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)

In a 55-year-old man, attacks of spontaneous angina were associated with dizziness and syncope. Holter ECG monitoring disclosed evidence of sinus node dysfunction. Dizziness and syncope were corrected by a permanent ventricular demand pacemaker. Coronary cineangiography showed spontaneous, severe, diffuse spasm in a dominant left coronary artery and localized spasm in a nondominant right coronary artery. The patient died of pump failure shortly after cardiac catheterization. An autopsy disclosed only minimal coronary atherosclerosis. This patient's condition shows that (1) coronary spasm may cause sinus node dysfunction, dizziness, and syncope, (2) severe spasm that involves all the coronary artery branches may be fatal, and (3) severe spasm occur in minimally diseased coronary arteries confirmed by pathologic examination.
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PMID:Coronary artery spasm with sinus node dysfunction and syncope. 711 92

Syncope is a brief sudden loss of consciousness and muscle tone secondary to cerebral ischaemia, inadequate oxygen or glucose delivery to the brain. The causes of syncope may be benign and require very little in the way of evaluation or treatment. However, syncope may be the harbinger of sudden death, and extensive evaluation, monitoring and detailed recommendations regarding advisability of participating in sports should be reviewed with the patient. The history is the most important clue when attempting to identify which patient with syncope is at risk for sudden death. A careful cardiac and neurological examination should be performed in any patient presenting with syncope. Selective use of laboratory testing and cardiac monitoring may assist the practitioner in making the diagnosis. Most often patients with syncope will have a benign cause such as vaso-vagal events, hyperventilation or orthostatic hypotension. Patients with a cardiac condition causing their syncope are at increased risk for sudden death. The ominous, cardiac-related causes of syncope in the younger population include hypertrophic cardiomyopathy, aberrant coronary arteries and aortic dissection secondary to Marfan's syndrome. In the older athletic population, coronary atherosclerosis may present with syncope. Dysrhythmias may be the cause of syncope in both populations.
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PMID:Syncope in athletes. 778 60

Unusual forms and causes of ischemic heart disease include angina pectoris in the presence of normal coronary arteries (syndrome X), congenital coronary abnormalities, vasculitic disorders, and graft atherosclerosis after cardiac transplantation. There is now evidence that endothelial dysfunction of coronary resistance vessels can account for abnormalities of the coronary microvasculature and possibly, myocardial ischemia and chest pain. The incidence of syndrome X appears to be higher in women, particularly those who have undergone hysterectomy. An intriguing hypothesis is that low estrogen levels may be associated with reduced expression of nitric oxide (reflecting endothelial dysfunction). The presence of coronary abnormalities in the young should not be underestimated. Syncope and arrhythmias are observed frequently in this patient population and warrant vigorous exploration. Worldwide, cardiac transplantation is now carried out in approximately 4500 patients yearly, with excellent (80% to 90%) 1-year survival due to improved immunosuppression. However, accelerated atherosclerosis develops rapidly postoperatively and is the main cause of late death. The link between cellular rejection of the myocardium and transplant coronary artery disease is not clear. The process of transplant coronary artery disease is believed to be due to chronic immune injury followed by intimal smooth-muscle proliferation and lipid deposition in the vascular wall. By the time it is detected by coronary angiography, the disease is far advanced and not susceptible to routine revascularization procedures. A prospective, randomized study of diltiazem versus no calcium blocker started early after transplantation has documented highly significant reductions in transplant atherosclerosis as measured by lumen narrowing, clinical events, and rates of retransplantation or death due to the process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unusual forms of ischemic heart disease. 791 90

Anomalous origin of the coronary artery can lead to angina pectoris, acute myocardial infarction or even sudden death in the absence of atherosclerosis. However, in Japan, this anomaly is usually treated medically rather than surgically. To clarify the clinical features of anomalous origin of the coronary artery in Japanese and the prognosis of such patients who are treated medically, we reviewed 56 patients with anomalous origin of the coronary arteries. The mean age of these patients was 55.9 +/- 11.5 years. Anomalous origin of the right coronary artery from the left sinus of Valsalva was seen most frequently (78.6%). In contrast, we found no cases of anomalous origin of the left coronary artery from the right sinus of Valsalva traversing between the aorta and the pulmonary trunk. A history of syncope (14.3%) and aorta regurgitation (21.4%) was frequent and serious complications during exercise stress testing occurred in 5 patients. These patients were treated medically, such as by limiting exercise or by the oral administration of medicine. During the follow up period (mean 5.6 +/- 4.2 years), death directly related to anomalous origin of the coronary artery was not found despite the lack of surgical treatment. Our results suggest that the prognosis of these middle-aged-to-elderly patients without atherosclerosis is relatively good, despite the lack of surgical treatment.
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PMID:Clinical features of prognosis of Japanese patients with anomalous origin of the coronary artery. 893 35

