Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Contrary to the present practice of measurement of cardio-vascular risk factors or inflammatory risk factors such as C-Reactive Protein (CRP) from a blood sample from the vein of one arm, by using the Bi-Digital O-Ring Test Resonance Phenomena between 2 identical substances, one can non-invasively detect the approximate location on the body of abnormally increased risk factors in just 2 minutes, by detecting the resonance with L-Homocystine, even when blood CRP failed to detect any abnormality. This is performed by projecting a 0.5 to approximately 5mW red spectral laser beam with 560-670nm wavelength, to at least 6 standard parts of the body, when one of the control risk markers placed next to the laser beam also exists in the part of the body tested. It is generally believed that CRP is increased in the presence of acute myocardial infarct, chronic rheumatoid arthritis, ulcerative colitis, metabolic abnormalities such as often detected in diabetes, inflammation and underlying infection of the cardio-vascular system, and in some cancers. However, in our study, when the clinical significance of CRP and L-Homocystine was compared, we found that CRP often was not increased when there was extensive infection of Mycobacterium Tuberculosis as well as asymptomatic infection by Cytomegalovirus, Herpes Simplex Virus Type I, Human Herpes Virus Type 6, Borrelia Burgdorferi, or Chlamydia Trachomatis in the heart (and other parts of the body), particularly when there was liver cell dysfunction such as an increase in ALT. In contrast, L-Homocystine was often increased in the presence of localized infections of the heart and other parts of the body. For screening of Cardio-Vascular diseases by this method, 0.5mg of L-Homocystine as a control marker was found to be the most sensitive and reliable, compared with most effective amount of CRP, 0.5ng, for detecting early Cardio-Vascular problems due to various localized infections. About 0.5ng of cardiac Troponin T and cardiac Troponin I were also useful for detecting early stages of heart disease but they are not as sensitive as L-Homocystine. Once the pathogenic factors were identified, the effective medication was given, and the Selective Drug Uptake Enhancement Method (originally discovered by the first author in 1990) was applied after the effective drug was administered, to selectively deliver the medication to the pathological area, while reducing drug uptake to the normal parts of the body. As a result, the therapeutic effect was markedly accelerated.
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PMID:2 minute non-invasive screening for cardio-vascular diseases: relative limitation of C-Reactive Protein compared with more sensitive L-Homocystine as cardio-vascular risk factors; safe and effective treatment using the selective drug uptake enhancement method. 1293 59

By the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherogenesis; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious. Yet it was the very inability of 'established' risk factors such as hypercholesterolemia, hypertension and smoking to completely explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago. Today, half of US heart attack victims have acceptable cholesterol levels and 25% or more have none of the "risk factors" associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection. Even the case of the traditionalist's latest 2003 JAMA assault to 'debunk' what they call the "50% risk factor myth" falls woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl, a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and elevated cholesteriol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed to tuberculosis but do not get the disease. In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible role of infectious agents beyond the three infections which have in recent years been the focus of research: Cytomegalovirus (CMV) Chlamydia pneumoniae and Helicobactor pylori. Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking similarity to those of State and regional TB case rates. Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander-Jackson all saw clinical and laboratory evidence of a causative relationship between the mycobacteria and heart disease. And Xu showed that proteins of mycobacterial origin actually led to experimental atherosclerosis in laboratory animals Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein (CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis. It therefore behooves us to explore the link between heart disease and typical and atypical tuberculosis.
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PMID:Heart disease: the greatest 'risk' factor of them all. 1508 5

