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

Qualitative and quantitative studies were performed on pulmonary blood vessels in lung tissue obtained by biopsy, pneumonectomy, or autopsy from 58 patients in the Registry of Primary Pulmonary Hypertension sponsored by the Heart, Lung, and Blood Institute of the National Institutes of Health. In 49 patients (84%), the hypertensive vascular disease involved predominantly or exclusively muscular pulmonary arteries and arterioles. In each of these 49 patients, pulmonary artery medial hypertrophy was observed, and in 48 patients, it was also associated with intimal or luminal lesions. On the basis of the predominant histopathologic features, 25 of the 48 patients were classified as having pulmonary arteriopathy with plexiform lesions characterized by a combination of concentric laminar intimal fibrosis, eccentric intimal fibrosis, and plexiform lesions; in nine of these 25, recanalized thrombi were also present. Pulmonary arteriopathy with thrombotic lesions, defined by the presence of both eccentric intimal fibrosis and recanalized thrombi but without plexiform lesions, was observed in 19 patients. Intimal fibrosis, either concentric or eccentric, without plexiform or thrombotic lesions was found in four patients. Among the remaining nine patients in the Registry, pulmonary veno-occlusive disease was present in seven and chronic pulmonary venous hypertension in one. Pulmonary blood vessels were microscopically normal in a lung biopsy specimen from another patient. In general, patients with plexiform lesions and those with veno-occlusive disease had a much poorer prognosis than patients with thrombotic lesions. The present study shows the existence of several distinct histopathologic patterns of pulmonary vascular disease in individuals with primary pulmonary hypertension diagnosed by standardized clinical and laboratory criteria.
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PMID:Histopathology of primary pulmonary hypertension. A qualitative and quantitative study of pulmonary blood vessels from 58 patients in the National Heart, Lung, and Blood Institute, Primary Pulmonary Hypertension Registry. 280 80

Pulmonary hypertension due to vasculitis is a rare complication of rheumatoid arthritis (RA). We describe 2 patients with RA and pulmonary hypertension who died with a clinical diagnosis of idiopathic pulmonary hypertension. In each case postmortem examination revealed severe pulmonary vasculitis as the actual cause of the hypertension. Subclinical systemic vasculitis was found in one case and hepatic nodular regenerative hyperplasia in both cases. Pulmonary vasculitis must be included in the differential diagnosis of pulmonary hypertension associated with RA. Open lung biopsy should be considered in this clinical setting in an attempt to identify this potentially treatable cause of pulmonary hypertension.
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PMID:The association of pulmonary hypertension with rheumatoid arthritis. 281 Feb 87

Clinical and pathologic findings in seven patients who died of severe pulmonary artery hypertension due to toxic oil syndrome are assessed. These cases correspond to a late stage of evolution of the disease characterized by progressive deterioration in clinical features--increasing dyspnea, chest pain, syncope, and death (in low-output heart failure). The main pathologic pulmonary vascular findings consisted of plexiform lesions, thromboses, and venous lesions. Endothelial damage induced by the toxic agents is suggested as an initial causative mechanism, perpetuated by intimal proliferation and in situ thrombosis. Plexiform lesions appear late and active histologically. This new cause of pulmonary artery hypertension, with pathologic findings similar to those found in primary pulmonary hypertension, may help in understanding the pathophysiology of this unknown disease.
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PMID:Pulmonary hypertension due to toxic oil syndrome. A clinicopathologic study. 291 83

A total of 249 patients with arterial hypertension taking a variety of clinical forms, primary pulmonary hypertension, dilatation cardiomyopathy, congenital heart diseases with secondary pulmonary hypertension were examined and allocated to 3 groups: 125 patients with left-ventricular hypertrophy (LVH) (group 1); 44 patients with right-ventricular hypertrophy (RVH) (group 2), and 80 patients with combined hypertrophy of both ventricles (CH). Eighty-one normal subjects were taken as controls. New parameters of diagnostic significance were identified by automated reproduction of vectorcardiographic spatial QRSxyz loop (the Macfee-Parungao system) and computer analysis of vectorcardiographic parameters, that improve electrocardiographic diagnosis of cardiac hypertrophies, as compared to the conventional criteria, bringing its accuracy to 88.8% for LVH, 100% for RVH, and 45% for CH. Typical features of myocardial hypertrophy at large are increased area enclosed by the spatial loop (SQRS greater than 3.4 mV2) and/or increased mean vector (LQRSxyz greater than 0.76 mV), while Lx greater than 0.6 mV and/or Lz less than -0.4 mV were specific for LVH; Lx less than 0.05 mV was specific for RVH, and the H angle ranging from -70 degrees to -140 degrees or H of -60 degrees to -140 degrees at Lz less than 1.1 mV, or -50 degrees to -140 degrees at Lz less than 1.5 mV were specific for CH.
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PMID:[Integral indices of the automatically reproduced spatial QRS loop in the diagnosis of different forms of myocardial hypertrophy]. 294

