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At least 469 records · Page 26Linked to original sources
PubMed2004

CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: clinical use of inflammatory markers in patients with cardiovascular diseases: a background paper.

Inflammation is a recognized key component of acute coronary syndromes. Such pathogenetic achievement has led to the use of inflammatory cells and proteins as prognostic markers in these syndromes. A number of markers have been proposed, including proinflammatory cytokines such as interleukin-6, interleukin-1RA, and tumor necrosis factor-alpha, adhesion molecules such as intracellular adhesion molecule-1 and vascular adhesion molecule-1 and markers of cell activation. Although all are of scientific interest, the clinical use of these markers is limited by their high cost, low availability, and unfavorable biological profile. Conversely, common markers of inflammation such as C-reactive protein (CRP), the prototypic acute phase protein, and to a lesser extent fibrinogen, have been proven to be reliable and important markers of risk in ischemic heart disease. CRP, in particular, has been found to be associated with short- and long-term prognosis in acute coronary syndromes, including ST-elevation myocardial infarction, and in stable angina, and to predict the risk of restenosis and major events, including death, after revascularization procedures. CRP has been consistently found to be independent from other risk factors and to have an incremental value beyond the common risk factors and biochemical markers of risk, including troponin. Whether CRP also should be used as a guide to therapy is still a matter of discussion that deserves further, properly designed studies.

Angioplasty, Balloon, Coronary↗
PubMed2006

Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: the American Academy of Neurology affirms the value of this guideline.

BACKGROUND AND PURPOSE: This guideline provides an overview of the evidence on various established and potential stroke risk factors and provides recommendations for the reduction of stroke risk. METHODS: Writing group members were nominated by the committee chair on the basis of each writer's previous work in relevant topic areas and were approved by the American Heart Association Stroke Council's Scientific Statement Oversight Committee. The writers used systematic literature reviews (covering the time period since the last review published in 2001 up to January 2005), reference to previously published guidelines, personal files, and expert opinion to summarize existing evidence, indicate gaps in current knowledge, and when appropriate, formulate recommendations based on standard American Heart Association criteria. All members of the writing group had numerous opportunities to comment in writing on the recommendations and approved the final version of this document. The guideline underwent extensive peer review before consideration and approval by the AHA Science Advisory and Coordinating Committee. RESULTS: Schemes for assessing a person's risk of a first stroke were evaluated. Risk factors or risk markers for a first stroke were classified according to their potential for modification (nonmodifiable, modifiable, or potentially modifiable) and strength of evidence (well documented or less well documented). Nonmodifiable risk factors include age, sex, low birth weight, race/ethnicity, and genetic factors. Well-documented and modifiable risk factors include hypertension, exposure to cigarette smoke, diabetes, atrial fibrillation and certain other cardiac conditions, dyslipidemia, carotid artery stenosis, sickle cell disease, postmenopausal hormone therapy, poor diet, physical inactivity, and obesity and body fat distribution. Less well-documented or potentially modifiable risk factors include the metabolic syndrome, alcohol abuse, drug abuse, oral contraceptive use, sleep-disordered breathing, migraine headache, hyperhomocysteinemia, elevated lipoprotein(a), elevated lipoprotein-associated phospholipase, hypercoagulability, inflammation, and infection. Data on the use of aspirin for primary stroke prevention are reviewed. CONCLUSIONS: Extensive evidence is available identifying a variety of specific factors that increase the risk of a first stroke and providing strategies for reducing that risk.

Brain Ischemia↗
PubMed1985

Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. I. Cardiovascular responses and blood gases.

We measured oxygen consumption (VO2), heart rate (HR), stroke volume (SV), cardiac output (CO) and mean arterial blood pressure (MBPa) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. PO2, PCO2, pH and oxygen content (CO2) of the arterial and mixed venous blood were also measured. VO2 during exercise was not significantly affected by Ta. Spinal cord cooling produced definite increases in VO2, CO and SV during 0.5 ms-1 exercise at 9 degrees C; otherwise, effects of spinal cord cooling were not significant. HR, SV and CO were all linearly related to VO2; these relationships were unaffected by spinal cord cooling or Ta. Blood pressure did not increase during exercise. PaCO2 and P-vCO2 did not increase significantly during exercise. The arterial-venous CO2 difference was increased by exercise only at 34 degrees C. The chickens generally hyperventilated at 34 degrees C Ta compared to the other Ta values. No consistent effect on blood gases or on pH and CO2 of the blood could be attributed to spinal cord cooling.

Animals↗