Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.
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PMID:Two cases of right ventricular ischemic injury due to massive pulmonary embolism. 1118 71

Systemic lupus erythematosus is known to have cardiac manifestations consisting of pericarditis, myocarditis, endocarditis, and coronary vasculitis. Pericarditis is the most common cardiac manifestation of systemic lupus erythematosus. Myocarditis may be suspected in patients presenting with unexplained tachycardia, conduction disturbances, unexplained systolic dysfunction with or without heart failure, or arrhythmias. The development of arrhythmias in systemic lupus erythematosus could be secondary to pericarditis, myocarditis, or ischemia caused by coronary vasculitis. The development of atrial fibrillation in systemic lupus erythematosus is not commonly reported. There have been few reports on the patients developing atrial fibrillation after being started on methylprednisolone therapy. Described here is a case of the development of atrial fibrillation in a newly diagnosed 37-year-old patient with systemic lupus erythematosus who was started on intravenous methylprednisolone therapy.
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PMID:Atrial fibrillation associated with systemic lupus erythematosus and use of methylprednisolone. 1144 30

An 86-year-old-woman presented with apical ballooning left ventricular dysfunction associated with therapy for acute pulmonary thromboembolism. She was referred to our hospital for advanced treatment for her shock state due to acute pulmonary embolism with normal left ventricular(LV) function. Her condition was stabilized using a percutaneous cardiopulmonary support system. Suction embolectomy was successfully carried out after pulmonary arteriography. After the therapy, echocardiography revealed apical ballooning and hyperkinesis of the base(LV ejection fraction = 28%), although coronary arteriography showed no fixed stenosis. LV wall motion significantly improved on day 3(LV ejection fraction = 45%). Pulmonary embolism relapsed on day 5 in spite of anticoagulation treatment. She died of multiple organ failure on day 9. Autopsy findings indicated no sign of myocardial infarction or myocarditis, patchy appearance of myocardial contraction band necrosis and few migrated lymphocytes. The mechanism for the flow mis-matched LV dysfunction remains unknown. The probable explanations include non-ischemic stress such as catecholamine or neurogenic stress, and possibly ischemic stress or ischemia/reperfusion injury.
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PMID:[Apical ballooning by transient left ventricular dysfunction (so-called "ampulla" cardiomyopathy) associated with therapy for acute pulmonary thromboembolism: a case report]. 1149 35

Heart failure is generally believed to begin with myocyte damage caused by a variety of insults, including ischemia, toxin or myocardial infection. The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been hypothesized to play a pathogenetic role in the transition from compensated to decompensated heart failure. Interleukin-18 (IL-18), a recently cloned cytokine synthesized by Kupffer cells, activates macrophages. We examined the therapeutic effect of IL-18 on the modulation of TNF-alpha gene expression in failing heart in a murine model of heart failure caused by viral myocarditis. The heart weight (HW)/ body weight (BW) ratio in IL-18 treated mice 7 days after viral inoculation was significantly lower (P<0.01) than in the untreated controls. Myocardial necrosis and inflammatory cell infiltration were significantly lower in IL-18 treated mice than untreated mice 5 and 7 days after inoculation. The expression of TNF-alpha mRNA in the myocardium was significantly lower on days 5 and 7 in IL-18 treated mice than in infected untreated mice. We conclude that concurrent systemic administration of IL-18 is beneficial in mice with myocarditis, and may be mediated through reduced expression of TNF-alpha in the heart.
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PMID:Interleukin-18 reduces expression of cardiac tumor necrosis factor-alpha and atrial natriuretic peptide in a murine model of viral myocarditis. 1188 1

Increased inducible nitric oxide synthase (iNOS) expression is a component of the immune response and has been demonstrated in cardiomyocytes in septic shock, myocarditis, transplant rejection, ischemia, and dilated cardiomyopathy. To explore whether the consequences of such expression are adaptive or pathogenic, we have generated a transgenic mouse model conditionally targeting the expression of a human iNOS cDNA to myocardium. Chronic cardiac-specific upregulation of iNOS in transgenic mice led to increased production of peroxynitrite. This was associated with a mild inflammatory cell infiltrate, cardiac fibrosis, hypertrophy, and dilatation. While iNOS-overexpressing mice infrequently developed overt heart failure, they displayed a high incidence of sudden cardiac death due to bradyarrhythmia. This dramatic cardiac phenotype was rescued by specific attenuation of transgene activity. These data implicate cardiomyocyte iNOS overexpression as sufficient to cause cardiomyopathy, bradyarrhythmia, and sudden cardiac death.
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PMID:Cardiomyocyte overexpression of iNOS in mice results in peroxynitrite generation, heart block, and sudden death. 1190 Nov 82

Heart failure is not a uniform disease entity, but a syndrome with various causes, including hypertension, ischemia and congenital heart disease, cardiomyopathy, myocarditis and intoxication. During the recent years a number of molecular and cellular alterations have been identified in the diseased heart, but a direct causative link between these changes and functional impairment, medical responsiveness, progression of the disease and the patients' outcome remains to be established. After an accumulation of large amounts of DNA sequence data in genomic projects, scientists have now turned their attention to the central executors of all programs of life, the proteins. In complementation of the genomic initiatives, proteomics based approaches have lined up not only for large-scale identification of proteins and their post-translational modifications, but also to study the function of protein complexes, protein-protein interactions and regulatory and signalling cascades in the cellular network. In concert with genomic data functional proteomics will hold the key for a better understanding and therapeutical management of cardiovascular diseases in the future.
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PMID:Separation and identification of human heart proteins. 1201 96