Resveratrol is a polyphenolic natural product that is present in red wine and peanuts and has inhibitory activity against inflammation, heart disease, and cancer. Here we describe its inhibition of human cytomegalovirus replication (IC50 = 1-2 microM). At least 50-fold higher concentrations of compound were required to produce cytotoxicity against growing or stationary human embryonic lung fibroblasts. Mechanism of action studies determined that resveratrol blocked virus-induced activation of the epidermal growth factor receptor (EGFR) and phosphatidylinositol-3-kinase signal transduction as well as NF-kappaB and Sp1 transcription factor activation shortly following infection. Resveratrol prevented the appearance of immediate-early, early, and late viral proteins. Human cytomegalovirus DNA replication was reduced to undetectable levels by treatment with resveratrol, as were the second (late) phases of virus-induced phosphatidylinositol-3-kinase signaling and transcription factor activation. Resveratrol lost substantial antiviral activity when its addition was delayed until 4 h postinfection. Compound reversibility and preincubation studies were inconsistent with a virucidal mechanism of action. These data indicated that this compound likely operated during attachment and entry. We hypothesize that the primary molecular target for resveratrol may be blockage of epidermal growth factor receptor activation and its downstream effectors.
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PMID:3,4',5-Trihydroxy-trans-stilbene (resveratrol) inhibits human cytomegalovirus replication and virus-induced cellular signaling. 1530 37

More than 150 epidemiological or clinical studies have reported on associations between vascular disease and the presence of certain persistent bacterial and viral agents, or of clinical conditions (e.g., periodontal disease) that are associated with persistent infection. This article provides a review of such studies, particularly in relation to Helicobacter pylori, Chlamydia pneumoniae, dental disease and cytomegalovirus (CMV), as well as references to possible mechanisms. The association between coronary heart disease and H. pylori or between heart disease and dental disease may be accounted for by residual confounding. Although markers of C. pneumoniae infection are around twenty times more common in atherosclerotic plaques than in disease-free blood vessels, the sequence of infection and disease is uncertain. For CMV, a limited number of patients with classic atherosclerotic coronary heart disease have been investigated in seroepidemiological studies. For all such agents, better and larger seroepidemiological and pathology-based studies are needed to resolve these uncertainties, as well as - at some stage - large-scale, randomised intervention studies.
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PMID:Persistent infection and vascular disease: a systematic review. 1599 62

Nonimmune hydrops fetalis (NIHF) or generalized soft tissue edema and cavity effusions may be due to cardiovascular diseases, congenital infections, genitourinary malformations, thoracic masses, placental conditions, chromosomal abnormalities, and idiopathic. We report 32 cases of NIHF from among 429 neonates who underwent autopsies (incidence 7.45%). Sixteen cases (50%) had cardiovascular disease; all were due to low output cardiac failure; 7 had structural congenital heart disease. Three of the children with congenital heart disease also had chromosomal abnormalities: 2 had trisomy 18 and 1 had Noonan syndrome. Among myocardial conditions were five subjects with cardiomyopathies (1 of each of the following types): oncocytic, dilated, endocardial fibroelastosis, cardiac glycogenosis, and carnitine deficiency; 3 had myocarditis, and 1 had cardiac rhabdomyomas. Congenital infections were due to cytomegalovirus in 3 cases, bacteria in 2, and parvovirus in 1. The mechanism of NIHF in these cases might be a combination of decreased myocardial contractility due to myocarditis and fetal anemia. Genitourinary diseases were present in 5 newborns: Two had congenital nephrotic syndrome, 1 had VACTER association, 1 had prune-belly syndrome, and 1 had urogenital sinus malformation. Intrathoracic lesions were found in 2 babies (pulmonary sequestration and diaphragmatic hernia). One twin died of volume overload due to twin transfusion syndrome. Only 2 newborns were classified as idiopathic. Our study shows that cardiovascular diseases that lead to heart failure or impaired venous return are more common in the liveborn (50%), whereas congenital infections are more common in the stillborn with NIHF.
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PMID:Nonimmune hydrops fetalis in the liveborn: series of 32 autopsies. 1601 Apr 81

