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

Right atrial hypertension has been considered to have a major physiologic influence on the formation of transudative pleural effusions. Since pleural fluid is thought to be cleared primarily by the parietal pleural lymphatic vessels that empty into the systemic veins, systemic venous hypertension secondary to right atrial hypertension should decrease the lymphatic drainage of the pleural space. We retrospectively studied nine patients and prospectively studied 18 patients with long-term right atrial or pulmonary arterial hypertension (or both). All patients had stable respiratory symptoms, and none had a significantly elevated pulmonary arterial wedge pressure. Our purpose was to determine the relationship of right atrial and pulmonary arterial hypertension to the development of transudative pleural effusions. Posteroanterior and bilateral decubitus chest roentgenograms and ultrasound were used to detect pleural effusions. Pleural effusions were not identified in any of the 27 patients, even in four patients with right atrial pressures greater than 20 mm Hg. We conclude that chronic elevation of right atrial pressure or pulmonary arterial pressure (or both) alone is not a cause of pleural effusion. In contrast, elevation of left atrial and pulmonary arterial wedge pressures is associated with the formation of transudative pleural effusions in man. Thus, if pleural effusions are detected in patients who have cor pulmonale, a search should be made for coexisting left heart failure or a primary cause of pleural inflammation, such as pulmonary emboli or infection.
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PMID:Lack of association of pleural effusion with chronic pulmonary arterial and right atrial hypertension. 367 41

The experiment has been performed in 124 non-inbred dogs by means of a complex of morphometrical methods in order to study compensatory-adaptive processes in the heart after pulmonary resection various in its volume. After 58% resection, and especially after 67-75% resection of the lung mass, a stable pulmonary arterial hypertension appears; it results in development of a chronic cor pulmonale and terminates in its decompensation. Application of extrapulmonary arterio-venous anastomosis, before 67-75% of the pulmonary parenchyma is resected, decreases hypertension in the pulmonary circulation, improves adaptive changes of the heart in the newly formed conditions of hemodynamics, preventing development of its failure.
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PMID:[Compensatory and adaptive changes in the heart after pulmonary resection (morphometric analysis)]. 370 74

The nerve density, expressed as total length of nerve fibers per square millimeter of tissue section, was measured in both carotid bodies from five subjects free from cardiopulmonary disease and from eight subjects with carotid body hyperplasia. Six of the cases with enlargement of the carotid body had been exposed to chronic hypoxemia in life (due to panacinar pulmonary emphysema in five instances and the pickwickian syndrome in one case), and the other two cases had had systemic hypertension. The cases of carotid body hyperplasia showed an increased nerve density associated with the characteristic proliferation of elongated cells. These findings confirm that the proliferating cells in carotid body hyperplasia are both sustentacular and Schwann's cells, not fibroblasts, and suggest that these cells develop to support an increased number of nerve axons. The mechanisms by which two such different stimuli as chronic hypoxemia and raised intravascular pressure bring about an increased nerve density are obscure.
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PMID:Nerve axons in carotid body hyperplasia. A quantitative study. 383 53

In order to not only survive, but to carry out our mission in health care delivery, nuclear medicine procedures will have to be competitive with the many other techniques that are available for assessing cardiopulmonary structure or function. Our tests must also be shown to be cost-effective. According to the American Heart Association, cardiovascular diseases alone had an economic cost of 56.9 billion dollars in 1983. Of this enormous sum only a very small percentage could be attributed to the performance of diagnostic nuclear medicine examinations. In addition to the economic cost, cardiovascular diseases accounted for 51% of all deaths in 1980. Statistics from the U.S. Department of Health show that 8.26 million (26.3%) of the national noninstitutionalized handicapped are the result of heart conditions and hypertension. These statistics are especially tragic since cardiovascular disease tends to strike a large proportion of persons in their most productive working years. We must avoid becoming penny wise and pound foolish when we decide whether or not to perform diagnostic examinations. Information obtained from these tests can be used to evaluate the effectiveness of therapy (or lack thereof), determine those patients who are at greatest risk of subsequent events and, therefore, require the most intensive investigation and therapy, and similarly identify that population at very low risk of having subsequent cardiac events and, therefore, requiring little, if any, therapy and no further investigation. Is such an approach economically feasible? An estimated 1.5 million Americans will have a heart attack this year, and about 550,000 of them will die. Of these persons, 350,000 will die before they reach the hospital. This leaves 1,150,000 persons who will be hospitalized due to myocardial infarction. As an example, if every one of these patients had a GBP study, at an estimated cost of +350.00 per examination, the cost would be about +400,000,000 or 0.7% of the total cost of cardiovascular diseases. This figure would roughly double if either a 201Tl or GBP study was performed with stress. Thus, our examinations constitute only a small percentage of the overall cost of cardiopulmonary disease. If one of these tests results in even a day early CCU to general bed transfer, early discharge, deferment of angiography, or surgery, or long-term medical therapy, then they will be cost-effective. We believe that a strong case can be made for optimism about the continued growth and expansion of nuclear techniques.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiopulmonary diagnoses by nuclear medicine techniques--where we have been, where we are, where we are going. 390 65

