Radcliffe Cardiology presents a selection of 60 second insights addressing current trends and opinion on the most recent advances in the field of cardiology by industry experts.
1. Are further studies needed?2. How will CABANA change your practice?3. What was the biggest weakness of CABANA?4. What was the biggest strength of CABANA?5. Why do you think CABANA misses its primary endpoint?6. Should we stop catheter ablation after CABANA?7. Can you describe CABANA in your own words?
Chronic Total Occlusions (CTO)
1. Are CTOs important to the management of angina in your patients?2. What trials are needed to advance the CTO field?3. What is your preferred imaging modality for CTOs?4. What is your preferred CTO wire strategy, and why?5. What is the biggest advance in CTO treatment in the past 5 years?6. What devices should be developed to further advance CTO management?7. The data for CTO is mixed, with clinical trials showing no clear benefit, should we keep on doing CTO's?8. Retrograde or anterograde? What is your preferred strategy?9. How would you recommend someone starts a CTO program?
1. Do you have a preferred strategy for patients with AF on OACs post-PCI?2. What factors do you consider when assessing when to switch?3. Which scenarios would you use I.V. antiplatelet such as cangrelor?4. Which scenarios do you typically use prasugrel +ASA?5. Which scenarios do you typically use clopidogrel +ASA?6. Which scenarios do you typically use ticagrelor +ASA?7. Do you have a preferred stent and does this alter the DAPT approach?8. Do you have a preferred approach to DAPT dosage and duration for ACS patients undergoing PCI?9. Do you have a preferred approach to DAPT dosage and duration for stable patients undergoing PCI?10. What are the major risk factors that should be considered before initiating DAPT in stable patients?
1. Describe the Define-FLAIR study in your own words?2. How has Define-FLAIR affected your clinical practice?3. Can you describe the DEFINE-FLAIR study in your own words?4. Are you surprised that DEFINE-FLAIR showed that iFR was non-inferior to FFR?5. After the results of Define-FLAIR should we stop using FFR?6. What is the biggest weakness to Define-FLAIR?7. What is the biggest strength to Define-FLAIR?8. Is there a need for further studies?9. How important is cost-effectiveness in your current clinical practice?
1. What can be done with physiologic guidance vs physiologic spot measurement?2. In what kind of scenarios would residual ischaemia be addressable or not?3. How does residual ischaemia impact the healthcare system?4. What has been your experience with tools like iFR co-registration?5. What's next in the research pipeline?6. How will it change your clinical practice?7. What were the key findings from DEFINE-PCI8. Do you think the broader interventional community believes post-PCI ischaemia is a real problem?9. How is DEFINE PCI different from earlier post-PCI ischaemia studies?10. Why was DEFINE PCI done, is there precedent for post-PCI ischaemia?11. What would be surprising to see from DEFINE PCI?12. What do we hope DEFINE PCI will shed light on?
1. What are the challeges of DOACs and are alternatives needed?2. What factors influence your choice of DOAC?3. Do you have a DOAC you prescribe more frequently?4. What are the most important anticoagulation clinical trials?5. Do you have a DOAC of choice?6. How important are reversal agents?7. Are you once-daily or twice-daily?8. Is RCT or real-world data more important to you?
1. What is the future for LAA closure?2. What is your measure of procedural/follow-up success?3. What is your anticoagulant regime for LAA?4. How would you advise someone to set up a LAA closure program?5. Do you use imaging? If so, What Imaging?6. What is your favourite LAA closure device, and why?7. Is there ever a need for a surgical LAA closure?8. What is the trial evidence to support the use of LAA closure devices?9. In which cases do you perform LAA closure?
1. Which emerging compounds show the most promise in reducing LDL?2. What is required for PCSK9s to get wider spread adoption?3. How important is inflammation in atherosclerosis?4. Are statins over (or under) prescribed?5. Is cholesterol being managed sub- optimally? If so, what needs to improve?6. How low should LDL go?7. Is HDL good cholesterol?8. What is the greatest unmet need in lipid management?
Multi-vessel disease (MVD)
1. How do manage patients with multi-vessel disease during PPCI?2. Do you think we should be doing multi-vessel revascularisation instead of CABG? If so, in which cases?3. Do you prefer Clopidogrel, Ticagrelor or Prasugrel?4. Do you have any concerns giving adenosine during PPCI or would your prefer and adenosine-free technique?5. Do you believe registry (i.e. culprit only) or RCT data (treat all vessels)?6. Do you believe coronary physiology has a role in non-culprit PPCI decision-making?7. Are you using G2B3A inhibitors like ReoPro?8. Are you using Bivalirudin or Heparin?9. What trials best support the use of MVD PCI?10. Should we balloon acutely and then returning to stent the following morning?11. Should PPCI be performed at large surgical centres only?
Optical Coherence Tomography (OCT)
1. Do you think the role of OCT has diminished following the withdrawal of BVS?2. What tips would you give for administering contrast?3. What is the most important trial to support the use of OCT?4. What disadvantages do you think OCT offers over other imaging modalities?5. What cases would you use OCT in?6. What cases would you not use OCT in?7. What advantages do you think OCT offers over other imaging modalities?8. Should we trust dimensions from OCT or IVUS, and why?
1. Is there a need for further studies?2. After the results of ORBITA should we stop stenting?3. Can you describe the ORBITA study in your own words4. Why do you think that ORBITA failed to show a significant improvement in exercise capacity post PCI?5. What was the biggest weakness of ORBITA?6. What is the biggest strength of ORBITA?7. How has ORBITA affected your clinical practice?
1. Do you use imaging? If so, What Imaging (ICE/TTE)?2. What is your measure of procedural/follow-up success?3. What is your favourite PFO closure device, and why?4. What is your anticoagulant regime for PFO?5. What is the trial evidence to support the use of PFO closure devices?6. Is there ever a need for a surgical PFO closure?7. In which cases do you perform PFO closure?8. How would you advise someone to set up a PFO closure program?
1. Thinking about patient preference, what role does RDN have in blood pressure control?2. What role do you see for renal denervation in control of blood pressure in your patients?3. Where does renal denervation fit in your current clinical practice?4. What are the biggest barriers to blood pressure control in your patients?5. Which patient groups are most receptive to RDN?6. What is needed to get widespread adoption into clinical practice?7. How have SPYRAL HTN-OFF and SPYRAL HTN-ON studies influenced your clinical practice?8. Thinking about the SPYRAL HTN-OFF and SPYRAL HTN-ON studies, what are the take-home messages for you?9. Thinking about the SPYRAL HTN-OFF and SPYRAL HTN-ON studies, for you, what are the key results?10. Can you give an overview of the RDN SPYRAL clinical trial program?11. Thinking about compliance, what are the advantages of RDN over pharmacological therapy?12. How does renal denervation work?13. Does renal denervation work?
1. Do you think it is necessary to perform coronary revascularisation pre-TAVR? Do you use FFR/iFR decision-making?2. Are we ready to be doing TAVR in low risk patients?3. Which patients are you performing TAVR in now (High/Medium risk)?4. Which is your preferred valve, and why?5. How would you recommend someone start a TAVR program?6. What is the most important clinical trial data and why?7. What is the biggest innovation in TAVR over the past 12-24 months?8. What proportion of your patients have a TAVR rather than and surgical AVR?