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 53-year-old male was admitted to the hospital due to electrocardiographic ST-segment elevation in V1-4 with ST-segment depression in the inferior leads, which suggested acute myocardial infarction. He had a cough and a slight fever without chest pain. Serum creatine kinase and its myocardial band were slightly elevated but creatine kinase value did not exceed twice the normal upper limit. Emergent coronary arteriography (CAG) revealed intact coronary arteries. The CAG in a chronic stage again revealed intact coronary arteries. Intracoronary administration of acetylcholine of 100 micrograms to the left coronary artery and 50 micrograms to the right coronary artery provoked diffuse spasm in the right and left coronary arteries. The electrocardiogram (ECG) during the right coronary artery spasm revealed ST-segment depression in the inferior leads with ST-segment elevation in V2 and V3, which resembled the ECG finding at the time of the patient's admission. With intracoronary isosorbide dinitrate, the spasm and ST-segment elevation were resolved. These findings strongly suggest that coronary spasm can cause myocardial injury indicated by a slight elevation of serum creatine kinase value.
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PMID:[A case of painless myocardial injury probably caused by coronary artery spasm]. 143 52

Captopril is widely used for congestive heart failure and arterial hypertension. Its main side effects are cough, neutropenia, and renal injury. Liver dysfunction has rarely been described. We present a 71-year-old man with an acute myocardial infarction who developed high fever and progressive disturbance of liver function tests, hepatocellular and cholestatic, after beginning captopril. When other, more likely causes for his condition were ruled out, captopril was discontinued and the fever and liver dysfunction then quickly resolved. We recommend periodic laboratory follow-up in patients treated with angiotensin-converting enzyme inhibitors.
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PMID:[Captopril-induced liver dysfunction]. 175 82

We study the hemodynamic effects of pressotherapy in 11 patients (mean age : 68 +/- 10 years) with uncomplicated acute myocardial infarction (n = 6) or with chronic ischemic heart failure (n = 5). We measure the right auricular pressure (RAP), the mean pulmonary arterial pressure (MPAP) and the pulmonary wedge pressure (PWP), before, during pressotherapy (MPAP) and the pulmonary wedge pressure (PWP), before, during pressotherapy (T 20 min) and 30 minutes after the end of pressotherapy (T 30 min). We use five-chambered leg garments with 80 mm Hg pressure during 20 minutes. The wavelike action (from the bottom to the top) is intermittent: the compression time is 10 second (sec); compression is maintained during 60 sec; deflation time is 15 sec. After 20 minutes pressotherapy (t 20) the 3 variables increase: RAP: from 3.6 +/- 5 to 7 +/- 7 mm Hg (P less than 0.001), MPAP: from 25 +/- 14 to 29 +/- 17 mm Hg (p less than 0.01) and the PWP from 10 +/- 8 to 17 +/- 11 Hg (p less than 0.01). This rise is particularly important in heart failure patients: from 18 +/- 8 to 29 +/- 8 mm Hg for the PWP, with cough in one patient. At T 30 these 3 variables decrease and return nearly to initial values: respectively 2.7 +/- 4.7 (RAP), 24 +/- 14 (MPAP), 12 +/- 8 mm Hg (PWP). In conclusion pressotherapy increases RAP and pulmonary pressures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic impact of pressotherapy]. 221 70

An p6-year-old man with anterior acute myocardial infarction was administered antimyosin antibody labeled with 74 MBq (2 mCi) 111In, and abnormal hot activity was observed in the left lung by immunoscintigraphy. 67Ga-citrate scintigraphy also showed abnormal uptake in this lesion. At this time, this patient complained of fever and cough with sputum, and roentgenography showed a coin lesion-like shadow at the same location of the lung. By treatment with antibiotics, his symptom was improved and coin lesion-like shadow disappeared. So we thought the RI uptake area in the left lung was inflammatory lesion. This case suggests that 111In-antimyosin antibody can be trapped to the focal site of inflammation.
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PMID:[Accumulation of 111In-antimyosin antibody at the focal site of inflammation]. 229 Feb 15

