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

Recent case reports suggest that pulmonary hypertension could be caused by minoxidil, a new potent vasodilating antihypertensive drug. Therefore, we evaluated the incidence and severity of pulmonary hypertension in 110 patients with systemic hypertension. Fourteen patients were treated with minoxidil for 2 to 35 months (mean 19.9 months), 15 were treated with no drugs, and the remaining 81 patients received conventional antihypertensive agents of several types. Pulmonary vascular resistance correlated positively (P is less than 0.05) with systemic vascular resistance. Minoxidil-treated patients with hypertension previously refractory to conventional therapy had slightly lower pulmonary vascular resistance than other hypertensive subjects. There was no correlation between pulmonary vascular resistance and duration of minoxidil therapy or other types of antihypertensive regimens. The positive correlation between pulmonary and systemic vascular resistance suggests the possibility of a causal hypertension relation in the two vascular beds.
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PMID:Increased pulmonary vascular resistance with systemic hypertension. Effect of minoxidil and other antihypertensive agents. 87 Nov 7

Pulmonary precapillary hypertension present only during exercise is the first stage of corpulmonale. Examination of the reaction of central haemodynamics to exercise is the only way to detect it. In a model situation like unilateral pulmonary artery occlusion (UPAO) in healthy subjects, an increase in pulmonary artery pressure (Ppa) during exercise is a linear function of restriction of the pulmonary vascular bed and blood flow increase. Central haemodynamics during exercise in younger subjects after pneumonectomy (PNE) resemble the situation with UPAO provided the remaining lung is intact. In older patients after PNE the same rise of blood flow is associated with a considerably greater rise of Ppa. PNE patients compared to healthy individuals increase their cardiac output during exercise more by increasing stroke volume. Patients with pulmonary fibrosis show a disproportionate rise in Ppa in relation to flow. This is due to reduced distensibility of the pulmonary system. Hypoxia also seems to be involved in pulmonary hypertension during exercise. Pulmonary wedge pressure rises at work but remains within the normal range, even in patients having marked hypoxaemia at rest and during exercise. In idiopathic intersitial pulmonary fibrosis (IIPF), pulmonary hypertension during exercise is greater than in other forms of pulmonary fibrosis. Inhalation of oxygen during exercise in patients IIPF leads to a reversal of hypoxaemia but the decrease of Ppa is small and due to a passive decrease of cardiac output. Finally right ventricular function in restrictive pneumopathies is discussed.
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PMID:Central haemodynamics during exercise in patients with restrictive pulmonary disease. 88 Mar 98

In the 4 studied patients presenting with an Halasz's syndrome, the disease was complicated since the neonatal period by pulmonary arterial hypertension and heart failure. Three out of the 4 infants rapidly died, one after pneumonectomy. The fourth is surviving and benefitted solely from medical cardiotonic treatment. The pathogenesis of early pulmonary arterial hypertension in Halasz's syndrome is complex. The possibly associated cardiac malformations, the persistance of fetal obstructive hypertension due to the increase of the flow in the left pulmonary artery, the left to right shunt induced by the abnormal venous return and predominantly by the systemic blood supply to the right lung, are responsible, at various degrees, for pulmonary hypertension. Among surgical procedures to be proposed, the simple ligation of abnormal arteries which take their origin from the aorta seems to be preferable to pneumonectomy.
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PMID:[Halasz syndrome revealed in the newborn infant by pulmonary arterial hypertension. Study of 4 cases]. 90 33

