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At least 19 recordsLinked to original sources
PubMed1990

[Cor pulmonale and cor pulmonale decompensation--what is the future of these terms?].

Decompensated cor pulmonale is a clinical syndrome manifested by signs of congestive heart failure in pulmonary disease. The authors emphasize that the haemodynamic characteristic of the syndrome differs substantially from the classical picture of chronic heart failure: the cardiac output is usually normal at rest and sometimes even during exercise, signs of impaired contractility of the right ventricle are absent and the effect of cardiac glycosides is minimal. It is possible that the clinical syndrome of decompensated cor pulmonale is caused mainly by respiratory failure and subsequent impaired function of some organs, in particular the kidney.

Heart Failure↗
PubMed2000

[Chronic cor pulmonale].

Cor pulmonale is defined as "hypertophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, as congenital heart disease". Pulmonary hypertension is a frequent hemodynamic complication associated with a wide variety of respiratory systems disorders whose only common physiologic abnormalities are alveolar hypoxia and consequent arterial hypoxemia of longterm duration. The sustained elevation in pulmonary arterial hypertension is thought to be mediated through two pathophysiologic vascular mechanism: 1) persistent vasoconstriction and 2) vascular structural remodeling. The combination of these processes causes vascular luminal narrowing and vessel obliteration that reduce pulmonary vascular surface area to the critical degree necessary for the development of the pulmonary hypertension. Cor pulmonale may be difficult to diagnose, particularly early in its course, when they symptoms manifested may be interpreted as representing progression of an underlying pathophysiological state, such as chronic obstructive airways disease. The treatment of cor pulmonale is directed toward reversing the pathogenetic process that can be directly treated, while at the same time relieving the hypoxemia, hypercapnia or acidosis. At present long-term oxygen therapy is the best treatment for pulmonary hypertension. Heart failure in cor pulmonale is usually transient once the initiating mechanism is controlled. The usual therapeutic measures for heart failure apply: a low-salt regimen, and diuretics.

Chronic Disease↗
PubMed1979

Congenital ankylosis of the temporomandibular joint: resultant upper airway obstruction and cor pulmonale.

Cor pulmonale and severe congestive heart failure secondary to chronic upper airway obstruction developed in a three-year-old girl with congenital ankylosis of the temporomandibular joint complicated by frequent respiratory infections. Nearly absent mouth opening, micrognathia, and mandibular retroposition with resultant glossoptosia obstructed the airway. Medical treatment followed by a tracheostomy and bilateral condylectomy relieved the obstruction allowing normal function of the temporomandibular joint. The clinical, electrocardiographic, radiologic, and hemodynamic findings returned to normal. Congenital ankylosis of the temporomandibular joint has not been previously reported as a cause of cor pulmonale secondary to upper airway obstruction.

Airway Obstruction↗
PubMed1990

[A pathological study on 662 autopsy cases of chronic cor pulmonale. The National Pathological Cooperative Group of Cor Pulmonale].

According to the unified diagnostic criteria and methods, 662 cases of cor pulmonale autopsy were accepted and the acceptable rate was 88.5%. Additionally, a data base with IBM PC/XT computer and dBASE-III was established in which the data of all cases accepted were stored, processed and analyzed. The results showed that chronic bronchitis and emphysema were the primary pulmonary diseases of chronic cor pulmonale in China. Chronic bronchiolitis and peribronchiolitis were considered as the late stage of bronchitis causing damage to lung tissues and constituting the central link of such complications as pulmonary hypertension and right ventricular hypertrophy. The authors emphasize also that the cellular elements and extracellular matrix were the major reason in decreasing pulmonary vascular compliance, while dilation of the lumen of pulmonary small arteries was probably the secondary change of pulmonary hypertension. According to the results obtained, it is considered that hypertrophy of the supraventricular crest can be used as one of the diagnostic criteria of right ventricular hypertrophy due to pulmonary hypertension.

Aged↗
PubMed1989

Chronic cor pulmonale.

Chronic cor pulmonale is defined as right heart hypertrophy and/or chronic right heart failure. There are many etiologies, but the common cause is increased right heart work from pulmonary hypertension. Etiology can be conveniently discussed by assuming two prototypes, the asphyxial or hypoxic type and the vascular obliterative type. A common cause of the asphyxial type is chronic obstructive pulmonary disease, and the obliterative type is represented by chronic pulmonary thromboembolic disease or primary pulmonary hypertension. Pathology is discussed, emphasizing the cardiac manifestations of chronic cor pulmonale including data of specific cardiac chamber size. An overview of hemodynamics is given, and the use and limitation of electrocardiography and chest x-rays are discussed. The exciting potential use of echocardiography for the serial non-invasive measurement of anatomical and pathophysiological features is outlined, along with the value of a careful physical examination and the proper utilization of laboratory tests in the diagnosis of chronic cor pulmonale. In the patient with the asphyxial type, the treatment of pulmonary infectious exacerbations, the role of corticosteroids, digoxin, diuretics, phlebotomy, bronchodilators (theophylline, beta adrenergic agonists, and anticholinergics), and long-term oxygen therapy is noted. The controversy surrounding the use of vasodilators and calcium blockers in these patients is discussed. Treatment aspects of the vascular obliterative type, including the role of vasodilators, calcium blockers, prostacyclin, anticoagulants, and overall strategy are discussed. A brief note is mentioned of the promising role of surgical therapy in chronic thromboembolic disease causing chronic cor pulmonale.

Adult↗
PubMed1993

[Pathophysiology of cor pulmonale].

Chronic cor pulmonale is defined as right-heart hypertrophy or right-ventricular dilatation and/or chronic right-heart failure, secondary to disorders of the respiratory system. Most cases of cor pulmonale are secondary to chronic obstructive pulmonary disease. Other etiologies include restrictive lung diseases (e.g. idiopathic pulmonary fibrosis) and multiple pulmonary emboli, with the important, although small group of patients with chronic major vessel thromboembolism. In some instances abnormal ventilatory drive, disorders of the thoracic cage or neuromuscular diseases will eventually lead to cor pulmonale. Pathogenetic mechanisms involve hypoxic pulmonary vasoconstriction, mechanical narrowing of vessels and obstruction of the pulmonary vascular bed, which are discussed in further detail.

Humans↗
PubMed1991

[The drug therapy of chronic cor pulmonale].

Chronic cor pulmonale is defined as right heart hypertrophy or right ventricular dilatation and/or chronic right heart failure. There are many etiologies which largely determine mortality and drug therapy, but the common cause is increased right ventricular work from primary or secondary pulmonary hypertension assuming two prototypes, the asphyxial and the vascular obliterative type. The main focus of this review concentrates on the various drugs to reduce pulmonary vascular pressure and resistance. The value to correct hypoxaemia is mentioned with regard to its demonstrated important effect of asthmatic patients with cor pulmonale. Continuous oxygen therapy and a potential therapy by almitrine, a respiratory stimulant, have been suggested. Phosphodiesterase inhibitors and dopaminergic drugs have been used successfully to improve right cardiac function in a small number of patients. The use of prostacyclin has a large potential to effectively correct pulmonary vascular haemodynamics but its use is fairly limited by the need of continuous intravenous application. New oral drugs under investigation which stimulate endogenous prostacyclin as well as thromboxane synthetase inhibitors still need further evaluation but might be of potential benefit. The comparison of the side-effects due to vasodilators and calcium antagonists argues for the use of calcium channel blockade for patients with pulmonary hypertension. To define the role of angiotensin converting enzyme inhibitors or the more recently introduced potassium channel openers for treatment of chronic cor pulmonale still await detailed, controlled studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1996

[The prospect of prevention and treatment of Cor pulmonale on a 20-year follow-up of 40 middle to old aged cases of COPD and Cor pulmonale].

OBJECTIVE: To study the outcome of current therapy for COPD and Cor pulmonale by long-term follow-up of COPD patients. METHOD: Forty cases of middle to old aged COPD and Cor pulmonale patients were followed up for a period of 20 years. RESULTS: The pulmonary function of all the patients reduced significantly more than healthy elderly, while no difference was noted in blood gas analysis. 23 patients with advanced COPD developed cor pulmonale, so that the number of cases with cor pulmonale increased significantly from 7 to 30. By the end of follow-up 19 cases survived (48%), 21 cases (Cor pulmonale 19, COPD 2) died (53%). CONCLUSIONS: In view of the high mortality of cor pulmonale and the tremendous treatment cost, it was considered that the prospect for cor pulmonale management should be put on treating COPD to avoid development of Cor pulmonale. The keys of treating COPD are stop of smoking, protection from cold, early treatment of respiratory infection and further establishment of pulmonary rehabilitation work.

Aged↗
PubMedDate not supplied

Serum soluble Fas in patients with Schistosomal cor pulmonale.

BACKGROUND: Schistosomal cor pulmonale is considered an important pathological condition in endemic areas. Few recent studies have reported the role of apoptosis in pulmonary hypertension. OBJECTIVES: The aim of this study was to assess serum levels of soluble Fas (sFas), an inhibitor of apoptosis, in patients with schistosomal cor pulmonale as compared to patients with cor pulmonale due to chronic obstructive pulmonary disease (COPD) and normal subjects. METHODS: Serum sFas was assessed in 15 men with schistosomal cor pulmonale (age 32 +/- 10 years), 15 men with chronic cor pulmonale secondary to COPD and 20 healthy men, matched for age. RESULTS: Serum levels of sFas were significantly higher in patients with schistosomal cor pulmonale (74 +/- 80 U/ml) than in patients with cor pulmonale due to COPD (15 +/- 10 U/ml) and normal subjects (19 +/- 11 U/ml, p < 0.001 in both). In patients with schistosomal cor pulmonale, sFas was significantly higher in patients with mean pulmonary artery pressure > 30 mm Hg as compared to patients with pressure < or = 30 mm Hg (109 +/- 97 vs. 34 +/- 20 U/ml, p = 0.01). There was a significant correlation between serum sFas and the mean pulmonary artery pressure in patients with bilharzial cor pulmonale (r = 0.4, p < 0.01), but not in patients with COPD (r = 0.1, p = NS). CONCLUSIONS: Serum sFas levels are elevated in patients with schistosomal cor pulmonale and they are related to the severity of pulmonary hypertension. These findings suggest a role of apoptosis in schistosomal cor pulmonale.

Adult↗