A 61-year-old man was admitted to our hospital with complaints of cough and left back and chest pain. He had suffered from left tuberculous pleurisy at the age of 20 years. Chest X-ray film and CT revealed atelectasis of the left lung, a left hilar mass and an irregular left atrial wall. Depressed P-Ta segment in the inferior limb and anterior chest leads and an abnormal P wave were found on ECG. Transbronchial lung biopsy showed squamous cell carcinoma. After radiation therapy, the patient complained of chest oppression. ECG revealed a normalized P-Ta segment deviation, markedly elevated ST segment in the inferior limb and lateral chest leads and a depressed ST segment in the anterior chest leads. These findings persisted until his death. An obscure appearance of the pericardium and an echogenic intramyocardial mass in the posteroinferior and lateral wall were evident by echocardiography. The patient died due to heart failure. Postmortem needle biopsy showed scattered intramyocardial tumor cell nests with keratinization. CPK, GOT and LDH were within normal limits throughout the course, but CPK-MB was slightly increased. Cardiac metastasis with an ECG appearance similar to that of acute myocardial infarction has been rarely reported. Our present case showed peculiar feature including 1) ECG findings similar to atrial and ventricular myocardial infarction, and 2) an echogenic intramyocardial mass and an ill-defined pericardium on echocardiography. These findings suggested direct invasion of squamous cell carcinoma of the lung to the ventricular myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Report of a case of lung cancer with metastasis to the myocardium which showed electrocardiographic findings similar to acute myocardial infarction and intramyocardial mass on echocardiography]. 274 Jun 46

Legionellosis is an important cause of severe pneumonia in the community. Inadequate therapy will lead to respiratory distress syndrome, disseminated intravascular coagulation (DIC) and finally fatal multiple organ failure. We encountered a rare case in which early manifestation included septic shock and DIC complicated by acute myocardial infarction (AMI) suspected to be derived from Legionnaires' disease. A 54-year-old healthy female complained of lumbago, high fever and dry cough 10 days after visiting a hot spring spa. She was emmergently admitted due to shock. Physical examination demonstrated hypotension, high fever, course creakle in the right lower lung. Hepatosplenomegaly, lymphadenopathy and eruption were not found. WBC count was 34600/microliters with nuclear shift. CRP elevated. FDP, D dimer and TAT also elevated CPK elevated with dominance of the MB isozyme. Chest roentogenography revealed congestive heart failure, pleural effusion and obscure pneumonic shadow and EKG showed ST segment elevation in leads I, II, III, aVF, V4, V5, and V6. The patient was diagnosed as having septic shock, DIC and AMI. She was treated with gabexate mesilate, high dose methyl prednisolone and dopamine hydrochloride as well as piperacillin, meropenem, isepamycin and fluconzaole. Despite intensive care, the blood pressure fell again and pneumonia had progressed on the 8th hospital day. These antibiotics appeared to be ineffective. Erythromycin was then administered and a dramatic effect. was obtained as the patient recovered. Serum titer of Legionella pneumophila (serogroup 1) rose to 128-fold 2 weeks after the onset. Other serum titers such as Chlamydia psittaci, Rickettsia, Mycoplasma were all negative. Cultures obtained from the sputum, throat swab, urine and blood did not yield any microorganisms. Although the diagnosis could not be confirmed because the titer did not elevate over 256-fold of 4-fold within 2 weeks after the onset, Legionella infection was highly suspected from the clinical features. This is a rare case in which septic shock and DIC with AMI preceded pulmonary symptoms in a non-immunocompromised patient.
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PMID:[Early manifestation of septic shock and disseminated intravascular coagulation complicated by acute myocardial infarction in a patient suspected of having Legionnaires' disease]. 958 3

This study examines whether there are differences between Mexican Americans and non-Hispanic whites in reported symptoms of acute myocardial infarction (AMI). The symptoms experienced by patients identified in a community-based surveillance program were examined to determine whether between-group differences existed by ethnicity, gender, and diabetic status. Data were available regarding the symptoms of 589 patients, between the ages of 25 and 74 years, who were hospitalized and diagnosed as either having definite or possible AMI in special care units at 1 of 7 hospitals in Corpus Christi, Texas. The most frequently reported symptoms were chest pain (83.2%), chest pressure or discomfort (67.6%), sweating (64.2%), fatigue (62.6%), dyspnea (60.3%), and arm or jaw pain (58.2%). After adjusting for age, diabetes mellitus, and gender, and relative to non-Hispanic whites, Mexican Americans were more likely to report chest pain, upper back pain, and palpitations, and less likely to report arm or jaw pain. Likewise, relative to men, women were more likely to report fatigue, dyspnea, dizziness, upper back pain, palpitations, and cough, and were less likely to report chest pain. Significant differences were also observed when older patients' symptoms were compared with younger patients' symptoms.
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PMID:Comparison of reported symptoms of acute myocardial infarction in Mexican Americans versus non-Hispanic whites (the Corpus Christi Heart Project). 985 14

