Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied by Echocardiographic-Doppler 114 consecutive intravenous drugs addicts (IVDA); 91 were positive human immunodeficiency virus (HIV+) and 23 negatives. We classified them in five groups; beginning the negative HIV as group 0, and groups I to IV stratified according the Central Disease Control (CDC) classification. We compared the cardiac abnormalities founded between themselves and a control group presumed healthy persons of similar age. The cardiac cavities dimensions showed a statistic significant increased left ventricular end-systolic and diastolic diameters, right ventricular diameter, posterior wall and interventricular septum thickness and aortic root diameter compared with the control group; but all were in the normal range for age. The left ventricular fractional shortening was statistically different from control group related the other groups, and the group IV related other. The existence and severity of pericardial effusions were directly related to the illness stage. We founded moderate pericardial effusions in 25% patients in the 0 to III groups, increasing until 50% in the group IV. The presence of valvular vegetations, nearly 30% in our series, ought to the IVDA. We did not found relationship between the severity of valvular incompetence and the illness stage. We recorded a excellent correlation between the ratio T4/T8 lymphocytes with the progress of illness and the existence and severity of cardiac abnormalities.
Rev Esp Cardiol 1992 Nov
PMID:[Doppler echocardiography assessment of cardiac abnormalities in parenteral drug addicts]. 147 92

Two hundred fifteen patients infected with human immunodeficiency virus (HIV) participated in a prospective longitudinal study of HIV-related heart disease. Evaluation included signal-averaged electrocardiography and echocardiography. Fifteen patients underwent endomyocardial biopsy, 5 had cardiovascular symptoms and 10 did not. Cardiac myocytes or dendritic cells were prepared by individual cell microdissection to sort them from other cell types such as interstitial cells or circulating blood elements. HIV proviral sequences were amplified in samples of 15 to 20 cells of each type by multiplex, nested, polymerase chain reaction and hybridized to 32P-labeled probes specific for regions within the gag and pol genes of HIV-1. The results showed the presence of HIV sequences in myocytes of 2 of 5 patients with cardiac symptoms and in 6 of 10 without. Thus, symptomatic HIV cardiomyopathy did not appear to be a direct consequence of the virus on myocardial cells. In dendritic cells, HIV sequences were detected in 5 of 5 patients with cardiac symptoms and in 8 of 10 with apparently normal ventricular function. Furthermore, dendritic cells were somewhat more numerous in the myocardium of symptomatic than asymptomatic patients. Our studies are the first to directly detect the HIV genome in purified cardiac myocytes from patients with and without cardiac dysfunction. Our findings do not support a direct role of the virus in myocardial dysfunction. However, the results do suggest that the interstitial dendritic cells may be involved in some manner in the development of cardiac dysfunction observed in HIV-infected patients.
Am J Cardiol 1991 Dec 01
PMID:Cardiac myocytes and dendritic cells harbor human immunodeficiency virus in infected patients with and without cardiac dysfunction: detection by multiplex, nested, polymerase chain reaction in individually microdissected cells from right ventricular endomyocardial biopsy tissue. 174 36

Seventy adults who tested positive for human immunodeficiency virus (HIV) were prospectively studied with serial echocardiography to better define the prevalence and progression of cardiac disease in such patients. Fifty outpatients (Group A), including 44 with acquired immunodeficiency syndrome (AIDS) and 6 with AIDS-related complex, and 20 additional patients (Group B) with asymptomatic HIV infection had baseline echocardiographic studies at a time when no patient had symptomatic heart disease. Follow-up studies were performed at 9 +/- 3 months in 52 patients (74%) and again at 15 +/- 3 months after baseline studies in 29 patients (41%). During the study, 22 patients (44%) in Group A and 1 patient (5%) in Group B died. Cardiac abnormalities were noted in 26 patients (52%) in Group A and 8 patients (40%) in Group B (p = NS) on initial or follow-up study. An abnormal left ventricular ejection fraction (less than 45%) or fractional shortening (less than 28%) was seen in seven patients in Group A; of these, three had normal left ventricular function on a later echocardiogram. One patient in Group B had persistent left ventricular dysfunction. All patients in Group A with left ventricular dysfunction on two serial studies died within 1 year after the initial echocardiogram. Ejection fraction did not change between baseline and two follow-up studies in either group (A: 52 +/- 9 vs. 56 +/- 9 vs. 55 +/- 5%, p = NS; B: 58 +/- 6 vs. 58 +/- 5 vs. 59 +/- 6%, p = NS). Right-sided cardiac enlargement resolved in 18 patients (44%), including 5 of 10 in Group A and 3 of 8 in Group B.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1991 May
PMID:Reversibility of cardiac abnormalities in human immunodeficiency virus (HIV)-infected individuals: a serial echocardiographic study. 182 90

