Ueber die genuine Arteriosklerose der Lungenarterie<sup>1</sup>)

Mönckeberg, J. G.

doi:10.1055/s-0029-1188911

Cited by 43 publications

(5 citation statements)

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“…Noted particularly were (1) interval from initial clinical manifestation to clinical and hemodynamic diagnosis, (2) roentgenographic evidence, including prominence of main pulmonary and hilar arteries and signs of cardiomegaly, and (3) electrocardiographic abnormalities, including right ventricular hypertrophy (R/S wave in lead V, >1 mm, R wave in lead V, plus S in lead V6 > 10 mm), right axis deviation (QRS axis >90 degrees), and large P wave (-2.5 mm in lead II).…”

mentioning

confidence: 99%

Primary pulmonary hypertension: natural history and the importance of thrombosis.

Fuster¹,

Steele²,

Edwards³

et al. 1984

Circulation

955

444

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A long-term retrospective follow-up study was made of 120 patients (33 male, 87 female patients) with primary pulmonary hypertension -diagnosed by strict clinical and hemodynamic criteria to obtain a better understanding of the natural history and possible pathogenetic mechanisms of the disease. The mean age at diagnosis was 34 (3 to 64) years, but only 24 patients (21 %) remained alive 5 years later. Lung tissue obtained at autopsy from 56 patients revealed two major pathologic types: thromboembolic pulmonary hypertension in 32 patients (57%) and plexogenic pulmonary arteriopathy in 18 (32%). Thus, in more than half the patients undergoing autopsy the major histologic feature was thrombi without any evidence of plexiform lesions. The two groups were similar with respect to their clinical and hemodynamic features and short survival. Of the variables tested for prognostic importance by stepwise multivariate analysis, only two were significant: pulmonary arterial oxygen saturation (p < .00001) and anticoagulant therapy (p = .01). Anticoagulant therapy is recommended for patients with primary pulmonary hypertension.

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mentioning

confidence: 99%

Primary pulmonary hypertension: natural history and the importance of thrombosis.

Fuster¹,

Steele²,

Edwards³

et al. 1984

Circulation

955

444

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“…Pathologic findings consistent with primary PHT were first noted in autopsy specimens as a form of arterial sclerosis by Romberg 6 and Monckeberg 7 over a century ago. However, the first diagnosis of primary PHT in a living human was not made until 1951, by Dresdale et al 8 Over the past 50 years it has become clear that primary PHT is largely a disease of the pulmonary circulation, and the pathology is focused in the small pulmonary arteries, which are characterized by intimal fibrosis, medial hypertrophy, adventitial proliferation, obliteration of small arteries, and, on occasion, vasculitis or changes in the walls of the pulmonary veins.…”

Section: Introduction and History Of The Pulmonary Circulationmentioning

confidence: 92%

Pulmonary Arterial Hypertension

Michelakis

Archer

2007

Cardiovascular Medicine

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“…The infection should be treated with vigor, since thereby one of the frequent precipitating causes of heart failure may be removed. 99 10 and may be based on a reduction of certain phases of the inflammatory response. The need for such therapy seems less well established, and the possibility of accelerating preexisting fibrosis by cortisone must be kept in mind.69 Postural drainage, advocated in young subjects with bronchiectasis and emphysema, is rarely feasible in patients with emphysema heart, but intermittent periods of positive-pressure breathing with air, oxygen, or oxygen-helium mixtures (80 per cent helium, 20 per cent oxygen) may be effective in improving alveolar ventilation.…”

Section: Pulmonary Diseasementioning

confidence: 99%

Heart Failure and Lung Disease

Hecht

1956

Circulation

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The confusing and complex interplay of factors leading to "cor pulmonale" may be somewhat clarified if the effects of excessive pulmonary hypertension causing right heart overloading ("pulmonary hypertensive heart disease") are separated from the ventilatory defects that result in arterial desaturation, erythrocytosis, and moderate pulmonary hypertension ("emphysema heart"). In the former group, heart failure dominates the clinical picture; in the latter, it is assumed that heart failure occurs on the basis of a "myocardial factor"—presumably arteriosclerotic heart disease—whose manifestations are colored and modified by the coexisting and contributing respiratory dysfunction. Overlapping of these two distinct forms occurs frequently, and pulmonary hypertension may be severe enough to be the chief precipitating cause of failure in emphysema, particularly in young subjects and in patients with kyphoscoliosis. Respiratory disturbances, fibrosis, and loss of pulmonary elasticity may accompany heart failure secondary to right ventricular overloading which may ultimately lead to significant arterial desaturation at rest and the development of polycythemia, even in this group. It is typical, however, that the disturbances leading to cor pulmonale rarely, if ever, involve the actual pulmonary function of alveolar-capillary gas exchange; they are confined to the abnormalities of the precapillary pulmonary vasculature and to the mechanical apparatus of the chest cage and of the pulmonary parenchyma concerned with breathing mechanisms. Pulmonary hypertensive heart disease, whatever its cause, has a monotonous symptomatology that is dominated by the signs of heart failure. In cor pulmonale due to emphysema and its allied types, the clinical picture is varied, and oxygen deficiency with arterial desaturation is of central significance. It raises pulmonary artery pressure by a mechanism not fully understood, and it stimulates erythropoiesis. When erythrocytosis has occurred, heart failure from cor pulmonale will soon make its appearance. Unless the arterial oxygen content falls sharply on exercise, resting oxygen saturation values in excess of 80 per cent do not cause this type of polycythemia; nor does polycythemia as such, as in erythremia ("vera"), result in significant arterial desaturation, pulmonary hypertension, or heart failure. However, little is known concerning the hemodynamic load imposed by an increase in blood viscosity. The management of cor pulmonale must recognize the multiplicity of factors that are concerned and should weigh their relative significance in any given subject. The kaleidoscopic appearance of cor pulmonale requires flexibility of therapy based on a grasp of the individual pathophysiologic interrelations, which may differ from patient to patient.

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Ueber die genuine Arteriosklerose der Lungenarterie¹)

Cited by 43 publications

References 0 publications

Primary pulmonary hypertension: natural history and the importance of thrombosis.

Primary pulmonary hypertension: natural history and the importance of thrombosis.

Pulmonary Arterial Hypertension

Heart Failure and Lung Disease

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Ueber die genuine Arteriosklerose der Lungenarterie1)

Cited by 43 publications

References 0 publications

Primary pulmonary hypertension: natural history and the importance of thrombosis.

Primary pulmonary hypertension: natural history and the importance of thrombosis.

Pulmonary Arterial Hypertension

Heart Failure and Lung Disease

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Product

Resources

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Ueber die genuine Arteriosklerose der Lungenarterie¹)