Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal values for left anterior descending coronary artery (LAD) flow velocity were assessed from a large number of normal children. In 303 healthy children, LAD peak flow velocity was measured by Doppler echocardiography. LAD peak flow velocities were calculated considering the angle between the Doppler beam and the coronary flow direction. The flow signals of LAD were recorded in 95% (288/303). The mean angle between the Doppler beam and Doppler flow signals of LAD was 42 +/- 8 degrees. The ratio of AT to total diastolic spectral duration was 0.19 +/- 0.088 and constant with age. LAD peak flow velocity correlated significantly with age (r = -0.57, p < 0.0001) and heart rate (r = 0.63, p < 0.0001). Multiple linear regression analysis showed that LAD peak flow velocity was associated with age and heart rate (LAD peak flow velocity = 20-0.34 (age) + 0.16 (heart rate), r2 = 0.41, p < 0 .0001). Normal data obtained in the present study provide a basis of the understanding and investigation in children with congenital heart disease or acquired heart disease such as atherosclerosis, left ventricular hypertrophy, or Kawasaki's disease.
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PMID:Normal values for left anterior descending coronary artery flow velocity assessed by transthoracic doppler echocardiography in healthy children. 1285 61

Myocardial blood flow (MBF) was investigated in children (14.2 +/- 5.01 years) with "resolved" coronary involvement after the onset of Kawasaki disease and angiographically normal epicardial coronary arteries. Ten asymptomatic children with a history of Kawasaki disease had electrocardiography, echocardiography, and positron emission tomography (PET) 10.3 +/- 6.01 years after onset of the acute illness. Myocardial perfusion was assessed by NH(3)- PET at rest and after vasodilatation and compared with that of 10 healthy volunteers (26.1 +/- 6.3 years). No patient had signs of myocardial ischemia; on echocardiography ventricular function was normal without dyskinetic areas or signs of enlargement or stenosis of the proximal coronary arteries. There was no statistical significant difference between patients and volunteers in MBF at rest (0.86 +/- 0.27 vs 0.77 +/- 0.17 ml/g/min), whereas MBF after vasodilatation (2.42 +/- 0.81 vs 3.10 +/- 0.8 ml/g/min) and coronary flow reserve (CFR) (2.89 +/- 0.26 vs 4.09 +/- 1.01 mmHg/ml/g/min) were significantly attenuated in the Kawasaki group. No stress-induced perfusion defects could be detected. In children with a history of Kawasaki disease and angiographically normal epicardial coronary arteries, there is a significant attenuation of MBF after vasodilatation and a significant reduction of CFR. Impairment of vasoreactive ability may indicate residual damage of the coronary arteries and may be a risk factor for atherosclerosis in adulthood.
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PMID:Myocardial blood flow and coronary flow reserve in children with "normal" epicardial coronary arteries after the onset of Kawasaki disease assessed by positron emission tomography. 1466 60

Coronary artery aneurysms are rare findings usually diagnosed incidentally at necropsy or at angiography in patients with symptoms of myocardial ischaemia. Even if atherosclerosis is a common cause of coronary aneurysms in the adult, other acquired diseases with inflammatory pathogenesis are associated with coronary artery aneurysms. We present three cases of patients with low probability of coronary artery atherosclerotic disease, due to their age, risk factors profile and history, complaining of chest pain suggestive of myocardial ischaemia and angiographic documentation of one or more coronary aneurysms. In all cases, although no patient had had a previous diagnosis of Kawasaki disease (KD), an unexplained febrile syndrome had occurred in childhood, which is compatible with misdiagnosed episode of KD causing the aneurysmatic lesions. The present reports highlight the potential clinical relevance of previously misdiagnosed KD in patients with ischaemic chest pain, low probability of atherosclerosis and coronary aneurysms.
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PMID:Clinical manifestations of coronary aneurysms in the adult as possible sequelae of Kawasaki disease during infancy. 1503 Jan 28

