In the first presentation, Prof. Paulus from Amsterdam (NL) questioned the reality of an adapted hypertrophy of the left ventricle. He showed clearly that at least 3 factors influence the evolution of hypertrophy to heart failure: the intensity of the stimulus with its speed of progression, the nature of the stimulus that may activate different genes and the characteristics of the recipient with, for example, the existence of a diabetes and gender differences.
These were discussed in detail in the ensuing talk by Prof. Regitz-Zagrosek from Berlin (Germany). She reminded the audience that apoptosis is present in old men but not in old women and the Euro Heart survey showed that heart failure is mostly of systolic origin in men and diastolic in women. The differences in response to ventricular overload may be due to the presence of X and Y chromosomes or to oestrogen receptors she studied.
Prof. Tarone from Turin (Italy) presented a sum of results from his laboratory concerning a protein, melusin, which is connected to integrins and senses the mechanical load. The demonstration of the role of melusin is shown by melusin knock-out mice which have a blunted response to aortic stenosis and develop a rapid cardiac dilatation . In contrast, melusin overexpressing mice maintain a normal ventricular function for a long time after aortic banding.
In the final presentation, Dr. Hilifiker-Kleiner from Hannover (Germany) presented her data evaluating the cellular pathways that lead to angiogenesis during the development of ventricular hypertrophy. She clearly showed that the intracellular pathways that induce angiogenesis are not the same as those that maintain it during the development of hypertrophy.
Conclusion
The classical evolution from an adaptive to a non-adaptive hypertrophy leading to heart failure is probably a too simplistic scheme since so many different factors contribute to the development of hypertrophy and no single index allows the prediction of the outcome of hypertrophy.
The content of this article reflects the personal opinion of the
author/s and is not necessarily the official position of the
European Society of Cardiology.