Imidapril hydrochloride (imidapril) is a long-acting, non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor, which has been used clinically in the treatment of hypertension, chronic congestive heart failure (CHF), acute myocardial infarction (AMI), and diabetic nephropathy. It has the unique advantage over other ACE inhibitors in causing a lower incidence of dry cough. After oral administration, imidapril is rapidly converted in the liver to its active metabolite imidaprilat. The plasma levels of imidaprilat gradually increase in proportion to the dose, and decline slowly. The time to reach the maximum plasma concentration (T(max)) is 2.0 h for imidapril and 9.3 h for imidaprilat. The elimination half-lives (t(1/2)) of imidapril and imidaprilat is 1.7 and 14.8 h, respectively. Imidapril and its metabolites are excreted chiefly in the urine. As an ACE inhibitor, imidaprilat is as potent as enalaprilat, an active metabolite of enalapril, and about twice as potent as captopril. In patients with hypertension, blood pressure was still decreased at 24 h after imidapril administration. The antihypertensive effect of imidapril was dose-dependent. The maximal reduction of blood pressure and plasma ACE was achieved with imidapril, 10 mg once daily, and the additional effect was not prominent with higher doses. When administered to patients with AMI, imidapril improved left ventricular ejection fraction and reduced plasma brain natriuretic peptide (BNP) levels. In patients with mild-to-moderate CHF [New York Heart Association (NYHA) functional class II-III], imidapril increased exercise time and physical working capacity and decreased plasma atrial natriuretic peptide (ANP) and BNP levels in a dose-related manner. In patients with diabetic nephropathy, imidapril decreased urinary albumin excretion. Interestingly, imidapril improved asymptomatic dysphagia in patients with a history of stroke. In the same patients it increased serum substance P levels, while the angiotensin II receptor antagonist losartan was ineffective. These studies indicate that imidapril is a versatile ACE inhibitor. In addition to its effectiveness in the treatment of hypertension, CHF, and AMI, imidapril has beneficial effects in the treatment of diabetic nephropathy and asymptomatic dysphagia. Good tissue penetration and inhibition of tissue ACE by imidapril contributes to its effectiveness in preventing cardiovascular complications of hypertension. The major advantages of imidapril are its activity in the treatment of various cardiovascular diseases and lower incidence of cough compared with some of the older ACE inhibitors.
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PMID:Protection of the cardiovascular system by imidapril, a versatile angiotensin-converting enzyme inhibitor. 1217 88

The causes and consequences of failed extubation in postoperative intensive care unit (ICU) patients were prospectively collected by clinical observation study in the surgical ICU Siriraj Hospital from 1st October 2000 to 31st March 2001. The failure rate was 1.7 per cent (9/477). Patients underwent the following types of surgery: abdominal surgery 66.67 per cent, orthopedic 22.22 per cent, and head-neck surgery 11.11 per cent. Reasons for reintubation were respiratory failure 55.56 per cent (5/9), inadequate cough reflex 22.22 per cent (2/9), congestive heart failure 11.11 per cent (1/9), and acute myocardial infarction 11.11 per cent (1/9). The consequences of failed extubation were worse outcomes:- the average length of stay in these patients increased from 3.67 days to 9.3 days. The mortality rate was 33.33 per cent. Tracheostomy was required in 55.56 per cent. From these observations we conclude that extubation should be performed at the appropriate time for each patient. This will differ according to the patient and his/her circumstances.
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PMID:Clinical outcomes of failed extubation in a postoperative intensive care unit. 1245 40

Non-invasive positive pressure ventilation (NIPPV) has been discussed comprehensively in the last years, but usage of non-invasive ventilation in Intensive Care Units is rare. The reasons may be uncertainty in indications and difficulties in handling the masks and ventilators. In the last years the introduction of full face masks and respiratory helmets has made it possible to ventilate patients with unusual facial forms and to avoid problems of pressure necrosis. Software components designed for NIPPV are available for standard respirators. Indications for NIPPV (neuromuscular diseases, spinal abnormalities, chest wall malformations, COPD, cardiogenic pulmonary edema) have been ensured in clinical trials. No sufficient data are available for the application of NIPPV in weaning and respiratory failure following extubation. Indication for NIPPV becomes apparent when therapy starts in early stage with sufficient ventilation pressure. Compared to standard therapy, no reliable advantage has been seen for NIPPV in hypoxic hypercapnia respiratory failure except for malignant diseases. However, prophylactic use in patients with high risk might be conceivable. For these patients strict criteria of termination are required to avoid missing the time point for intubation. Gas exchange disturbances in advanced lung fibrosis, pneumonia and ARDS are not amenable to NIPPV. Contraindications for NIPPV are non-compliant patients, absence of cough- and pharyngeal reflexes as well as retention of secretions and malignant ventricular arrhythmia. Relative contraindications are catecholamine-dependent circulatory collapse and acute myocardial infarction, since sufficient data for NIPPV are missing.
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PMID:[Noninvasive ventilation in the intensive care unit -- is it still negligible?]. 1267 84


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