Relationship Between the Temporal Profile of Plasma microRNA and Left Ventricular Remodeling in Patients After Myocardial Infarction

Zile, Michael R.; Mehurg, Shannon M; Arroyo, Jazmine E.; Stroud, Robert E.; DeSantis, Stacia M.; Spinale, Francis G.

doi:10.1161/circgenetics.111.959841

Cited by 129 publications

(101 citation statements)

References 24 publications

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“…However, they also showed that there was no difference in incidence of HF between patients with lower and higher levels of miR-133a (4 of 108 patients [3.7%] for the lower miR-133a group versus 3 of 108 patients [2.8%] for the higher miR-133a group; P=NS). Overall, however, we totally agree with the last sentence by Devaux et al 1 that the studies by us 2 and others [5][6][7][8] suggest that the potential of miRs as a prognostic biomarker in the secondary prevention setting of AMI deserves further testing. …”

supporting

confidence: 86%

“…5,7,8 In this context, Eitel et al 6 demonstrated that plasma miR-133a levels predicted a composite of death, HF, and reinfarction within 6 months after AMI. However, they also showed that there was no difference in incidence of HF between patients with lower and higher levels of miR-133a (4 of 108 patients [3.7%] for the lower miR-133a group versus 3 of 108 patients [2.8%] for the higher miR-133a group; P=NS).…”

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confidence: 99%

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Response to the Letter by Devaux et al

Sakata

Matsumoto

Hamasaki

et al. 2013

Circulation Research

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We thank Devaux et al 1 for their interest in our work published in a recent issue of Circulation Research. 2 We have carefully read their comments and replied to them.First, we are afraid that there are some misunderstandings about our studies, including the study design. For the first screening in the study, we randomly selected 7 patients who experienced development of heart failure (HF) within a year after discharge from the hospital after acute myocardial infarction (AMI) and 7 matched control subjects who did not experience any cardiac events for 2 years after AMI using propensity score, as described in the Supplemental Materials of the original article. 2 In the validation phase, we examined associations between HF development and circulating levels of candidate microRNAs (miRs) selected on the basis of the results of the first screening in a total of 86 post-AMI patients. Through these processes and additional experiments, we concluded that circulating levels of p53-responsive miRs were increased from the early convalescent stage (median, 18 days after onset) in post-AMI patients who survived the acute stage of AMI but developed HF within a year.2 Devaux et al 1 claimed that our study had a limitation of statistical underpower without any calculation of statistical power of our study. However, if the statistical power was retrospectively calculated on the basis of the results of our study, the estimated sample size was 49 to detect a correlation of 0.35 (or −0.35) using a 1-sided hypothesis test with a significance level of 0.05 and a power of 80%, suggesting that our sample size (n=86) had enough power. Furthermore, it should be understood that the statistical power is the probability of the event of rejecting the null hypothesis in a future study (prospective power) and thus that post hoc (retrospective) calculation of the statistical power is meaningless, particularly once statistical significance is detected, regardless of sample size. 3,4 As for the second comment, we agree with the point that the change in left ventricular diastolic dimension (LVDd) is another important factor to evaluate cardiac remodeling. However, cardiac remodeling should be assessed with several viewpoints. In our study, the absolute values of LVDd and left ventricular ejection fraction (LVEF) at 1 year were more excellently correlated with the development of HF than the change in LVDd from a median of 18 days after onset to 1 year (area under the receiveroperating characteristic curve [AUC]=0.746, r=0.335, P=0.010 for LVDd at 1 year; AUC=0.688, r=−0.334, P=0.010 for LVEF at 1 year; and AUC=0.679, r=0.236, P=0.086 for the change in LVDd), which was the reason why we showed the association between miR levels and LVDd or LVEF at 1 year but not the change in LVDd in the article.2 Indeed, the association of the change in LVDd with miR levels was less robust compared with those of absolute values of LVDd and LVEF at 1 year in the present study.The third comment is somewhat misleading because our conclusions were that the levels of ...

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confidence: 86%

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confidence: 99%

Response to the Letter by Devaux et al

Sakata

Matsumoto

Hamasaki

et al. 2013

Circulation Research

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“…Takotsubo cardio- [79] . [80] . miR-1, miR-208b and miR-499-5p were further measured in plasma samples from 424 patients for discrimination of a clinical diagnosis of MI and for association with 30-d mortality and for diagnosis of HF.…”

Section: Plasma Mirnas For Differentiating MI From Other Cardiovasculmentioning

confidence: 99%

miRNome in myocardial infarction: Future directions and perspective

Boštjančič

Glavač

2014

WJC

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MicroRNAs (miRNAs), which are small and non-coding RNAs, are genome encoded from viruses to humans. They contribute to various developmental, physiological and pathological processes in living organisms. A huge amount of research results revealed that miRNAs regulate these processes also in the heart. miRNAs may have cell-type-specific or tissue-specific expression patterns or may be expressed ubiquitously. Primary studies of miRNA involvement in hypertrophy, heart failure and myocardial infarction analyzed miRNAs that are enriched in or specific for cardiomyocytes; however, growing evidence suggest that other miRNAs, not cardiac or muscle-specific, play a significant role in cardiovascular disease. Abnormal miRNA regulation has been shown to be involved in cardiac diseases, suggesting that miRNAs might affect cardiac structure and function. In this review, we focus on miRNAs that have been found to contribute to the pathogenesis of myocardial infarction (MI) and the response post-MI and characterized as diagnostic, prognostic and therapeutic targets. The majority of these studies were performed using mouse and rat models of MI, with a focus on the identification of basic cellular and molecular pathways involved in MI and in the response post-MI. Much research has also been performed on animal and human plasma samples from MI individuals to identify miRNAs that are possible prognostic and/or diagnostic targets of MI and other MI-related diseases. A large proportion of research is focused on miRNAs as promising therapeutic targets and biomarkers of drug responses and/or stem cell treatment approaches. However, only a few studies have described miRNA expression in human heart tissue following MI.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: MicroRNAs; Myocardial infarction; Human; Animal models; Biomarkers and targets Core tip: MicroRNAs (miRNAs) contribute to various developmental, physiological and pathological processes in the heart. Cardiac diseases show abnormal miRNA regulation. Primary studies of miRNA involvement in cardiac disease analyzed mainly miRNAs that enriched in or specific for cardiomyocytes; however, growing evidence suggests that other cell-type-specific or ubiquitously expressed miRNAs are also involved in cardiovascular disease. miRNAs were found to contribute to the pathogenesis of myocardial infarction (MI) and post-MI. The majority of studies focused on miRNAs in animal models of MI, in human and animal plasma samples of MI (prognostic and diagnostic targets), and on miRNAs as promising therapeutic targets.Boštjančič E, Glavač D. miRNome in myocardial infarction: Future directions and perspective. World J Cardiol 2014; 6(9): 939-958 Available from:

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“…12,15,16 In the acute phase of MI, levels of miR-1 and miR-133a increase and can be detected in the circulation. 17 However, these miRs quickly decline, 18,19 and lead to chronically depressed levels. 20 Myocardia from patients with ischemic heart failure exhibited decreased levels of miR-1 and miR-133a which were restored after implantation of a left ventricular assist device (LVAD).…”

Section: Introductionmentioning

confidence: 99%