Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the span of two or three days in August, 1972, in two separate communities in eastern Massachusetts two men, one aged 39, the other 66, each without previous overt heart disease, were stung by wasps. Each went into shock rapidly after an interval of over a half-hour developed chest pain and, later, sequential electrocardiographic changes diagnostic of acute myocardial infarction. Each survived; each had normal electrocardiograms before the sting. Though preexistent coronary artery disease can be excluded in neither, the view is favored that acute myocardial infarction in each was caused by deficient coronary perfusion secondary to anaphylactic shock induced by the wasp stings. An intriguing case was just recently reported58 of a 62-year-old man with previous angina who developed pulmonary edema but no chest pain following wasp sting and went on to show rapidly reversed electrocardiographic changes attributable to subendocardial ischemia or infarction. In a sense, this sequence fills the gap as an intermediate phase between the normal and the two individuals described here who developed pain after anaphylactic shock, then proceeded, perhaps through this phase, to develop transmural infarction.
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PMID:Acute myocardial infarction following wasp sting. Report of two cases and critical survey of the literature. 125 36

Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.
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PMID:Stress failure of pulmonary capillaries: role in lung and heart disease. 809 42

A 21 month old female had voluntarily ingested 0.5-1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema. Right heart failure was improved after administering vitamin B1. However, 5 days after the shock, hypoxemia and diffuse radiographic infiltrates progressed, and a diagnosis of adult respiratory distress syndrome (ARDS) was made. After the occurrence of an air leak, the patient died of respiratory failure. The cardiogenic shock and pulmonary edema due to cardiac beriberi may have triggered the ARDS.
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PMID:Cardiac beriberi (shoshin beriberi) caused by excessive intake of isotonic drink. 141 37

The frequency, clinical characteristics, and outcome of patients admitted with heart failure to a district general hospital in North-West London serving a population of approximately 155,000 was assessed over a six-month period. The number of patients with heart failure was determined by both a prospective ward survey and a retrospective study of all patient records with diagnostic codes for heart failure or pulmonary oedema. During those six months, 2,877 patients were admitted to the medical and geriatric services of whom 140 (4.9%) had heart failure. Only 29 patients in heart failure were under the age of 65 years. In 86 patients the mode of presentation was acute pulmonary oedema. Fifty-two (37%) patients had an arrhythmia at the time of admission of whom 48 had atrial fibrillation. An electrocardiogram, a chest X-ray, and an echocardiogram were performed in 137, 136, and 81 patients respectively. The aetiology of heart failure was considered to be coronary artery disease (41%), valve disease (9%), hypertension (6%), cor pulmonale (4%), a dilated cardiomyopathy (1%), congenital heart disease (1%), thyrotoxicosis (1%), and unknown (36%). During the period of hospital stay 42 patients (30%) died; a further 20 patients (14%) died in a one-year follow-up. In a district general hospital heart failure is a common reason for admission and patients remain in hospital for a considerable time. Arrhythmias are commonly associated with heart failure. The prognosis is poor and the hospital mortality high. The management of heart failure is an important consideration in allocating hospital resources in a district general hospital.
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PMID:Heart failure in a district general hospital. 842 54

The discrimination of the pathogenesis of the clinical picture "heart failure" as caused by a dominant systolic or diastolic LV-dysfunction is of a special importance in the elderly patient because of the consequences for the choice of pharmacological therapy, resulting from the age-related physiological increase of stiffness of the myocardium. The pathophysiology of diastolic dysfunction is characterized by a prolonged relaxation period as well as by compromised passive filling properties, caused by myocardial and external determinants. Typical clinical signs of diastolic dysfunction are dyspnea or pulmonary edema. Cardiac disorders with a dominance of diastolic dysfunction are coronary and hypertensive heart disease as well as hypertrophic or uremic cardiomyopathies. Diagnosis of diastolic dysfunction easily can be performed noninvasively by means of Doppler-echocardiography. Pharmacological therapy in diastolic dysfunction should prefer beta blocking drugs and calcium-antagonists against vasodilators or digitalis.
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PMID:[Diastolic left ventricular dysfunction--significance for differential diagnosis and therapy of heart failure in the aged]. 160 44