Signal-averaged electrocardiograms were performed in 225 patients with serologic evidence of human immunodeficiency virus infection as part of a prospective longitudinal study of patients with HIV-associated heart disease and 12 seronegative control subjects. The duration of signal-averaged QRS vector, root-mean-square voltage of the terminal 40 ms of the vector magnitude and the duration of the low-amplitude (less than 40 microV) signal were determined during serial visits at 4-month intervals. One or more of these variables was abnormal on initial visit in 59 of patients (26%); QRS duration was greater than 114 ms in 9 patients (4%), root-mean-square voltage less than 20 microV in 55 patients (24%) and low-amplitude signal duration greater than 39 ms in 43 (19%). In contrast, none of the seronegative control subjects had any abnormal variables (p less than 0.03). During follow-up (mean 10 +/- 8 months), 26 patients with initially normal studies developed abnormal variables and 24 with abnormal signal-averaged electrocardiograms reverted to normal. Left ventricular contractility was assessed by echocardiography using the rate-corrected velocity of fiber shortening-end-diastolic wall stress relation. Late potentials were not related to contractile abnormalities. Clinical arrhythmias were rare and did not appear more frequent among patients with late potentials. Thus, late potentials were both common and evanescent in patients infected with human immunodeficiency virus.
Am J Cardiol 1991 Nov 01
PMID:Late potentials and their relation to ventricular function in human immunodeficiency virus infection. 195 Oct 82

We present 1 case of right sided endocarditis caused by Fusobacterium nucleatum in a patient with intravenous drug addiction and human immunodeficiency. The clinical features were fever, anemia, and pulmonary embolism. The echocardiogram showed a giant vegetation originated from the right atrial wall prolapsing in diastole into the right ventricle which disappeared after the patient presented pulmonary embolism. The clinical course was uncontrolled with empiric antimicrobial therapy but it was good with metronidazol. The cases previously described in the literature caused by gram-negative anaerobic bacteria are discussed and compared with the present case.
Rev Esp Cardiol 1991 Mar
PMID:[Right-sided endocarditis due to Fusobacterium nucleatum]. 204 51

A wide variety of organisms and conditions have been reported to cause pericarditis in patients that present and die with AIDS. Although pericarditis is remarkably common in patients dying of AIDS, no consistent pattern of cause emerges. Patients with AIDS are susceptible to pericarditis as a concomitant of the terminal condition, but it seldom contributes to the patient's death. Alternatively, pericarditis (as opposed to silent pericardial effusion) as a cardinal symptom in a patient's illness is likely to have an origin that can be ascribed to organisms typically associated with infectious pericarditis in those patients who have profound cellular immunodeficiency. Thus, it is important to make the diagnosis of infectious or neoplastic pericarditis in the setting of AIDS, since control of the agent has the potential of influencing the clinical course. In the absence of signs of hemodynamic compromise or inflammation, pericardial effusion may be accepted as an accompaniment of pleural effusions or ascites in the appropriate clinical context. Invasive diagnostic measures may be reserved for those cases in which pericardial disease is a prominent feature of the symptom complex or of accompanying pleural effusion. The study of epidemiology and biology of AIDS is a rapidly changing field. Explanations of the high incidence of pericardial disease in terminal disease may emerge with broad-ranging studies of the incidence of myocarditis in AIDS as well as the relative contribution to pericardial disease of agents used in the treatment of the illness.
Cardiol Clin 1990 Nov
PMID:Pericarditis in AIDS. 224 23

The anatomopathological study of the heart, carried out during the autopsy of a series of 38 subjects seropositive for the human immunodeficiency virus, has enabled the observation of histological lesions in 23 cases (60%). The heart affection is more often asymptomatic since it has been clinically suspected in only four cases. A myocarditis is present in 42 p. cent of the cases, and lesions specific to a pathogenic agent are visible in half of the myocarditis cases. These pathogenic agents are: toxoplasma (2 cases), cryptococcus (2 cases), candida (1 case), aspergillus (1 case) and cytomegalovirus (1 case). Lymphocytic myocarditis, with no isolated aetiological agent, and without viral inclusion, has been observed in 9 cases. The histological affection of the pericardium is observed in 4 cases and that of the endocardium in 3 cases. The lesions are not specific. The cardiotropism of the HIV is suspected, but not established. It could explain the frequency of lymphocytic myocarditis and dilated cardiomyopathies observed in HIV positive patients. The frequency of heart localizations in HIV positive subjects, even strictly asymptomatic as observed in this study, leads us to advise a systematic specialized cardiac examination.
Ann Cardiol Angeiol (Paris) 1990 Nov
PMID:[Cardiac involvement in carriers of the human immunodeficiency virus. Report of 38 cases]. 229 17