Clinical and morphologic observations are described in two patients with severe pulmonary arterial hypertension without pulmonary venous hypertension from fibrosing mediastinitis. In one patient, both main pulmonary arteries and one major pulmonary vein were severely narrowed by dense fibrous tissue; in the second patient, only the right main pulmonary artery was severely narrowed. Both patients had normal intrapulmonary arteries and normal pulmonary parenchyma. Of nine previously described necropsy patients with pulmonary hypertension due to fibrosing mediastinitis, seven had severe narrowing of multiple large pulmonary veins and in six of them the pulmonary hypertension was entirely due to pulmonary venous obstruction. In one other patient, the pulmonary hypertension was due to obstruction of one main pulmonary artery and several large pulmonary veins. Each of these seven previously described patients had severe changes in the small intrapulmonary arteries. Of the other two previously described patients with pulmonary hypertension from fibrosing mediastinitis, one had severe narrowing of only the main right pulmonary artery, and the other, of both main pulmonary arteries. Thus, although pulmonary arterial hypertension in patients with fibrosing mediastinitis is usually due to obstruction of multiple large pulmonary veins and to severe secondary changes in small intrapulmonary arteries, fibrosing mediastinitis can cause severe pulmonary hypertension by obstructing the right or both main pulmonary arteries.
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PMID:Fibrosing mediastinitis causing pulmonary arterial hypertension without pulmonary venous hypertension. Clinical and necropsy observations. 91 Aug 11

Between 1967 and 1970 primary pulmonary arterial hypertension was diagnosed in 52 patients. Menocil had been taken by 36 patients. Overall survival rate after 9 years was 0.58. Mortality was particularly high within 2 years after the diagnosis was established (22%). Survival rate was low in the group with pulmonary vascular resistance exceeding 1000 dynes-sec-cm-5 (0.42 after 9 years). Initially slight pulmonary hypertension generally had a good prognosis but even severe pulmonary hypertension can regress or even disappear. With respect to survival rate, there were no significant differences between patients with and without Menocil intake.
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PMID:[Course and prognosis of primary pulmonary hypertension]. 92 44

Between September 1967 and April 1975, a total of 120 patients between one day and 20 years of age underwent surgery for coarctation of the thoracic aorta. Thirty-two patients were below two years of age (group 1) and 88 were above two years (group 3). All patients in group 1 initially had congestive heart failure. Twenty-eight had associated cardiac defects, and 18 had signficant pulmonary arterial hypertension (greater than 50 mm Hg). Operative deaths occurred only in group 1, all in infants below five months of age. Common features in the 13 deaths were congestive heart failure, pulmonary hypertension, patent ductus arteriosus, large ventricular septal defect, concomitant pulmonary arterial bandling or open-heart procedures. The only recurrence occurred in an infant first operated at 14 days of age. Resection of aortic coarctation can be safely performed as an elective procedure; however, it still presents a high surgical risk in infants with associated intracardiac defects. Late follow-up shows the salutary effects of repair of the coarctation on hypertension.
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PMID:Coarctation of the aorta in children and adolescents. Surgical treatment and review of 120 patients. 97 79

Minoxidil has a direct dilator effect on the systemic arterial smooth muscle. It is potentially an important drug in the treatment of systemic hypertension, especially when combined with beta blockade, which is used to control the associated tachycardia and increase in cardiac output. However, recent observations have suggested that minoxidil might cause pulmonary hypertension. Consequently, we examined the acute effect of monoxidil and propranolol, separately and in combination, on the pulmonary vasculature of the anesthetized dog and the awake calf during normoxia and hypoxia. In both species minoxidil reduced pulmonary vascular resistance. In the dogs this appeared to be the result of a direct action on the pulmonary vascular smooth muscle and in the cattle it was secondary to beta-receptor stimulation. Propranolol alone in the cattle increased the pulmonary pressor response to hypoxia. While we have not examined the possibility that chronic administration of minoxidil might cause pulmonary hypertension by some other mechanism, our acute studies suggest that it reduces, rather than increases, pulmonary vascular resistance. Furthermore, there seems to be a species difference in the mode of its action in dogs and cattle.
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PMID:Minoxidil reduces pulmonary vascular resistance in dogs and cattle. 99 42

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

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
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PMID:Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. 99 7

The case of a 32-year-old woman who had used oral contraceptives and died from primary vascular pulmonary-hypertension (PVPH) is discussed. A case of this type had never been reported before and the relationship between the occurrence of PVPH and oral contraceptive use is discussed. A relationship between oral contraceptive use and venous thrombosis of the lower extremities has been demonstrated. The direct effect of oral contraceptives on blood vessels has been shown in animal experiments and pathological-histological studies. Clinical studies indicate a relationship between pulmonary hypertension and oral contraceptive use.
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PMID:[Primary vascular pulmonary hypertension and ovulation inhibitors]. 101 83


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