Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major cardio-circulatory events, defined as circulatory death, myocardial infarction, unstable angina, or stroke, sometimes occur unexpectedly in patients who apparently have no evident increase in risk (absence of overt heart failure, hypertrophy, uncontrolled or severe hypertension, previous or present myocardial infarction, angina, myocarditis, infectious or any other pericardial, valvular or great vessel disease, heart malformation, significant arrhythmia or conduction disturbances). To investigate whether 2D-guided M-mode echocardiographic variables have predictive value in such patients, a retrospective analysis of 1,965 cases was performed. Twenty-one patients were found who on the day of echocardiographic examination fulfilled the above criteria, but suffered major cardio-circulatory events during the first following year (1 yr group), 12 during the second year (2 yr group), and 16 during the third year (3 yr group). Twenty-eight patients who fulfilled the same criteria, but were followed-up free of major cardio-circulatory events for 935 +/- 144 days constituted the control group. Multivariate analysis of variance (MANOVA) of echocardiographic data was used to select the final set of 11 variables from 30 measurements and calculations which enabled satisfactory discrimination between the four groups (Hotelling T2 = 3.979, Fisher F = 7.596 > Ftab = 1.585). Extension of MANOVA with the leave-one-out method revealed that none of 28 control patients was predicted to be at risk of major cardio-circulatory events in the next year, and only one of 21 patients from the 1 yr group was misdiagnosed as not being at risk. Patients at risk were older, had slightly greater body size (particularly weight), and slightly increased diastolic diameter and volume of the left ventricle. The left ventricular mass, mean wall thickness, and estimated cross-sectional area indexes were also slightly increased. The peak systolic stress was slightly increased and contractility index (BPS/ESVI) was slightly decreased. Our preliminary results suggest that easily obtained echocardiographic measurements and calculations contain clinically useful predictive information.
 ...
PMID:Prediction of lethal or life-threatening cardio-circulatory events in patients who apparently are not at risk : a preliminary retrospective echocardiographic study. 884 Feb 15

The prevalence of myocardial damage after coronary artery bypass grafting is related to the criteria of its evaluation. Indium-111 monoclonal antimyosin antibody scintigraphy has been shown to be highly sensitive and specific for even small areas of myocardial necrosis or injury like those of myocarditis or transplant rejection. Our purpose was to evaluate, by using this method, myocardial damage after uncomplicated coronary artery bypass grafting. Uptake of this radio tracer was evaluated after coronary artery bypass grafting in 14 informed and consenting consecutive patients without previous myocardial infarction, with no post-surgical complications and a favorable postoperative course, following coronary artery bypass grafting for stable angina pectoris. Monoclonal antimyosin antibody indium-111 74 MBq (Myoscint Centocor) was injected on the third postoperative day; planar images in the anterior, left anterior oblique 45 degrees and 70 degrees projections were obtained 24 and 48 h later and analyzed for myocardial uptake. Indium-111 antimyosin uptake was present in 10 out of 14 patients (71.4%); it was diffuse in 6 and localized in 4. The ratio of the maximal counts in the myocardium to the counts in the adjacent lung background was measured and found elevated: 1.94 +/- 0.23, higher than the normal values reported in the literature. Indium-111 antimyosin uptake was clear in a group of patients after uncomplicated coronary artery bypass grafting. No correlation was observed between indium-111 antimyosin uptake or heart to lung ratio and creatine kinase, creatine kinase isoenzyme MB, glutamic oxalacetic transferase levels, duration of cardiopulmonary bypass or aortic cross-clamp time, while elevated serum beta myosin heavy chain fragments (IRMA Pasteur) were observed (1378 +/- 238 microU/l). This study suggests that some degree of myocardial damage, though silent, is common after coronary artery bypass grafting.
 ...
PMID:Myocardial indium-111 antimyosin uptake after uncomplicated coronary artery bypass surgery. 887 23

Chest pain with normal coronary angiograms is a relatively common syndrome. The mode of presentation of this syndrome includes patients with syndrome X and patients with an acute myocardial infarction and angiographically normal coronary arteries. Different mechanisms have been proposed to elucidate the exact cause and to explain the various clinical presentations in these patients. Abnormalities of pain perception and the presence of oesophageal dysmotility have all been reported in patients with syndrome X. In situ thrombosis or embolization with subsequent clot lysis and recanalization, coronary artery spasm, cocaine abuse, and viral myocarditis have been described as potential mechanisms responsible for an acute myocardial infarction in patients with angiographically normal coronary arteries. Recent data suggest that both microvascular and epicardial endothelial dysfunction may play an important role in the pathophysiological mechanism of the syndrome of stable angina or acute myocardial infarction with normal coronary arteries.
 ...
PMID:Role of the vascular endothelium in patients with angina pectoris or acute myocardial infarction with normal coronary arteries. 1062 74

