Author + information
- Karin A.L. Mueller, MD,
- David Heinzmann, MD,
- Karin Klingel, MD,
- Petra Fallier-Becker, MD, PhD,
- Jörg Kumbrink, MD, PhD,
- Harald Langer, MD,
- Jürgen Schreieck, MD,
- Michael Gramlich, MD,
- Meinrad Gawaz, MD and
- Peter Seizer, MD∗ ()
- ↵∗Medizinische Klinik, Innere Medizin III, Kardiologie und Kreislauferkrankungen, Universitätsklinikum Tuebingen, Otfried-Mueller-Strasse 10, 72076 Tuebingen, Germany
Gaining insight into the diverse etiology of different cardiomyopathies in a clinical setting is a notoriously difficult task. In the current study, we established histological and immunohistochemical features of patients with clinically diagnosed tachycardiomyopathy, all of which showed a severely impaired left ventricular function at study entry. We thank Dr. Wijesurendra and colleagues for raising important questions stimulating further research in this field.
It is intriguing to speculate in clinical settings whether atrial fibrillation itself, tachycardia (of any reason), or the combination of both leads to severely reduced left ventricular ejection fraction. Underlying cardiomyopathies, among others, could indeed predispose cardiomyocytes and other heart-resident cells to be more susceptible for left ventricular impairment under any of these conditions, in particular, in the presence of any tachycardia or AF alone.
We observed no significant differences in patients with AF compared with patients with other tachycardic arrhythmias in our patient cohort. However, our study describes a group of patients with severely impaired left ventricular function and pronounced heart failure symptoms, compared with the almost untainted study cohort described in the analysis of Dr. Wijesurendra and colleagues. In this context, differences regarding left ventricular dysfunction resulting from AF alone might be below the detection threshold, especially in a patient cohort in which severe ventricular dysfunction is present. Highly sophisticated analytical tools that gather evidence about the energetic changes within the myocardium, as used by Dr. Wijesurendra and colleagues (1), could prove beneficial for detecting occult or clinically inapparent cardiomyopathies. In our opinion, it might also be possible to detect such subtle cardiomyopathies in endomyocardial specimens by using novel bioptic and analytic tools such as site-directed sampling or gene expression profiling (2).
The focus of our study was to further characterize tachycardia-induced cardiomyopathy in patients with symptomatic heart failure and left ventricular impairment. We have demonstrated relevant inflammation, fibrosis, and changes in apoptosis, which could lead to irreversible damage. To date, little is known about the (complete) reversibility of cardiomyopathies and their underlying mechanisms. Thus, the absence of a complete normalization of left ventricular function arguments is not against the fact that arrhythmia alone could be the cause of cardiomyopathy and heart failure. In our opinion, the data of Dr. Wijesurendra and colleagues do not establish a clear causative relationship between a postulated underlying occult cardiomyopathy inducing atrial fibrillation or atrial fibrillation inducing (ir)reversible changes in left ventricular metabolism.
We postulate that precise diagnostic criteria are of fundamental importance for developing adequate treatment strategies for different patient subgroups, which could be of interest in AF therapy; in particular, identifying subjects more likely to benefit from rhythm control and subjects at high risk to develop progressive heart failure is of vital interest. Our study helps to identify patients with symptomatic heart failure in which tachycardia is the cause of the impaired left ventricular function, especially in difficult cases (3). For the detection of mild or clinically inapparent cardiomyopathies induced by rhythm disturbances, further studies using highly sophisticated analytical tools involving endomyocardial biopsies and distinct myocardial imaging are needed.
Please note: The original study was supported by the Deutsche Forschungsgemeinschaft, the Tuebingen Platelet Investigative Consortium (TuePIC), the TUEFF Frauenfoerderungsprogramm of the University of Tuebingen (Dr. Mueller), and Sonderlinie Medizin BW (Dr. Seizer). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
- Wijesurendra R.S.,
- Liu A.,
- Eichhorn C.,
- et al.
- Elliott P.