Although syncope has been shown to reduce quality-of-life, its impact on resource costs has not been documented. The objective of this study was to quantify the annual medical costs of caring for elderly patients with syncope, especially recurrent syncope of unknown origin. Administrative data from the Health Care Financing Administration were obtained on 7,959 Medicare patients who had at least one inpatient admission with a diagnosis of syncope in 1993. The costs of any inpatient admissions, outpatient procedures, or physician visits with an ICD-CM-9 diagnosis for syncope were summed for a 365-day period from the date of the initial hospitalization for syncope. Patients who had at least two hospitalizations with admission and discharge diagnosis of syncope were deemed to have recurrent syncope of uncertain origin. To better estimate syncope costs for those whose syncope costs could have been attributed to other diagnoses, a regression analysis was performed including variables representing the most frequent secondary diagnoses. The average annual costs of those who were admitted with syncope but who were discharged with another diagnosis was $4,942 in 1993. The average annual cost of patients with recurrent syncope deemed to be of unknown origin was $5,165. For those patients with secondary diagnoses of atherosclerosis, urinary tract infections, or hypokalemia, the annual costs of syncope averaged $6,820, $7,013, or $7,949, respectively.
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PMID:The costs of recurrent syncope of unknown origin in elderly patients. 1052 21

A 68-year-old man was admitted to St Marianna University Hospital on account of loss of consciousness with left hemiplegia. During the hospital recovery course with a rehabilitation procedure, the patient's blood pressure was very unstable, fluctuating between high (210/110 mmHg) and low (110/70 mmHg) values accompanied by a fainting sensation. A second stroke of left hemiplegia took place 1 month later. Afterwards, his condition worsened to tetraplegia with dysarthria. Three months later, lung cancer with multiple metastasis including his left neck was found and he died from adynamic ileus 6 months after the onset of the present illness. Autopsy revealed nearly complete atheromatous obstruction and more than 50% stenosis, respectively, of his right common and internal/external carotid arteries. His intracranial arterial trunks and main branches were all patent with localized atherosclerosis of only moderate degree. The pathology of the brain existed predominantly in the right hemisphere in the border zone area between the anterior and middle cerebral arteries systematically with numerous disseminated foci of complete or incomplete necrosis, white matter and gray matter being involved independently. Involvement of centrum semiovale white matter is more extensive and intensive than that of gray matter. Of the gray matter, cerebral cortex as well as striatum, periventricular (the third ventricle) gray and cerebellar cortex was involved. The specific characteristic topography and distribution of the lesions together with their histopathology are described in detail with illustration. It is concluded that this case represents an outstanding example of hemodynamic cerebral circulatory insufficiency doubly caused by hemilateral carotid artery stenosis and repeated episodes of systemic hypotension.
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PMID:An autopsy case of hemilaterally dominant and systematic/extensive border zone infarction: sequela of preceding atherosclerotic obstruction of one common carotid artery followed by repeated episodes of systemic hypotension. 1183 34

Aortic stenosis in the elderly is related to calcification of either a bicuspid valve or a morphologically normal tricuspid valve. There is increasing evidence that factors relating to atherosclerosis are involved in valvular calcification and that it is an actively regulated process rather than a degenerative one. With severe aortic stenosis left ventricular hypertrophy occurs, decreasing wall stress and supporting the left ventricular ejection fraction. However, with pathologic hypertrophy there is a dropout of myocardial cells, subendocardial ischemia, and fibrosis. Eventually, symptoms of angina, non-Q wave myocardial infarction, exertional syncope, and heart failure occur. Once symptoms begin, the prognosis is poor, with sudden death occurring in about one third of patients who die. In the elderly, symptoms can be recognized very late in the course of the disease since they can be attributed to other problems and since the elderly patient may have reduced physical activity to a minimum. The more comorbidities that exist, the greater the risk of valve replacement. Symptomatic patients with severe aortic stenosis even over age 80 can be operated upon with a relatively low mortality and morbidity. In patients over age 80, prolongation of life for any meaningful length of time is not as important as relief of symptoms and improvement in the quality of life. Thus, it is unlikely that any truly asymptomatic patient over age 80, even with severe aortic stenosis, should be sent to surgery.
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PMID:Pathophysiology of valvular aortic stenosis in the elderly. 1273 12