Inflammatory processes induced by viral or bacterial infections are believed to be one of the major pathogenetic mechanisms in myocardial diseases. Although the reason for progression to myocardial failure is not fully understood, postulated mechanisms include persistent viral infection alone or in combination with autoimmune processes. A variety of cardiotropic viruses have been identified to elicit myocarditis, with enteroviruses and adenoviruses as the most frequent causative agents in children and adolescents. However, parvovirus B19 (PVB19) has recently emerged as another potential pathogen in adult patients associated with inflammatory heart disease. Many dimensions of inflammatory heart disease coexist while different phases of the disease progress simultaneously: phase 1 is dominated by viral infection, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation without the role of an infectious agent and cardiac inflammation. Taking these mechanisms into account, screening for viral and bacterial genome by polymerase chain reaction (PCR) and detection of inflammatory infiltrates by immunohistochemistry are considered crucial for establishing an aetiological diagnosis, thereby allowing initiation of specific therapeutic strategies. In a large cohort of 3345 consecutive patients with left ventricular dysfunction evaluated over a period of 10 years, prevalence of PVB19, coxsackievirus (CVB), human cytomegalovirus (HCMV), influenza A virus and adenovirus (ADV) genome was assessed by PCR. Inflammatory infiltrates within the myocardium were detected by immunohistochemistry according to the WHF criteria and by histopathology according to the Dallas criteria of myocarditis. For control, endomyocardial samples of patients with arterial hypertension were studied. Parvovirus B19 was the most often detected virus in all patient subgroups, with positivity ranging from 17% to 33%. Except for PVB19, CVB RNA (3%), ADV (2%) and CMV (3.9%) were the most frequently detected viral genomes. Interestingly, detection of PVB19 genome was significantly correlated with inflammatory heart disease and reduced ejection fraction. Importantly, an aetiological diagnosis requires the immunohistochemical and molecular biological investigation of endomyocardial biopsies. Such an approach may change the management of these diseases in the future. One of the aims of the study was to reveal the underlying dominant pathophysiological mechanisms in a for deciding on the most approriate therapy.
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PMID:Pathophysiology and aetiological diagnosis of inflammatory myocardial diseases with a special focus on parvovirus B19. 1631 98

CMV infection causes morbidity and mortality after transplantation. Despite a wide range of prevention strategies among pediatric lung transplant programs, the optimal duration of prophylactic therapy against CMV infection in pediatric lung transplantation is unknown. To assess the feasibility, safety, and short-term efficacy of extending intravenous ganciclovir administration from six wk duration to 12 wk duration in pediatric lung transplant recipients. An open-label pilot study was performed in primary pediatric lung transplant recipients with donor and/or recipient CMV seropositivity. Intravenous ganciclovir was given for 12 wk post-transplantation. Subjects were tracked for protocol completion. Toxicities monitored included renal dysfunction, myelosuppression, gastrointestinal and neurological complications, as well as infection related to indwelling catheter placement. Serial CMV levels were measured to determine short-term efficacy of the intervention. Nine of nine subjects enrolled completed the pilot study. Subjects' ages ranged from six to 18 yr. Indications for lung transplantation included cystic fibrosis (n = 7), idiopathic pulmonary hypertension (n = 1), and complex congenital heart disease with pulmonary hypertension (n = 1). Seven subjects underwent deceased donor bilateral lung transplantation and two subjects underwent heart-lung transplantation. No subjects had protocol-defined drug toxicity. No episodes of neutropenia, thrombocytopenia, or renal toxicity occurred. Five subjects had catheter-related infections (three after week 12 of ganciclovir). Seven of nine subjects had CMV detected by PCR (four prior to ganciclovir completion) with only one subject having a positive viral culture for CMV viremia (prior to ganciclovir completion). No subjects had UL-97 mutation for ganciclovir resistance detected. The use of prolonged prophylactic administration of ganciclovir for 12 wk duration is a feasible, safe, and effective treatment to prevent CMV viremia based on viral culture in at risk pediatric lung transplant recipients. Further clinical studies are underway to determine optimal CMV prevention strategies.
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PMID:Safety and efficacy of prolonged cytomegalovirus prophylaxis with intravenous ganciclovir in pediatric and young adult lung transplant recipients. 1743 Apr 89

