Key result
Peak endocardial acceleration monitoring during pharmacological stress was feasible, detecting an increase from 0.26 g at baseline to 0.5 g at peak stress (MD 0.24 g; 95% CI 0.14-0.34; p<0.01).
Why the study?
Does peak endocardial acceleration monitoring detect left ventricular inotropic response in patients undergoing pharmacological stress echocardiography?
Does peak endocardial acceleration monitoring detect left ventricular inotropic response in patients undergoing pharmacological stress echocardiography?
Mean Difference: 0.24 (95% CI 0.14–0.34)
Absolute Event Rate: 0.5% vs 0.26%
p-value: p=<0.01
Transcutaneous peak endocardial acceleration monitoring is a feasible, non-invasive method to quantitatively assess left ventricular inotropic response during pharmacological stress echocardiography.
Supports non-invasive inotropic monitoring during stress echo; leaves open diagnostic utility versus standard parameters.
BACKGROUND: As the myocardium contracts isometrically, it generates vibrations that can be measured with an accelerometer. The vibration peak, peak endocardial acceleration (PEA), is an index of contractility. OBJECTIVE: To evaluate the feasibility of PEA measured by the cutaneous precordial application of the accelerometer sensor; and to assess the usefulness of PEA monitoring during pharmacological stress echocardiography. DESIGN: Feasibility study. SETTING: Stress echo laboratory. PATIENTS: 34 consecutive patients underwent pharmacological stress (26 with dipyridamole; 8 with dobutamine) and PEA monitoring simultaneously. INTERVENTIONS: A microaccelerometer was positioned in the precordial region and PEA was recorded. Dipyridamole was infused up to 0.84 mg/kg in 10 minutes, and dobutamine up to 40 microg/kg/min in 15 minutes. RESULTS: A consistent PEA signal was obtained in all patients. Overall mean (SD) baseline PEA was 0.26 (0.15) g (g = 9.8 m/s(2)), increasing to 0.5 (0.36) g at peak stress (+0.24 g, 95% confidence interval (CI) 0.14 to 0.34 g; p < 0.01). PEA increased from 0.26 (0.16) to 0.37 (0.25) g in the dipyridamole group (+0.11 g, 95% CI 0.08 to 0.16 g; p < 0.01), and from 0.29 (0.1) to 0.93 (0.37) g in the dobutamine group (+0.64 g, 95% CI 0.37 to 0.91 g; p < 0.01). CONCLUSIONS: Using precordial leads this method offers potential for diagnostic application in the short term monitoring of myocardial function. PEA monitoring is feasible during pharmacological stress and documents left ventricular inotropic response quantitatively in a non-invasive and operator independent fashion.
No takes yet. Share an insight, caveat, or question.
Tonino Bombardini (2001) studied Pharmacological stress echocardiography (n=34). Peak endocardial acceleration (PEA) monitoring vs. Baseline was evaluated on Peak endocardial acceleration (PEA) at peak stress (MD 0.24, 95% CI 0.14-0.34, p=<0.01). Peak endocardial acceleration monitoring during pharmacological stress was feasible, detecting an increase from 0.26 g at baseline to 0.5 g at peak stress (MD 0.24 g; 95% CI 0.14-0.34; p<0.01).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: