S20 Journal of Cardiac Failure Vol. 14 No. 6S Suppl. 2008 and LVSw (2.8 6 1.1 vs. 4.1 6 1.0; p ! 0.004) were lower than Group I. There was no difference in terms of QRS duration between Group I (105 6 20 ms and 123 6 26 ms) and Group II. We found no correlation between peak TDI LVLw velocity and QRS duration (p 5 0.25) as seen in Figure 1. However, as seen in Figure 2, a significant correlation was noted between QRS duration and LVSw velocities (r 5 e0.55). Conclusion: In this analysis we found that even though QRS duration correlates with reduction in LVSw peak velocity; such correlation was not present when assessing LVLw velocities. Therefore, analysis of LVSw might be an early marker of sub clinical LV systolic function in patients depending on the QRS duration.
Conclusion: Before death we observed a decline in body temperature in cardiomyopathic hamsters. Slope of this decline alone or in combination with the low frequency spectrum are significant predictors prior to death. Information from continuous temperature monitoring may be useful as an indicator of decompensation and the need to add further therapy in CHF patients.
058 Acute and Chronic Hemodynamic Effects of Biventricular Pacing in Patients with Coronary Artery Disease and Lateral LV Wall Infarct Dusan Kocovic1, Nancy Britton1, Scott Cox1, Mark Heimann1, Glen Miske1, Steven Rothman1; 1Lankenau Hospital, Wynnewood, PA
057 Utility of Continuous Body Temperature Monitoring in Predicting Prognosis in Cardiomyopathic Hamsters Amany Ahmed Sreedevi Gondi1, Muhammad Munir, Casey Cox, K.J. Shankar, Igor Stupin, Ed Sobash, Sabrina Engel, Shubha Asopa, Dejian Lai, Alan Brewer, James Wilson, S. Ward Casscells; 1Texas Heart Institute, Houston, TX Introduction: Previously, we found that hypothermia is a significant predictor of death in heart failure patients. We hypothesized that continuous temperature monitoring is useful in predicting death in cardiomyopathic hamsters. Methods: We prospectively observed 48 male Bio-TOe2 Syrian dilated cardiomyopathic hamsters whose temperatures were monitored continuously with an intraperitoneally implanted Data Sciences International transmitter, until their death. Temperatures and frequency domain analysis of those temperatures were analyzed, after the point body temperature started to decline (changing point or CP). We used logistic regression, multiple logistic regression and ROC curves to study the ability to predict death 3, 5, 7 and 9 days prior to the event. Results: Of the hamsters, 98% had a decline in body temperature before death. On frequency domain analysis, a rise in the low frequency (LF) spectrum was observed, coinciding with temperature decline. Logistic regression of slope of the temperature curve within 24 hours after CP, showed a declining slope could predict death in 3 and 5 days OR 5 1.791, 95% CI: (1.16, 3.13), p 5 0.02 and OR 5 1.82, 95% CI: (1.15, 2.91), p 5 0.01, respectively. The predictability became insignificant for 7 and 9 days. However, using the slope within median time after CP (7 days), logistic regression predicted death at day 7 (OR 5 1.34, 95% CI: (0.995, 1.81), p 5 0.054, c 5 0.74) and more significantly at day 9 (OR 5 1.81, 95% CI: (1.15, 2.86), p 5 0.01). Multiple logistic regression with slope and LF within the median at day 7 showed OR 5 3.49, 95% CI: (1.57, 7.73), p 5 0.002 and OR 5 4.56, 95% CI: (1.33, 15.70), p 5 0.02 respectively, for predicting death. Area under the ROC curve was 0.90.
Background: Up to one third of patients treated with cardiac resynchronization therapy (CRT) do not respond clinically. The lack of response to CRT may be explained by the presence of scar tissue in the lateral left ventricular (LV) segments, which may result in ineffective LV pacing. We compared the effect of LV pacing, using acute hemodynamic measurements, among patients with an ischemic cardiomyopathy and varying regions of transmural scar. Methods and Results: 65 consecutive patients with end-stage heart failure (NYHA class III/IV), LV ejection fraction # 35%, QRS duration O120 ms, left bundle-branch block, and chronic coronary artery disease were included. The localization and depth of scar tissue were evaluated with nuclear imaging and echocardiography. LV dyssynchrony and the optimal pacing site were assessed at implantation using pressure-volume loops obtained with a conductance catheter. Clinical parameters, LV volumes, and LV ejection fraction were assessed at baseline and at a 6-month follow-up. 18 of 65 patients (28%) had a transmural (O50% of LV wall thickness) lateral scar. Patients with lateral scar had an acute increase in stroke volume of only 15% compared with 36% (p ! 0.05) in patients with either an anterior or inferior scar at their optimal pacing site. Lateral scar pts also had a diminished improvement in their maximum dP/dT (+11% vs +27% p ! 0.05) at implant and LV ejection fraction at 6 months (EF +2.2% vs EF +5%, p !0.05). Conclusions: CRT is less effective in patients with transmural scar tissue in the lateral LV segments, resulting in decreased clinical and echocardiographic response to CRT.
059 Resting Heart Rate Does Not Reflect the Degree of betae1 Receptor Sensitivity in Subjects with Heart Failure on Chronic Beta Blocker Therapy Andrea Mignatti1, Gabriel Sayer1, Ulrich P. Jorde1; 1Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY Background: Guideline recommended dosing versus the more ‘‘physiological’’ endpoint of resting heart rate have been proposed as targets for beta blockade in subjects with congestive heart failure (CHF). Whether resting heart rate truly reflects the degree of beta blockade, however, is unknown. Accordingly, we examined the relationship of resting heart rate and two measures of betae1 receptor sensitivity/blockade: (1) The percentage of maximal age predicted heart rate reached during exercise (%MPHR) and (2) the heart rate increase per unit circulating norepinehrine ( 5 chronotropic responsiveness index - CRI). Methods and Results: 19 men and 9 women with systolic CHF (LVEF ! 40%) on chronic beta blocker therapy underwent cardiopulmonary exercise testing; NE levels were measured before and at peak exercise. The chronotropic responsiveness index was calculated using the following formula: (baseline heart rate-peak heart rate)/Log (baseline norepinephrine-peak