PubMed · 11628434
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A Carreras Panchón. [Not Available].. https://pubmed.ncbi.nlm.nih.gov/11628434/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
In the recent World Health Organization (WHO) classification the group of pulmonary arterial hypertension (PH) comprises the classic primary pulmonary hypertension and several conditions with definite or very high risk factors to develop pulmonary arterial hypertension. Therapeutic advances drive the need for a comprehensive pre-therapeutic evaluation for optimal treatment. Furthermore, follow-up examinations need to be performed to monitor changes in disease status and response to therapy. Up to now, the diagnostic imaging work-up of PH comprises mainly echocardiography, invasive right heart catheterization and ventilation/perfusion scintigraphy. Due to technical advances helical computed tomography (CT) and magnetic resonance imaging (MRI) became more important in the evaluation and for differential diagnosis of pulmonary arterial hypertension. Both modalities are reviewed and recommendations for clinical use are given.
Ischemic heart disease is the major cause of morbity and mortality in the Western world, with chronic heart failure as one complication. Ischemia-reperfusion injury may induce cardiomyocyte cell death by necrosis or apoptosis. The heart can be adapted to tolerate an ischemic event by preceeding brief episodes of ischemia and reperfusion, called preconditioning. Innate immunity has the latest years surfaced as important for the development of cardiovascular pathology as well as for myocardial protection. Nuclear factor kappa B (NFkappaB) is a redox sensitive transcription factor which contributes to the regulation of innate and adaptive immunity. NFkappaB regulates a battery of inflammatory genes, and has been indicated to play a role in the development of numerous pathological states. Activation of NFkappaB induces gene programs leading to transcription of factors which promote inflammation, among them leukocyte adhesion molecules, cytokines such as tumor necrosis factor alpha, and chemokines, but may in some situations also promote tissue remodelling, the resolution of inflammation, and transcription of some few substances with possible antiinflammatory effects. The present paper reviews the basic regulation of NFkappaB, and the possible role of NFkappaB activation in ischemia-reperfusion injury, in adaptation to ischemia-reperfusion injury, and in chronic heart failure.
During the first wave of the 2003 smallpox vaccination campaign, two ischemic cardiac deaths occurred in civilian vaccinees aged 55 and 57 years, and one occurred in a military vaccinee aged 55 years, 4-17 days after vaccination with the New York City Board of Health (NYCBOH) vaccinia strain. Whether these and 13 other recognized military and civilian nonfatal ischemic events among vaccinees were associated with smallpox vaccination is unclear. The same NYCBOH strain was used in 1947 to vaccinate approximately six million New York City (NYC) residents (80% of the population) during a 4-week period (April 4-May 2) after a smallpox outbreak. To determine whether smallpox vaccination increased the risk for cardiac death in 1947, the NYC Department of Health and Mental Hygiene (DOHMH) analyzed data from NYC death certificates during that period. This report summarizes the results of that analysis, which found no increases in cardiac, atherosclerotic, or all-cause deaths. The findings are consistent with a growing body of evidence suggesting that ischemic cardiac deaths observed after the 2003 campaign might have been unrelated to vaccine.