Dr RR Baliga's Internal Medicine Podkasts for Physicians: GOT KNOWLEDGE DOC Podkasts about Long-Term Risk of HF with Chemotherapy with Trastuzumab

Long-Term Risk of Heart Failure in Breast Cancer Patients After Adjuvant Chemotherapy With or Without Trastuzumab. JACC Heart Fail 2019;7:217-224.

Not Medical Advice or Opinion

Why Combination Lipid-Lowering Therapy Should be Considered Early in the Treatment of Elevated LDL-C For CV Risk Reduction Mini G Varughese, MD; Matthew Deshotels, MD; Christie M. Ballantyne, MD, FACC

Long-Term Evolocumab in Patients with Established Atherosclerotic Cardiovascular Disease

With Chiara Bucciarelli-Ducci, Bristol Heart Institute, Bristol - United Kingdom, Leslie Cooper, Mayo Clinic, Jacksonville - USA & Matthias Friedrich McGill University Health Centre, Montreal - Canada.

Link to paper

Link to editorial

In this special meeting edition of the Cardiocast, MDedge Cardiology editor Catherine Hackett is joined by MDedge reporters Mitchel L. Zoler, Bruce Jancin, and Richard Mark Kirkner. 

The MDedge cardiology team reviews three big stories from the 2019 annual scientific sessions of the American Heart Association in Philadelphia. 

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Help us make this podcast better! Please take this short listener survey: https://www.surveymonkey.com/r/podcastsurveyOct2019

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ISCHEMIA trial hailed as practice changing

The results of the ISCHEMIA trial were emphatically declared practice changing by interventional cardiologists and noninterventionalists alike at the AHA meeting. 

Bruce Jancin discusses the story.

DAPA-HF: Dapagliflozin's HFrRF efficacy confirmed in nondiabetes

The results in nondiabetics from the practice-changing DAPA-HF trial gives clinicians strong evidence that the diabetes drug dapagliflozin is equally effective at reducing cardiovascular death and acute exacerbations in heart failure patients regardless of diabetes status. 

Mitchel L. Zoler discusses this report. 

Weakness exposed in valsartan recall

ED visits for hypertension in the month after the 2018 recall spiked 55%. The 2018 recall of generic forms of the antihypertensive drug valsartan exposed weaknesses in the recall systems for generics in both the U.S. and Canada that caused many patients who were on the drug to fall through the cracks. 

Richard Mark Kirkner goes deeper into this story. 

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For full coverage of AHA 2019 visit MDedge Cardiology

For more MDedge Podcasts, go to mdedge.com/podcasts

Email the show: podcasts@mdedge.com

Interact with us on Twitter: @MDedgeCardio

We introduce a brand new format with Jerome Dwyer, MD, brother of our host, Jim Dwyer, MD, for a new segment that we're calling 'Card Talk' where Dr. Jim and Dr. Jerry talk about the current clinical state of cardiology and take a peek into the future. 

This week in cardiology news:

• Survival at ‘overweight’ BMI surpasses ‘normal’
  Data from more than 142,000 middle-aged people worldwide show those with a BMI of 25-29 outlast those at 20-24.
• Visceral fat linked to sixfold increase in masked hypertension
  The body mass index trend was not significant.
  New class of drug safely halved LDL cholesterol in ORION-11
  Inclisiran potently cut LDL cholesterol by inhibiting the PCSK9 enzyme with biannual injections.

1. Statins crush early seizure risk poststroke
   Statin initiation upon hospitalization for acute ischemic stroke was linked to a major antiseizure benefit in a Japanese study.
2. Atherosclerotic disease risk persists after smoking cessation
   Clinicians should reinforce smoking cessation with awareness that risk for several atherosclerotic diseases remains significant for decades.
3. Air pollution levels correlated with cardiorespiratory mortality; reduced life expectancy
   Fine particulate matter pollution is associated with increased cardiorespiratory mortality, particularly in lower-income areas.
4. Exercise counters astronauts' dizziness after space flight
   Two hours of daily activity during space flight eliminated hypotension after landing. 

