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)

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

Recent investigations allow a controversial but convincing interpretation of the pathogenesis of atherosclerosis (arteriosclerosis). Atherosclerosis can be apparently the result of ultrachronic persistent infection by Chlamydia pneumoniae and not the result of heterogenous risk factors. The main arguments for the chlamydial genesis are: Correlation of coronary heart disease and other atherosclerotic diseases and antibodies against Chlamydia pneumoniae. Chlamydia pneumoniae could be detected with different techniques (PCR, ICC, immunohistology, electromicroscopy, culture) in a high percentage in atheromas from different sites. Three successful international studies with macrolides in coronary heart disease. Target cells of atherosclerosis (endothelia, macrophages, muscle cells) can be infected by Chlamydia pneumoniae in vitro. Provocation of an arteriitis in animal experiments. The reduction of incidence of atherosclerotic diseases since the 1960s, probably due to advanced antibiotic therapy. Elevated acute-phase proteins and other inflammatory signs (CRP, WBC count, fibrinogen) briefly before occurrence of myocardial infarction. There are good arguments for intervention studies in coronary heart disease and other manifestations of atherosclerosis. The relevant antibiotics are licensed for chlamydial infections, cheap and safe. Meticulous records and long-term observation of patients need to be developed, sometimes contrary to interests of the pharmaceutical industry.
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PMID:[Atherosclerosis--a chronic infectious disease caused by Chlamydia pneumoniae]. 1020 Jun 11

Inflammation has recently been shown to be an important pathogenetic component of atherosclerosis in general and of acute coronary syndromes in particular. Not only activated inflammatory cells have been found in the plaques, but, more interestingly, also activated circulating inflammatory cells as well as elevated levels of systemic markers of inflammation have been described. Among these, C-reactive protein is of clinical value, as its levels are associated with the outcome. Inflammation is important also in triggering the mechanisms of restenosis and CRP has been recently described as a useful pre-procedure marker of risk of restenosis. The cause of inflammation, what triggers the shift from an indolent disease to the acute coronary syndromes and the more appropriate therapies are still a matter of debate.
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PMID:The variable role of inflammation in acute coronary syndromes and in restenosis. 1054 16

In recent years it has been established that inflammation is a key mechanism in the pathogenesis of atherosclerosis and in coronary artery disease progression. Inflammation is a host response to a wide variety of tissue injuries. A persistent or continually repeated insult will lead to chronic inflammation which may result in tissue destruction and/or loss of normal organ function. Atherosclerosis and other pathologies involving inflammation are associated with increased levels of cytokines, which in turn raise acute-phase proteins levels in blood (acute inflammation markers, i.e. fibrinogen and C-reactive protein). It has been shown recently that concentrations of these proteins are higher in individuals at increased risk of developing cardiac events in the years to come. This is true both in apparently healthy men and women and in ischaemic heart disease patients. CRP is currently the inflammatory marker which appears to have captured the investigators' attention around the globe. In this report we review the current data on the relationship between atherosclerosis and inflammation, with special attention to cytokines and acute phase reactants. The use of acute phase reactants as prognostic risk markers in ischaemic heart disease is also discussed.
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PMID:[Ischemic cardiopathy: inflammation markers and the cardiovascular risk]. 1061 9

We found a novel G-->C change at nucleotide 1059 within exon 2 of the CRP gene encoding the C-reactive protein. The CRP 1059G/C polymorphism could be detected by digestion with endonuclease MaeIII. The frequency of the CRP 1059C allele was 0.109 in Caucasians, but it was absent from Canadian Oji-Cree. Because of the importance of the CRP gene product in inflammation and its recent association with ischemic heart disease syndromes, this polymorphism may be useful in the association studies of atherosclerosis and its related phenotypes.
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PMID:Human C-reactive protein (CRP) 1059G/C polymorphism. 1072 74

Leptin receptors are supposed to have signal effects and are located in most tissues in the organism but we failed to find literary data on concentration (measurement) of leptin receptors in the system circulation. We examined by the method of randomized selection the group of 20 patients with manifested atherosclerosis in whom BMI was calculated. Then we analyzed concentration of leptin receptor (double sandwich ELISA, standard recombinant human leptin), leptin, glucose, insulin, proinsulin, CRP and uric acid in the serum. The control group consisted of 103 probands without signs of atherosclerosis or other manifested diseases. The control group was subjected to determination of BMI, leptin and leptin receptor in the serum. Concentration of leptin receptor does not differ significantly between the patients with atherosclerosis and normal population. Probands with atherosclerosis showed a very close negative correlation between concentration of leptin receptor and leptinemia which is absent in normal population.
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PMID:Determination of leptin receptor in the serum and relations to laboratory and anthropological parameters in patients with atherosclerotic complications. 1074 33

