Systolic tissue Doppler measurements (s') have been used to measure the velocity in myocardial motion and are a valuable tool for evaluating the systolic function of the left and right ventricles. Digestion of food is known to significantly alter hemodynamics and may therefore affect s'. The effect of food intake on s' parameters has not yet been studied. We assessed whether s' is affected by food intake. Nineteen healthy subjects aged 26·2 ± 4·2 years were investigated. s' was measured with pulsed tissue Doppler imaging in the right and left ventricles before the subjects ate a standardized meal and also 30 and 110 min after the meal. Three measurements were taken in each projection, and a mean value was calculated for each. s' increased significantly (P<0·05) from fasting to 30 min after food intake in every measured site except in the left inferolateral wall (P = 0·15, NS). Several, but not all, variables returned to base value 110 min after food intake. This study shows that food intake affects the tissue Doppler variables used to evaluate systolic heart function. Further studies are needed in older healthy subjects and older subjects with various cardiovascular diseases.

BackgroundMyocardial performance index (MPI) has been investigated in a variety of populations, but the effect of food intake has not been evaluated. We assessed whether myocardial performance index is affected by food intake in healthy subjects.MethodsTwenty-three healthy subjects aged 25.6 ± 4.5 years were investigated. MPI was measured before, 30 min after, and 110 min after a standardized meal.ResultsMPI decreased significantly (P < 0.05) from fasting values 30 min after the meal, and had almost returned to baseline after 110 min. MPI decreased from 0.28 ± 0.06 (fasting) to 0.20 ± 0.07 30 min after eating. At 110 min after eating the index value was almost back to the baseline value 0.26 ± 0.06. (P = 0.15).ConclusionsThis study shows that myocardial performance index is affected by food intake in healthy subjects.

OBJECTIVE While existing evidence supports beneficial cardiovascular effects of glucagon-like peptide 1 (GLP-1), emerging studies suggest that glucose-dependent insulinotropic peptide (GIP) and/or signaling via the GIP receptor may have untoward cardiovascular effects. Indeed, recent studies show that fasting physiological GIP levels are associated with total mortality and cardiovascular mortality, and it was suggested that GIP plays a role in pathogenesis of coronary artery disease. We investigated the associations between fasting and postchallenge GIP and GLP-1 concentrations and subclinical atherosclerosis as measured by mean intima-media thickness in the common carotid artery (IMTmeanCCA) and maximal intima-media thickness in the carotid bifurcation (IMTmaxBulb). RESEARCH DESIGN AND METHODS Participants at reexamination within the Malmö Diet and Cancer–Cardiovascular Cohort study (n = 3,734, mean age 72.5 years, 59.3% women, 10.8% subjects with diabetes, fasting GIP available for 3,342 subjects, fasting GLP-1 available for 3,299 subjects) underwent oral glucose tolerance testing and carotid ultrasound. RESULTS In linear regression analyses, each 1-SD increment of fasting GIP was associated with increased (per mm) IMTmeanCCA (β = 0.010, P = 0.010) and IMTmaxBulb (β = 0.014; P = 0.040) in models adjusted for known risk factors and glucose metabolism. In contrast, each 1-SD increment of fasting GLP-1 was associated with decreased IMTmaxBulb (per mm, β = −0.016, P = 0.014). These associations remained significant when subjects with diabetes were excluded from analyses. CONCLUSIONS In a Swedish elderly population, physiologically elevated levels of fasting GIP are associated with increased IMTmeanCCA, while GLP-1 is associated with decreased IMTmaxBulb, further emphasizing diverging cardiovascular effects of these two incretin hormones.