Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A possible relationship between heart disease, oesophageal dysfunction (OD) and symptomatology was studied in 47 patients with valvular heart disease. They were investigated with oesophageal manometry and oesophageal acid perfusion test. OD was found in 32 percent of the patients. A local pressure increase in the middle part of the oesophagus, probably an effect of cardiac enlargement and compression of the oesophagus, was found at manometry in 38 percent. The incidence of OD and of oesophageal symptoms was the same in patients with and without oesophageal compression. We did not find any indications that valvular disease in itself provokes OD, nor that symptoms of chest pain and cough in patients with valvular heart disease are due to OD.
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PMID:Oesophageal symptoms and manometry in valvular heart disease. 52 38

Clinical, biochemical, bacteriological, x-ray, electrocardiographic, ultrasonic and morphological examinations for pulmonary pathology were made in 230 patients with infectious endocarditis (IEC) treated in 1982-2001. Pulmonary involvement was found in 30% of the examinees. Pulmonary onset of IEC caused misdiagnosis in 11% cases. Its appearance can be recognized by fever (100% cases), chest pain (73%), cough (50%) and dyspnea (46%). Pulmonary affection and pulmonary onset of IEC were associated with disorders of the mitral (26 and 27%, respectively), aortic (17 and 8%, respectively), tricuspis (5 and 8%, respectively) valves or compound valvular heart disease (43 and 50%, respectively). Bacterial vegetations of the heart valves were detected in 60% patients with pulmonary lesions and 62% patients with pulmonary onset of IEC in transthoracic ultrasonography. Pulmonary lesions and pulmonary onset of IEC were caused primarily by staphylococci (73 and 67%, respectively).
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PMID:[Engagement of the lungs in infectious endocarditis]. 1510 8

The autopsy protocols of 560 patients were studied in order to detect the incidence of pulmonary embolism, 83 cases were found (15%). The clinical data was analyzed to establish the existence of differentiating points between subjects with pulmonary infarcts and those with embolism but without infarction. The necropsy findings were further scrutinized to determine the effect of the anatomic localization of the embolus upon the production of infarction. Pulmonary infarctions were present in 60% of the cases with pulmonary embolus. The presence of cardiac failure, valvular heart disease and left ventricular hypertrophy was significantly more frequent in patients with pulmonary infarcts. In subjects with or without infarction the age, sex and the presence of medical debilitating diseases, recent trauma, surgical interventions or postpartum, cardiac diseases, arteriosclerotic heart disease, clinical evidence of thrombophlebitis, prolonged bed rest and atrial fibriliation preceding the pulmonary embolism, did not evidenciate any significant difference. In the cases with infarction the pulmonary embolus was significantly more frequently located in the small and sublobar pulmonary artery branches, while when pulmonary infarction was not found the embolic process was more frequently located in the main, right or left pulmonary arteries; occlusion of the lobar arteries had approximately the same incidence in the two groups. The most common clinical signs of pulmonary thromboembolism were dyspnea, tachycardia, cough and shock. The presence of hyperthermia, cough, jaundice, bloody sputum, pleuritic pain, pleural friction rub and pleural effusion was significantly more frequent in those cases with pulmonary infarction; the last five features were present only in the presence of infarction. The electrocardiogram was strongly suggestive of pulmonary embolism in the 6% of all cases, while the chest X-ray in 30% of those with pulmonary infarct. The diagnosis was established antemortem in 40% of the cases with infarction and in 20% of the cases with embolus but without pulmonary infarction. In 23% adequate anticoagulant therapy was established.
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PMID:[Anatomoclinical study of pulmonary embolism in patients with or without pulmonary infarction]. 1515 31

Pulmonary hypertension (PH) decreases resistance to fatigue and life expectancy. The aim of this study was to correlate some indirect Doppler indices of PH with tricuspid and pulmonary regurgitation criteria and to relate PH on different indices with the severity of clinical signs. Furthermore the pathogenetic mechanisms associated to PH development were discussed. Dogs with Doppler echocardiographic evidence of PH diagnosed by assessment of pulmonary and tricuspid regurgitant jet velocity were selected, their clinical records were reviewed and a clinical score was computed. Seventeen cases of PH were identified. The degree of PH was assessed based on systolic or diastolic pulmonary pressure and the indirect Doppler indices (AT/ET and Tei Index) were calculated; data were statistically evaluated. Indirect Doppler indices were calculated also in a control group of seven healthy dogs. The most common clinical signs were coughing, dyspnea and syncope; the most common condition associated to PH development was the left-sided valvular heart disease. A significant positive correlation was found between Tei Index and both the systolic pressure and the severity of PH while no correlations were found between PH on different indices and clinical score and/or severity of clinical signs. Results of this study suggest that Tei-index could be an useful support not only to reveal PH but also to give information on the severity of PH. The clinical picture in dogs with PH is apparently unpredictable and not strictly correlated with the severity of PH.
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PMID:Doppler echocardiographic evidence of pulmonary hypertension in dogs: a retrospective clinical investigation. 2441 41

A 65-year-old woman, with valvular heart disease, atrial fibrillation, and depression, presented to the emergency room due to dyspnea with shock state accompanied by agitation. An electrocardiogram showed ST segment elevation in leads II, III, aVF, I, aVL, and V4-6. An echocardiography revealed extensive akinesis in the apex, but hyperkinesis in the base, with apical ballooning appearance. An emergent coronary angiography showed no obstructive disease. The patient required intubation under mechanical ventilator, and an intra-aortic balloon pump to recover from shock state. She had been taking maprotiline, a tetracyclic antidepressant, and had added dextromethorphan, a cough suppressant, just before admission. The patient was diagnosed with takotsubo cardiomyopathy associated with serotonin syndrome due to serotonergic drug interactions. After discontinuation of these drugs and administration of serotonin antagonist under mechanical supportive care, she became hemodynamically stable. Apical ballooning was completely resolved 2 weeks later, and she was discharged well. We diagnosed serotonin syndrome manifesting as excessive serotonin toxicity that resulted in a hyperserotonergic and hyperadrenergic state, causing takotsubo cardiomyopathy. Here, we report a case of takotsubo cardiomyopathy associated with serotonin syndrome. This case suggests that serotonin syndrome should be recognized promptly and complications, including takotsubo cardiomyopathy, need to be treated appropriately. <Learning objective: We must closely monitor serotonergic agents because serotonin syndrome can occur from a combination some serotonergic drugs, even when each is used at a therapeutic dose. Serotonin syndrome can lead to not only serotonergic but also hyperadrenergic state that may be a trigger of takotsubo cardiomyopathy. Serotonin syndrome should be diagnosed surely to ensure the prompt initiation of the treatment included discontinuation of the precipitating drugs because the disease occasionally progresses rapidly to fatal condition.>.
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PMID:Cardiogenic shock due to takotsubo cardiomyopathy associated with serotonin syndrome. 3053 5