The Cardiovascular Effects of a Meal: J-T and T -T Assessment and Further Insights Into the Physiological Effects.

Meal intake leads to a significant and prolonged increase in cardiac output to supply the splanchnic vasculature. A meal is associated with sympathetic activation of the cardiovascular system, and food ingestion is correlated with an increase in heart rate, an increase in cardiac stroke volume, and QTc interval shortening for up to 7 hours. Given the complexity of the system, one or several of many mechanisms could explain this observation. The shortening of the QTc interval was correlated with a rise of C-peptide following food ingestion, but the mechanisms by which C-peptide may be involved in the modulation of cardiac repolarization are still unknown. This shortening of the myocardial action potential caused by the ingestion of food was further investigated in the present study by measuring the QRS, J-T , and T -T intervals in search of further clues to better understand the underlying mechanisms. A retrospective analysis was conducted based on data collected in a formal thorough QT/QTc study in which 32 subjects received a carbohydrate-rich "continental" breakfast, moxifloxacin without food, and moxifloxacin with food. We assessed the effect of food on T-wave morphology using validated algorithms for measurement of J-T and T -T intervals. Our findings demonstrate that a standardized meal significantly shortened J-T for 4 hours after a meal and to a much lesser extent and shorter duration (up to 1 hour) prolonged the T -T and QRS intervals. This suggests that the QTc shortening occurs mainly during phase 2 of the cardiac action potential. As there was no corresponding effect on T -T beyond the first hour, we conclude that a meal does not interfere with the outward correcting potassium channels but possibly with Ca currents. An effect on mainly Ca aligns well with our understanding of physiology whereby an increase in stroke volume, as observed after a meal, is associated with changes in Ca cycling in and out of the sarcoplasmic reticulum during cardiac myocyte contraction.