Ischemic preconditioning is thought to evoke cell survival programs in the heart in large part via the activation of G(I)-protein coupled receptor signal transduction pathways. However, the identification and characterization of G(I)-protein coupled receptor independent pathways would enable researchers to pursue novel cellular events that could direct or promote preconditioning. In this regard recent work has begun to explore the role of the innate immune system in intrinsic cardioprotection against both viral myocarditis and ischemia. Interestingly, cytokines such as TNFalpha, IL-1beta and leukemia inhibitory factor, which are components of innate immunity, have been shown to mimic ischemic preconditioning. Thus as the innate immune system functions via a diverse array of G(I)-protein independent receptors, the study of this immunological system in the heart may provide new insight into mechanisms driving and promoting ischemic preconditioning. We propose that innate immunity is indeed an integral part of ischemic preconditioning. In this review, we provide an overview of the innate immune system, describe the studies whereby cytokines mimic ischemic preconditioning and finally postulate some mechanisms whereby innate immunity may promote cardioprotection as a component of preconditioning.
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PMID:Innate immunity and cardiac preconditioning: a putative intrinsic cardioprotective program. 1216 Sep 44

The functional role of tumor necrosis factor (TNF)-alpha in the heart has been extensively studied over the last 15 years. Collectively, these studies have demonstrated that TNF-alpha has both diverse and potentially conflicting roles in cardiac function and pathology. These include beneficial effects, such as cardioprotection against ischemia, myocarditis, and pressure overload, as well as potentially adverse effects, such as the development of atherosclerosis, reperfusion injury, hypertrophy, and heart failure. TNF-alpha antagonist therapy recently has been demonstrated to be clinically applicable in inflammatory conditions, and clinical trials are currently in progress in the use of these agents in cardiovascular diseases. The scope for clinical applications of anti-TNF-alpha therapy in cardiovascular diseases is potentially extensive. Hence, this review has been undertaken to evaluate the cardiovascular effects of this pleiotropic cytokine and to evaluate the potential of targeting this cytokine in cardiovascular therapeutics. An overview of the TNF-alpha peptide and its associated signaling are described. This is followed by a discussion of the known roles of TNF-alpha in cardiac physiology and in a diverse array of cardiac pathologies. Reference to experimental and clinical studies using anti-TNF-alpha therapies are described where applicable. The postulated role of TNF-alpha signaling concerning innate cardiac cellular processes that may have direct adaptive effects in the heart will be reviewed with respect to future research directions. Finally, the author postulates that attenuation of TNF-alpha biosynthesis in selected individuals will need to be tested if true benefits of this therapeutic approach are to be realized in the management of cardiovascular diseases.
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PMID:Tumor necrosis factor-alpha in cardiovascular biology and the potential role for anti-tumor necrosis factor-alpha therapy in heart disease. 1219 98

10 specimens of heart in autopsy were immunohistochemically studied by using anti-actin(At) antibody. In 5 cases with definite or suspected viral myocarditis according to Dallas criteria, actin in myocardium showed focal or diffuse weak staining, and occasionally showed focal absence of staining. In 2 cases with myocardial infarction, actin showed large pieces absent of staining, while actin in 3 cases with non-cardiac death showed strongly positive, well-distributed staining. The results indicated the immunohistochemical observation of actin in myocardium is useful for improving the sensitivity in diagnosing viral myocarditis and differentiating the slight injuries of myocytes caused by ischemia or inflammation.
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PMID:[Immunohistochemical observation of actin in viral myocarditis]. 1253 1

Myocardial contractile dysfunction accompanies both systemic and cardiac insults. Septic shock and burn trauma can lead to reversible contractile deficits, whereas ischemia and direct inflammation of the heart can precipitate transient or permanent impairments in contractility. Many of the insults that trigger contractile dysfunction also activate the innate immune system. Activation of the innate immune response to infection is coordinated by the conserved Toll/interleukin-1 (IL-1) signal transduction pathway. Interestingly, components of this pathway are also expressed in normal and failing hearts, although their function is unknown. The hypotheses that Toll/IL-1 signaling occurs in the heart and that intact pathway function is required for contractile dysfunction after different insults were tested. Results from these experiments demonstrate that lipopolysaccharides (LPS) activate Toll/IL-1 signaling and IL-1 receptor-associated kinase-1 (IRAK1), a critical pathway intermediate in the heart, indicating that the function of this pathway is not limited to immune system tissues. Moreover, hearts lacking IRAK1 exhibit impaired LPS-triggered downstream signal transduction. Hearts from IRAK1-deficient mice also resist acute LPS-induced contractile dysfunction. Finally, IRAK1 inactivation enhances survival of transgenic mice that develop severe myocarditis and lethal heart failure. Thus the Toll/IL-1 pathway is active in myocardial tissue and interference with pathway function, through IRAK1 inactivation, may represent a novel strategy to protect against cardiac contractile dysfunction.
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PMID:IRAK1 deletion disrupts cardiac Toll/IL-1 signaling and protects against contractile dysfunction. 1286 May 65


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