During the pre-event smallpox vaccination program, the U.S. Department of Defense (DOD) and CDC have received reports of cardiac events after vaccination. A case definition for myo/pericarditis as a smallpox vaccine--associated adverse event has been developed in conjunction with DOD, the joint Smallpox Vaccine Safety Working Group of the Advisory Committee on Immunization Practices (ACIP) and the Armed Forces Epidemiology Board (AFEB), and consulting cardiologists, immunologists, and epidemiologists. The term myo/pericarditis is used for surveillance purposes to refer to patients who have myocarditis, pericarditis, or both (myopericarditis). Myo/pericarditis cases are classified into suspected, probable, and confirmed categories. Suspected cases include those that are investigated and reported, although the level of certainty for the diagnosis is lower. These definitions were used to categorize all cardiac-related reports among civilian vaccinees received through May 9, 2003; a total of 21 cases of myo/pericarditis were ascertained. All have been reported previously; however, some have been reclassified. In addition, nine cases of ischemic cardiac events (i.e., myocardial infarction [MI] or angina) among civilian vaccinees have been reported previously. This report includes the case definition of myo/pericarditis and updates information on all reports of cardiac adverse events among 36,217 civilian vaccinees since the beginning of the civilian smallpox vaccination program reported through May 9 to CDC from the Vaccine Adverse Event Reporting System (VAERS).
 ...
PMID:Update: cardiac-related events during the civilian smallpox vaccination program--United States, 2003. 1280 10

The antiviral effect of nitric oxide (NO)-releasing compounds was investigated. Using bacterially expressed and purified proteinases 2A and 3C of coxsackievirus B3, in vitro assays demonstrated the inhibition of the 2A proteinase activity in the presence of S-nitroso- N-acetyl-penicillamine (SNAP), 3-morpholinosydnonimine (SIN-1), 4-phenyl-3-furoxancarbonitrile (PFC), glyceryl trinitrate (GTN), and isosorbide dinitrate (ISDN). Sodium nitroprusside (SNP), which releases NO after metabolization, had no effect. The 3C proteinase was inactivated by SNAP, GTN, and ISDN. The vasodilators GTN and ISDN, widely used in the treatment of angina pectoris, exhibited antiviral activity in CVB3-infected GMK cells. CVB3-infected NMRI outbred mice showed significantly reduced signs of myocarditis after treatment with GTN or ISDN. Inhibitors of the cellular inducible NO synthase (iNOS) such as N(G)-nitro-L-arginine methyl ester (L-NAME), N(G)-nitro-L-arginine (L-NNA), and S-methyl-isothiourea (SMT), had no deleterious effect on CVB3-infected NMRI mice, indicating that endogenous NO synthesis is unlikely to be a major defense mechanism after enterovirus infection of outbred mice.
 ...
PMID:Nitric oxide donors inhibit the coxsackievirus B3 proteinases 2A and 3C in vitro, virus production in cells, and signs of myocarditis in virus-infected mice. 1451 74

