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From 1982 to 1991, we experienced 76 patients with Mycoplasma pneumoniae pneumonia which were confirmed by serologic tests. There were 32 (42%) male and 44 (58%) female patients. One patient had underlying disease of diabetes mellitus while the other patients were in good health. The age ranged from 9 months old to 72 years old. All the patients complained of fever and coughing; 63% had dry cough and 37% had sputum production. Upper respiratory tract complaints such as rhinorrhea, sore throat, or earache were noted in 57% of the patients. Fifty-five percent of the patients had GI symptoms of anorexia, nausea, vomiting, or diarrhea. Other complaints included myalgia/arthralgia (29%), headache (30%), and general malaise (32%). Dyspnea (17%) and chest pain (20%) were occasional complaints. Seventy-one percent of the patients had WBC counts < 10000/cu mm and 29% > 10000/cu mm. The mean value of C-reactive protein (CRP) was 53.1 micrograms/ml, while 16% of the patients had a CRP value above 100 micrograms/ml. Thirty-one percent of the patients were noted to have a transient elevation of serum transaminase. Four different patterns of infiltration were seen in chest radiographic manifestation: 1) peribronchial and perivascular interstitial infiltrates (18.4%), 2) nonhomogeneous patchy consolidations (22.4%), 3) homogeneous acinar consolidations (27.6%), and 4) mixed interstitial and alveolar infiltrates (27.6%). Interstitial infiltration was more commonly seen in pediatric than adult patients (46% vs 20%). Other features of the radiologic manifestation were as follows: unilateral lesions in 80% of patients, single lobe lesions in 77%, lower lobe predominant in 69%, pleural effusion in 7%, and radiographic deterioration in 10%. Mycoplasmal pneumonia should be considered in the differential diagnosis of community-acquired pneumonias.
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PMID:Clinical study of Mycoplasma pneumoniae pneumonia. 832 Jul 55

We report the history of a 38-year-old male native of Sri Lanka admitted to the emergency ward because of chest pain and shortness of breath. On physical and radiographic examination a bilateral predominantly right-sided pneumonia was found. The patient was admitted to the medical ICU and an antibiotic regimen with amoxicillin/clavulanic acid and erythromycin was initiated. Shortly afterwards septic shock developed. The patient was intubated and received high doses of catecholamines. He died 30 hours after admission to the hospital. Cultures from sputum, tracheal aspirate and blood grew Acinetobacter baumanni. Acinetobacter is an ubiquitous gram-negative rod with coccobacillary appearance in clinical specimens, that may appear gram-positive due to poor discoloration on Gram-stain. It is a well known causative agent of nosocomial infections, particularly in intensive care units. Community-acquired pneumonias, however, are quite rare. Sporadic cases have been reported from the US, Papua-New Guinea and Australia. Interestingly, these pneumonias are fulminant and have a high mortality. Chronic obstructive lung disease, diabetes, and tobacco and alcohol consumption appear to be predisposing factors. Due to the rapid course and poor prognosis, prompt diagnosis and adequate antibiotic treatment are indicated. Antibiotics use for community-acquired pneumonias, such as amoxicillin/clavulanic acid or macrolides, are not sufficient. Appropriate antibiotics for the initial treatment of suspected Acinetobacter infections include imipenem and carboxy- and ureidopenicillins combined with an aminoglycoside.
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PMID:[Community-acquired Acinetobacter pneumonia]. 837 43

Silent myocardial ischemia is a marker in patients with coronary artery disease identifying those at high risk for subsequent cardiac events. During provoked myocardial ischemia some patients with angina pectoris do not develop chest pain. Are there clinical, angiographic or electrocardiographic differences between patients with chest pain as compared with patients without chest pain during provoked myocardial ischemia? Coronary angioplasty is a well-established method for the treatment of coronary stenosis, but it is also an interesting model for the study of myocardial ischemia as a result of coronary occlusion. We monitored 114 patients with angina pectoris during coronary angioplasty with dynamic, computerized vectorcardiography. During inflation of the balloon 33 of 114 patients had silent ischemia. Patients with silent myocardial ischemia had similar reasons for terminating the preangioplasty exercise test and where on similar anti-ischemic drug regimes. Silent myocardial ischemia was significantly associated with a history of diabetes, presence of collaterals, a history of less severe previous angina and less ST segment changes during angioplasty as compared with patients with painful ischemia. It is suggested that during coronary angioplasty silent ischemia may be caused by a less severe degree of ischemia, possibly as a result of the protective effect of collaterals.
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PMID:Silent myocardial ischemia during coronary angioplasty. 837 30