You can contact the MDedge Cardiocast by emailing us at podcasts@mdedge.com or following us on Twitter @MDedgeCardio

You can find more of our podcasts on our website at http://www.mdedge.com/podcasts.

This week in cardiology:

1. Novel cardiogenic shock, PCI protocol nets 72% acute survival
2. Energy drinks increase BP and disrupt the heart's electrical activity
3. Syncope during pregnancy increases risk for poor outcomes
4. Ethnicity seems to affect predisposition to components of metabolic syndrome

Find more podcasts from MDedge on our website: https://www.mdedge.com/podcasts

This week's top stories in cardiology:

1. Risk score developed for cardiac-device infection
2. AFib screening cuts hospitalizations and ED visits
3. Arsenic exposure increases risk of left ventricular hypertrophy
4. Ankylosing spondylitis patients taking COX-2 inhibitors may see fewer cardiovascular events

You can contact the show be emailing us at podcasts@mdedge.com and you can interact with us on Twitter at @MDedgeCardio

The MDedge Cardiology team is back this week for part II of their conversation on the 2018 annual scientific session of the American Heart Association. 

A new definition in myocardial infarction. Also today, aspirin and fish oil flap in patients with diabetes, CT angiography cuts MI in patients with stable chest pain, and rivaroxaban is no help for heart failure outcomes.

New data from an observational study show that breastfeeding was linked with a lower risk of stroke later in life. Also today, a new Valsalva maneuver is tops at converting supraventricular tachycardia to sinus rhythm, and a warning about the growing occurrence of finding about a key component of some artificial hearts

Alan Wu

This episode covers chapter 82 of Rosen's Emergency Medicine. Take a listen for all those juicy pericardial-pump-pearls!

1. List eight causes of pericarditis.
2. Describe typical pain of pericarditis, expected lab work abnormalities,
3. What is the typical sequence of ECG changes in pts with pericarditis? (the stages)
4. Describe the treatment of pericarditis associated with: Uremia, Neoplasm, and SLE
5. Outline the management of Dressler's syndrome.
6. What is the pathophysiology of cardiac tamponade? Describe the mechanism of hypotension in pericardial tamponade and list 4 expected findings on physical examination.
7. Describe the procedural steps in pericardiocentesis
8. List 4 causes of pneumopericardium and one specific PEX finding
9. List five causes of constrictive pericarditis.
10. What is the pathophysiology of purulent pericarditis?  List 5 organisms responsible for infectious pericarditis? How is it managed?
11. Describe the pathophysiology of hypertrophic cardiomyopathy
12. Describe the clinical exam and ECG findings associated with HCM
13. List 5 RFs for sudden death in HCM
14. A pt with known hypertrophic cardiomyopathy presents to the ED with acute cardiogenic pulmonary edema causing mild hypoxia.  What is the general approach to management in the ED?  Explain your choices.
15. List four causes of dilated cardiomyopathy.
16. Describe ECG findings of dilated cardiomyopathy
17. List 5 RFs for developing a dilated cardiomyopathy
18. In what time frame would one expect peripartum DCM?
19. List 5 causes of restrictive cardiomyopathy
20. List 8 common pathogens responsible for myocarditis, and 3 non-infectious causes of myocarditis
21. Describe the stages of viral myocarditis and the management at each stage

Wisecracks:

1. What are some functions of the pericardium?
2. What are Chagas Disease and Trichinosis, list bizz-buzz features for each?
3. What are the expected cardiac findings in Lyme disease and how is it treated?
4. How does sarcoid affect the heart?
5. Amyloidosis?

This episode covers chapter 82 of Rosen's Emergency Medicine. Take a listen for all those juicy pericardial-pump-pearls!

1. List eight causes of pericarditis.
2. Describe typical pain of pericarditis, expected lab work abnormalities,
3. What is the typical sequence of ECG changes in pts with pericarditis? (the stages)
4. Describe the treatment of pericarditis associated with: Uremia, Neoplasm, and SLE
5. Outline the management of Dressler's syndrome.
6. What is the pathophysiology of cardiac tamponade? Describe the mechanism of hypotension in pericardial tamponade and list 4 expected findings on physical examination.
7. Describe the procedural steps in pericardiocentesis
8. List 4 causes of pneumopericardium and one specific PEX finding
9. List five causes of constrictive pericarditis.
10. What is the pathophysiology of purulent pericarditis?  List 5 organisms responsible for infectious pericarditis? How is it managed?
11. Describe the pathophysiology of hypertrophic cardiomyopathy
12. Describe the clinical exam and ECG findings associated with HCM
13. List 5 RFs for sudden death in HCM
14. A pt with known hypertrophic cardiomyopathy presents to the ED with acute cardiogenic pulmonary edema causing mild hypoxia.  What is the general approach to management in the ED?  Explain your choices.
15. List four causes of dilated cardiomyopathy.
16. Describe ECG findings of dilated cardiomyopathy
17. List 5 RFs for developing a dilated cardiomyopathy
18. In what time frame would one expect peripartum DCM?
19. List 5 causes of restrictive cardiomyopathy
20. List 8 common pathogens responsible for myocarditis, and 3 non-infectious causes of myocarditis
21. Describe the stages of viral myocarditis and the management at each stage

Wisecracks:

1. What are some functions of the pericardium?
2. What are Chagas Disease and Trichinosis, list bizz-buzz features for each?
3. What are the expected cardiac findings in Lyme disease and how is it treated?
4. How does sarcoid affect the heart?
5. Amyloidosis?

Here is the follow-up to the mammoth ACS chapter. This one has some key factoids to put into your mind map / memory pallace / organic computer.

1. List Sgarbossa criteria for AMI in pre-existing LBBB
2. What is Takotsubo cardiomyopathy and how does it present?
3. Describe the kinetics of cardiac biomarkers (Troponins and CK)
4. List DDx for ↑ Troponin
5. What is the utility of CTA in the diagnosis of MI?
6. What is the role of ED-based chest pain centers?
7. List 3 phases of delay in the management of AMI; and describe the time-points in ED management of AMI.
8. What are door-to-needle and door-to-balloon timelines by AHA recommendations?
9. Describe the mechanism of action and indications/contraindications for
   1. Nitroglycerin
   2. Morphine
   3. BBlockers
   4. ACE-I
   5. Antiplatelet Therapies
   6. Anti-thrombins
10. Describe eligibility criteria for Fibrinolytics
11. List contraindications to Fibrinolytic therapy in MI
12. What is the utility of Rescue PCI and Facilitated PCI?
13. List 5 indications for Rescue PCI
14. Describe factors assisting with decision to utilize PCI or thrombolytics
15. In NSTEMI, who will benefit from an early invasive strategy of management?
    
    

Wise Cracks:

1. What is the HEART Score?
2. What is the management of ACS in the setting of recent cocaine use?
3. How is STEMI diagnosed in the setting of LBBB?
4. How is STEMI diagnosed in the setting of a ventricular pacemaker?
5. When should you be getting a 15 lead ECG?

Here is the follow-up to the mammoth ACS chapter. This one has some key factoids to put into your mind map / memory pallace / organic computer.

1. List Sgarbossa criteria for AMI in pre-existing LBBB
2. What is Takotsubo cardiomyopathy and how does it present?
3. Describe the kinetics of cardiac biomarkers (Troponins and CK)
4. List DDx for ↑ Troponin
5. What is the utility of CTA in the diagnosis of MI?
6. What is the role of ED-based chest pain centers?
7. List 3 phases of delay in the management of AMI; and describe the time-points in ED management of AMI.
8. What are door-to-needle and door-to-balloon timelines by AHA recommendations?
9. Describe the mechanism of action and indications/contraindications for
   1. Nitroglycerin
   2. Morphine
   3. BBlockers
   4. ACE-I
   5. Antiplatelet Therapies
   6. Anti-thrombins
10. Describe eligibility criteria for Fibrinolytics
11. List contraindications to Fibrinolytic therapy in MI
12. What is the utility of Rescue PCI and Facilitated PCI?
13. List 5 indications for Rescue PCI
14. Describe factors assisting with decision to utilize PCI or thrombolytics
15. In NSTEMI, who will benefit from an early invasive strategy of management?
    