Angiotensin-converting enzyme inhibitors are potent vasodilators acting by inhibition of production of the vasoconstrictor angiotensin II. In adults, they are used for treatment of systemic hypertension and congestive heart failure and investigated for treatment of primary pulmonary hypertension. In infants and children, saralasin and captopril were found to be useful in treatment of systemic arterial hypertension, especially when associated with high plasma renin activity. Captopril has failed in the treatment of congestive heart failure associated with complex congenital heart diseases and in most cases of primary pulmonary hypertension. It has a clear beneficial effect in coarctation of the aorta and may have such an effect in endomyocardial diseases and ventricular septal defect. In adults, serious side effects have limited the use of captopril. New converting enzyme inhibitors, devoid of a sulfhydryl group, are expected to have a better safety profile.
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PMID:Cardiovascular drugs in children: angiotensin-converting enzyme inhibitors. 304 87

This review discusses the role of three mediators, synthesized by vascular endothelial cells, that help to keep the surface of the normal endothelium nonthrombogenic. 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 clinically for use in cardiovascular diseases such as primary pulmonary hypertension. 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 that stimulate the release of EDRF include acetylcholine, bradykinin, and adenosine 5'-diphosphate. EDRF is even more labile than prostacyclin, with a half-life of about 6 seconds, and it has recently been identified as nitric oxide. Prostacyclin and EDRF are released together following stimulation of endothelial receptors and synergize to inhibit platelet aggregation. 13-Hydroxy-9,11-octadecadienoic acid, a third suggested mediator, is not released but acts from inside the cell to make the endothelial surface nonadhesive for circulating blood cells. It is proposed that these three mediators form the endothelial defense mechanism against blood-borne cells and chemicals and that breakdown of this barrier results in diseases such as hypertension and atherosclerosis.
Hypertension 1988 Dec
PMID:Mediators produced by the endothelial cell. 306 Apr 28

In primary pulmonary hypertension of recent clinical onset, pulmonary endothelial cells show injury. To characterize this phenomenon, we measured plasma von Willebrand factor (vWF) by immunologic and ristocetin cofactor assays in 6 patients with primary pulmonary hypertension, 17 patients with secondary pulmonary artery hypertension associated with congenital heart disease or cystic fibrosis, and 13 patients with congenital heart disease and normal pulmonary artery pressure. In selected cases, we also determined the vWF multimer pattern. In all 6 cases of primary pulmonary hypertension, the ristocetin cofactor activity was increased relative to the vWF antigen (vWF:Ag) concentration (a ratio of 2.55 +/- 0.36; normal range, 0.8 to 1.4); 4 of the 6 also had a similar and abnormal vWF multimer pattern--an increased proportion of the fastest moving bands. In the other 2, the multimer pattern was normal. Of the other 30 patients, a mild increase in ristocetin cofactor/vWF:Ag was seen in only 2 with secondary pulmonary hypertension and 1 with normal pulmonary artery pressure: these also had an abnormal vWF multimer pattern that was different from that observed in patients with primary pulmonary hypertension. The vWF abnormalities we describe in primary pulmonary hypertension offer a marker of the disease and could be helpful in understanding its pathogenesis.
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PMID:von Willebrand factor abnormalities in primary pulmonary hypertension. 310 58

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

The pulmonary arteries dilate in response to many factors, principally increased pressure and flow. In patients who have pulmonary arterial hypertension but no increase in flow, we have compared main pulmonary artery size at computed tomography with pulmonary haemodynamic data obtained during right heart catheterisation. In patients with primary pulmonary hypertension and chronic thromboembolic pulmonary hypertension, dilatation correlated with raised pulmonary vascular resistance and reduced cardiac output but not with mean arterial pressure. In patients with chronic lung disease no correlations were shown though a trend between raised pressure and size was observed. We speculate that pulmonary artery compliance is an important factor which determines the degree of dilatation in response to raised pressure. Estimations of pressure cannot be made from measurements of pulmonary artery size without knowledge of the underlying lung disease.
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PMID:The relationship between pulmonary artery pressure and pulmonary artery diameter in pulmonary hypertension. 318 Jun 68

There is hesitancy, based on the perceived risk, to do pulmonary angiography in patients believed to have primary pulmonary hypertension. Yet pulmonary hypertension due to major-vessel, chronic thromboembolism mimics primary pulmonary hypertension clinically and on standard laboratory tests. Because thromboembolic pulmonary hypertension is potentially remediable by thromboendarterectomy and primary pulmonary hypertension is not, differentiating between these disorders is essential. Angiography is required in patients with thromboembolic pulmonary hypertension to define the anatomic location of the thrombi. In evaluating perfusion lung scans of 110 patients with pulmonary hypertension to determine whether the scan might provide a guide to selecting those patients who merit angiography, no segmentalsize perfusion defects were noted on the scans of 64 patients with primary pulmonary hypertension, whereas all 46 patients with thromboembolic hypertension had one or more defects that were segmental in size or larger. These data indicate that a perfusion lung scan should be done in patients with pulmonary hypertension of uncertain cause and that those with one or more segmental or larger defects merit pulmonary angiography before being diagnosed as having primary pulmonary hypertension.
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PMID:Perfusion lung scans provide a guide to which patients with apparent primary pulmonary hypertension merit angiography. 334 25


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