Heart muscle disease in the acquired immune deficiency syndrome (AIDS), characterized by electrocardiographic changes or congestive cardiomyopathy, is a documented clinical problem, but its pathogenesis is obscure. In AIDS the heart is known to be involved by a variety of opportunistic infections as well as Kaposi's sarcoma, but no causative relation with the development of cardiomyopathy has been established. This study reports evidence for direct infection of the heart in AIDS, not by an opportunistic pathogen but by the AIDS, not by an opportunistic pathogen but by the AIDS virus itself, the human immunodeficiency virus (HIV). For this study the technique of in situ deoxyribonucleic acid hybridization was applied to cardiac tissues obtained at autopsy from AIDS patients. Using sulfur-35-labeled ribonucleic acid probes encompassing the entire HIV genome, HIV nucleic acid sequences were detected in cardiac tissue sections from 6 of 22 patients examined who died of AIDS. The hybridization targets appeared to be cardiac myocytes, although their precise morphology was often obscured by the intensity of the signal. The myocardial cells showing a positive hybridization signal were sparse, often comprising only 1 or a few cells per section, and their number and location did not correlate obviously with any histopathologic or clinical evidence of heart muscle disease in these patients. It is conceivable that the presence of HIV nucleic acid sequences may represent a preclinical marker of impending AIDS-associated heart muscle disease. This sequela would not be recognized in many patients, including those in this series, who died rapidly of Pneumocystis carinii pneumonia, Kaposi's sarcoma and other well-documented manifestations of AIDS.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1990 Jul 15
PMID:Infection of the heart by the human immunodeficiency virus. 237 52

Acquired immunodeficiency syndrome (AIDS) has become an increasingly important health problem worldwide. This review focuses on its cardiac complications. The key elements in the clinical syndrome are the opportunistic infections and the cancer that occur as a by-product of the immunodeficiency process. However, as early diagnosis, aggressive therapy and better supportive care become increasingly available, with consequently longer survival rates, cardiac lesions other than those due to opportunistic infections or malignancy should be seen. Cardiac complications are described in terms of the pathologic lesions, the clinical manifestations that ensue as a result of the pathologic lesions and the cardiac abnormalities that can occur from administration of the various therapeutic agents in the syndrome.
J Am Coll Cardiol 1989 Apr
PMID:Cardiac complications in acquired immunodeficiency syndrome (AIDS): a review. 252 70

The prevalence of cardiac abnormalities in the spectrum of human immunodeficiency virus (HIV) infection is unknown. Sixty consecutive HIV-infected patients were studied using echocardiograms, electrocardiograms (50 patients) and ambulatory electrocardiographic monitoring (43 patients). Group A (25 patients) were seropositive but pre-AIDS, whereas group B (35 patients) had AIDS and included 24 with an active opportunistic infection (group B1) and 11 without it (group B2). Abnormalities were identified in 32 of 60 patients (53%) and were more frequent in group B (23 of 35, 66%) than in group A (9 of 25, 36%, p less than 0.05) but independent of active opportunistic infection (15 of 24, 62%, in group B1 vs 8 of 11, 73%, in group B2). Echocardiographic abnormalities were identified in 21 of 60 patients (35%), including 7 of 25 (28%) in group A vs 14 of 35 (40%) in group B (difference not significant), and 7 of 24 (29%) in group B1 vs 7 of 11 (64%) in group B2 (difference not significant). Those patients with an absolute CD4 lymphocyte count less than or equal to 100/mm3 had a higher prevalence of echocardiographic abnormalities (12 of 22) than those with CD4 counts greater than 100/mm3 (1 of 14, p less than 0.01). Left ventricular dilation or hypokinesis was identified in 14 of 60 patients (23%), including 4 of 25 (16%) in group A and 10 of 35 (29%) in group B. Electrocardiographic abnormalities were seen in 22 of 50 patients (44%) including 5 of 18 (28%) in group A and 17 of 32 (53%) in group B (difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1989 Jan 01
PMID:Prevalence of cardiac abnormalities in human immunodeficiency virus infection. 256 18


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