NF-kappaB is a pleiotropic transcription factor implicated in the regulation of diverse biological phenomena, including apoptosis, cell survival, cell growth, cell division, innate immunity, cellular differentiation, and the cellular responses to stress, hypoxia, stretch and ischemia. In the heart, NF-kappaB has been shown to be activated in atherosclerosis, myocarditis, in association with angina, during transplant rejection, after ischemia/reperfusion, in congestive heart failure, dilated cardiomyopathy, after ischemic and pharmacological preconditioning, heat shock, burn trauma, and in hypertrophy of isolated cardiomyocytes. Regulation of NF-kappaB is complicated; in addition to being activated by canonical cytokine-mediated pathways, NF-kappaB is activated by many of the signal transduction cascades associated with the development of cardiac hypertrophy and response to oxidative stress. Many of these signaling cascades activate NF-kappaB by activating the IkappaB kinase (IKK) complex a major component of the canonical pathway. These signaling interactions occur largely via signaling crosstalk involving the mitogen-activated protein kinase/extracellular signalregulated kinase kinases (MEKKs) that are components of mitogen activated protein kinase (MAPK) signaling pathways. Additionally, there are other signaling factors that act more directly to activate NF-kappaB via IkappaB or by direct phosphorylation of NF-kappaB subunits. Finally, there are combinatorial interactions at the level of the promoter between NF-kappaB, its coactivators, and other transcription factors, several of which are activated by MAPK and cytokine signaling pathways. Thus, in addition to being a major mediator of cytokine effects in the heart, NF-kappaB is positioned as a signaling integrator. As such, NF-kappaB functions as a key regulator of cardiac gene expression programs downstream of multiple signal transduction cascades in a variety of physiological and pathophysiological states. We show that genetic blockade of NF-kappaB reduces infarct size in the murine heart after ischemia/reperfusion (I/R), implicating NF-kappaB as a major determinant of cell death after I/R. These results support the concept that NF-kappaB may be an important therapeutic target for specific cardiovascular diseases.
 ...
PMID:NF-kappaB as an integrator of diverse signaling pathways: the heart of myocardial signaling? 1455 89

Angiogenic gene therapy for stable angina is aimed at promoting new blood vessel formation in the heart, thus providing enhanced cardiac perfusion, symptom relief, increased exercise capacity, improved quality of life, and reduced risk of coronary events. Ad5FGF-4 is a replication-deficient serotype 5 adenovirus encoding the gene for fibroblast growth factor-4 (FGF-4) driven by a cytomegalovirus promoter. In preclinical studies using a pig model of myocardial ischemia, a single intracoronary infusion of Ad5FGF-4 improved cardiac contractile function and regional blood flow in the ischemic region during stress. These effects were apparent after 2 weeks and maintained for > or =12 weeks. Histologic evidence of capillary angiogenesis was observed. FGF-4 gene expression was detected in the heart but not at extracardiac sites. Placebo-controlled trials in humans with chronic stable angina indicate that Ad5FGF-4 increases treadmill exercise duration and improves stress-related ischemia measured by perfusion sestamibi single-photon emission computed tomography. More patients receiving Ad5FGF-4 than placebo reported complete resolution of their angina and no nitroglycerin use. Ad5FGF-4 gene therapy was well tolerated. The administration procedure did not cause any adverse events, although mild, transient fever, a transient modest fall in platelet count, and a transient mild elevation in hepatic enzymes and uric acid levels occurred in a few patients. This adverse event profile concurs with other adenoviral gene trials. There was no evidence of myocarditis, retinal neovascularization, or angioma formation. FGF-4 was not detected in venous blood. Larger clinical trials will assess Ad5FGF-4 with regard to cardiovascular prognosis, symptom relief, and safety profile in patients with chronic stable angina.
 ...
PMID:Angiogenic gene therapy with adenovirus 5 fibroblast growth factor-4 (Ad5FGF-4): a new option for the treatment of coronary artery disease. 1461 23

The basis for life is the ability of the cell to maintain ion gradients across biological membranes. Such gradients are created by specific membrane-bound ion pumps [adenosine triphosphatases (ATPases)]. According to physicochemical rules passive forces equilibrate (dissipate) ion gradients. The cholesterol/phospholipid ratio of the membrane and the degree of saturation of phospholipid fatty acids are important factors for membrane molecular order and herewith a determinant of the degree of non-specific membrane leakiness. Other operative principles, i.e. specific ion channels can be opened and closed according to mechanisms that are specific to the cell. Certain compounds called ionophores can be integrated in the plasma membrane and permit specific inorganic ions to pass. Irrespective of which mechanism ions leak across the plasma membrane the homeostasis may be kept by increasing ion pumping (ATPase activity) in an attempt to restore the physiological ion gradient. The energy source for this work seems to be glycolytically derived ATP formation. Thus an increase in ion pumping is reflected by increased ATP hydrolysis and rate of glycolysis. This can be measured as an accumulation of breakdown products of ATP and end-products of anaerobic glycolysis (lactate). In certain disease entities, the balance between ATP formation and ion pumping may be disordered resulting in a decrease in inter alia (i.a.) cellular energy charge, and an increase in lactate formation and catabolites of adenylates. Cardiac syndrome X is proposed to be due to an excessive leakage of potassium ions, leading to electrocardiographic (ECG) changes, abnormal Tl-scintigraphy of the heart and anginal pain (induced by adenosine). Cocksackie B3 infections, a common agent in myocarditis might also induce an ionophore-like effect. Moreover, Alzheimer's disease is characterized by the formation of extracellular amyloid deposits in the brain of patients. Perturbation of cellular membranes by the amyloid peptide during the development of Alzheimer's disease is one of several mechanisms proposed to account for the toxicity of this peptide on neuronal membranes. We have studied the effects of the peptide and fragments thereof on 45Ca2+-uptake in human erythrocytes and the energetic consequences. Treatment of erythrocytes with the beta 1-40 peptide, results in qualitatively similar nucleotide pattern and decrease of energy charge as the treatment with Ca2+-ionophore A23187. Finally, in recent studies we have revealed and published in this journal that a rare condition, Tarui's disease or glycogenosis type VII, primarily associated with a defect M-subunit of phosphofructokinase, demonstrates as a cophenomenon an increased leak of Ca2+ into erythrocytes.
 ...
PMID:Imbalance of plasma membrane ion leak and pump relationship as a new aetiological basis of certain disease states. 1464 92

