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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
Am J Cardiol 1978 Aug
PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

For the first time in the world we take surfactant scan in 3 normal volunteers and in one patient with pneumonia lobar, using 400 microCuries of surfactant Iodine-131. No intolerance, or radiotoxicity was found in 3 months of clinical follow up of the subjects. The results are very encorageous. A great variety of clinical situations could be now examinated with this new technic and radiocompound and given new perspectives in its study and diagnoses and a better knowledge of its physiophatology.
Arch Inst Cardiol Mex
PMID:[Scentilleography of the pulmonary tensive active Iodine-131 in humans]. 57 82

Symptomatic myocardial infarction without chest pain was identified in 26 of 102 patients (25.5%) admitted to the hospital with acute myocardial infarction. As a group, these patients had a significantly lesser prevalence of a history of angina (P less than 0.05) and cigarette smoking (P less than 0.01). Their mean age was 69.1 years compared with 58.7 years for patients with chest pain (P less than 0.001). The group had a significantly greater median delay between the onset of symptoms and (1) arrival at the hospital (P less than 0.05), (2) examination by a physician in the emergency room (P less than 0.05), (3) diagnosis of possible myocardial infarction (P less than 0.001), and (4) transfer from the emergency room to the intensive care unit (P less than 0.001). They had significantly higher admission values for mean heart rate, respiratory rate, temperature and white blood cell count and more frequent in-hospital complications of pneumonia (P less than 0.001) and cardiogenic shock (P less than 0.05). Mortality in the group was 50% compared with 18% in the group with chest pain (P less than 0.05). Discriminant function analysis identified an at-risk population with 80% reliability.
Am J Cardiol 1977 Oct
PMID:Symptomatic myocardial infarction without chest pain: prevalence and clinical course. 91 Jul 14

ECG and Bcg studies have been carried out on 40 youths, aged 18-23, suffering from mycoplasmic pneumonia; in 19 of them mild Bcg changes were established. The frequencyof ECG changes is less-12 patients. The pathological deflections in Ecg and Bcg in all patients normalize before the control examination, which takes place 30 days after discharge of the patients from hospital.
Bibl Cardiol 1975
PMID:The ballistocardiogram in myocardial infarction. 113 Dec 1

ECG and Bcg studies have been carried out on 40 youths, aged 18-23, suffering from mycoplasmic pneumonia; in 19 of them mild Bcg changes were established. The frequency of ECG changes is less - 12 patients. The pathological deflections in Ecg and Bcg in all patients normalize before the control examination, which takes place 30 days after discharge of the patients from hospital.
Bibl Cardiol 1975
PMID:Cardiac lesions caused by mycoplasmic pneumonia in youths according to ballistocardiographic and electrocardiographic data. 113 Dec 2

The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the hypoxia is associated to acute pulmonary edema and shock. Mechanic ventilators, and intermitent possitive pressure are recommended even though they have a posenous effect on the cardiac output. Always keep the air ways permeable: changing position, breathing exercises, humidifications, aspiration of secretions, intubation, or traqueostomy depending upon the various cases.
Arch Inst Cardiol Mex
PMID:[Pulmonary complications of acute myocardial infarct. Therapeutic orientation]. 115 8

Sixteen patients with pericarditis caused by Histoplasma capsulatum were studied. Fourteen were less than 30 years old, and no patient had an underlying illness or was receiving immunosuppressive therapy. All patients experienced a flu-like prodromal illness lasting from 2 weeks to 4 months. Pneumonitis or hilar adenopathy, or both, was found in 12; pleural effusion, uncommon in primary pulmonary histoplasmosis, was found in seven patients. Pericardial fluid, pleural fluid and bone marrow cultures yielded no growth. All patients demonstrated a fourfold or greater change in complement-fixing antibody titers. No patient had disseminated disease, and only one required treatment with ampholericin B. The illness ran a protracted course, and in six patients symptomatic pericarditis recurred. Ultimately all recovered. Ten patients were restudied 6 months to 12 years after recover. Only one patient had pericardial calcification, and none had constrictive pericarditis. This form of granulomatous pericarditis, unlike that caused by Mycobacterium tuberculosis, appears to carry a good prognosis.
Am J Cardiol 1976 Jan
PMID:Pericarditis caused by Histoplasma capsulatum. 124 38

