Background: Many patients with appropriate indications fail to respond to cardiac resynchronization therapy (CRT).
Objective: The purpose of our study was to determine the relationship between CRT response and preimplantation apical wall motion abnormality.
Methods: We analyzed data from 83 patients with ischemic cardiomyopathy who underwent CRT. All patients had New York Heart Association class III or IV symptoms despite maximal medical therapy, left ventricular ejection fraction (LVEF) < or =35%, and QRS duration > or =130 ms or <130 ms with left ventricular dyssynchrony. CRT responders at 6 months were defined as surviving patients with: (1) no hospitalization for heart failure, and (2) improvement of New York Heart Association classification. Patients underwent echocardiography before and 6 months after implantation to assess changes in regional wall motion and LVEF.
Results: At baseline, CRT responders (n = 39) and nonresponders (n = 44) had similar LVEF (22.9% +/- 6.9% vs 23.1% +/- 8.3%), QRS duration (159 +/- 43 ms vs 159 +/- 36 ms), and medical treatment. CRT nonresponders had a higher prevalence of preimplantation apical wall motion abnormality (68% vs 33%, P = .003). Patients with baseline apical wall motion abnormalities (n = 43) were less likely than others (n = 40) to show improvement in wall motion at 6 months (30% vs 81%, P < .001) or clinical response to CRT (31% vs 64%, P = .003).
Conclusion: The presence of a preimplantation apical wall motion abnormality was associated with a lower rate of CRT response in patients with ischemic cardiomyopathy.
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http://dx.doi.org/10.1016/j.hrthm.2007.06.020 | DOI Listing |
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Diabetic cardiomyopathy (DMCM), defined as left ventricular dysfunction in the setting of diabetes mellitus without hypertension, coronary artery disease or valvular heart disease, is a well-recognized entity whose prevalence is certainly predicted to increase alongside the rising incidence and prevalence of diabetes mellitus. The pathophysiology of DMCM stems from hyperglycemia and insulin resistance, resulting in oxidative stress, inflammation, cardiomyocyte death, and fibrosis. These perturbations lead to left ventricular hypertrophy with associated impaired relaxation early in the course of the disease, and eventually culminating in combined systolic and diastolic heart failure.
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