; scleroderma) who were first evaluated during 1984-1988. All sera were tested for antinuclear antibodies by immunofluorescence staining using HEp-2 cells as substrate. We excluded 219 sera showing dark nucleoli and screened for antibodies to Th in the remaining 152 sera by immunoprecipitation of a 32P-labeled HeLa cell extract. Fifteen (4.0%) of 371 sera were anti-Th+. Anti-Th antibodies were present in 14 (8.4%) of 167 SSc patients with limited cutaneous involvement, in 1 of 167 with diffuse cutaneous involvement, and in 0 of 37 with SSc overlap syndrome. Among 244 controls with other connective tissue diseases, anti-Th was detected in only 3 patients, all having primary Raynaud's phenomenon of less than 2 years duration. In the subgroup with SSc with limited cutaneous involvement, the 14 anti-Th+ patients had a significantly greater frequency of puffy fingers, small bowel involvement, and hypothyroidism, and a significantly lower frequency of arthralgia and/or arthritis. Their cumulative survival rate from the time of onset of symptoms was lower than that for anti-Th- patients (78% versus 91% at 10 years), primarily due to 3 deaths from pulmonary arterial hypertension (2 from primary pulmonary hypertension and 1 from pulmonary hypertension secondary to pulmonary interstitial fibrosis). Serum anti-Th antibodies are present almost exclusively in patients with SSc with limited cutaneous involvement or in those with primary Raynaud's phenomenon whose disease may evolve to SSc with limited cutaneous involvement, and these antibodies may identify those patients who are at greater risk for reduced survival.
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PMID:Autoantibody to Th ribonucleoprotein (nucleolar 7-2 RNA protein particle) in patients with systemic sclerosis. 170 94

The conventional chest radiographs were studied of 18 patients with primary pulmonary hypertension, waiting for, or treated with lung transplantation in the Papworth Hospital. The goal of the study was to find out whether there is a pattern characteristic of primary pulmonary hypertension. The following points were considered: a) pulmonary transparency; b) the hila; c) the left hemidiaphragm; d) the pulmonary artery; e) the right ventricle; f) the right atrium; g) the left ventricle. A score was assigned for any degree of abnormality of the points mentioned above. As a result, a radiological pattern was found that can: 1) confirm the presence of pulmonary hypertension; 2) exclude that this hypertension has a detectable cause; 3) measure the severity of the disease, particularly with regard to hypertension degree. The conclusion is that there is a radiological pattern strongly suggestive of primary pulmonary hypertension and that conventional radiology can help in detecting and monitoring this rare disease, which today can only be treated by means of transplantation.
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PMID:[Is there a typical radiologic picture of primary pulmonary hypertension? Study of 18 cases]. 194 63

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

Since Shumway carried out the first successful heart-lung transplant (HLT) in Stanford in 1981, HLT has become a new therapeutic means for patients with end-stage pulmonary disease or arterial hypertension. However, it is still rarely carried out because of a lack of donors and the complexity of the surgery and postoperative course. This review described the criteria for proper donor and recipient selection, as well as the anaesthetic and postoperative management of HLT patients at Marie Lannelongue Hospital. The lack of suitable organ grafts results, at least in part, from improper donor management. Pulmonary oedema by fluid overloading and excessive haemodilution should be carefully prevented. Low doses of catecholamines and vasopressin maintain circulatory stability and convenient organ function. The indications for HLT (primary pulmonary hypertension, Eisenmenger's complex, and end-stage bronchopulmonary disease) are all characterized by severe pulmonary hypertension, hypoxaemia and cardiac failure. Careful anaesthetic induction is required to avoid circulatory collapse. Cardiopulmonary bypass (CPB) should be started early, so that mediastinal dissection may be carried out in satisfactory haemodynamic conditions. After unclamping the aorta, circulatory support with fluid and catecholamine infusion is often required. High inspired oxygen fraction and end-expiratory positive pressure may be required because of reperfusion pulmonary oedema. Blood transfusion is often needed as there are major blood losses due to dissection of the posterior mediastinum during CPB. Postoperative catecholamine administration is prolonged over several days. Negative fluid balance is often necessary to reduce pulmonary oedema. Improvement in surgical technique, early extubation, and late prescription of steroids have reduced the incidence of tracheal complications. Acute renal failure often occurs as a result of prolonged CPB, hypovolaemia, drug nephrotoxicity and sepsis. Bacterial complications (pneumonia, mediastinitis) are the main causes of early death. After the 15th postoperative day, opportunistic infections and allograft rejection are the main complications. Since 1981, major advances in HLT recipient management resulted in improved survival rates (70-80% at 1 year, and 60-70% at 2 years for the best teams). Despite the complexity of management, and the longterm threat of obliterative bronchiolitis, HLT is, at present time, the only possibility for these young patients to recover a normal quality of life.
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PMID:[Anesthesia and intensive care for heart-lung transplantation]. 205 32

