Open Access
Open Peer Review

This article has Open Peer Review reports available.

How does Open Peer Review work?

Prediction of left ventricular reverse remodeling after therapy with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers and β blockers in patients with idiopathic dilated cardiomyopathy

  • Yoshihisa Matsumura1Email author,
  • Eri Hoshikawa-Nagai2,
  • Toru Kubo2,
  • Naohito Yamasaki2,
  • Hiroaki Kitaoka2,
  • Jun Takata3,
  • Yoshinori Doi4 and
  • Tetsuro Sugiura1
Cardiovascular Ultrasound201513:14

https://doi.org/10.1186/s12947-015-0009-4

Received: 10 February 2015

Accepted: 10 March 2015

Published: 25 March 2015

Abstract

Background

Predictors of left ventricular reverse remodeling (LVRR) after therapy with angiotensin converting enzyme inhibitors or angiotensin-receptor blockers and β blockers in patients with idiopathic dilated cardiomyopathy (IDC) remains unclear.

Methods

We studied 44 patients with IDC who had been treated with the therapy. LVRR was defined as LV end-diastolic dimension ≤ 55 mm and fractional shortening ≥ 25% at the last echocardiogram.

Results

During a mean follow-up period of 4.7 ± 3.3 years, LVRR occurred in 34% (15/44) of the patients. We divided the patients into 2 groups: (1) patients with LVRR (n = 15); (2) patients without LVRR (n = 29). The presence of atrial fibrillation was 40% in patients with LVRR and 14% in those without (p = 0.067). Initial LV end-diastolic dimension was significantly smaller (62 ± 6 vs. 67 ± 6 mm, p = 0.033) in patients with LVRR than in those without. Initial LV end-diastolic dimension of 63.5 mm was an optimal cutoff value for predicting LVRR (sensitivity: 67%, specificity: 59%, area under the curve: 0.70, p = 0.030). When patients were further allocated according to initial LV end-diastolic dimension ≤ 63.5 mm with atrial fibrillation, the combined parameter was a significant predictor of LVRR by univariate logistic regression analysis (odds ratio, 5.78, p = 0.030) (sensitivity: 33%, specificity: 97%, p = 0.013).

Conclusions

Combined information on LV end-diastolic dimension and heart rhythm at diagnosis is useful in predicting future LVRR in patients with IDC.

Keywords

RemodelingAtrial fibrillationCardiomyopathyHeart failure

Introduction

Idiopathic dilated cardiomyopathy (IDC) is characterized by left ventricular (LV) dilatation with systolic dysfunction [1]. Reverse remodeling (RR), which is a decrease in LV size with an improvement in systolic function, has an important role in prognosis of IDC [2-10]. Recently, occurrence of LVRR during follow-up has been reported to identify patients who will have a favorable future prognosis [5,8]. Therefore, prediction of future LVRR at initial diagnosis is of prognostic significance. Nevertheless, predictors of LVRR remain unclear in IDC [11]. The aim of the present study was to identify predictors of LVRR in patients with IDC after therapy with angiotensin converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) and β blockers.

Methods

We retrospectively studied 44 patients with IDC who were treated with therapy with ACE inhibitors or ARBs and β blockers. ACE inhibitors or ARBs and β blockers were continued during follow-up in all patients, although there were some changes of the other concomitant drugs, such as diuretics, when clinically indicated. All patients were admitted to our hospital for confirmation of diagnosis, risk assessment, and symptom management during the period from 1994 to 2006. The study was approved by the Ethics Committee on Medical Research of the Kochi Medical School. All patients gave informed consent. On admission, an exhaustive clinical evaluation including medical history, physical examination, 12-lead electrocardiography, ambulatory 24-hour electrocardiography, laboratory studies, echocardiography, and cardiac catheterization was performed, in each patient to identify cause of cardiomyopathy as precisely as possible. The diagnostic criteria were: (1) dilated LV end-diastolic dimension (Dd) > 55 mm with fractional shortening (FS) < 25%; (2) exclusion of patients with acute myocarditis, infiltrative myocardial disease, connective-tissue disease, endocrine dysfunction, neuromuscular disease, general systemic disease, significant coronary artery stenosis (defined as diameter narrowing of > 50% in any of the major coronary arteries or their branches), valvular disease, sensitivity/toxic reactions and a history of excessive alcohol intake. LVDd, LV end-systolic dimension (Ds), thicknesses of the interventricular septum, LV posterior wall, and left atrial dimension were measured by M-mode echocardiography as recommended by the American Society of Echocardiography [12]. LVFS was calculated as ((LVDd – LVDs)/LVDd) × 100. Echocardiography was performed in routine clinical practice. The study patients underwent echocardiography at baseline and within 1 year of the last visit, death, or transplantation. LV reverse remodeling (LVRR) was defined as described previously (LV end-diastolic dimension (Dd) ≤ 55 mm and fractional shortening (FS) ≥ 25% at the last echocardiogram) [5,10]. Follow-up data were obtained by regular visits and chart reviews, and telephone contact with the patients or their relatives.

Statistical analysis

Categorical variables are presented as total number and % of patients, and continuous variables are presented as means ± standard deviation. Fisher’s exact test was used to analyze categorical variables. Differences in continuous variables were analyzed by the unpaired Student’s t test or Mann–Whitney test, as appropriate. Receiver operating characteristic curve analysis was used to determine the discriminating cutoff value for predicting LVRR. Univariate logistic regression analysis was used to determine a significant predictor of LVRR. A p value of < 0.05 was considered statistically significant.

Results

The incidence of LVRR and clinical outcomes during a mean follow-up period of 4.7 ± 3.3 years (range 5 months to 12 years) are shown in Figure 1. LVRR occurred in 34% (15/44) of the patients. LVRR occurred at 6 months in 2 patients, and after 12 months in 13 patients. All patients who showed LVRR survived. Of the remaining 29 patients without LVRR, 8 patients died (heart failure death in 5 patients, sudden cardiac death in 3), 1 underwent heart transplantation, and 20 survived. The incidence of cardiac death and heart transplantation was significantly higher in patients without LVRR than in those without (p = 0.018).
Figure 1

Occurrence of LVRR and clinical outcomes during a follow-up period of 4.7 ± 3.3 years. LVRR, left ventricular reverse remodeling; IDC, dilated cardiomyopathy.

We divided the patients into 2 groups: (1) patients with LVRR, (2) patients without LVRR. There were no significant differences in the frequency of use of ACE inhibitors or ARBs. We most frequently used enalapril (83%) (30/36) as an ACE inhibitor and losartan (63%) (5/8) as an ARBs. There were no significant differences in these maintenance doses between the 2 groups. Carvedilol was administered in 37 patients and metoprolol in 7 patients. There were no significant differences in the frequency of use of these drugs. There were no significant differences in these maintenance doses between the 2 groups (Table 1).
Table 1

Initial clinical characteristics

Variables

LVRR (+)

LVRR (−)

p value

(n = 15)

(n = 29)

Age (years)

60 ± 11

58 ± 13

0.512

Men

13 (87%)

26 (89%)

0.767

New York Heart Association class

I – II

11

24

0.207

III – IV

5

5

 

Diabetes mellitus

4 (27%)

3 (10%)

0.206

Atrial fibrillation

6 (40%)

4 (14%)

0.067

Nonsustained ventricular tachycardia

6 (40%)

11 (38%)

0.894

Serum creatinine (mg/dl)

0.87 ± 0.16

0.81 ± 0.25

0.406

Estimated glomerular filtration rate (ml min-1 1.73 m-2)

80.3 ± 12.2

79.8 ± 12.1

0.738

Complete left bundle brunch brock

2 (13%)

6 (21%)

0.549

QRS duration (ms)

101 ± 14

111 ± 32

0.173

Follow-up periods (years)

5.9 ± 3.2

4.4 ± 2.8

0.220

Pharmacological treatments

β blockers

15 (100%)

29 (100%)

>0.99

Carvedilol

13 (87%)

24 (83%)

0.737

Dose (mg/day)

11.3 ± 4.8

10.8 ± 5.3

0.761

Metoprolol

2 (13%)

5 (17%)

0.735

Dose (mg/day)

60.0 ± 28.2

56.0 ± 21.9

0.879

Angiotensin converting enzyme inhibitors/angiotensin II receptor blockers

12 / 3 (100%)

24/5 (100%)

>0.99

Enalapril

10 (67%)

20 (69%)

0.877

Dose (mg/day)

5.2 ± 1.8

4.6 ± 0.9

0.318

Losartan

2 (13%)

3 (20%)

0.767

Dose (mg/day)

37.5 ± 17.7

41.7 ± 14.4

0.738

Loop diuretics

13 (87%)

27 (93%)

0.596

Spironolactone

7 (45%)

15 (52%)

0.751

Digitalis

11 (73%)’

20 (67%)

0.763

Amiodarone

1 (7%)

4 (14%)

0.647

Data are presented as mean ± SD or n (%). LVRR, left ventricular reverse remodeling.

Atrial fibrillation was found in 40% (6/15) of patients with LVRR, and in 14% (4/29) of those without LVRR (p = 0.067). The initial heart rate was 87 ± 21 (60–105) beats/min in 6 patients with LVRR, and that was 98 ± 28 (80–140) beats/min in 4 patients without LVRR. No difference was found in the initial heart rate between the 2 groups (P = 0.390). The heart rate was > 100 beats/min was found in 2 patients with atrial fibrillation; 1 patient with heart rate of 105 beats/min showed LVRR, and 1 patient with heart rate of 140 beats/min did not show LVRR. Atrial fibrillation recovered to sinus rhythm in 2 patients who did not show LVRR. Initial LVDd was significantly smaller in patients with LVRR than in those without LVRR (Table 2). No other differences were found between the 2 groups. Initial and last echocardiographic parameters are shown in Table 3. Initial LVDd of 63.5 mm was an optimal cutoff value for predicting LVRR (sensitivity: 67%, specificity: 59%, area under the curve: 0.70, p = 0.030) by receiver operating characteristic curve analysis. When patients were further allocated according to initial LVDd ≤ 63.5 mm in combination with atrial fibrillation, initial LVDd ≤ 63.5 mm with atrial fibrillation was a significant predictor of LVRR by univariate logistic regression analysis (odds ratio, 5.78; 95% confidence interval, 1.19 – 28.0, p = 0.030) (sensitivity: 33%, specificity: 97%, p = 0.013).
Table 2

Initial echocardiographic and cardiac catheterization findings

Variables

LVRR (+)

LVRR (−)

p value

Left ventricular end-diastolic dimension (mm)

62 ± 6

67 ± 6

0.033

Left ventricular end-systolic dimension (mm)

53 ± 6

57 ± 8

0.093

Left ventricular fractional shortening (%)

15 ± 4

14 ± 5

0.574

Interventricular septal thickness (mm)

10 ± 2

10 ± 1

0.727

Left ventricular posterior wall thickness (mm)

10 ± 2

9 ± 2

0.165

Relative wall thickness

0.32 ± 0.01

0.29 ± 0.06

0.106

Left atrial dimension (mm)

43 ± 6

42 ± 7

0.653

Left ventricular mass index (g/m2)

204 ± 58

196 ± 68

0.703

Left ventricular end-diastolic volume index (ml/m2)

144 ± 72

169 ± 43

0.197

Left ventricular end-systolic volume index (ml/m2)

100 ± 66

119 ± 42

0.274

Left ventricular ejection fraction (%)

34 ± 13

31 ± 9

0.357

Left ventricular end-diastolic pressure (mm Hg)

12 ± 6

12 ± 7

0.819

Pulmonary capillary wedge pressure (mm Hg)

11 ± 8

11 ± 8

0.929

Systolic pulmonary artery pressure (mm Hg)

30 ± 12

29 ± 9

0.672

Mean pulmonary artery pressure (mm Hg)

19 ± 8

19 ± 9

0.961

Right ventricular end-diastolic pressure (mm Hg)

8 ± 3

7 ± 4

0.806

Mean right atrial pressure (mm Hg)

6 ± 2

6 ± 4

0.963

Systolic aortic pressure (mm Hg)

112 ± 22

112 ± 19

0.985

Mean aortic pressure (mm Hg)

87 ± 15

84 ± 12

0.614

Cardiac index (ml/min/m2)

2.1 ± 0.6

2.2 ± 0.6

0.486

Data are presented as mean ± SD. LVRR, left ventricular reverse remodeling.

Table 3

Initial and last echocardiographic findings

Variables

LVRR (+)

LVRR (−)

Initial

Last

Initial

Last

Left ventricular end-diastolic dimension (mm)

62 ± 6

49 ± 4

67 ± 6

62 ± 9

Left ventricular end-systolic dimension (mm)

53 ± 6

33 ± 4

57 ± 8

50 ± 11

Left ventricular fractional shortening (%)

15 ± 4

32 ± 4

14 ± 5

20 ± 8

Interventricular septal thickness (mm)

10 ± 2

10 ± 1

10 ± 1

10 ± 1

Left ventricular posterior wall thickness (mm)

10 ± 2

10 ± 1

9 ± 2

9 ± 1

Relative wall thickness

0.32 ± 0.01

0.41 ± 0.06

0.29 ± 0.06

0.30 ± 0.08

Left atrial dimension (mm)

43 ± 6

42 ± 6

42 ± 7

41 ± 7

Left ventricular mass index (g/m 2)

204 ± 58

140 ± 30

196 ± 68

176 ± 54

Data are presented as mean ± SD. LVRR, left ventricular reverse remodeling.

Discussion

The present study had major 2 findings. First, initial LVDd was significantly smaller in patients with LVRR than in those without. Second, when patients were further allocated according to initial LV end-diastolic dimension ≤ 63.5 mm with atrial fibrillation, the combined parameter was a significant predictor of LVRR by univariate logistic regression analysis (odds ratio: 5.78, p = 0.030).

LVRR has a key role in favorable prognosis of IDC [2-10]. Although many predictors of LVRR in patients with IDC have been reported, inconsistent results exist in the past studies [2,8,11,13-19]. This was probably because of differences in the definition of LVRR and in clinical factors such as pharmacological therapy. Although the ACE inhibitors or ARBs and β blockers that block the neurohormonal activation play an important role in inducing LVRR, there is no report on prediction of LVRR after therapy with ACE inhibitors or ARBs and β blockers in patients with IDC. In the present study, initial LVDd was smaller in patients with LVRR than in those without LVRR. Initial LVDd of ≤ 63.5 mm was significantly associated with future LVRR by receiver operating characteristic curve analysis. In a past study, myocardial recovery was evident in 32% of the patients on a LV assist device who had initial LVDd < 60 mm [20]. In contrast, myocardial recovery was not evident in all patients who had initial LVDd > 70 mm. More recently, in the multicenter IMAC-2 study, LVDd at presentation predicted a better LV systolic function at 6 months [21]. The authors have stated that smaller LV size is likely a marker of a more reversible cardiac pathological condition. Similarly, the present study suggests that initial LVDd could provide important information in predicting future LVRR.

Atrial fibrillation is a common arrhythmia in patients with IDC. The presence of atrial fibrillation tended to be associated with LVRR in the present study. When patients were further categorized according to initial LVDd ≤ 63.5 mm with concomitant atrial fibrillation, this combined parameter was a significant predictor of LVRR by univariate logistic regression analysis. The parameter of initial LVDd ≤ 63.5 mm with concomitant atrial fibrillation had high specificity and low sensitivity. These results suggest that the combined parameter is useful for predicting future LVRR, but not useful for denying future LVRR.

It is problematic to determine whether atrial fibrillation is the primary cause of the cardiomyopathy (tachycardia-induced cardiomyopathy), or secondary to IDC [22,23]. We are still in this old dilemma of “which came first”: chicken, or egg [24]? Tachycardia-induced cardiomyopathy is retrospectively diagnosed by marked improvement in LV function typically seen in 4 – 6 weeks [23]. Prolonged heart rate > 100 beats/min has been reported to be also important in its diagnosis [23]. However, there are no absolute parameters which distinguish between tachycardia-induced cardiomyopathy and IDC. In the present study, the patients with atrial fibrillation had not typical feature of tachycardia-induced cardiomyopathy in view of the initial heart rate and time of appearance of LVRR. Also, no significant difference was found in initial LVDd between patients with atrial fibrillation and those without (data not shown). Although these results indicate that patients of the present study with atrial fibrillation had IDC but not tachycardia-induced cardiomyopathy, initial LV end-diastolic dimension ≤ 63.5 mm with atrial fibrillation was a significant predictor of LVRR, suggesting that atrial fibrillation might be associated with future LVRR.

The targeting doses of ACE inhibitors, ARBs, and β blockers were lower in the present study than those in the United States’ guidelines [25]. A low dose of carvedilol of 5 mg/day was beneficial in Japanese patients with heart failure in the Multicenter Carvedilol Heart Failure Dose Assessment (MUCHA) trial [26]. We have previously reported that low doses of ACE inhibitors, ARBs, and β blockers had favorable effects on the prognosis of Japanese patients with IDC [27,28]. The Japanese Guidelines (available at the Japanese Circulation Society Web site (http://www.j-circ.or.jp/) have recommended a targeting dose of enalapril of 5 to 10 mg/day and of carvedilol of 5 to 20 mg/day.

The present study has several limitations as follows: (1) The study was retrospective, and the number of patients was small; (2) Although all patients showed basically diffuse LV wall motion abnormalities, calculated LVFS would not be a representative estimate of systolic function, particularly when regional abnormalities were present; (3) Because these limitations could affect the results of the present study, care should be taken when applying the results to the individual patients; (4) There are no currently available parameters that can accurately distinguish between tachycardia-induced cardiomyopathy and IDC; (5) Further studies especially with a large number of patients are required to confirm the results of the present study.

Conclusions

Initial LVDd was significantly smaller in patients with LVRR than in those without. Initial LVDd ≤ 63.5 mm in combination with atrial fibrillation was a significant predictor of future LVRR. Combined information on LVDd and heart rhythm at diagnosis is useful in predicting future LVRR in patients with IDC.

Abbreviations

LV: 

Left ventricular

RR: 

Reverse remodeling

IDC: 

Idiopathic dilated cardiomyopathy

ACE: 

Angiotensin converting enzyme

ARBs: 

Angiotensin-receptor blockers

Dd: 

End-diastolic dimension

Ds: 

End-systolic dimension

FS: 

Fractional shortening

Declarations

Authors’ Affiliations

(1)
Department of Laboratory Medicine, Kochi Medical School, Kochi University
(2)
Department of Cardiology, Neurology, and Aging Science, Kochi Medical School, Kochi University
(3)
Center to Promote Creativity in Medical Education, Kochi Medical School, Kochi University
(4)
Chikamori Hospital

References

  1. Dec GW, Fuster V. Idiopathic dilated cardiomyopathy. N Engl J Med. 1994;331:1564–75.View ArticlePubMedGoogle Scholar
  2. Kawai K, Takaoka H, Hata K, Yokota Y, Yokoyama M. Prevalence, predictors, and prognosis of reversal of maladaptive remodeling with intensive medical therapy in idiopathic dilated cardiomyopathy. Am J Cardiol. 1999;84:671–6.View ArticlePubMedGoogle Scholar
  3. Udelson JE, Konstam MA. Relation between left ventricular remodeling and clinical outcomes in heart failure patients with left ventricular systolic dysfunction. J Card Fail. 2002;8:S465–71.View ArticlePubMedGoogle Scholar
  4. Konstam MA. Reliability of ventricular remodeling as a surrogate for use in conjunction with clinical outcomes in heart failure. Am J Cardiol. 2005;96:867–71.View ArticlePubMedGoogle Scholar
  5. Hoshikawa E, Matsumura Y, Kubo T, Okawa M, Yamasaki N, Kitaoka H, et al. Effect of left ventricular reverse remodeling on long-term prognosis after therapy with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers and β blockers in patients with idiopathic dilated cardiomyopathy. Am J Cardiol. 2011;107:1065–70.View ArticlePubMedGoogle Scholar
  6. Kramer DG, Trikalinos TA, Kent DM, Antonopoulos GV, Konstam MA, Udelson JE. Quantitative evaluation of drug or device effects on ventricular remodeling as predictors of therapeutic effects on mortality in patients with heart failure and reduced ejection fraction: a meta-analytic approach. J Am Coll Cardiol. 2010;56:392–406.View ArticlePubMedPubMed CentralGoogle Scholar
  7. Konstam MA, Kramer DG, Patel AR, Maron MS, Udelson JE. Left ventricular remodeling in heart failure: current concepts in clinical significance and assessment. JACC Cardiovasc Imaging. 2011;4:98–108.View ArticlePubMedGoogle Scholar
  8. Merlo M, Pyxaras SA, Pinamonti B, Barbati G, Di Lenarda A, Sinagra G. Prevalence and prognostic significance of left ventricular reverse remodeling in dilated cardiomyopathy receiving tailored medical treatment. J Am Coll Cardiol. 2011;57:1468–76.View ArticlePubMedGoogle Scholar
  9. Udelson JE, Konstam MA. Ventricular remodeling fundamental to the progression (and regression) of heart failure. J Am Coll Cardiol. 2011;57:1477–9.View ArticlePubMedGoogle Scholar
  10. Matsumura Y, Hoshikawa-Nagai E, Kubo T, Yamasaki N, Furuno T, Kitaoka H, et al. Left ventricular reverse remodeling in long-term (>12 years) survivors with idiopathic dilated cardiomyopathy. Am J Cardiol. 2013;111:106–10.View ArticlePubMedGoogle Scholar
  11. Kubanek M, Sramko M, Maluskova J, Kautznerova D, Weichet J, Lupinek P, et al. Novel predictors of left ventricular reverse remodeling in individuals with recent-onset dilated cardiomyopathy. J Am Coll Cardiol. 2013;61:54–63.View ArticlePubMedGoogle Scholar
  12. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. A report from the American Society of echocardiography’s guidelines and standards committee and the chamber quantification writing group, developed in conjunction with the European Association of echocardiography, a branch of the european society of cardiology. J Am Soc Echocardiogr. 2005;18:1440–63.View ArticlePubMedGoogle Scholar
  13. Failure Levine TB, Levine AB, Bolenbaugh J, Stomel RJ. Impact of left ventricular size on pharmacologic reverse remodeling in heart. Clin Cardiol. 2000;23:355–8.View ArticlePubMedGoogle Scholar
  14. Naqvi TZ, Goel RK, Forrester JS, Davidson RM, Siegel RJ. Usefulness of left ventricular mass in predicting recovery of left ventricular systolic function in patients with symptomatic idiopathic dilated cardiomyopathy. Am J Cardiol. 2000;85:624–9.View ArticlePubMedGoogle Scholar
  15. Metra M, Nodari S, Parrinello G, Giubbini R, Manca C, Dei Cas L. Marked improvement in left ventricular ejection fraction during long-term beta-blockade in patients with chronic heart failure: clinical correlates and prognostic significance. Am Heart J. 2003;145:292–9.View ArticlePubMedGoogle Scholar
  16. Kang SJ, Song JK, Song JM, Kang DH, Lee EY, Kim J, et al. Usefulness of ventricular longitudinal contractility assessed by Doppler tissue imaging in the prediction of reverse remodeling in patients with severe left ventricular systolic dysfunction. J Am Soc Echocardiogr. 2006;19:178–84.View ArticlePubMedGoogle Scholar
  17. Binkley PF, Lesinski A, Ferguson JP, Hatton PS, Yamokoski L, Hardikar S, et al. Recovery of normal ventricular function in patients with dilated cardiomyopathy: predictors of an increasingly prevalent clinical event. Am Heart J. 2008;155:69–74.View ArticlePubMedGoogle Scholar
  18. Park SM, Kim YH, Ahn CM, Hong SJ, Lim DS, Shim WJ. Relationship between ultrasonic tissue characterization and myocardial deformation for prediction of left ventricular reverse remodelling in non-ischaemic dilated cardiomyopathy. Eur J Echocardiogr. 2011;12:887–94.View ArticlePubMedGoogle Scholar
  19. Bhat PK, Ashwath ML, Rosenbaum DS, Costantini O. Usefulness of left ventricular end-systolic dimension by echocardiography to predict reverse remodeling in patients with newly diagnosed severe left ventricular systolic dysfunction. Am J Cardiol. 2012;110:83–7.View ArticlePubMedGoogle Scholar
  20. Simon MA, Primack BA, Teuteberg J, Kormos RL, Bermudez C, Toyoda Y, et al. Left ventricular remodeling and myocardial recovery on mechanical circulatory support. J Card Fail. 2010;16:99–105.View ArticlePubMedGoogle Scholar
  21. McNamara DM, Starling RC, Cooper LT, Boehmer JP, Mather PJ, Janosko KM, et al. Clinical and demographic predictors of outcomes in recent onset dilated cardiomyopathy: results of the IMAC (Intervention in Myocarditis and Acute Cardiomyopathy)-2 study. J Am Coll Cardiol. 2011;58:1112–8.View ArticlePubMedGoogle Scholar
  22. Umana E, Solares CA, Alpert MA. Tachycardia-induced cardiomyopathy. Am J Med. 2003;114:51–5.View ArticlePubMedGoogle Scholar
  23. Khasnis A, Jongnarangsin K, Abela G, Veerareddy S, Reddy V, Thakur R. Tachycardia-induced cardiomyopathy: a review of literature. Pacing Clin Electrophysiol. 2005;28:710–21.View ArticlePubMedGoogle Scholar
  24. Gallagher JJ. Tachycardia and cardiomyopathy: the chicken-egg dilemma revisited. J Am Coll Cardiol. 1985;6:1172–3.View ArticlePubMedGoogle Scholar
  25. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, et al. 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines: developed in collaboration with the international society for heart and lung transplantation. Circulation. 2009;119:e391–479.View ArticlePubMedGoogle Scholar
  26. Hori M, Sasayama S, Kitabatake A, Toyo-oka T, Handa S, Yokoyama M, et al. Low-dose carvedilol improves left ventricular function and reduces cardiovascular hospitalization in Japanese patients with chronic heart failure: the Multicenter Carvedilol Heart Failure Dose Assessment (MUCHA) trial. Am Heart J. 2004;147:324–30.View ArticlePubMedGoogle Scholar
  27. Matsumura Y, Takata J, Kitaoka H, Kubo T, Baba Y, Hoshikawa E, et al. Long-term prognosis of dilated cardiomyopathy revisited: an improvement in survival over the past 20 years. Circ J. 2006;70:376–83.View ArticlePubMedGoogle Scholar
  28. Kubo T, Matsumura Y, Kitaoka H, Okawa M, Hirota T, Hamada T, et al. Improvement in prognosis of dilated cardiomyopathy in the elderly over the past 20 years. J Cardiol. 2008;52:111–7.View ArticlePubMedGoogle Scholar

Copyright

© Matsumura et al.; licensee BioMed Central. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Advertisement