OBJECTIVE: We sought to evaluate in patients with type 1 diabetes mellitus (DM1): (1) whether myocardial afterload correlates with left ventricular (LV) circumferential and longitudinal systolic function at rest and during low-dose dobutamine (LDD) infusion, and whether longitudinal and circumferential LV systolic function reserves are correlated; and (2) to explore relations between LV systolic mechanics and LV chamber output reserves. METHODS: A total of 20 patients with DM1 underwentechocardiography to assess LV systolic function at rest and at peak LDD (7.5 microg/kg/min). At rest, echocardiographic data of patients with DM1 were compared with those from 24 healthy control subjects. LV afterload was estimated by computing circumferential end-systolic stress (ESS). LV chamber systolic function was assessed by computing ejection fraction and ESS/end-systolic volume index; LV circumferential myocardial contractility was explored by computing midwall fractional shortening (MWS) and ESS-corrected MWS. Longitudinal LV systolic function was assessed using color Doppler tissue (DTI) to assess peak systolic velocities and maximal displacement of the lateral and medial mitral annulus in apical 4-chamber view; regional deformation analyses were computed at the midportion of the posterior interventricular septum (peak strain and peak strain rate); strain/ESS was assessed as an alternative indicator of longitudinal myocardial contractility. LV chamber output was assessed by computing stroke index. RESULTS: DM1 and control groups did not differ in terms of sex distribution, mean age, blood pressure, LV mass index and geometry, and at-rest parameters of LV systolic function (all P > .1), whereas body mass index was higher and systolic lateral mitral annulus velocity was lower in the DM1 than control group (both P < .01). At rest, in both groups, higher ESS correlated with lower ejection fraction and lower MWS; ESS did not show significant correlation with longitudinal systolic function parameters. At peak LDD in DM1, heart rate changed minimally; ESS decreased significantly (P < .01); circumferential and longitudinal LV systolic functions increased significantly but did not show intercorrelation; higher ESS correlated with lower ejection fraction; longitudinal LV systolic function parameters did not show correlation with ESS. In a multivariate analysis, percent increase in stroke index correlated with percent change of MWS (beta = 0.74, P < .01), and to a lesser extent with the percent increase of systolic lateral mitral annulus velocity (beta = 0.47, P = .04), independent to age, sex, percent change of ESS, and heart rate. CONCLUSIONS:LV longitudinal systolic function (DTI) parameters did not fall into the paradigm of the stress-shortening relationship used to describe LV contractility. However, both LV circumferential contractility and longitudinal systolic function reserves correlated with stroke index reserve during LDD.
RCT Entities:
OBJECTIVE: We sought to evaluate in patients with type 1 diabetes mellitus (DM1): (1) whether myocardial afterload correlates with left ventricular (LV) circumferential and longitudinal systolic function at rest and during low-dose dobutamine (LDD) infusion, and whether longitudinal and circumferential LV systolic function reserves are correlated; and (2) to explore relations between LV systolic mechanics and LV chamber output reserves. METHODS: A total of 20 patients with DM1 underwent echocardiography to assess LV systolic function at rest and at peak LDD (7.5 microg/kg/min). At rest, echocardiographic data of patients with DM1 were compared with those from 24 healthy control subjects. LV afterload was estimated by computing circumferential end-systolic stress (ESS). LV chamber systolic function was assessed by computing ejection fraction and ESS/end-systolic volume index; LV circumferential myocardial contractility was explored by computing midwall fractional shortening (MWS) and ESS-corrected MWS. Longitudinal LV systolic function was assessed using color Doppler tissue (DTI) to assess peak systolic velocities and maximal displacement of the lateral and medial mitral annulus in apical 4-chamber view; regional deformation analyses were computed at the midportion of the posterior interventricular septum (peak strain and peak strain rate); strain/ESS was assessed as an alternative indicator of longitudinal myocardial contractility. LV chamber output was assessed by computing stroke index. RESULTS: DM1 and control groups did not differ in terms of sex distribution, mean age, blood pressure, LV mass index and geometry, and at-rest parameters of LV systolic function (all P > .1), whereas body mass index was higher and systolic lateral mitral annulus velocity was lower in the DM1 than control group (both P < .01). At rest, in both groups, higher ESS correlated with lower ejection fraction and lower MWS; ESS did not show significant correlation with longitudinal systolic function parameters. At peak LDD in DM1, heart rate changed minimally; ESS decreased significantly (P < .01); circumferential and longitudinal LV systolic functions increased significantly but did not show intercorrelation; higher ESS correlated with lower ejection fraction; longitudinal LV systolic function parameters did not show correlation with ESS. In a multivariate analysis, percent increase in stroke index correlated with percent change of MWS (beta = 0.74, P < .01), and to a lesser extent with the percent increase of systolic lateral mitral annulus velocity (beta = 0.47, P = .04), independent to age, sex, percent change of ESS, and heart rate. CONCLUSIONS:LV longitudinal systolic function (DTI) parameters did not fall into the paradigm of the stress-shortening relationship used to describe LV contractility. However, both LV circumferential contractility and longitudinal systolic function reserves correlated with stroke index reserve during LDD.