Most patients suffering from systemic lupus erythematosus develop secondary heart disease at some time during the course of the primary illness. The most common forms of this type of heart disease are acute fibrinous pericarditis and hypertension. By means of echocardiography, an increased incidence of pericardial effusion has been demonstrated. Although commonly noted at autopsy, myocarditis is often clinically silent. However, endomyocardial biopsy may confirm its presence during life. Libman-Sacks endocarditis, although encountered in 40 to 50% of hearts at autopsy, is rarely diagnosed during life. When significant valve dysfunction such as aortic insufficiency or mitral regurgitation develops during the course of systemic lupus erythematosus, then Libman-Sacks endocarditis should be strongly suspected. Cardiac arrhythmias, first degree AV block, and acquired complete heart block may develop either de novo or in association with lupus pericarditis, myocarditis, vasculitis, etc. Complete congenital heart block has been reported in newborns of mothers with systemic lupus erythematosus, particularly those who have an antibody to a soluble tissue ribonucleoprotein antigen called RO(SS-A). Coronary arteritis and premature coronary atherosclerosis manifesting in either angina pectoris or myocardial infarction in young adults, particularly women suffering from systemic lupus erythematosus, have received attention recently. The development of hypertension and hyperlipidemia while such patients are receiving prolonged corticosteroid therapy has been incriminated as the significant risk factor in premature coronary atherosclerosis. Longstanding hypertension and congestive heart failure have unfavorable prognoses. This report is based on a cumulative review of 50 patients with acute and chronic systemic lupus erythematosus seen at our institution and in private practice during the last 10 years.
 ...
PMID:Heart disease in systemic lupus erythematosus: diagnosis and management. 1522 37

Human immunodeficiency virus (HIV) and acute immunodeficiency syndrome are known to be associated with cardiac involvement. In this respect, a relation between HIV and dilated cardiomyopathy has been described. Additionally, highly active antiretroviral therapy (HAART) may independently contribute to cardiac impairment. We here report two cases of severely reduced left ventricular function detected in the context of a recent standardized screening of 132 HIV+ individuals of the German heart failure network. Both patients presented in a poor overall condition and progressive exercise-induced dyspnea accompanied by edema or angina pectoris, respectively. Subsequent examinations revealed left bundle-branch blockade, ventricular arrhythmia, elevated serum BNP-levels as well as pathologic transthoracic echocardiography, left ventricular angiography, electron beam tomography and cardiac magnetic resonance imaging without significant coronary stenoses or immunohistological signs of an ongoing or prior myocarditis. Clinical signs of progressive chronic heart failure developed slowly but constantly following initiation of the HAART regimen. Patients were treated by an implantation of a biventricular implantable cardioverter defibrillator beside conventional conservative standard therapy followed by a significant improvement of clinical symptoms. Antiviral medication could be maintained in both patients. Taking all data into account, the diagnosis of a HAART-associated dilated cardiomyopathy could be assessed. Even though the pathogenesis of secondary heart failure after HAART is still object of investigation a mitochondrial impairment by antiviral drugs is thought to contribute the development of dilated cardiomyopathy. However, due to the coexistence of an eminent HIV infection, a direct effect of the HI virus itself can not be completely excluded.
 ...
PMID:Dilated cardiomyopathy in two adult human immunodeficiency positive (HIV+) patients possibly related to highly active antiretroviral therapy (HAART). 1618 52


<< Previous 1 2 3 4 5 6 7 Next >>