We present the case of a 30-year-old female patient with few coronary risk factors for atherosclerosis but with 3-vessel coronary artery disease possibly secondary to Kawasaki disease. Coronary angiography showed total occlusion of the left anterior descending artery and a right coronary artery aneurysm. Quadruple coronary artery bypass was performed. The postoperative course was uneventful.
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PMID:Coronary bypass in an adult with Kawasaki disease. 1513 88

Systemic arterial stiffness is increased in patients after Kawasaki disease (KD). Recently, associations between mannose-binding lectin (MBL) gene mutation and coronary complications in infants with KD and atherosclerosis in adults have been reported. We tested the hypothesis that MBL genotype modulates arterial stiffness in children after KD. Seventy-one KD patients (42 with and 29 without coronary aneurysms), aged 9.5 +/- 3.7 y, and 41 age-matched controls were studied. We determined and compared their blood pressure, brachioradial arterial stiffness as determined by pulse wave velocity (PWV), fasting total cholesterol, serum MBL level, and MBL genotype. Additionally, the modulating effects of different MBL expression genotypes [high level (HL) versus intermediate or low level (IL/LL)] on arterial stiffness in different groups were assessed. The MBL genotype distributions did not differ between patients and controls (p = 0.41) or between patients with and without coronary aneurysms (p = 0.42). Patients with IL/LL expression genotypes had significantly faster PWV than those with HL expression genotypes (7.93 +/- 1.38 m/s versus 6.67 +/- 2.28 m/s, p = 0.027). This genotype-modulating effect is more pronounced in patients without (HL 8.86 +/- 0.77 m/s versus IL/LL 6.48 +/- 2.32 m/s, p = 0.02) than those with (HL 7.50 +/- 1.41 m/s versus IL/LL 6.80 +/- 2.28 m/s, p = 0.32) coronary aneurysms. Multiple linear regression analysis identified age (beta = 0.26, p = 0.012), being a Kawasaki patient (beta = 0.22, p = 0.015), and MBL IL/LL genotype subgroup (beta = 0.20, p = 0.03) as significant determinants of arterial stiffness in the entire cohort. In conclusion, MBL genotype modulates arterial stiffness, an important cardiovascular risk factor, in children after KD.
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PMID:Modulating effects of mannose binding lectin genotype on arterial stiffness in children after Kawasaki disease. 1529 97

Kawasaki disease (KD) is an acute febrile syndrome of childhood, characterized by vasculitis of the medium-sized arteries. White blood cell counts and the inflammatory parameter C-reactive protein (CRP) are known to be elevated in the acute phase of the disease. In this study we investigated the course of inflammatory cell type-specific parameters in KD over a longer period of time. Plasma levels of human neutrophil elastase (HNE), matrix metalloproteinases-2 and -9 (MMP2, MMP9), and neutrophil gelatinase-associated lipocalin (NGAL), macrophage neopterin and CRP were measured. Plasma samples were collected in the acute, subacute and early convalescent stage, and three months after the onset of disease. Median CRP and neopterin normalized within two weeks. In contrast, six weeks and three months after onset of disease, levels of HNE were still elevated, with median values of 163 ng/ml and 156 ng/ml, respectively (control children median < 50 ng/ml; for all time-points P < 0.0001). Values of NGAL correlated with the levels of HNE (r = 0.39, P = 0.013). These results demonstrate a longer state of neutrophil activation in KD than was previously assumed. The potential relationship between this prolonged neutrophil activation, coronary artery lesion formation and their persistence, as well as the risk of premature atherosclerosis warrants further evaluation.
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PMID:Sustained activation of neutrophils in the course of Kawasaki disease: an association with matrix metalloproteinases. 1595 85

