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At least 19 recordsLinked to original sources
PubMed1979

A possible causal relationship between defective fibrinolysis and pulmonary hypertension.

Pulmonary hypertension may be associated with multiple thrombi in the pulmonary arteries or with diffuse microembolization from a cryptic source. A 27-year-old man without any of the recognized clinical risk factors for venous thrombo-embolic disease presented with repeated attacks of chest pain and dyspnoea. Haemodynamic studies were compatible with the diagnosis of primary pulmonary hypertension. Despite intensive study there was no evidence of peripheral venous thrombosis. A survey of the plasma fibrinolytic profile showed unequivocal evidence of low spontaneous plasma fibrinolytic activity. The plasminogen activator activity of the venous wall was also markedly reduced. From these findings it would seem that a defective fibrinolytic defence mechanism may be an important predisposing factor in the pathogenesis of 'primary' pulmonary hypertension.

Adult↗
PubMed1976

Takayasu's arteritis: an unrecognized cause of pulmonary hypertension.

Pulmonary arteritis and secondary pulmonary hypertension are common in patients with Takayasu's arteritis. These sequelae of arteritis have not been previously emphasized in the literature. In some patients, particularly young and middle-aged women, disproportionately severe involvement of the pulmonary arteries may be the cause of pulmonary hypertension of unknown etiology.

Adolescent↗
PubMed1977

Changes in the pulmonary arteries of the rat during recovery from hypoxia-induced pulmonary hypertension.

Pulmonary hypertension has been induced in rats by 2 weeks' exposure to hypoxia, equivalent to an altitude of approximately 5500 m, in a hypobaric chamber. The rats were removed from the chamber and allowed to recover for up to 8 weeks at atmospheric pressure. Precise quantitative microscopic techniques after injection of the pulmonary artery have been used to estimate the regression in the pulmonary artery of the structural changes associated with pulmonary hypertension. During recovery the degree of muscularization of the pulmonary arteries decreases by disappearance of muscle cells from the small arteries and a drop in arterial wall thickness of larger vessels. These changes do not seem to reflect pulmonary artery pressure directly, since right ventricular hypertrophy regresses at a faster rate. In hypertensive rats there is a "loss" of small arteries in the alveolar region and little filling of precapillary vessels. On recovery, some of the vessels fill, suggesting that encroachment on the lumen by muscle and endothelial cells has lessened. Even after 8 weeks' recovery, however, some arteries do not return, suggesting they have completely disappeared and that regions are left with relatively little perfusion. This reduction of vascular reserve presents without there being right ventricular hypertrophy.

Angiography↗
PubMedDate not supplied

Pulmonary hypertension, "plexogenic pulmonary arteriopathy" and the appetite depressant drug aminorex: post or propter?

An epidemic of chronic pulmonary hypertension of vascular origin (CPHVO) has occurred in Austria, the Federal Republic of Germany, and Switzerland. The epidemic started in 1967 and reached its peak in 1968 and 1969. Since 1972, the prevalence of patients with CPHVO among individuals investigated by cardiac catheterization is again as low as in the pre-epidemic years. In Bern the prevalence of CPHVO during the peak of the epidemic was 20 times higher than during the 12-year period preceding the epidemic. The clinical, physical, electrocardiographic, radiologic, haemodynamic and respiratory findings of the patients observed in Bern (n = 102) are summarized. There has been a mortality between 12 and 20% at the time of the epidemic. Most patients observed for the first time during the epidemic have remained severely disabled over the years. A minute fraction seems to have recovered. There is a close geographic as well as temporal relation of the epidemic to the marketing and intake of the appetite depressing drug aminorex fumarate (Menocil). Acute administration of aminorex leads to a transient rise of the pulmonary artery pressure and vascular resistance in a number of animal species. It has not been possible to produce sustained precapillary pulmonary hypertension and chronic cor pulmonale vasculare under the conditions of chronic administration of the drug in the species tested. Morphologic examination of lung biopsy and autopsy material of patients who have died from CPHVO after the intake of aminorex reveals the presence of "plexogenic pulmonary arteriopathy". The vascular lesions are identical with those observed in pulmonary hypertension due to large congenital left-to-right shunts. In balancing the pros and cons, it appears that the arguments in favour of a cause-effect relationship between aminorex and pulmonary hypertension, which are derived from epidemiological evidence, outweigh the results of "negative" animal experiments. A "propter" in the title of this paper, therefore, seems to be more appropriate than a post".

