European Heart Journal Advance Access originally published online on January 4, 2008
European Heart Journal 2008 29(4):565; doi:10.1093/eurheartj/ehm591
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Diabetic cardiomyopathy: a controversial entity: reply
Department of Coronary Disease
Jagiellonian University School of Medicine
ul. Pradnicka 80
Krakow 31-202
Poland
Department of Coronary Disease
Jagiellonian University School of Medicine
ul. Pradnicka 80
Krakow 31-202, Poland
Department of Coronary Disease
Institute of Cardiology
Jagiellonian University School of Medicine
John Paul II Hospital
ul. Pradnicka 80
Krakow 31-202
Poland
E-mail address: prostoff{at}vp.pl
Department of Metabolic Diseases
Jagiellonian University School of Medicine
Krakow
Poland
Department of Pathology
The John Paul II Hospital
Krakow
Poland
Department of Coronary Disease
Jagiellonian University School of Medicine
ul. Pradnicka 80
Krakow 31-202
Poland
We are most grateful to Dr Karamitsos et al. for showing such an avid interest in our paper.1 Upon its submission, we were acutely aware that we might well shake things up, as prior to confronting the actual study results we also used to support the notion of diabetic cardiomyopathy (DC). By way of addressing some of Dr Karamitsos's queries,2 let me point out that our results were clearly owed to rather stringent inclusion criteria; a prerequisite condition for diagnosing/ruling out DC. All patients with microalbuminuria (with both normal and abnormal renal function) were excluded from the study due to arterial hypertension (AH), for fear of causing an undue bias.
Neither the diabetics nor the controls were at the time on any medication affecting the serum level of NT-proBNP and diastolic function. Finding patients with long-term diabetes without concomitant medications proved rather challenging and so an adequately sized population took 3 years to assemble. Presently, most of them remain on ACE-inhibitors or ARAs, with a view to retarding microalbuminuria.
A vast majority of echocardiographic parameters for the estimation of diastolic function (apart from those used specifically for diagnosing the restriction) is of little specificity and of rather dubious value in terms of adequately reflecting the left ventricular end-diastolic pressure. In our view, the best marker is actually the E/E' ratio correlating with the left ventricle end-diastolic pressure. Importantly, according to the recently published ESC consensus document,3 ventriculography is not recommended at all, as a diagnostic tool for diastolic dysfunction.
In assessing our study population, we used diverse echocardiographic techniques, as well as the serum level of NT-proBNP (biochemical marker), in line with applicable guidelines. Furthermore, not only were the structural changes observed by ourselves in the histological samples found non-compliant with the criteria for specific cardiomyopathy recognition, but they also clearly proved heart non-specific, being routinely encountered in other organs in diabetics. It might well be, their incidence alone does not seem to be of sufficient haemodynamic significance to promote diastolic dysfunction (unless AH or coronary heart disease should also enter into the equation).
In our study (despite long-term diabetes, frequent retinopathy, and cardiac autonomic neuropathy), we did not observe any differences in echocardiographic parameters between diabetics and the controls. On the other hand, we tentatively hypothesized that the results of other studies conducted on much smaller populations may actually have been impacted by the influence of exogenous insulin (in different dosages) on vascular resistance; the speculative character of this hypothesis notwithstanding.
It should nevertheless be noted at this juncture that even if echocardiographic parameters in a particular population (i.e. diabetics here) should remain well within normal values, while differing slightly from another population (i.e. the actual basis for diagnosing DC in the reports to date), this gives no grounds whatsoever for diagnosing diastolic dysfunction, let alone contravening applicable guidelines.
We might then have to resign ourselves with Dr Karamitsos to accepting, even if reluctantly so, there is in fact no mystery about DC.
References
- Konduracka E, Gackowski A, Rostoff P, Galicka-Latala D, Frasik W, Piwowarska W. Diabetes-specific cardiomyopathy in type 1 diabetes mellitus: no evidence for its occurrence in the era of intensive insulin therapy. Eur Heart J (2007) 28:2465–2471.
[Abstract/Free Full Text] - Karamitsos TD, Tsapas A, Arnold JR. Diabetic cardiomyopathy: a controversial entity. Eur Heart J (2008) 29:564.
[Free Full Text] - Paulus WJ, Tschöpe C, Sanderson JE, Rusconi C, Flachskampf FA, Rademakers FE, Marino P, Smiseth OA, De Keulenaer G, Leite-Moreira AF, Borbély A, Edes I, Handoko ML, Heymans S, Pezzali N, Pieske B, Dickstein K, Fraser AG, Brutsaert DL. How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J (2007) 28:2539–2550.
[Abstract/Free Full Text]
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