Impact of left ventricular size on pharmacologic reverse remodeling in heart failure

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Abstract

Background and hypothesis: Although medical therapy may normalize echocardiographic left ventricular (LV) systolic function in selected patients with cardiomyopathy, other patients experience no change or a further deterioration in heart failure remodeling. Our aim was to determine what clinical or echocardiographic parameters predict a beneficial therapeutic response. Methods: We prospectively followed biannual clinical and echocardiographic assessments in 215 patients. Forty-six of these patients ('Nonresponders') experienced no change or a decline in LV ejection fraction at 6 months. Of the 148 patients who improved LV function, 21 ('Responders') normalized LV systolic function at 6 months. Only Responders (n = 21) and Nonresponders (n = 46) were compared. Results: On average, these 67 patients were 54 ± 12 years old with 4.5 ± 3.3 years of heart failure. At 6 months, following uptitration of angiotensin-converting enzyme inhibitors and nitrates, Responder LV ejection fraction rose from 22 ± 6 to 50 ± 5% with improvement in New York Heart Association classification (2.6 ± 0.8 to 1.5 ± 0.8, p = 0.001). These patients had significantly more favorable clinical and echocardiographic outcomes versus Nonresponders despite comparable medical therapy. All baseline demographic, clinical, and echocardiographic variables were equivalent, except for initial LV end- diastolic diameter which differentiated Nonresponders (7.1 ± 0.7 cm) from Responders (6.1 ± 0.8 cm), p = 0.007. Conclusion: Thus, although heart failure therapy improves LV systolic function in a majority of patients, with normalization in up to 10% of patients, significant LV enlargement may render remodeling unresponsive to pharmacologic intervention, with a potential future need for alternative mechanical or surgical intervention.

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Levine, T. B., Levine, A. B., Bolenbaugh, J., & Stomel, R. J. (2000). Impact of left ventricular size on pharmacologic reverse remodeling in heart failure. Clinical Cardiology, 23(5), 355–358. https://doi.org/10.1002/clc.4960230510

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