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

Neoplastic thrombosis of the pulmonary artery is a rare and little known cause of pulmonary arterial hypertension. The clinical picture is one of acute respiratory failure and progressive right ventricular failure caused by pre-capillary pulmonary hypertension. In the living patient there is no way of distinguishing this condition from that of subacute cor pulmonale due to embolism, especially as the primary tumour is not always found either because it is too small or because it has already regressed by the time it has metastasised. The diagnosis usually rests on histological examination of the lungs, and two pathological types can be distinguished: carcinomatous lymphangitis with secondary invasion and thrombosis of the pulmonary arterioles on the one hand, and the neoplastic arterial emboli of a chorio-epithelioma on the other.
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PMID:[Pulmonary arterial hypertension caused by neoplastic thrombosis of the pulmonary artery]. 10 82

1) A systematic search was made for cardiac abnormalities (clinical, radiological and EKG) and for haemodynamic disorders (catheterisation of the right side of the heart and pulmonary artery). It was generally found that: -- 14 patients (37.8%) had no symptoms; -- 8 patients (21.6%) had pulmonary arterial hypertension (PAHT) with the corresponding cardiac signs; -- 15 patients (40.5%) had cardiac signs with no evidence of PAHT. 2) The 8 patients with PAHT (21.6%) had precapillary type of PAHT with an arteriocapillary gradient. The symptoms were those of PAHT and of the right ventricular failure; but this desorder could be latent. PAHT can be in relation with inflammatory lesions. In these 8 patients, S. Mansoni was to blame in 6 cases and 5 S. Hematobium in 2. 3) In 9 patients (24.3%), cardiac signs were connected indirectly with bilharziasis by anemia, iatrogenic injury or hypertensive myocardial disease of renal origin. 4) In 3 patients (8.1%), cardiac signs were found because of coexistant disease. 5) In 3 patients (8.1%), cardiac signs could have been due to bilharzia myocarditis. The authors reviewed the experimental and clinical discussions for such a possibility.
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PMID:[Systematic cardiologic study in 37 schistosomiasis patients]. 21 89

Two adult patients are described with pure right heart failure and chronically elevated systemic venous pressure. Neither patient had evidence of pulmonary venous hypertension, but both had septal lines. This unusual finding may be the result of impaired centripetal lymph flow in the lungs due to obstruction of the drainage of the thoracic duct by raised systemic venous pressure.
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PMID:Septal lines in pure right heart failure. 93 28

A study was made, at the altitude of Mexico City, of the clinic aspects and of the pulmonary function of 26 obese subjects more than 45% overweight. This excess weight habitually produces severe disturbances in pulmonary and/or heart function. In 50% of the patients, clinic, radiologic and electrocardiographic manifestations were found which suggested the existence of pulmonary arterial hypertension. This provoked right heart failure in 19% of the cases. The most constant alterations in the pulmonary volumes was the decrease in the VER, which occurred in 96% of the cases. Most of the patients had hypoxemia (92.5), which was produced mainly by the increase in venoarterial shunts. Although the clinic manifestations were similar to those described in Pickwick's syndrome, alveolar hypoventilation was presented in only a minority of the cases. No relationship was found between the degree of obesity and alveolar hypoventilation. Altitudes of 2,200 meters or more apparently favor hypoxemia in obese patients, and "protects" them from the hypercapnea. The altitude of Mexico City may be one of the reasons why alveolar hypoventilation is observed in only 15% of the cases.
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PMID:[Respiratory changes in obesity. Functional and clinical aspects. Study of 26 cases]. 113 Sep 8

A previously unreported combination of critical pulmonary valve stenosis and mitral stenosis is described. The initial clinical presentation was one of right ventricular failure that obscured the evidence of pulmonary venous hypertension. Following pulmonary valvulotomy, pulmonary edema ensued because of the increased pulmonary blood flow. The importance of urgent cardiac catheterization postoperatively following an operation that increases pulmonary blood flow is discussed.
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PMID:Pulmonary edema following pulmonary valvulotomy. 119 Aug 90

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

Symptoms and signs in 12 patients with severe obstructive sleep apnea (OSA) syndrome have been presented. The most common symptoms were snoring , increased motor activity during sleep and excessive daytime somnolence. The factors predisposing to OSA syndrome were obesity and anatomic abnormalities of the upper airway structure. In some cases the signs of OSA syndrome included hypertension, right heart failure, chronic alveolar hypoventilation and polycythemia. Polysomnography showed sleep fragmentation and the prevalence of light sleep stages. Obstructive sleep apneas repeated 73 +/- 23 times per hour of sleep. The mean apnea duration was 19 +/- 8 s. The mean arterial oxygen saturation during apnea was 72 +/- 14%.
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PMID:[Diagnosis of obstructive sleep apnea syndrome]. 148 56

An 18-year-old black woman presented with marginally compensated right heart failure, severe pulmonary hypertension, tricuspid incompetence, and right atrial myxoma. Catheterization suggested a substantial reactive component to her P-HTN, especially to nifedipine. Initial management consisted of excision of two right atrial myxomas and tricuspid annuloplasty, and postdischarge management with nifedipine, 30 mg four times daily. Emergency pulmonary thromboendarterectomy was required two weeks later for acute cor pulmonale. It is suggested that concomitant procedures are mandatory in this setting because of the otherwise accelerated adverse pathophysiology of obliterative pulmonary vascular obstructive disease.
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PMID:Long-term severe pulmonary hypertension associated with right atrial myxoma. 162 75

Abnormal pulmonary function that causes pulmonary artery hypertension increases right ventricular work. To compensate, the right ventricle enlarges, and cor pulmonale develops. Right ventricular failure occurs when these adaptive mechanisms cannot compensate for the hemodynamic burden. The various pulmonary diseases that are associated with right ventricular overload and the physiologic responses of the right ventricle to increased afterload are discussed in this article.
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PMID:The right ventricle in pulmonary disease. 173 54

In contrast to pulmonary parenchyma metastases or lymphangitic carcinomatosis, neoplastic emboli of small pulmonary arteries and capillaries frequently go unrecognized and are only discovered at autopsy. Five patients (48 +/- 12 years old) were admitted to 3 intensive care units for severe acute respiratory failure and died between the first and the tenth day following hospitalization. Each patient had a history of rapidly progressive dyspnea, and physical examination showed clinical evidence of right ventricular failure. The lungs were clear on chest X-rays and the ECG revealed sinus tachycardia with a right QRS axis. The mean partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were, respectively, 50.8 +/- 9.1 mm Hg and 22.2 +/- 2.4 mm Hg. A swan-Ganz catheter, inserted into 4 patients, revealed pulmonary arterial hypertension (55, 43, 37, 28) with capillary wedge pressure within the normal limits and cardiac output normal or low (3.0, 3.8, 4.4, 5.0 l/min). Pulmonary angiograms from each patient showed decreased distal lung perfusion without any proximal defects suggestive of pulmonary embolism. The inferior vena cava always appeared clear. Malignant cells were found upon autopsy (4 cases) in the lumina of the pulmonary arterioles and the primary site of the cancer was determined in 3 patients (2 hepatomas and 1 pancreatic carcinoma). The last patient had a known breast cancer with bone marrow metastases and clinical, hemodynamic and angiographic evidence of neoplastic emboli. The clinical course of neoplastic emboli can suggest acute pulmonary embolism, but the diagnosis can only be advanced after pulmonary angiography, especially if the patient is to have a cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress caused by distal neoplastic pulmonary emboli]. 209 8


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