Adolescent↗
PubMed1975

Hypertensive pulmonary vascular disease associated with patent ductus arteriosus. Primary or secondary?

In an infant with patent ductus arteriosus and pulmonary hypertension, elevated pulmonary vascular resistance persisted following ligation of the ductus. Histologic examination of a pulmonary biopsy at two years of age and tissue obtained at autopsy at three years of age showed obstructive pulmonary vascular disease. The question as to whether the organic vascular lesions are secondary to the effects of the patent ductus or part of pulmonary hypertension cannot be resolved. The age of the patient favors a primary etiology.

Age Factors↗
PubMed1978

Influence of pulmonary hypertension on pulmonary diffusing capacity in patients with mitral stenosis.

The pulmonary diffusing capacity (DLCO--steady state method according to Bates and coworkers) was measured at the time of heart catheterization in 12 patients with mitral stenosis without mitral incompetence. DLCO correlates with the tidal volume at rest and during exercise and with pulmonary vascular resistance during exercise only. DLCO and left atrial pressure exhibit a positive correlation up to 22.5 mm Hg only. In patients with mitral stenosis DLCO depends on the alveolar surface area and DLCO is influenced by regional changes in the pulmonary vascular resistance.

Adult↗
PubMed1979

Hypertensive pulmonary vascular disease in Down syndrome.

Clinical studies have suggested that patients with Down syndrome have precocious development of pulmonary hypertension, even in the absence of congenital heart disease. To examine the pathologic basis of this impression, we studied 82 patients with Down syndrome autopsied at The Johns Hopkins Hospital from 1913 to present. The patients ranged in age from 26 hours to 25 years; 41 (50%) were female. Atrioventricular canal defect was present in 40 patients, nine of whom also had pulmonary stenosis. Eight had isolated ventricular septal defect and seven had other malformations. Histologic sections of the lung from each patient were studied and the degree of hypertensive pulmonary vascular disease graded. Age and sex-matched controls without cardiovascular manifestations, all other autopsied patients with atrioventricular canal defect not associated with Down syndrome, and age-matched patients with ventricular septal defect or other malformations were similarly studied for pulmonary vascular changes. Comparison of the 27 patients with Down syndrome and no cardiovascular malformations with normal controls showed no differences, with one notable exception: an 8-month-old child with Down syndrome had severe HPVD secondary to idiopathic pulmonary hypertension. HPVD in patients with the various cardiovascular malformations was similar for those groups with Down syndrome and those without, when HPVD was considered as a function of the patients' age and the type of malformation. We conclude that, in general, patients with Down syndrome have no predisposition to develop severe or precocious hypertensive pulmonary vascular disease.

Adolescent↗
PubMed1979

Quantitative evaluation of hypertensive pulmonary arterial change.

A new method to quantitatively evaluate pulmonary arterial change in pulmonary hypertension is presented in this paper. Hypertensive pulmonary arterial changes are classified into four grades according to severity and a score from 1 to 4 is given to each arterial change according to the grading. An index of pulmonary vascular disease is then defined as a relative mean value of all scores. It is concluded that this index accurately expresses the grade of pulmonary arterial change in the whole pulmonary arterial system in any given case and makes possible a detailed statistical analysis of large numbers of cases.

Adult↗
PubMed1978

Pulmonary hypertension secondary to minor pulmonary embolism.

The response of pulmonary arterial pressure to minor degrees of pulmonary embolism was examined in 18 patients with embolic occlusion of less than 25% of the pulmonary vascular bed. Patients with pulmonary embolism were compared to normal controls matched for age and sex and to patients with a variety of acute pulmonary disorders without pulmonary embolism. Patients with pulmonary embolism and patients with other acute pulmonary diseases had significantly higher pulmonary arterial pressures and significantly lower values for arterial oxygen tension (PaO2) than did normal subjects. The degree of pulmonary hypertension correlated with the PaO2. Pulmonary hypertension occurring after minor degrees of pulmonary embolism may be a response to mild arterial hypoxemia.

Adult↗
PubMed1979

Effects of isosorbide dinitrate on pulmonary hypertension in chronic obstructive pulmonary disease.

