Lee Stylos

Feasibility of using an implantable system to measure thoracic congestion in an ambulatory chronic heart failure canine model.

Background: Noninvasive measures of impedance reflect alterations in thoracic fluid and pulmonary edema in acute animal and human studies.

Comparison of electrocardiogram and intrathoracic electrogram signals for detection of ischemic ST segment changes during normal sinus and ventricular paced rhythms.

ST Segment Changes in ECG and EGM Signals. Introduction: The aim of this study was to compare surface ECGs with electrograms (EGM) that are available from implanted devices for the ability to detect ischemic ST segment changes during normal sinus (NS) and ventricular paced (VP) rhythms.

Detection of Acute Myocardial Ischemia During Percutaneous Transluminal Coronary Angioplasty by Endocardial Acceleration

The first heart sound is generated by vibrations from the myocardium during isovolumic contraction. Peak endocardial acceleration (PEA) has been used previously to measure these vibrations in humans and correlates with myocardial contractility during inotropic interventions. It is unknown if changes in PEA can be used to characterize a reduction in contractility during ischemic episodes. This study was designed to evaluate the use of an endocardial accelerometer for the detection of acute myocardial ischemia. Thirteen patients undergoing routine percutaneous transluminal coronary angioplasty (PTCA) consented to having a single‐axis, lead‐based accelerometer positioned in the right ventricular apex. PEA was defined as the maximum peak‐to‐peak amplitude during a window 50 ms before to 200 ms following the peak R wave. Time of endocardial acceleration (TEA) was defined as the time from the peak R wave to the maximum accelerometer signal within this window. To obtain a more robust estimate of the strength of vibrations, a 100‐beat template of the accelerometer signal was constructed at baseline and applied as a matched filter during ischemia. The peak magnitude of the filtered endocardial accelerometer signal (Max Filtered EA) was used as an index of signal intensity. Median baseline PEA, TEA, and Max Filtered EA were 0.91 ± 0.35 g, 75.2 ± 16.2 ms, and 0.40 ± 0.20 g, respectively. PEA and Max Filtered EA significantly decreased by 7% during ischemia (0.91 to 0.85 g and 0.40 to 0.37 g, both P < 0.05, respectively). TEA did not significantly change from baseline (77.0 ms, P = ns). The results of this study suggest that acute ischemia can be detected with an endocardial accelerometer in humans. (PACE 2004; 27:621–625)