The author presented data obtained in Bangladesh, to elucidate the role of hypertension as a risk factor along with others such as smoking, cholesterol and diabetes mellitus as cofactors in ischaemic heart disease (IHD). There was a series of 100 cases with IHD admitted within 12 hours after the onset of chest pain observed in this study. They all were diagnosed as IHD for the first time. Of them, 94 were male and 6 female, with an age range of 25-77 years (mean 50.16 +/- 14 years). On grouping of IHD, 21 had angina pectoris and 79 acute myocardial infarction. 31% cases of IHD had hypertension. The blood pressure ranged between 168.54 +/- 24.85 and 106.29 +/- 16-80 mmHg. 74 out of the 100 cases with IHD were smokers. The mean value of serum cholesterol in this series was 6.48 +/- 1.66 mmol/L and that among 50 normal controls was 4.76 +/- 1.28 mmol/L (P < 0.01). The serum triglyceride determinations between the 94 cases of IHD and 50 normal controls showed values with statistically significant difference. The author concluded in this study that, hypertension, smoking and hyperlipidemia are the most important risk factor of IHD in Bangladesh.
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PMID:Evaluation of hypertension and other risk factors in ischemic heart disease. 840 84

The prevalence of risk factors for atherosclerosis in 488 consecutive patients undergoing cardiac catheterization for the investigation of chest pain was compared with that in 868 subjects from a population sample. The presence and severity of angiographic coronary artery disease (CAD) (defined as mean diameter stenosis > 50%), total and high-density lipoprotein (HDL) cholesterol, triglycerides, history of systemic hypertension, smoking, diabetes mellitus, family history and drug therapy were assessed. Low HDL cholesterol (< 0.9 mmol/liter [35 mg/dl]) was more prevalent in patients with CAD than in the population sample in both men (44% [95% confidence interval 38 to 48] vs 21% [12 to 28]; p < 0.01) and women (12% [9 to 15] vs 1% [0 to 3]; p < 0.01). There were no differences in total cholesterol levels between these 2 groups. Total:HDL cholesterol ratios were significantly greater in patients with CAD. History of systemic hypertension was more prevalent in both men and women with CAD than in the population sample (47% [37 to 57] vs 20% [16 to 25] for men, and 31% [26 to 36] vs 21% [17 to 26] for women; p < 0.01). The prevalence of other risk factors was not significantly different between the 2 groups. In patients with CAD, the severity of disease was inversely correlated with levels of HDL cholesterol in both men and women (p < 0.01), and positively correlated with total cholesterol in men aged < 55 years (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of angiographically detected coronary artery disease with low levels of high-density lipoprotein cholesterol and systemic hypertension. 843 34

To determine the long-term prognosis of patients (pts) with angina-like chest pain and normal coronary arteriograms, 178 pts (61 women, 117 men; mean age 48.1 years) were followed for an average of 9.8 years (5.5-13.1 years). Eight pts (4.5%) died during follow-up: One pt from acute myocardial infarction, one pt suddenly, one pt from chronic cor pulmonale and 5 pts from non-cardiac diseases. Chest pain remained constant in 137/170 surviving pts (80.6%), but disappeared in 33 pts (19.4%). Nine of the 178 pts (5.1%) developed manifest coronary artery disease (CAD): four of them (2.2%) acute myocardial infarctions including one death, after an average of 7.2 years; in five pts (2.8%) with continued chest pain a second coronary angiogram showed typical CAD. These pts with manifest CAD averaged 2.1 risk factors: six pts were smokers, two pts had elevated cholesterol levels (> 7.5 mmol/l), three pts had elevated triglyceride levels (> 2.4 mmol/l), two pts had a diabetes mellitus type IIa and six pts were hypertensives. Patients without manifestation of CAD averaged only 1.4 risk factors (p < 0.05). Our data show that pts with angina-like chest pain and normal coronary angiograms have an excellent long-term prognosis (only 0.51% of patients with new manifestations of CAD per year). However, angina-like chest pain can persist over many years.
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PMID:[Long-term follow-up of patients with angina pectoris-like chest pain and normal coronary angiogram]. 847 Apr 21

This study was undertaken to determine if there is an association between increased titers of five different antiphospholipid antibodies (aPLA) in young patients' sera and the occurrence of acute myocardial infarction (AMI). Antibodies to anticardiolipin (aCL), anti-phosphatidylserine (aPS), antiphosphatidylinositol (aPI), anti-phosphatidylcholine (aPC), and anti-phosphatidylethanol amine (aPEA) were measured in 214 patients (102 patients, 102 healthy controls and 10 patients with antiphospholipid syndrome). These antibodies were measured twice (within 4h of onset of acute myocardial ischemic chest pain and 3 months after the myocardial infarction) by enzyme linked immunosorbent assay (ELISA). Elevated titers of four different aPLA were detected in 6.9% of all patients with AMI on hospitalization. Titers of aPLA in AMI were elevated in the younger age group < 50 years old (P < 0.001) and in men only (not statistically significant). No correlation was found between the presence of aPLA and cardiovascular risk factors (smoking, hypertension, diabetes mellitus and hyper-cholesterolemia). Three of the seven patients with increased titers of aPLA did not have any other cardiovascular risk factors. The titers of aPLA were within normal range 3 months after AMI. Evidence of significantly elevated titers of different aPLA at the early stage of AMI suggests that these autoantibodies are present before the AMI and are not secondary to them. The disappearance of the elevated aPLA 3 months after AMI may be due to an absorption effect or possibly a cyclic phenomenon similarly found in other autoimmune diseases. aPLA may be an additional risk factor for AMI, and should especially be considered in a patient of the younger age group without apparent cardiovascular risk factors.
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PMID:The presence of antiphospholipid antibodies in acute myocardial infarction. 852 29

Controversy persists about whether hyperinsulinemia and hyperproinsulinemia are independent risk markers for coronary atherosclerosis. A common limitation of most previous studies has been imprecise categorization of disease status in normal and coronary artery disease (CAD) groups. We assessed the relationship of pancreatic beta-cell secretory products and premature CAD in a case-control study of 134 nondiabetic subjects, aged < or = 55 years old, carefully defined for CAD status by catheterization and/or thallium stress studies. Case patients comprised 66 patients with premature CAD, and control subjects (non-CAD group) included 68 patients without CAD but with traditional CAD risk factors and chest pain and/or abnormal electrocardiograms but normal catheterization and/or thallium stress studies. In addition to the CAD and non-CAD group comparison, both groups were compared with a reference group of 27 mixed lean and obese control volunteers. All CAD and non-CAD patients had a 3-h 75-g oral glucose tolerance test with measurement of fasting and post-glucose load immunoreactive insulin (IRI), specific insulin (INS), proinsulin-like material (PI), and C-peptide. Increased fasting insulin and fasting proinsulin levels both were statistically significantly associated with higher odds of being in either the premature CAD and the non-CAD groups when compared with the reference group in a polychotomous logistic regression model (odds ratio of at least 1.20 for a 20% increase in each beta-cell secretory product in both comparisons, P < 0.05). However, increased pancreatic beta-cell secretory hormone levels did not show a statistically significant relative risk for being in the premature CAD group when compared with the non-CAD group. After adjustment for BMI, all statistically significant associations disappeared for IRI, INS, and PI when the odds favoring being in the CAD and non-CAD groups were compared versus the reference group. Furthermore, the odds of being in the premature CAD and non-CAD groups when compared with the reference group were not significantly associated to the ratio of PI to insulin and C-peptide. Thus, although there is a statistically significant association between the odds of having premature CAD with elevated insulin and proinsulin levels compared with the reference group, these findings are equally common in subjects with traditional CAD risk factors without detectable CAD. Furthermore, the association of higher insulin and proinsulin levels with the likelihood of a patient having or not having CAD disappears after adjustment for BMI, suggesting that insulin and proinsulin are not independent risk markers but are primarily dependent on obesity.
Diabetes 1996 Jun
PMID:Are insulin and proinsulin independent risk markers for premature coronary artery disease ? 863 46

Coronary artery disease (CAD) is the leading cause of adult mortality in the United States. Data collected from the era preceding contemporary revascularization techniques indicated that chest pain syndromes among women carried a more favorable cardiac prognosis than such symptoms in men. More recent information indicates that many women with chest pain do not have CAD and that, among those who do, clinical manifestations first appear an average of 10 years later than in men, at a time when risk factors and comorbidities such as diabetes, hypertension, and hypercholesterolemia are more prevalent. The toll that this disease exacts among women catches up with that among men after women go through menopause, so that coronary heart disease accounts for nearly equal annual mortality rates in the two genders and for more deaths among women than is attributable to all cancers. The initial, widely held impression that chest pain is more benign in women is being replaced by a growing awareness that coronary disease is not. It appears from published experience that any potential bias in the management of women with possible CAD is overcome once the diagnosis is established. It is clear that a reliable method for the evaluation of women with known or suspected CAD is required. Stress electrocardiography, perfusion imaging, and radioventriculography suffer from a number of limitations, particularly in women. This paper discusses the rationale for and performance of stress echocardiography. Although the specific application of this method in females has been the subject of relatively limited clinical investigations, we believe that it holds great promise as the diagnostic test of choice for women.
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PMID:Are there gender differences related to stress or pharmacological echocardiography? 868 Jan 35

The aim of this study was to analyse the influence of patient characteristics on delay between onset of symptoms and hospital admission (patient delay) in acute myocardial infarction, and especially to assess the impact of risk factors for acute myocardial infarction on patient delay. A group of 6676 consecutive patients with enzyme-confirmed acute myocardial infarction, admitted alive to 27 Danish hospitals over a 26 month period from 1990 to 1992, were studied. Due to missing information on delay or in-hospital acute myocardial infarction 698 patients were excluded, leaving 5978 patients for analysis. Mean patient delay was 9.1 h, median delay 3.25 h (5 to 95 percentiles: 0.67-40.0 h). Thirty-four percent were admitted within the first 2 h, 68% within 6 h and 81% within 12 h of onset of symptoms. In multivariate logistic regression analysis, a greater than 2 h patient delay was independently associated with male gender (odds ratio (OR) = 0.809, P = 0.003), increased age (P = 0.0001), diabetes mellitus (OR = 1.269, P = 0.03), left ventricular systolic function (wall motion index) (P = 0.02), onset from midnight to 0600h (OR = 1.434, P = 0.0001), onset on a weekday (OR = 0.862, P = 0.04), history of angina pectoris (OR = 1.198, P = 0.02), chest pain as initial symptom (OR = 1.293, P = 0.02), ventricular fibrillation (OR = 0.562, P = 0.0001), ventricular tachycardia (OR = 0.620, P = 0.0001), Killip class > or = 3 (OR = 0.709 P = 0.002), presence of ST elevation (OR = 0.810, P = 0.01) and ST depressions (OR = 0.847, P = 0.01). All these variables, except history of diabetes mellitus, angina pectoris, and chest pain as an initial symptom were also associated with a delay of more than 6 h. Thrombolytic therapy was administered to 55.8% of patients admitted within 2 h of an acute myocardial infarction, 48.5% of patients admitted within 2-6 h, 31.5% of patients admitted after 6-12 h and 11.9% of patients arriving later than 12 h after start of symptoms. CONCLUSION. Patient delay continues to be disappointingly long. This also applies for patients at a high risk of acute myocardial infarction (notably those with a history of diabetes mellitus and angina pectoris).
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PMID:Determinants of delay between symptoms and hospital admission in 5978 patients with acute myocardial infarction. The TRACE Study Group. Trandolapril Cardiac Evaluation. 873 7


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