Cardioembolic stroke accounts for approximately 15% of all strokes and is thought to be one of the more preventable types of strokes. Features that have been reported to support cardioembolism as a mechanism for ischemic stroke have included documented cardiac source of embolism, maximal neurologic deficit at onset, multiple cerebrovascular territories involved, enhanced tendency toward hemorrhagic transformation, enhanced risk of syncope or seizure associated with presentation, and lower likelihood of premonitory transient ischemic attacks. Features that tend to make cardioembolic stroke less likely include significant cerebral atherosclerosis, step-wise progression of the neurologic deficit within a finite period of time, vascular distribution such as entire internal carotid artery territory with combined middle cerebral artery and anterior cerebral artery involvement or watershed distribution, and premonitory transient ischemic attacks. A number of cardiac conditions can promote thromboembolism, and there is risk stratification reflective of the specific condition or coexistent conditions. Anticoagulant therapy generally has been found to be the most effective means of preventing cardiogenic brain embolism, but the intensity of anticoagulation needs to be optimized to reflect the risk-to-benefit ratio for the particular patient.
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PMID:Cardioembolic stroke: an update. 1291 51

Toll-like receptors (TLRs) initiate and maintain host defenses and inflammation, and directly contribute to diseases such as atherosclerosis. It is not completely understood in what cell types proatherogenic TLR-induced signaling arises and, particularly, there is uncertainty regarding the potential functional role of TLR2 in endothelial cells (ECs). We determined TLR2 and TLR4 gene expression in four different human and two different murine primary ECs using gene array analysis, RT-PCR, and flow cytometry and confirmed these data by functional studies by stimulating ECs with the corresponding TLR ligands. TLR4 was expressed in all human and murine ECs and these cells responded to stimulation with LPS. Faint expression of TLR2 was observed in human ECs, whereas murine ECs express considerable amounts of TLR2 mRNA. Human ECs failed to respond to TLR2 ligands while murine ECs responded to TLR2 ligands. Furthermore, in murine ECs, TLR2 was located on the cell surface while in human ECs, TLR2 was sequestered in intracellular compartments. After IFN-gamma or IL-1beta stimulation, TLR2 translocated to the cell surface of human ECs. In conclusion, TLR2 is expressed intracellularly in human ECs and, therefore, TLR2 ligands are inaccessible to the receptor. Murine ECs express membrane TLR2 and respond to TLR2 ligands, but human ECs normally will not respond unless they are first primed with inflammatory stimulation, which appears to trigger translocation of TLR2 to the cell surface.
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PMID:Differential expression of Toll-like receptor 2 (TLR2) and responses to TLR2 ligands between human and murine vascular endothelial cells. 1798 87

Sudden cardiac death in athletes is an uncommon but extremely visible event because of the high profile of amateur and professional athletes and the expected excellent health of these athletes. However, paradoxically, athletic performance may immediately increase the risk of ventricular arrhythmias and sudden cardiac death while run reducing atherosclerosis, which thus improves cardiovascular health and longevity. In athletes younger than 30 years, the most common underlying causes are due to inherited heart disease. In the older athletes, sudden death is generally due to arrhythmias in the context of coronary artery disease. Many athletes with aborted sudden death, arrhythmia-related syncope, or high-risk genetic disorders benefit from therapy with implanted cardioverter/defibrillators (ICDs) . Although ICD therapy can effectively abort sudden death, implantation of an ICD generally prohibits an individual from all competitive athletics except low-intensity sports. The screening of athletes has been notoriously inadequate; however, the optimal screening strategies have yet to be determined. Recommendations for participation in competitive athletics generally follow the recently published 36th Bethesda Conference Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities.
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PMID:Sudden cardiac death in athletes. 1863 17


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