Meet the ESC Gold Medallists: Professor Peter J. Schwartz
31 Aug 2024
ESC Gold Medallist With over half a century of research to his name, Professor Peter J. Schwartz (Istituto Auxologico Italiano IRCCS - Milan, Italy) is a world-leading expert in the relationship between the autonomic nervous system and life-threatening cardiac conditions, especially long-QT syndrome (LQTS), an area in which his work has revolutionised patient care.
What inspired you to specialise in cardiology research?
Probably it was the chance event of having started to work as a medical student in a department that was a world-leading place for studies on the autonomic nervous system. This was exciting and stimulating. In the morning, I was treating patients and in the afternoon, I was recording the activity of single fibres in the cardiac nerves of cats. This double culture – with the patients providing the questions and the laboratory offering the answers – was fundamental for my approach to always link clinical issues to basic science.
What are your main career achievements to date?
Having worked on LQTS since 1971 when very little was known, the list is not short. In 1975, as a 32-year-old ‘rookie’ writing my first review article on LQTS, I boldly stated that beta-blockers were the choice of therapy.1 Everyone knows that today, but 50 years ago there had been great uncertainty about how to treat these patients. In 1979, with Arthur Moss at the University of Rochester Medical Center, USA, we created the International Registry for LQTS, then thought to be a rare disease, although we now know it affects at least 1 in 2,000 persons. The registry has since provided ground-breaking data on the natural history of the disease and its response to therapy. Crucially, two decades since it was first established, it provided molecular biologists with the large pedigrees of clearly affected and unaffected individuals that were essential for the discovery of the first genes associated with the syndrome. It was also in the late 1970s that, with a series of experimental studies, I provided the rationale for the use of left cardiac sympathetic denervation for high-risk LQTS patients.2 This surgical approach has since become a key tool for therapy, used in leading centres around the world to reduce the need for an implantable cardioverter defibrillator (ICD).
In 1995, following the discovery of the first LQTS genes, with my group I introduced the concept of gene-specific therapy, using the sodium channel blocker mexiletine, which has become a standard treatment for LQT3 patients.3 Some years later, in 2001, I documented that there was a genotype–phenotype correlation specific for the triggers of the life-threatening arrhythmias, and this resulted in the first recommendations for gene-specific management to complement traditional therapy for the different types of LQTS.4 For example, it became clear that loud noises in the early morning were creating a major risk for LQT2 patients, whereas LQT1 patients were at greater risk during physical or emotional stress and while swimming.
What are you working on at the moment?
During the last 20 years, my work has focused on the study of modifier genes, common genetic variants that can influence the risk of developing a cardiac arrest in patients with LQTS. We are currently trying to understand how protective variants work so that we can exploit this mechanism of action in the search for new therapies. Another key area for me is to raise awareness about the value of conservatively treating patients with LQTS. Our experience shows that the overwhelming majority of patients – if assessed on a yearly basis to optimise therapy5 – can safely and effectively be protected using the treatments that we already have and that ICDs, which can impact in a negative way on quality of life, are seldom required.
“Research is competitive and demanding. Taking the middle ground is not worth it – don't be shy, aim high!”
References
- Schwartz PJ, et al. Am Heart J. 1975;89:378–390.
- Schwartz PJ, et al. Am J Cardiol. 1976;37:1034–1040.
- Schwartz PJ, et al. Circulation. 1995;92:3381–3386.
- Schwartz PJ, et al. Circulation. 2001;103:89–95.
- Dusi V, et al. Eur Heart J. 2024;45:2647–2656.