In a retrospective study, patients with end-stage renal failure from analgesic-associated nephropathy - 55 on regular dialysis treatment and 12 after renal transplantation - were under observation for 57 and 33 months, respectively. Of these 34 patients on chronic hemodialysis had suffered from different cardiovascular diseases. Hypertriglyceridemia was diagnosed in 62% of the patients, arterial hypertension requiring antihypertensive therapy in 44%. In three patients (5%) carcinoma of the urinary bladder were diagnosed. The leading causes of death in 21 patients included cardiovascular diseases (29%), hyperkalemia (19%), sepsis, and malignant tumors (14% each). Rejection occurred in 3 out of 12 patients after renal transplantation. Again, cardiovascular morbidity was high (58%) with coronary heart disease being present in 33% of the patients. Hypertriglyceridemia was observed in 5 out of 6 patients, antihypertensive therapy was needed in 50%. One patient died from primary pulmonary hypertension.
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PMID:Morbidity of patients with analgesic-associated nephropathy on regular dialysis treatment and after renal transplantation. 210 98

We evaluated the effect of verapamil therapy on left ventricular hypertrophy and left ventricular diastolic function in 13 patients with mild to moderate hypertension. Left ventricular hypertrophy was determined by M-mode echocardiographic measurements of interventricular septal thickness (IVST), posterior wall thickness (PWT) and left ventricular mass index (LVMI) both before (T0) and after 3 months (T3) of verapamil therapy. Left ventricular diastolic transmitral flow was measured by pulsed Doppler indices of early (E) and atrial (A) velocity, E/A ratio, total area (Ta), A area (Aa), Aa/Ta ratio, E-pressure half-time (E-PHT). A-pressure half-time (A-PHT) and E-PHT/A-PHT ratio both before and after 3 months of verapamil therapy. No significant changes occurred in mean heart rate, systolic function or body weight. We conclude that 3 months' therapy with verapamil resulted in an improvement in left ventricular hypertrophy and left ventricular diastolic function and a normalization of blood pressure, without a corresponding deterioration in left ventricular systolic function.
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PMID:Improvement in left ventricular hypertrophy and left ventricular diastolic function following verapamil therapy in mild to moderate hypertension. 214 51

CCB are a diverse group of drugs that bind to specific glycoprotein receptors associated with the cell membrane that are most likely identical to the voltage-sensitive calcium channel. By inhibiting the influx of calcium into myocardial, pacemaker, and conducting tissues and vascular smooth muscle, these agents modify excitation-contraction coupling in muscle and electrical impulse transmission in the heart. The vasodilating and electrophysiologic actions of these drugs have been harnessed for the treatment of coronary vasospasm, angina pectoris, and supraventricular arrhythmias. They also have great potential for the treatment of hypertension, cerebrovascular disorders, and Raynaud's phenomenon. Their utility in hypertrophic cardiomyopathy, congestive heart failure, myocardial preservation, and primary pulmonary hypertension has not been convincingly established. Future second-generation CCB may offer greater selectivity, improved side effect profiles, and an even wider range of actions.
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PMID:Calcium channel blocking drugs. Part II: Clinical applications. 241 54

Two of the many mediators synthesized by vascular endothelial cells (EC), are involved in maintaining the surface of the normal, healthy endothelium in a non-thrombogenic state. The first is prostacyclin, a product of arachidonic acid metabolism, discovered in 1976. This labile prostanoid, with a half life of approximately 3 minutes, relaxes vascular smooth muscle and inhibits the aggregation of blood platelets. Prostacyclin and its analogues are currently being tested in the clinic for cardiovascular diseases such as primary pulmonary hypertension. A number of drugs including defibrotide, nafazatrom, ronicol and cicletanine may exert their therapeutic effects by releasing prostacyclin from the EC. The second mediator discussed is endothelium-derived relaxing factor (EDRF), discovered in 1980, which also relaxes smooth muscle and inhibits the aggregation and adhesion of platelets. Substances which stimulate release of EDRF include acetylcholine, bradykinin and ADP. EDRF is even more labile than prostacyclin with a half life counted in seconds. It has recently been identified as nitric oxide formed from L-arginine by an unknown mechanism. Prostacyclin and EDRF are released together following stimulation of endothelial receptors and synergize to inhibit platelet aggregation. It is suggested that these mediators form the endothelial defence mechanism against blood-borne cells and chemicals and that breakdown of this barrier results in diseases such as hypertension and atherosclerosis. The peptide, endothelin is the third mediator under discussion. Characterised and synthesised in 1988, it is the most potent vasoconstrictor so far discovered. Three isomers of endothelin have been identified. Paradoxically, endothelin strongly releases both prostacyclin and EDRF thus modulating its own vasoconstrictor actions.
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PMID:Vasoactive mediators derived from the endothelium. 251 50


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