[Precision medicine enhances personalized medicine in cardiology]. / Präzisionsmedizin vertieft die personalisierte Medizin in der Kardiologie.

Personalized medicine and precision medicine, frequently used synonymously, shall be clearly differentiated. Accordingly, personalization in cardiac medicine is based on the clinical presentation of a patient, as well as his/her cardiovascular risk factors and comorbidities, electrocardiography, imaging, and biomarkers for myocardial load and ischemia. Personalization is based on large clinical trials with detailed subgroup analyses and is practiced on the basis of guidelines. Further in depth personalization is achieved by precision medicine, which is based on innovative imaging for myocardial structure, coronary morphology, and electrophysiology. From the clinical perspective, genome analyses are relevant for comparatively rare monogenetic cardiovascular diseases. While these as well as transcriptome and metabolome analyses play a significant role in cardiovascular research with great translation potential, they have not yet been broadly introduced in the diagnosis, prevention, and treatment of complex cardiovascular diseases. Furthermore, digital technologies have considerable potential in cardiovascular precision medicine. On the one hand, this is based on the frequency of the diseases with the availability of Big Data and, on the other hand, on the availability of bio-signals and sensors of those signals in cardiovascular diseases.

Effects of different proton pump inhibitors on cardiac contractility in isolated human failing myocardium.

AIM: Proton pump inhibitors (PPI), e.g. pantoprazole (PP), esomeprazole (EP) and omeprazole (OP), work as anti-ulcer/gastrointestinal reflux drugs. Also, they are widely used in postoperative care of patients in cardiac surgery to prevent upper gastrointestinal bleeding. Therefore, in western industrial countries they play a major economic role, representing one of the most important drugs in open heart cardiac surgery. METHODS: Intact muscle strips (n=32) were isolated from the right ventricle wall of failing human hearts. In four different groups (PP, EP, OP, control group, each n=8), force amplitudes were recorded at a frequency of 60 beats per minute (bpm) with increasing PPI concentrations (0 to 320 µm/mL). RESULTS: In isometrically contracting muscle strips, significant negative inotropic effects were observed in the presence of all three PPI-groups (PP, EP and OP) with doses of 2.5 µg/mL and higher compared to the control group (p < 0.05 each). With high doses (320 µm/mL), force amplitudes could be almost completely depressed. The half maximal inhibitory concentration (IC50) for EP was 35.7 (confidence interval: 17.3-73.6) vs. OP 29.3 (6.8-126.6) vs. PP 25.1 (14.6-43.1) µg/mL (n.s.). No significant differences were found between the different proton pump inhibitors (PP, EP, OP) throughout the range of all concentrations. Relaxation was impaired in all PPI subgroups with prolonged time to 90% relaxation (RT90%) and maximum relaxation velocity (­df/dt) was reduced, too. These effects were partially reversible after wash-out of the drugs. CONCLUSION: We conclude that proton pump inhibitors show significant negative inotropic effects on isolated human failing myocardium. There is no apparent difference seen in the magnitude of the effects of each PPI-group. Further, in-vivo investigations are necessary to reveal the clinical evidence of PPI's negative inotropic effects, e.g. in cardio-surgical patients with heart failure.