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Response to the letter regarding the article, “Late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol”
Letters to the Editor
4351
Response to the letter regarding the article, “Late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol” Keisuke Kida a,⁎, Kihei Yoneyama a, Yasuyuki Kobayashi b, Makoto Takano a, Yoshihiro J. Akashi a, Fumihiko Miyake a a b
Department of Cardiology, St. Marianna University School of Medicine, Japan Department of Radiology, St. Marianna University School of Medicine, Japan
a r t i c l e
i n f o
Article history: Received 4 May 2013 Accepted 4 May 2013 Available online 29 May 2013 Keywords: Beta blockers Renin-angiotensin system blockers Hypertension Ejection fraction De novo heart failure
To the Editor We are really grateful that Dr. Sarli and his colleagues [1] are interested in our cardiac magnetic resonance (CMR) imaging study report [2]. To address their concerns on the effect of our statistical method, we reanalyzed our data using the Mann–Whitney U test as they recommended the comparison between the two groups. Overall, the result of the reanalysis was similar to that of our previously-published report. We also appreciate their comments and suggestions and the opportunity to provide our data associated with their second concern, the etiology of systolic dysfunction would affect left ventricular reverse remodeling (LVRR). First, in our study, all participants with systolic heart failure underwent invasive coronary angiography and right ventricular endomyocardial biopsy in the subacute phase of heart failure. Patients who were suspected as having coronary artery disease, myocarditis, and postpartum cardiomyopathy were excluded from our study. Second, one of the possible explanations of significant increases in left ventricular ejection fraction (LVEF) might be the influence of hypertension. We consider that favorable improvement in LVEF in our study was associated with the medical history of our study population, including patients with de novo congestive heart failure and 60% of those had a history of hypertension. It is well known that hypertension is associated with the development of clinical heart failure, although the percentage of reduced LVEF heart failure associated with hypertension is unknown. It is also uncertain whether such patients subsequently develop
⁎ Corresponding author at: Department of Cardiology, St. Marianna University School of Medicine, 2-16-1 Sugao Miyamae, Kawasaki, Kanagawa, 216-8511, Japan. Tel.: +81 44 977 8111; fax: +81 44 976 7093. E-mail address: [email protected] (K. Kida).
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.05.073
ventricular dilatation. However, Choi et al. reported that higher systolic blood pressure and use of beta blockers were independently related with LVRR at the median 16-month follow-up in patients with nonischemic dilated cardiomyopathy [3]. One study has reported significantly increased LVEF (27 ± 8% to 57 ± 11%) in Japanese patients with de novo acute decompensated heart failure due to nonischemic dilated cardiomyopathy [4], which is similar to our study result. We agree with the suggestion by Dr. Sarli et al. [1] that reninangiotensin system (RAS) blockers may improve LVEF and we should focus on the dose of RAS blockers which may influence our study result. We did not present our results sufficiently because of the limited space in publication, however, the dosage of enalapril, candesartan and spironolactone was similar between the two groups. Mann et al. [5] have described the efficacy of medication; beta blockers lead to a decrease in LV dilatation while RAS blockers stabilize it. Heart rate (HR) reduction improved chamber contractility and afterload reduction, and these factors helped carvedilol improve LVEF [6]. Of interest, higher HR at baseline was a strong predictor for LVRR even after the adjustment of the absence of late gadolinium enhancement (LGE) and the area under the curve of delta HR (HR reduction) predicting LVRR was 0.85 in our study. Accordingly, we would like to highlight that beta blockers, rather than RAS blockers, influenced our study result because of HR reduction after medical therapy. Consequently, the absence of LGE assessed by CMR can be considered as an indicator of LVRR because changes in left ventricular structure and function may occur before irreversible tissue damage. The presence of myocardial scar may limit LVRR. References [1] Sarli B, Celik T, Kaya MG. Letter to editor: late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol. Int J Cardiol 2013;168(3):3134–5. [2] Kida K, Yoneyama K, Kobayashi Y, et al. Late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol. Int J Cardiol 2013;168(2):1588–9. [3] Choi JO, Kim EY, Lee GY, et al. Predictors of left ventricular reverse remodeling and subsequent outcome in nonischemic dilated cardiomyopathy. Circ J 2013;77(2):462–9. [4] Ishii S, Inomata T, Ikeda Y, et al. Clinical significance of heart rate during acute decompensated heart failure to predict left ventricular reverse remodeling and prognosis in response to therapies in nonischemic dilated cardiomyopathy. Heart Vessels Mar. 22 2013. [5] Mann DL, Barger PM, Burkhoff D. Myocardial recovery and the failing heart: myth, magic, or molecular target? J Am Coll Cardiol 2012;60(24):2465–72. [6] Maurer MS, Sackner-Bernstein JD, El-Khoury Rumbarger L, et al. Mechanisms underlying improvements in ejection fraction with carvedilol in heart failure. Circ Heart Fail 2009;2(3):189–96.
