Abstract
BackgroundAlthough it has been shown that acute beta-blocker administration may reduce the presence or severity of myocardial perfusion defects with dipyridamole stress, little information is available about the potential effect of chronic beta-blocker treatment on the sensitivity of dipyridamole myocardial perfusion imaging (DMPI).MethodsAs a randomized clinical trial, one hundred twenty patients (103 male and 17 female) with angiographically confirmed CAD who were on long-term beta blocker therapy (≥3 months) enrolled in a randomized clinical trial study. The patients were allocated into two groups: Group A (n=60) in whom the beta-blocker agent was discontinued for 72h before DMPI and Group B (n=60) without discontinuation of beta-blockers prior to DMPI.ResultsNo significant difference was noted between the groups concerning age, sex, type of the injected radiotracer and number of involved coronary vessels. The mean rank of total perfusion scores for whole myocardium (irrespective of reversibility or irreversibility) in group B was not significantly different from that of group A, (65.75 vs. 55.25, P=0.096). Regarding the only irreversible perfusion defects, the mean rank of perfusion score in group B was higher than that of group A for whole myocardium (72 vs. 49, P=0.0001); however, no difference was noted between two groups for only reversible perfusion defects (61.0 vs. 60.0, P=0.898). The overall sensitivity of DMPI for the diagnosis of CAD in group A (91.7%) was not statistically different from group B (90%).ConclusionBeta-blocker withholding before DMPI did not generally affect the sensitivity of the test for the diagnostic purposes in our study. Thus, beta-blocker withdrawal for just the purpose of diagnostic imaging is not mandatory particularly when medication discontinuation may cause the patients to face increased risk of heart events.
Highlights
Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide
Obesity is associated with chronic activation of low-grade inflammation [3], which is implicated in the pathogenesis of obesity-associated diseases including insulin resistance, type-2 diabetes (T2D) [4, 5] and cardiovascular disease [6, 7]
A numerous of studies has been shown that shortchain fatty acids (SCFAs) inhibit inflammation with focus on butyrate and to a lesser extent on acetate and Propionic Acid (PA), [16]
Summary
Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide. In Palestine the prevalence of obesity has been shown to be approximately 4. The etiology of obesity and low-grade inflammation is complex and involves intrinsic and extrinsic factors. The colonization of germ-free mice with microbiota derived from obese mice results in significantly greater adiposity than colonization with microbiota from lean mice [12]. Prebiotic diets such as fructans [13] are associated with general better health, including the decrease in body weight, fat mass and the severity of T2D [14,15,16]. The factors that influence the composition and metabolism of intestinal
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