Eighteen patients with chronic obstructive pulmonary disease with pulmonary hypertension were studied to assess the hemodynamic response to acute oxygen administration and to oral isosorbide dinitrate (ISDN). All 18 patients had baseline hemodynamic measurements and hemodynamic measurements during low-flow nasal oxygen. Following a second baseline measurement, patients received either oral ISDN (11 patients) or placebo (7 patients) in a randomized, double-blind protocol. Heart rate decreased with oxygen administration but there were no other significant hemodynamic changes. With oral ISDN, there was a significant fall in pulmonary artery and brachial artery pressure. Cardiac output, right atrial pressure, pulmonary wedge pressure, and pulmonary vascular resistance all fell but not significantly. We conclude that oral ISDN is effective in reducing pulmonary hypertension in patients with chronic obstructive pulmonary disease.

Blood Pressure↗
PubMed1978

Hypertensive pulmonary vascular disease in alpha-transposition of the great arteries.

In subjects with classic complete transposition (d-transposition) of the great arteries, the pulmonary arterial plexiform lesion, characteristic of chronic high levels of pulmonary arterial pressure, was observed in those with an intact ventricular septum as well as in those with a ventricular septal defect. The lesion was not observed before age 12 months. Among 16 patients aged 12 to 30 months, the plexiform lesion was observed in 6 of 12 patients (50 percent) with an intact ventricular septum and a closed ductus arteriosus and in 1 of 4 patinets with an associated ventricular septal defect. The basis of the plexiform lesion, which is considered a sign of chronic severe pulmonary hypertension, occurring in subjects with an intact ventricular septum and a closed ductus arteriosus is not explained. The phenomenon observed in this study confirms the earlier observations of others.

Arteritis↗
PubMed1978

Pulmonary hypertension in sepsis: measurement by the pulmonary arterial diastolic-pulmonary wedge pressure gradient and the influence of passive and active factors.

To examine the relative roles of passive factors (flow; filling pressures of left side of heart) and active factors (acidosis; arterial unsaturation) in the genesis of pulmonary hypertension when associated with sepsis, 37 patients with sepsis and 24 patients without sepsis were examined. Pulmonary hypertension was measured by the pulmonary arterial diastolic-pulmonary wedge pressure gradient (PAd-PWP gradient) and correlated reasonably with a standard formula for calculated resistance ([PA--PWP]/CI, where PA is mean pulmonary artery pressure and CI is cardiac index). In 22 of 37 patients, sepsis was associated with a significant degree of resistance to flow in the pulmonary circulation, as measured by the PAd-PWP gradient: and the higher the PAd--PWP gradient, the greater the likelihood of early death. None of the examined passive or active factors appeared to be adequate to explain pulmonary hypertension when present. By the use of previously derived formulae to estimate the compliance of the elastic pulmonary arteries, factors affecting this part of the pulmonary microcirculation could not be held accountable for apparent pulmonary hypertension. Therefore, the presence of pulmonary hypertension in sepis appears to be an active, rather than a passive, phenomenon and unrelated to arterial oxygen saturation or acid-base imbalance. Although the exact cause is unknown, pulmonary hypertension in sepis is associated with a high mortality and may be clinically followed by measurement of the PAd-PWP gradient.

Bacterial Infections↗
PubMed1979

The extraction of circulating catecholamines by the lungs in normal man and in patients with pulmonary hypertension.

We directly measured the net pulmonary extraction of circulating norepinephrine, epinephrine and dopamine in control patients and patients with primary or secondary pulmonary hypertension. Mixed pulmonary artery norepinephrine, epinephrine and dopamine were 314 +/- 13 pg/ml, 102 +/- 9 pg/ml, 51 +/- 5 pg/ml, respectively, for the control group; values were similar in patients with pulmonary hypertension. The pulmonary extraction of norepinephrine was 25.4 +/- 2.6% (clearance 266 +/- 62 ng/min) in control patients; epinephrine and dopamine were not extracted. There was no net extraction or production of any of the three catecholamines by the lungs in any of the patients with pulmonary hypertension. We conclude that the lungs play a significant role in the inactivation of circulating norepinephrine in man. This metabolic function of the lungs appear to be lost in pulmonary hypertension.

Adult↗