4351
Response to the letter regarding the article, “Late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol” Keisuke Kida a,⁎, Kihei Yoneyama a, Yasuyuki Kobayashi b, Makoto Takano a, Yoshihiro J. Akashi a, Fumihiko Miyake a a b
Department of Cardiology, St. Marianna University School of Medicine, Japan Department of Radiology, St. Marianna University School of Medicine, Japan
a r t i c l e
i n f o
Article history: Received 4 May 2013 Accepted 4 May 2013 Available online 29 May 2013 Keywords: Beta blockers Renin-angiotensin system blockers Hypertension Ejection fraction De novo heart failure
To the Editor We are really grateful that Dr. Sarli and his colleagues [1] are interested in our cardiac magnetic resonance (CMR) imaging study report [2]. To address their concerns on the effect of our statistical method, we reanalyzed our data using the Mann–Whitney U test as they recommended the comparison between the two groups. Overall, the result of the reanalysis was similar to that of our previously-published report. We also appreciate their comments and suggestions and the opportunity to provide our data associated with their second concern, the etiology of systolic dysfunction would affect left ventricular reverse remodeling (LVRR). First, in our study, all participants with systolic heart failure underwent invasive coronary angiography and right ventricular endomyocardial biopsy in the subacute phase of heart failure. Patients who were suspected as having coronary artery disease, myocarditis, and postpartum cardiomyopathy were excluded from our study. Second, one of the possible explanations of significant increases in left ventricular ejection fraction (LVEF) might be the influence of hypertension. We consider that favorable improvement in LVEF in our study was associated with the medical history of our study population, including patients with de novo congestive heart failure and 60% of those had a history of hypertension. It is well known that hypertension is associated with the development of clinical heart failure, although the percentage of reduced LVEF heart failure associated with hypertension is unknown. It is also uncertain whether such patients subsequently develop
⁎ Corresponding author at: Department of Cardiology, St. Marianna University School of Medicine, 2-16-1 Sugao Miyamae, Kawasaki, Kanagawa, 216-8511, Japan. Tel.: +81 44 977 8111; fax: +81 44 976 7093. E-mail address: [email protected] (K. Kida).
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.05.073
ventricular dilatation. However, Choi et al. reported that higher systolic blood pressure and use of beta blockers were independently related with LVRR at the median 16-month follow-up in patients with nonischemic dilated cardiomyopathy [3]. One study has reported significantly increased LVEF (27 ± 8% to 57 ± 11%) in Japanese patients with de novo acute decompensated heart failure due to nonischemic dilated cardiomyopathy [4], which is similar to our study result. We agree with the suggestion by Dr. Sarli et al. [1] that reninangiotensin system (RAS) blockers may improve LVEF and we should focus on the dose of RAS blockers which may influence our study result. We did not present our results sufficiently because of the limited space in publication, however, the dosage of enalapril, candesartan and spironolactone was similar between the two groups. Mann et al. [5] have described the efficacy of medication; beta blockers lead to a decrease in LV dilatation while RAS blockers stabilize it. Heart rate (HR) reduction improved chamber contractility and afterload reduction, and these factors helped carvedilol improve LVEF [6]. Of interest, higher HR at baseline was a strong predictor for LVRR even after the adjustment of the absence of late gadolinium enhancement (LGE) and the area under the curve of delta HR (HR reduction) predicting LVRR was 0.85 in our study. Accordingly, we would like to highlight that beta blockers, rather than RAS blockers, influenced our study result because of HR reduction after medical therapy. Consequently, the absence of LGE assessed by CMR can be considered as an indicator of LVRR because changes in left ventricular structure and function may occur before irreversible tissue damage. The presence of myocardial scar may limit LVRR. References [1] Sarli B, Celik T, Kaya MG. Letter to editor: late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol. Int J Cardiol 2013;168(3):3134–5. [2] Kida K, Yoneyama K, Kobayashi Y, et al. Late gadolinium enhancement on cardiac magnetic resonance images predicts reverse remodeling in patients with nonischemic cardiomyopathy treated with carvedilol. Int J Cardiol 2013;168(2):1588–9. [3] Choi JO, Kim EY, Lee GY, et al. Predictors of left ventricular reverse remodeling and subsequent outcome in nonischemic dilated cardiomyopathy. Circ J 2013;77(2):462–9. [4] Ishii S, Inomata T, Ikeda Y, et al. Clinical significance of heart rate during acute decompensated heart failure to predict left ventricular reverse remodeling and prognosis in response to therapies in nonischemic dilated cardiomyopathy. Heart Vessels Mar. 22 2013. [5] Mann DL, Barger PM, Burkhoff D. Myocardial recovery and the failing heart: myth, magic, or molecular target? J Am Coll Cardiol 2012;60(24):2465–72. [6] Maurer MS, Sackner-Bernstein JD, El-Khoury Rumbarger L, et al. Mechanisms underlying improvements in ejection fraction with carvedilol in heart failure. Circ Heart Fail 2009;2(3):189–96.