1. To test the hypothesis that the number, size, location, and severity of myocardial perfusion defects and scar distribution dictate the pattern of LV dyssynchrony by tissue Doppler echocardiography and speckle tracking. An extensive body of literature exists describing the predictors of response to BIV pacing in HF patients. Our group and others have established a clear association between the presence of mechanical cardiac dyssynchrony and the response to BIV pacing. Also, our group and others have examined the effect defects on myocardial perfusion imaging (MIBI) scan on response to BIV pacing. What remains unclear is the relationship between the number, size, distribution, and severity of these perfusion defects and the pattern of dyssynchrony by echo. It seems plausible that the distribution of scar and/or perfusion abnormalities dictates the pattern of mechanical delay and the relative timing of contraction of the various parts of the LV. Approach: In this first phase of the proposal, we will utilize some of the techniques that are available to our group to correlate the patterns of perfusion defects with the patterns of mechanical dyssynchrony. For that purpose, patients with clinical indications for BIV pacing will undergo nuclear perfusion imaging at rest as well as echocardiographic (echo) imaging with tissue Doppler assessment and speckle tracking. The site of latest mechanical activation and pattern of mechanical contraction will then be compared to the sites of scar and/or perfusion defects on the resting MIBI scan. Anticipated Results: The purpose of this first phase of the proposal would be to identify if the dyssynchrony pattern is a downstream manifestation of the myocardial injury scheme and therefore, if it can be predicted based on the number, size, severity, and distribution of the perfusion abnormalities.
2. To test the hypothesis that LV lead positioning away from dense scars as determined by resting nuclear perfusion imaging and close to the site of latest LV mechanical activation translates into improved response after BIV pacing. Our group and others have demonstrated improved acute hemodynamics and long term response to BIV pacing if the LV lead position was concordant with the site of latest mechanical activation of the LV. Also, our group and others have shown that an LV pacing lead positioned at the site of a scar or in the vicinity of a high scar density area is associated with little echocardiographic and clinical response after BIV pacing. To date, standard clinical practice continues to consist of placing the LV lead tip in the most lateral and posterior position. Maintaining this approach in all cardiomyopathy patients regardless of the nature of the myocardial insult or the sites of scaring may not be optimal and may account for the lack of response to BIV therapy in a significant number of patients. The primary objective of this specific aim is to demonstrate that MIBI/echo-guided LV lead placement is superior to standard lead placement and that patients who are randomized to the MIBI/echo-guided arm will exhibit greater improvement in the symptoms of HF and greater improvement of LV function at the 6-month interval compared to patients receiving standard LV lead placement. Approach: Heart failure patients (n=210) enrolled in this study will be randomly assigned in a 2:1 fashion to one of two study arms:
