BACKGROUND: The hemodynamic effects of enhanced external counterpulsation (EECP) and its mechanism(s) were investigated in relation to neurohumoral factors in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Twenty-four patients with AMI were studied before, during and after EECP treatment for 60 min. Heart rate (HR), right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) were determined. In addition, circulating concentrations of neurohumoral factors were determined at each time point. HR did not change following EECP treatment. However, RAP and PCWP increased significantly and CI was significantly elevated during EECP and thereafter. Blood atrial natriuretic peptide (ANP) concentration was significantly increased 15 and 60 min after the start of EECP treatment, but brain natriuretic peptide (BNP) did not change. Renin, aldosterone and catecholamine concentrations also did not change. CONCLUSION: Treatment with EECP resulted in an increased preload because of increased venous return, and CI was increased thereafter. In patients with AMI, EECP increased blood ANP concentration, but not BNP, which suggests that an increase in ANP without an increase in BNP is an important mechanism for the effects of EECP treatment.
BACKGROUND: The hemodynamic effects of enhanced external counterpulsation (EECP) and its mechanism(s) were investigated in relation to neurohumoral factors in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Twenty-four patients with AMI were studied before, during and after EECP treatment for 60 min. Heart rate (HR), right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) were determined. In addition, circulating concentrations of neurohumoral factors were determined at each time point. HR did not change following EECP treatment. However, RAP and PCWP increased significantly and CI was significantly elevated during EECP and thereafter. Blood atrial natriuretic peptide (ANP) concentration was significantly increased 15 and 60 min after the start of EECP treatment, but brain natriuretic peptide (BNP) did not change. Renin, aldosterone and catecholamine concentrations also did not change. CONCLUSION: Treatment with EECP resulted in an increased preload because of increased venous return, and CI was increased thereafter. In patients with AMI, EECP increased blood ANP concentration, but not BNP, which suggests that an increase in ANP without an increase in BNP is an important mechanism for the effects of EECP treatment.
Authors: Kama Z Guluma; David S Liebeskind; Rema Raman; Karen S Rapp; Karin B Ernstrom; Andrei V Alexandrov; Reza B Shahripour; Kristian Barlinn; Sidney Starkman; Ileana D Grunberg; Thomas M Hemmen; Brett C Meyer; Anne W Alexandrov Journal: J Stroke Cerebrovasc Dis Date: 2015-09-04 Impact factor: 2.136
Authors: Keren Constantini; Abigail S L Stickford; Jeffery L Bleich; Paul D Mannheimer; Benjamin D Levine; Robert F Chapman Journal: Med Sci Sports Exerc Date: 2018-05 Impact factor: 5.411