Migraine and patent foramen ovale: transesophageal echocardiography study. should we exclude migraine without aura?

The prevalence and size of patent foramen ovale [PFO] in migraine without aura have never been assessed directly using Transesophageal echocardiography [TEE] and compared with migraine with aura. We sought to assess the prevalence and the size of patent foramen ovale in patients suffering from migraine with [MA] and without [MoA] aura using TEE. consecutive patients with migraine with and without aura were asked to participate in the study. Impact of migraine on daily life was assessed using the Migraine Disability Assessment [MIDAS] questionnaire. Contrast transesophageal echocardiography was performed to all participants and the presence of a patent foramen ovale and their size were assessed. forty consecutive patients with migraine headache were included in our study. The majority of participants were women, mean age was 26.7 [18-38 year]. Family history of migraine was encountered in 65% of patients. The mean Migraine severity using MIDAS was 16.2 [5-28] half of the patients were higher than the score of 21. Out of the 40 studied patients, 18 [45%] showed patent foramen ovale in TEE examination. Twenty patients [50%] had migraine with aura. There was no statistical difference between MA and MoA patients regarding age, sex, and MIDAS. The prevalence of patent foramen ovale was significantly higher in MA patients 11 out of 20 [55%] compared with 7 out of 20 [35%] MoA patients [OR 2.7, p = 0.005]. The presence of PFO was significantly related to the migraine disability severity score. Large PFO size was found in 45% of patients with MA while 42% of patients with MoA [p = NS]. although prevalence of PFO is higher in migraine with aura, the prevalence of large PFO is nearly the same in both subtypes of migraine and more related to severity of migraine disability and family history of migraine

Pro and antiinflammatory cytokines in unstable angina

Recent studies suggest that inflammation may play an important role in the pathogenesis of acute coronary syndromes. Several inflammav tory markers are increased in acute coronary syndromes as the nonspecific hepatically synthesized CRP, instead, several cytokines are direct inflammatory mediators as lL-6 and TNF-alpha which increase in many disease states, including the acute coronary syndromes. lL-10 is an anti-inflammatory cytokine, is produced by Th2 lymphocytes, B cells, and monocytes. It inhibits macrophagedependent cytokine synthesis by Th1 cells thus regulate balance between ceII-and humeral-mediated immune response. The proinflammatory cytokines play a role in acute coronary syndrome. however. the potential role of anti-inflammatory cytokines in the modulation of atherosclerotic process remains unknown. The objective of this study is to assess the value of pro and entiinilammatory cytokines in patients with unstable angina. The present work assessed the serum level of proinflammatory cytokines lL-6 and TNF-alpha and anti-inflammatory cytokine lL-10 in 36 patients, 20 patients had chronic stable angina, their ages ranged between 48-62 years with mean age 53 years and 16 patients with unstable angina class IIIB according to Braunwald classification, their ages ranged between 4861 years and their mean age is 54 years. All patients were diagnosed by coronary angiography. A control group comprise 10 subjects oi matched age and sex also included in this study. Serum lL-6 end TNF-alpha show a highly significant elevation in unstable angina versus the other two groups [P<0.001], these proinflammatory cytokines are positively correlated with serum cholesterol, LDL-c. TG and negatively correlated with mm in whole groups. Serum anti-inflammatory cytokine IL-10 shows a highly significant decrease in patients with unstable angina when compared to the control group [P=0.002] and also shows significant decrease when compared to patients with stable angina group [P=0.02]. Also serum lL-10 shows a negative correlation with lL-6, TNF-alpha, serum cholesterol, LDL-c, TG and PPBS in whole groups. These results indicate that the level at antiinlammatory cytokine lL-10 decrease in patients with unstable angina and this decrease may be the cause of plaque instability and rupture