    

Wise Cracks:

1. What is the HEART Score?
2. What is the management of ACS in the setting of recent cocaine use?
3. How is STEMI diagnosed in the setting of LBBB?
4. How is STEMI diagnosed in the setting of a ventricular pacemaker?
5. When should you be getting a 15 lead ECG?

Paul Young discusses remote ischaemic preconditioning and along he delves into the pitfalls of clinical research. 2016 was the 30th anniversary of ischaemic preconditioning. Remote ischaemic preconditioning is the magical offspring of ischaemic preconditioning and refers to the phenomenon whereby brief periods of ischaemia in one organ can protect other organs from subsequent prolonged ischaemic insults. Ischaemic preconditioning rose to prominence after a seminal paper in 1986 that demonstrated the protective effects of ischaemic preconditioning in dogs who had coronary ischaemia. This effect had been appreciated in humans. For instance, pre-infarct angina leads to smaller infarcts that in heart attacks without preceding angina. Remote preconditioning is for more magical. Paul takes you through the basics. The idea is simple enough. Blockage to one site leading to ischaemia preconditions another site to subsequent ischaemia. This was first demonstrated by blocking the circumflex artery in the first instance with a series of temporary occlusions. The left anterior descending was then blocked for a prolonged period. This preconditioned the heart to the prolonged ischaemia and decreased deleterious effects. This effect was then repeated with transient renal ischaemia protecting the heart from prolonged cardiac ischaemia. This effect was demonstrated with different organs – with almost any organ being able to protect another organ. The clinical application? Inflate a blood pressure cuff on an arm (to above systolic blood pressure) for five minutes and you will protect the opposite limb… or the heart. Remote ischaemic preconditioning is a reproducible phenomenon. However, as Paul explains, no one knows how it works. In this talk Paul describes his research – a double blind trial on remote ischaemic preconditioning; the first of its kind. He also describes a systematic review and meta-analysis he conducted. He found conflicting results in his trial and heterogeneity across other studies. When considering further research Paul concluded that it nothing was convincing and there were many pitfalls in the papers. What matters? What the patient can do, how they feel, whether they live and to a lesser extent does the intervention save money. In the end it seems that it is the relationship between ischaemia and reperfusion that makes a difference. That is, apply the remote ischaemic preconditioning after the primary ischaemia but before the reperfusion.

This has potential clinical implications for the following:

1. Heart surgery with cardiopulmonary bypass

2. Planned percutaneous coronary interventions

3. Acute myocardial infarction

4. CBA being treated with lysis or clot retrieval

5. Carotid endarterectomy surgery

6. Hypoxic ischaemic encephalopathy

7. Organ transplantation

8. abdominal aortic aneurysm surgery While this technique is not yet ready for clinical application, it remains an exciting potential therapeutic modality for the future. Finally, Paul finished with his top tips. Don’t believe single centre studies, consider biological plausibility, be sceptical about secondary endpoints and don’t be misled by surrogate endpoints.

For more like this, head to https://codachange.org/podcasts/ 

This week on Humerus Hacks, Dr Bridget is back! In a heart stopping episode about arterial traffic, when the beat trops and all things AMI. 

Combined testing of high-sensitivity cardiac troponin T (hs-cTnT) and copeptin at presentation provides a very high—although still imperfect—negative predictive value (NPV) for the early rule-out of acute myocardial infarction (AMI). We hypothesized that a second copeptin measurement at 1 h might further increase the NPV.

Early detection of acute myocardial infarction is crucial for deciding the course of treatment to preserve and prevent further damage to the myocardial tissue. During the last several years there has been a burgeoning interest in circulating microRNAs as potential novel biomarkers for acute myocardial infarction.