The patient presented is a 27-month-old male with complex congenital heart disease consisting of severe left ventricular outflow tract obstruction and ventricular septal defect who had undergone a pulmonary trunk-to-aorta graft and a pulmonary artery banding procedure as a neonate. Sometime after this repair, but at least 15 months prior to presentation to this institution for placement of an aortic homograft, the pulmonary trunk band apparently slipped and migrated over the right pulmonary artery, severely limiting blood flow to the right lung and increasing flow to the left. Severe pulmonary hypertension developed, with a main pulmonary artery pressure of 94/53 mm Hg. We present clinical and radiographic evidence that the resulting chronic high blood flow and pressure in the left lung ultimately resulted in hypoperfusion of that lung, presumably secondary to chronic vascular changes with greatly increased vascular resistance. Upon surgical repair and removal of the constrictive band from the previously banded right PA, blood flow was increased to the low resistance right lung causing right-sided unilateral pulmonary edema, ventilation/perfusion mismatching, and severe hypoxemia. Perfusion studies documented that less than 10% of blood was directed to the left lung, with greater than 90% to the right. Perfusion studies 9 months postoperatively continued to demonstrate minimal blood flow to the left lung. Discussion focuses on the effects of mechanical forces and the interaction with hypoxia in causing pulmonary vascular remodeling.
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PMID:Unilateral pulmonary hypertension as a result of chronic high flow to one lung. 169 72

Cardiac diseases of cattle may involve valvular structures, myocardium, pericardium, or blood vessels and are manifested by the clinical signs of cardiac dysrhythmias, cardiac murmurs, generalized edema, muffled heart sounds, jugular venous distention, jugular venous pulsations, pulmonary edema, pleural effusion, or ascites. Digoxin, quinidine, and furosemide can be used effectively to control signs of CHF and cardiac arrhythmias. Combination antimicrobial therapy can be successful for cows with infective endocarditis and thrombophlebitis. Pericardial fluid drainage may temporarily improve cattle with traumatic pericarditis or lymphosarcoma so that short-term goals may be reached.
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PMID:Treatment of cardiovascular disease in cattle. 176 Jul 59

Acute ipsilateral pulmonary edema following reexpansion of the lung after pleurocentesis or pneumothorax is a well described entity. We report the unusual occurrence of bilateral pulmonary edema following unilateral pleurocentesis in a young male without heart disease. Various hypotheses regarding the mechanism of reexpansion pulmonary edema include increased capillary permeability due to hypoxic injury, decreased surfactant production, altered pulmonary perfusion and mechanical stretching of membranes. This case suggests that forces leading to ipsilateral reexpansion pulmonary edema also affect the contralateral lung.
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PMID:Bilateral reexpansion pulmonary edema following unilateral pleurocentesis. 198 21

Fifty-two cases of acute phase subarachnoid hemorrhage were studied by brain CT scanning to determine the presence and incidence of ischemic myocardial disorder, the relationship between ischemic change and severity, disease prognosis, and the relationship between acute phase circulatory dynamics and so-called neurogenic pulmonary edema. In all cases, ECGs were carried out and CPK-MB determined. Some of the patients underwent Tl myocardial scintigraphy, echocardiography, cardiac catheterization, as well as circulatory dynamic investigation (by Swan-Ganz catheter) and arterial blood gas analysis. In 31 of the 52 cases (59.6%), 3-day ECG series revealed ischemic changes. These findings were backed up by other cardiac function tests, thus suggesting that myocardial ischemia was present. Results in cases undergoing cardiac catheterization revealed that the myocardial ischemic changes were not due to organic constriction of the coronary artery. Included in those cases in which ECG markedly changed and CPK-MB rose substantially were many patients for whom the prognosis was poor. Evaluation of respiratory function and circulatory dynamics in cases of so-called neurogenic pulmonary edema seemed to indicate decline in cardiac function owing to myocardial ischemic change. This could account for onset of symptoms. These findings support the need for adequate circulatory management in cases of acute subarachnoid hemorrhage with pulmonary edema and/or changes on ECG. In such cases, concurrent catheterization and cerebral angiography (cerebro-cardiac catheterization: CCC) proved effective for evaluating cardiac function and determining whether heart disease was also present.
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PMID:[Ischemic myocardial disorder in acute phase subarachnoid hemorrhage: clinical study of 52 patients]. 204 49

Heart disease is the most important nonobstetric cause of maternal death; however, most young women with heart disease do well during pregnancy. If the physician is uncertain of the effects of pregnancy on a particular heart condition, needless restrictions may be imposed. The main hazards are: pulmonary edema when it occurs suddenly in mitral stenosis; pulmonary hypertension (because pulmonary vascular disease tends to be exacerbated by pregnancy); infective endocarditis (this is rare); and fulminating peripartum cardiomyopathy. The practical management of the pregnant patient with various concomitant heart conditions (congenital heart disease, pulmonary hypertension, rheumatic heart disease, anticoagulants and artificial valves, constrictive pericarditis, kyphoscoliosis, Marfan's syndrome, mitral prolapse, hypertrophic cardiomyopathy, dilated cardiomyopathy, infective endocarditis, and arrhythmias) is discussed. An absolute indication for therapeutic abortion is severe pulmonary vascular disease; discretionary indications include 'chronic thromboembolic pulmonary hypertension,' cardiomyopathies (depending on the hemodynamic disturbance), and Marfan's syndrome.
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PMID:Cardiovascular disease in pregnancy. 218 16


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