Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We described an anesthetic management of a patient with abdominal aortic aneurysm associated with dilated cardiomyopathy (DCM) focusing on preanesthetic evaluation of cardiovascular reserve and on intraoperative continuous circulatory monitoring with transesophageal echocardiography (TEE) and continuous cardiac output measurement (CCO). Based on echocardiographic and hemodynamic measurements after a 50 m-walk load, we predicted the allowable range of alteration of preload (LV diastolic dimension; Dd), myocardial performance (arterial blood pressure and ejection fraction) and of heart rate. During anesthesia and operation, we continuously monitored Dd, arterial blood pressure, heart rate and cardiac output, and maintained these variables within the allowable range. The changes in preload after clamping or unclamping of the aorta was promptly reflected by Dd as compared to pulmonary capillary wadge pressure. The CCO was also usuful in detecting abrupt changes in myocardial performance. In conclusion, we suggest preanesthetic stress test to be performed to evaluate cardiovascular reserve and to predict the allowable range of alteration of hemodynamic variables. Continuous monitoring of preload (Dd) by TEE and of myocardial performance by CCO is useful to detect early changes in these variables.
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PMID:[Preanesthetic evaluation of cardiovascular reserve in a patient with dilated cardiomyopathy]. 872 9

We report on a case of idiopathic dilated cardiomyopathy with aortic aneurysm involving the aortic root and thoraco-abdominal aorta. This patient presented with exertional chest pain and backache radiating to both the upper limbs. His echocardiogram revealed dilated cardiomyopathy with mild to moderate aortic regurgitation and a hugely dilated aortic root. His angiogram showed normal coronary arteries, a dilated aortic root and thoraco-abdominal aortic aneurysm.
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PMID:Annulo-aortic ectasia with thoraco-abdominal aortic aneurysm in a case of dilated cardiomyopathy. 1899 89

This case report details our experience with endovascular stent-graft repair for an abdominal aortic aneurysm (AAA) in a patient who was previously treated by left ventricular remodeling for dilated cardiomyopathy. Renal dysfunction with an elevated creatinine level (1.59 mg/dl) was managed by reducing the dose of contrast medium utilizing intravascular ultrasonography. Using a Zenith AAA endovascular device, the aneurysmal sac was successfully excluded and was thrombosed. Endovascular stenting is a good treatment option for abdominal aneurysm repair in patients with poor heart function and renal impairment.
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PMID:Endovascular stent-graft repair for abdominal aortic aneurysm in a patient with cardiac and renal dysfunction. 1936 53

Inflammation is essential in the initial development and progression of many cardiovascular diseases involving innate and adaptive immune responses. The role of CD4(+)CD25(+)FOXP3(+) regulatory T (TREG) cells in the modulation of inflammation and immunity has received increasing attention. Given the important role of TREG cells in the induction and maintenance of immune homeostasis and tolerance, dysregulation in the generation or function of TREG cells can trigger abnormal immune responses and lead to pathology. A wealth of evidence from experimental and clinical studies has indicated that TREG cells might have an important role in protecting against cardiovascular disease, in particular atherosclerosis and abdominal aortic aneurysm. In this Review, we provide an overview of the roles of TREG cells in the pathogenesis of a number of cardiovascular diseases, including atherosclerosis, hypertension, ischaemic stroke, abdominal aortic aneurysm, Kawasaki disease, pulmonary arterial hypertension, myocardial infarction and remodelling, postischaemic neovascularization, myocarditis and dilated cardiomyopathy, and heart failure. Although the exact molecular mechanisms underlying the cardioprotective effects of TREG cells are still to be elucidated, targeted therapies with TREG cells might provide a promising and novel future approach to the prevention and treatment of cardiovascular diseases.
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PMID:Regulatory T cells in cardiovascular diseases. 2652 43

Mitochondria are vital in providing cellular energy via their oxidative phosphorylation system, which requires the coordinated expression of genes encoded by both the nuclear and mitochondrial genomes (mtDNA). Transcription of the circular mammalian mtDNA depends on a single mitochondrial RNA polymerase (POLRMT). Although the transcription initiation process is well understood, it is debated whether POLRMT also serves as the primase for the initiation of mtDNA replication. In the nucleus, the RNA polymerases needed for gene expression have no such role. Conditional knockout of Polrmt in the heart results in severe mitochondrial dysfunction causing dilated cardiomyopathy in young mice. We further studied the molecular consequences of different expression levels of POLRMT and found that POLRMT is essential for primer synthesis to initiate mtDNA replication in vivo. Furthermore, transcription initiation for primer formation has priority over gene expression. Surprisingly, mitochondrial transcription factor A (TFAM) exists in an mtDNA-free pool in the Polrmt knockout mice. TFAM levels remain unchanged despite strong mtDNA depletion, and TFAM is thus protected from degradation of the AAA(+) Lon protease in the absence of POLRMT. Last, we report that mitochondrial transcription elongation factor may compensate for a partial depletion of POLRMT in heterozygous Polrmt knockout mice, indicating a direct regulatory role of this factor in transcription. In conclusion, we present in vivo evidence that POLRMT has a key regulatory role in the replication of mammalian mtDNA and is part of a transcriptional mechanism that provides a switch between primer formation for mtDNA replication and mitochondrial gene expression.
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PMID:POLRMT regulates the switch between replication primer formation and gene expression of mammalian mtDNA. 2753 55

Inflammation and fibrosis play an important role in the development and progression of cardiovascular diseases. Acute coronary syndrome (ACS) is caused by rupture of inflamed atherosclerotic plaque and subsequent atherothrombosis. Recent studies have shown that inflammatory markers such as C-reactive protein (CRP) can predict ACS development and have demonstrated the effectiveness of new therapeutic approaches targeting inflammation. Studies have also shown that an enhanced inflammatory response after myocardial infarction (MI) is associated with cardiac rupture, ventricular aneurysm formation, and exacerbation of left ventricular (LV) remodeling. Inflammation is a physiological reaction in which fibrosis is induced to facilitate the healing of tissue damage. However, when an excessive inflammatory response consisting mainly of monocytes/macrophages is induced by various factors, impaired reparative fibrosis and resulting pathological remodeling processes may occur. A similar phenomenon is observed in abdominal aortic aneurysm (AAA) expansion. In contrast, myocardial diseases such as inflammatory dilated cardiomyopathy (DCMI) and valvular diseases such as aortic valve stenosis (AS) are characterized by chronic inflammation mediated mainly by T lymphocytes and the associated enhancement of reactive fibrosis. Thus, inflammation can take 2 paths (the inhibition or promotion of fibrosis), depending on the phase of inflammation, inducing pathological cardiovascular remodeling. Elucidation of the regulatory mechanisms of inflammation and fibrosis will contribute to the development of new therapeutic approaches for cardiovascular diseases.
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PMID:Inflammatory Mechanisms of Cardiovascular Remodeling. 2941 11