Despite recent renewed interest in the detection of tricuspid valve regurgitation by echocardiographic and Doppler techniques, little morphologic information is available on dysfunctioning tricuspid valves. This report describes 45 necropsy patients with clinical and morphologic evidence of pure (no element of stenosis) tricuspid regurgitation and provides morphometric observations (anular circumference, leaflet area) of the tricuspid valve useful in determining the etiology of pure tricuspid regurgitation. Of 45 patients, 24 (53%) had pure tricuspid regurgitation resulting from an anatomically abnormal valve (prolapse in 7, papillary muscle dysfunction in 6, rheumatic disease in 5, Ebstein's anomaly in 3, infective endocarditis in 2, carcinoid tumor in 1), and 21 (47%) had an anatomically normal valve with systolic pulmonary artery hypertension (cor pulmonale in 12, mitral stenosis in 9). Anular circumference was dilated (greater than 12 cm) in patients with various causes of pulmonary hypertension, floppy valve and Ebstein's tricuspid anomaly. Leaflet area was increased in floppy valve and Ebstein's anomaly. Of the 45 patients, 24 had pulmonary systolic artery pressure measurements available for correlation with tricuspid valve morphology. Pulmonary artery pressures accurately predicted morphologically normal from abnormal valves in 16 patients (89%). Morphologic overlap occurred in six patients with pulmonary pressures of 41 to 54 mm Hg. Of these six, the additional knowledge of normal or dilated anular circumference correctly separated valves with normal and abnormal leaflets.
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PMID:Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation. 395 62

Hydralazine was administered short-term to 13 patients who had stable interstitial lung disease (ILD), pulmonary arterial hypertension (PAH); mean pulmonary arterial pressure ( [PAP]=26 +/- 9 mm Hg), and cor pulmonale (CP). All patients were studied at rest and during exercise. After intravenous hydralazine at rest, there were statistically significant increases in cardiac index (CI) (p less than 0.001), arterial oxygen saturation (SaO2) (p less than 0.01), and mixed venous saturation (S-vO2) (p less than 0.01). Pulmonary vascular resistance (Rp) (p less than 0.005) and systemic resistance (Rs) decreased (p less than 0.001), and PAP did not change. During exercise, PAP did not change; however, CI (p less than 0.01), PaO2 (p less than 0.001), and S-vO2 (p less than 0.01) increased further. The increase in Rp was significantly reduced (p less than 0.01). After continuation of oral hydralazine therapy in 12 patients for 7 days, PAP at rest was not statistically different from control; Rp and Rs remained decreased (p less than 0.001). The same results were found for CI, PaO2, S-vO2, and Rs during exercise. Although PAP did not change from control values, the drug significantly reduced the increase in Rp (p less than 0.005). Vasodilator therapy with hydralazine could be useful in patients with stable ILD who have inflammation with minimal to moderate fibrosis and PAH and might be used as an adjunct to conventional therapy for ILD and CP.
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PMID:Hemodynamic effect of hydralazine in interstitial lung disease patients with cor pulmonale. Immediate and short-term evaluation at rest and during exercise. 398 68

