Nausea and vomiting as predictors of presence, location and size of acute myocardial infarction

In a trial to assess the value of nausea and/or vomiting in prediction presence, location and/or size of acute myocardial infarction [AMI] in patients presenting with acute chest pain and electrocardiographic [ECG], changes suggestive of coronary heart disease [CHD], 220 patients were included in the present work. They classified into AMI group [G1], [which was further classified into anterior Q-wave infarction [G[1a]], inferior Q-wave infarction [G[1b]] and non-Q-wave infarction [G[1c]] and noninfarction group [G[11]]. Nausea and/or vomiting were good predictors of AMI [85% positive predictive value]. They had no relation to infract site [67% in anterior infarction group VS. 65% in inferior infarction group with insignificant difference between them]. Using peak serum creatine kinase [CK] level, as an index of infect size, nausea and/or vomiting were good predictors of larger infarction [nausea and/or vomiting were present in 54%, 70%, 79% and 86% in patients with peak serum CK level < 1.000 IU/liter, > 1000 IU/liter, > 1.500 IU/liter, and > 2.000 IU/liter, respectively]. Thus, nausea and/or vomiting are important predictors in diagnosing AMI and are associated with larger myocardial infarctions but do not suggest infarctions in a particular location

Neutrophil chemotaxis in localized and generalized juvenile periodontitis

The aim of the present investigation was to study the defect of neutrophil chemotaxis in the disease compared individuals. Patients with juvenile periodontitis were grouped into one of the two recognized form of the disease, the localized form and the generalized type. Periodontitis, 17 patients having the generalized form of the disease and 10 healthy individuals were assessed for chemotaxis using a Boyden diffusion chamber. The results showed that neutrophil chemotaxis in juvenile periodontitis, especially the localized form is less than normal individuals. The defect of neutrophils may be related to the high concentration of endotoxins in the disease or due to absence of glycoprotein on the surface membrane which interferes with neutrophil migration. Also, the defect may be genetic or due to presence of lysozymes in a high concentration inhibiting neutrophil chemotaxis by binding the cell wall of neutrophils. The decrease of neutrophil chemotaxis in the localized than the generalized forms of the disease may be related to the difference of pathogenic microorganisms between the two forms of the disease