Register
Community
Overview
Experts
Editors
Fellows
Code of conduct
Company
About Us
FAQs
Privacy Policy
Terms of Use
Careers
Programs
News
News Releases
Press Coverage
Publications
Blog
Contact Us
Sign in
Topics:
Cardiology
•
Preventive Cardiology
When would you consider adding an SGLT2 inhibitor, MRA, and/or ARNI (in lieu of ACE inhibitor or ARB) when discharging patients following revascularization for acute MI with newly reduced LV systolic function?
Related Questions
Should low-intensity statins be favored to minimize the risk of diabetes onset while still offering cardiovascular benefit for patients with prediabetes where a statin is indicated?
What is your approach to prescribing GLP-1 agonists for patients who would otherwise have CV benefits from this therapy, but who also have co-morbid GI problems such as Barrett's esophagus, severe GERD?
With the recent trials such as SELECT and STEP-HFpEF demonstrating benefits of GLP1-agonists in terms of CV risk reduction and improved exercise function, have you begun to incorporate this class of medications into routine CV health maintenance for patients with HFpEF and/or pre-existing CAD?
Is there a role of prophylactic aspirin in patients with incidental findings of aortic atherosclerosis but no history CAD or CVA?
What other considerations for hyperlipidemia management would you have for a patient with multiple prior PCIs whose LDL remains above goal on high intensity statin, ezetimibe, and evolocumab (assuming compliant with medications)?
What are your top takeaways from ACC 2024?
Would you consider opting for beta blocker withdrawal to improve exercise capacity in patients with heart failure with preserved ejection fraction and chronotropic incompetence?
Are there any ongoing clinical trials related to endothelial dysfunction and accelerated or premature CAD that patients might be able to enroll in nationwide?
How does the TACTiC trial's success with a web app for statin self-management influence your stance on nonprescription statins for primary prevention amidst statin underuse?
What would be your approach to working up possible autoimmune/coagulopathic etiologies for accelerated, rapidly progressive CAD in spite of medical therapy compliance?