The physiopathology of chronic bronchitis consists of sequential reactions which progressively result in respiratory failure, blood gas abnormalities and finally, post-hypoxia cor pulmonale. Airway obstruction produces maldistribution of inspired gas and starts off a series of compensatory mechanisms with increased resting lung volume and prolonged expiration time resulting in diminution of tidal volume. Abnormal ventilation/perfusion ratios result in shunt and dead space effects, determine blood gas disorders and hypoxia due to reflex vasoconstriction and ultimately lead to pulmonary arterial hypertension with elevated cardiac output and increased vascular resistances. These physiopathological chain-mechanisms account for the clinical symptoms observed, including dyspnoea, episodes of acute bronchitis and in the end, signs of chronic cor pulmonale. They also indicate that the primary objective of treatment is to correct hypoxaemia. This can be achieved by continuous low flow rate oxygen therapy, by drugs capable of redistributing more evenly the ventilation/perfusion ratios and, accessorily, by respiratory analeptic agents. As regards the treatment of pulmonary arterial hypertension, one must admit that many uncertainties are still surrounding the use of vasodilators.
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PMID:[Physiopathology of chronic bronchitis]. 614 30

The histopathology of hyperplasia of the carotid bodies was studied in 6 cases of hypoxaemia and right ventricular hypertrophy secondary to pan-acinar emphysema, and in five cases of systemic hypertension with left ventricular hypertrophy. The features of the hyperplasia were the same in the two groups. There was proliferation of sustentacular (type II) cells and compression of central cores of chief (type I) cells. It is speculated that the hyperplasia of sustentacular cells is associated in some way with the prevention of retention of sodium ions and water which characterises hypoxic cor pulmonale in "blue bloaters", systemic hypertension, and ascent to high altitude with the complications of acute mountain sickness, and pulmonary and cerebral oedema.
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PMID:Hyperplasia of the carotid body. 621 75

Massive cardiomegaly (heart weight above 400 g in females and 450 g in males) was studied in 26 Zambians examined post mortem. The aetiologies found were: hypertensive heart disease alone in six cases; hypertensive and alcoholic heart disease in two cases; alcoholic heart disease alone in five; alcoholic and pulmonary heart disease in one; alcohol with possible hypertensive heart disease in one. Eleven cases were classified as being idiopathic mainly due to lack of data and in five of these hypertension was suspected as being the cause. The series qualitatively represented the spectrum of non-rheumatic heart disease seen in patients admitted to the Central Hospital, Ndola, Zambia. Hypertension had a central role in the causation of massive cardiomegaly. Follow-up of several patients enabled observations on the cardiac effects of hypertension and alcoholism operating simultaneously and on the relationship between hypertension and congestive cardiomyopathy.
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PMID:Cardiomegaly in Northern Zambia: clinico-pathological observations. 622 32

The chest X-ray films of 251 patients with cardiovascular lesions, collected in the major hospitals of Papua New Guinea, were reviewed. Cor pulmonale (18%) and rheumatic heart disease (16%) were the predominant cardiac disorders, and cor pulmonale was the most common cause of cardiac failure (58%). Cardiomegaly or cardiac failure of unknown cause, possibly due to cardiomyopathy or myocarditis, made up 9% of the group and may be more important than has been thought previously. Aortic-arch calcification typical of atheroma was present in 21% of the patients, and is thus quite common, even though ischaemic heart disease remains very rare (1%). More than half of the patients with aortic atheroma had chronic lung disease, and though this could be explained by the coincidental frequency of both conditions, the possibility of an association or link in pathogenesis between them deserves further consideration. Anaemia was a common cause of cardiac enlargement (14%), and sometimes led to cardiac failure. Only 16 patients had hypertension (essential in 10 patients and renal in six), and this may indicate a change from the previously reported predominance of renal hypertension in Papua New Guinea towards a more equal incidence of the two conditions. Aneurysms of unknown cause were encountered in three fairly young patients. They had some resemblance to the aneurysms in arteritis of obscure origin described in Africa. There were also two dissecting aneurysms and one syphilitic aneurysm of the aorta. Congenital lesions (8%), pericarditis due to various causes (including tuberculosis), bacterial endocarditis (in four patients with rheumatic heart disease), and miscellaneous conditions made up the remainder of the series.
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PMID:Cardiovascular disease in Papua New Guinea. 644 34


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