Heart transplantation has emerged as the therapy of choice for selected patients with life-threatening, irremediable heart disease. Infectious complications are frequent, but are no longer the leading cause of death. Late infections (particularly viral infections), however, are still a threat to long-term graft survival in these patients. Bacterial infections are the most common, particularly of the respiratory tract, which usually appear in the first month or after one year following transplantation in patients with previous COPD. Catheter-related infection is also common, whereas postoperative mediastinitis is much less frequent. The overall incidence of fungal infections has decreased considerably in recent years (2%-15%), but associated mortality remains high. Pulmonary aspergillosis is the most common. Cytomegalovirus is the most important pathogen in heart transplantation, currently affecting 7%-35% of patients. Antiviral prophylactics and pre-emptive therapy have reduced the incidence of acute CMV disease, but the potential role of this microorganism as a cofactor in allograft vascular disease, the most common cause of death in these patients, is a cause for concern. Toxoplasmosis, a particularly severe entity in heart transplant recipients, has decreased with the use of routine prophylaxis in seronegative recipients.
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PMID:[Infection in heart transplantation]. 1795

Increasing evidences have shown that pathogens might promote atherosclerosis and trigger acute myocardial infarction (AMI). But the conclusions from various studies on the correlation between previous influenza virus (IV) infection and AMI were inconsistent. We conducted a case-control study to assess the association of previous IV infection and AMI. Questionnaire survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood sample was obtained to measure IgG antibodies to influenza virus A(IV-A), influenza virus B(IV-B), cytomegalovirus (CMV), herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2), adenovirus (ADV), rubella virus (RV) and Chlamydia pneumoniae (CP) and measure the level of some biochemistry markers. Compared to controls, cases were more likely to have positive IgG antibodies to IV-A and IV-B (IV-A: OR, 3.3; 95%CI, 1.5 to 7.4; IV-B: OR, 17.2; 95%CI, 7.7 to 38.0). After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR, 7.5; 95%CI, 1.3 to 43.0) and IV-B (adjusted OR, 27.3; 95%CI, 6.6 to 113.8). The study supported the hypothesis that previous IV infection took part in the development of atherosclerosis and trigger the occurrence of AMI.
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PMID:Influenza virus infection and risk of acute myocardial infarction. 1856 94

Heart disease is the leading cause of morbidity and mortality. Cardiac gene transfer may serve as a novel therapeutic approach. This investigation was undertaken to compare cardiac tropisms of adeno-associated virus (AAV) serotypes 1, 6, 7, 8, and 9. Neonatal mice were injected with 2.5 x 10(11) genome copies (GC) of AAV serotype 1, 6, 7, 8, or 9 expressing LacZ under the control of the constitutive chicken beta-actin promoter with cytomegalovirus enhancer promoter via intrapericardial injection and monitored for up to 1 year. Adult rats were injected with 5 x 10(11) GC of the AAV vectors via direct cardiac injection and monitored for 1 month. Cardiac distribution of LacZ expression was assessed by X-Gal histochemistry, and beta-galactosidase activity was quantified in a chemiluminescence assay. Cardiac functional data and biodistribution data were also collected in the rat. AAV9 provided global cardiac gene transfer stable for up to 1 year that was superior to other serotypes. LacZ expression was relatively cardiac specific, and cardiac function was unaffected by gene transfer. AAV9 provides high-level, stable expression in the mouse and rat heart and may provide a simple alternative to the creation of cardiac-specific transgenic mice. AAV9 should be used in rodent cardiac studies and may be the vector of choice for clinical trials of cardiac gene transfer.
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PMID:Adeno-associated virus (AAV) serotype 9 provides global cardiac gene transfer superior to AAV1, AAV6, AAV7, and AAV8 in the mouse and rat. 1879 39


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