The etiology of Kawasaki disease (KD) remains unknown despite several years of dedicated research in this direction. Recently coronavirus infection and genetic polymorphisms have been implicated. Since first description of the disease there have been few changes in the diagnostic criteria except for newer recommendations of fever of at least 4 instead of 5 days duration. Recently, Echocardiography Criteria and Laboratory Criteria have been added to aid in the diagnosis of incomplete KD where all the historical diagnostic criteria are not present; this is now called the "incomplete form of KD" as opposed to "atypical form of KD". The word "atypical" is reserved for unusual presentations of KD such as those with hemophagocytic syndrome or nerve palsy. The treatment of KD includes infusion of high dose immunoglobulin. Patients non-responsive to immunoglobulin therapy are labeled as having "immunoglobulin resistant KD". The treatment of immunoglobulin resistant KD can be challenging and new therapies that have tried with some success. Late outcomes after 4 decades of treating these patients have recently been published. There has been some concern about increased risk for premature atherosclerosis in patients with childhood KD who had coronary artery abnormalities.
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PMID:Current perspectives on Kawasaki disease. 1607 48

Cardiac sequelae of Kawasaki disease are an important cause of ischemic heart disease in young adults. The possibility of early progression of atherosclerosis following Kawasaki disease is therefore of great concern. We examined whether preclinical atherosclerotic changes are seen in patients with a history of Kawasaki disease, and whether these changes appear in all or in only a proportion of patients. Sixty-five patients with a history of Kawasaki disease, aged 13.1 +/- 2.1 years, and 20 aged-matched controls participated in the study. All subjects underwent flow-mediated dilatation (FMD) of the brachial artery and analysis of carotid artery size and pulse-wave transmission. Patients were classified into four groups depending on the severity of the maximum coronary artery lesion: group 0 (normal), group 1 (mild), group 2 (moderate), and group 3 (severe). There was no statistical difference in the carotid artery analyses between the four groups. FMD (mean +/- SD) was significantly lower in groups 2 and 3 than in groups 0 and 1 and the control group (group 0, 19.4 +/- 3.9%; group 1, 19.5 +/-4.1%; group 2, 8.9 +/- 2.8%; group 3, 4.2 +/- 1.5%; control group, 18.8 +/- 2.8%; p < 0.0001). There was a significantly negative correlation between the severity of the coronary artery lesion and FMD (p < 0.0001 for both). Endothelial dysfunction was revealed by FMD in patients with persistent coronary artery lesions subsequent to Kawasaki disease. Preclinical atherosclerosis may be present only in patients with coronary aneurysms.
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PMID:Evaluation of preclinical atherosclerosis by flow-mediated dilatation of the brachial artery and carotid artery analysis in patients with a history of Kawasaki disease. 1613 79

Coronary mycotic aneurysms are rare with a poor prognosis. Atherosclerosis often predisposes to aneurysmal dilatation. In children, Kawasaki disease and in adults trauma, vasculitis, syphilis, dissection, and postcoronary angioplasty contribute to coronary mycotic aneurysms. Radiolabeled leukocytes have been used in the diagnosis of prosthetic valve endocarditis and vascular graft infections. Abnormal accumulation of radiolabeled leukocytes have also been reported in infra renal aortic aneurysms. We present a case of a coronary mycotic aneurysm where delayed Tc-99m HMPAO labeled leukocyte imaging played an important role leading to the diagnosis.
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PMID:Role of delayed Tc-99m HMPAO labeled leukocyte scintigraphy in the diagnosis of coronary mycotic aneurysm. 1616 43

Coronary artery aneurysms are uncommon, usually associated with atherosclerosis and rarely involve all 3 main coronary arteries. Sudden death from documented thrombosis within large coronary aneurysms has been rarely reported. The authors report a case of a previously healthy 36-year-old male who presented with myocardial infarction complicated by sudden cardiac death. The patient was successfully resuscitated, and coronary angiography revealed diffuse, severe aneurysmal disease without evidence of atherosclerosis. A thrombus was visualized in a large aneurysm of the proximal left anterior descending artery, and there was total occlusion of a second diagonal branch, presumably due to thrombus embolization. The patient had no history of Kawasaki disease, and evaluation revealed no inflammatory or autoimmune condition. Optimal treatment and prognosis for patients with nonatherosclerotic coronary aneurysms remains unclear. Our patient was treated medically with chronic warfarin and low-dose aspirin therapy and recovered without complication.
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PMID:Diffuse nonatherosclerotic coronary aneurysms: an unusual cause of sudden death in a young male and a literature review. 1623 Aug 89


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