It is sometimes very difficult to diagnose dissecting aortic aneurysms (DAA), particularly in its early stage, due to manifold signs and symptoms. The purpose of this study is to clarify the reasons for such erroneous diagnoses. A total of 41 patients with DAA were referred to our hospitals for further examination and/or surgery from April 1986 to August 1989. In 18 of these patients, the diagnostic possibility of an underlying DAA was overlooked by the referring physicians. Among these 18 patients, 2 were mistakenly diagnosed as uncomplicated myocardial infarction (MI), one as pneumonia, 2 as cerebral infarction, 6 as acute abdominal disease, one as cholelithiasis, 5 as thrombosis of the lower extremities, and one as malignant metastasis to the pericardium. The following is the detail: In 2 cases thought to be uncomplicated MI, an expanding dissecting ascending aorta had crushed the lumen of the left coronary artery, causing MI, in turn, wasting clinical treatment and consuming precious time. In one case, enlargement of the descending aorta on the chest radiography was overlooked and the patient's symptoms were mistakenly attributed to pneumonia. In 2 cases in which symptoms of cerebral ischemia were thought to be attributed to cerebral thrombosis, the real cause turned out to be occlusion of the brachiocephalic artery following aortic dissection. Among 6 cases which were initially considered to have only acute abdominal disease, 3 presented with symptoms and signs of ileus, and their exploratory laparotomies yielded no positive findings.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiol 1992
PMID:[The pitfalls in the clinical diagnosis of dissecting aortic aneurysm]. 133 5

Atrial fibrillation and atrial flutter are common arrhythmias after coronary artery bypass grafting. Although the consequences of the arrhythmia are generally not life-threatening, it constitutes a major clinical problem often requiring conversion to sinus rhythm. Atrial fibrillation or flutter can result in hypotension, heart failure, pneumonia, and stroke. This article reviews the literature on epidemiology, electrophysiology, risk factors, and preventive trials. The major conclusions are: (1) In patients undergoing coronary artery bypass surgery, the incidence of postoperative atrial fibrillation or flutter is 20-30%, the peak incidence being on the second or third postoperative day. (2) The strongest independent preoperative predictor for atrial fibrillation or flutter is the patients' age. (3) Intra-atrial conduction delay recorded pre and peroperatively may predict development of atrial fibrillation. (4) Peroperative inducibility of atrial fibrillation by pacing the right atrium may identify patients at risk for postoperative atrial fibrillation. (5) Development of postoperative atrial fibrillation or flutter has not been associated with peroperative or postoperative events. (6) The specificity and sensitivity of age and other possible relevant factors for prediction of atrial fibrillation or flutter after coronary artery bypass grafting is low. (7) No effective prophylactic regimen has yet been established.
Int J Cardiol 1992 Sep
PMID:Atrial fibrillation and flutter after coronary artery bypass surgery: epidemiology, risk factors and preventive trials. 135 29

The prognostic risk factors in 4323 patients with rheumatic heart disease, admitted from 1970 to 1990, were analysed. The overall mortality was 31.75% in this group of patients. Single factor analysis indicated that cardiac functional classification, time of death, month of death, cardiothoracic ratio, valvular lesions, cardiogenic shock, digitalis-induced arrhythmias, intercurrent pneumonia, pleurorrhea, and hypotension were related to the overall mortality and cardiac death. Multiple factor logistic analysis indicated that for the overall mortality, the independent prognostic factors included presence of cardiac functional classification, cardiothoracic ratio and cardiogenic shock; for cardiac death, the independent factors included cardiac functional classification, cardiothoracic ratio, cardiogenic shock, digitalis-induced arrhythmias and valvular lesions. The data analysis showed that these five factors were contributory to rheumatic heart disease with synergism.
Int J Cardiol 1992 Jun
PMID:Nonconditional logistic regression analysis of risk factors in rheumatic heart disease. 844 96


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