Atherosclerosis remains the leading cause of morbidity and mortality in Western countries. Recent evidence has demonstrated that atherosclerosis is not simply a disease of lipid deposition. Inflammation plays a major role in the initiation, progression, and destabilization of atheromas. High-sensitivity C-reactive protein (hs-CRP) is a circulating acute-phase reactant that reflects active systemic inflammation. Large prospective trials have shown hs-CRP to be a strong predictor of future cardiovascular events. Increased hs-CRP concentration is in fact associated with higher cardiovascular events in individuals with and without clinical evidence of atherosclerotic disease. The relative risk associated with hs-CRP is independent of other cardiovascular disease risk factors. Assays for hs-CRP measurement are currently available but must be standardized because patients' results will be interpreted by using population-based cutpoints. A risk-stratifying algorithm incorporating hs-CRP and total cholesterol to high-density lipoprotein cholesterol ratio has been proposed. Further research into the mechanisms and pharmacological treatment of vascular disease will provide novel management strategies in the very near future.
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PMID:High-sensitivity C-reactive protein and atherosclerosis: from theory to therapy. 1116 6

Homocysteine, inflammatory markers (e.g. CRP), hemostatic factors (fibrinogen, PAI-1, factor VII and factor VIII) and lipoprotein (a) are independent risk factors for atherosclerotic disease. Although the association between these factors and atherosclerosis is clear, it is uncertain whether this signals a causal relationship, or whether the parameters simply represent markers of atherosclerosis. Currently, there are no reports on interventional studies demonstrating a benefit from correcting these risk factors. The determination of homocysteine, fibrinogen and lipoprotein should therefore be restricted to certain situations, such as atherosclerosis or a family history of the disease without classical risk factors, or uncertainty about the need for primary pharmacological prevention. An increase in these parameters should prompt the early use of lipid-lowering drugs or aspirin. In exceptional cases only (homocysteine), correction of the risk factors should be considered.
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PMID:[Homocysteine--CRP--lipoprotein (a). When do you evaluate the "new" risk factors]. 1121 76

CRP (C-reactive protein) is an acute-phase reactant, the levels of which increase dramatically in response to severe bacterial infection, physical trauma, and other inflammatory conditions. CRP is found in human atherosclerotic lesions. Atherosclerosis is clearly multifactorial in origin, and chronic inflammation is an important component in its pathogenesis. Focus on inflammation is critical in research on atherosclerosis. Elevated levels of CRP have been associated with increased risk of future coronary artery disease (CAD) events. I have summarized the recent literature on CRP studies in CAD. Both coronary heart disease and dilated cardiomyopathy(DCM) result in congestive heart failure due to myocardial damage. The inflammatory state produced by myocarditis of viral or other origin may induce advanced myocardial damage, resulting in heart failure with a poor prognosis. Routine CRP measurement proved to be valuable for identifying high-risk patients with DCM and lymphocytic myocarditis. I suggest that measurement of circulating CRP would be useful for the diagnosis of and for selecting therapeutic strategies for cardiovascular disorders.
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PMID:C-reactive protein (CRP) in the cardiovascular system. 1139 55

Cardiac valve calcification (VC) has long been regarded as a consequence of aging and abnormal calcium-phosphate metabolism in uremic patients. In view of the recent recognition of association among inflammation, malnutrition, and atherosclerosis, the possible role of inflammation and malnutrition in VC was investigated. Inflammatory markers (including C-reactive protein [CRP], fibrinogen, and basal metabolic rate) and nutritional status (assessed using serum albumin, subjective global nutrition assessment, and handgrip strength) were examined, in addition to calcium phosphate parameters and other traditional cardiovascular risk factors, including gender, smoking habits, BP, and lipid profile, in relation to VC in 137 patients who were on continuous ambulatory peritoneal dialysis. Compared with patients with no VC, patients with VC not only were older (60 [10] versus 54 [12] yr; P = 0.005), had higher plasma phosphate (1.89 [0.52] versus 1.64 [0.41] mmol/L; P = 0.003), and had higher parathyroid hormone (83 [40, 145] versus 38 [16, 71] pmol/L; P = 0.001) but also had higher CRP (4.5 [0.1, 13.4] versus 0.2 [0.1, 4.4] mg/L; P = 0.004), had higher fibrinogen (6.6 [1.9] versus 5.7 [1.3] g/L; P = 0.002), and had lower serum albumin (26 [4] versus 29 [3] g/L; P = 0004). Twenty-three percent of patients with VC versus 17% of patients with no VC were moderately to severely malnourished according to subjective global nutrition assessment (P = 0.05). Even after adjustment for patients' age, duration of continuous ambulatory peritoneal dialysis, diabetes, and calcium x phosphate product, cardiac VC remained strongly associated with CRP (odds ratio, 1.05; P = 0.026) and albumin (odds ratio, 0.85; P = 0.01). The data suggest that VC not only is a passive degenerative process but also involves active inflammation, similar to that seen in atherosclerosis. The presence of uncontrolled hyperphosphatemia and hyperparathyroidism further accelerates the progression of calcification. The data also indicate that VC and atherosclerosis should be considered as associated syndromes, sharing similar pathogenic mechanisms, namely active inflammation.
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PMID:Association of inflammation and malnutrition with cardiac valve calcification in continuous ambulatory peritoneal dialysis patients. 1151 87


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