Category Archives: Cardiovascular Medicine

Moffitt Pearls 6.20.2017 – Cardiology Report – MINOCA and Heart Failure

Thank you to Caroline for presenting a diagnostic mystery in Cardiology report. She presented a middle aged woman born in Russia presenting with progressive shortness of breath, PND and orthopnea found to have new heart failure. Despite some mild evidence of wall motion abnormalities and an EF of 35% she had nonobstructive CAD on diagnostic ! We discussed the possibilities which include microvascualr disease and Takotsubo cardiomyopathy which both fall under the bucket category known as MINOCA or Myocardial infarction with nonobstructive coronary arteries (see article below)!!



  1. Approach to new heart failure starts with 2 broad categories: ischemic vs. non-ischemic.
    1. Top 4 causes of heart failure include the following: 1) CAD 2) HTN 3) Valve disease 4) Toxin/EtoH
  2. Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a large bucket term that includes many diagnoses: Coronary spasm, coronary, microvascular dysfunction,
    1. Occurs in as many as 10% of patients and represents a condundrum because the underlying cause of their MI is not immediately apparent.
    2. Further work-up for these patient include cardiac MR

 Approach to new heart failure:

  • Ischemic (40% of new heart failure in older series)
    • CAD
    • bridge
  • Nonischemic
    • HTN (11% of new heart failure)
    • Toxic: EtOH, cocaine, other stimulants (up to 5% – though EtOH probably under-recognized as much HTN heart disease may be explained by chronic EtOH use as well)
    • Other meds: classically doxirubicin
    • Valvular (12% of new heart failure): AR, AS, MR
    • Infiltrative: sarcoid, amyloid, hemochromatosis
    • Infectious: post-myocarditis (often viral) up to 10% of cases, Chagas, HIV (4%)
    • Arrhythmia: tachycardia-mediated
    • High output:
      • Anemia
      • Hyperthyroidism
      • Beriberi
      • AV fistulas
        • Congenital: hepatic hemangiomas, HHT
        • Acquired: ESRD
      • Paget’s disease
      • Pregnancy
    • Post-partum Cardiomyopathy
    • Hypothyroidism
    • Stress-induced
    • Untreated OSA
    • Connective Tissue Disease
    • Idiopathic – in some series up to 50% of cases!

Another approach to the etiology of heart failure is by classification of cardiomyopathy as seen on TTE:

  • Hypertrophic cardiomyopathy
  • Dilated cardiomyopathy
  • Restrictive cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy
  • Left ventricular noncompaction

Common First Pass Assessment of New Heart Failure:

  • History – special focus on HF symptoms, arrhythmias, presyncope, syncope, family history
  • Physical Exam – special attention to cardiac and skeletal muscle
  • TTE, ECG
  • Labs: CBC, BMP, LFTs, TSH, HIV, Utox, iron studies
  • Risk assessment: lipid profile, diabetes screen
  • Evaluation for ischemia – coronary angiography

Second Pass for New Heart Failure (often guided by findings noted in first pass):

  • Further evaluation for arrhythmia: Event monitor
  • Advanced imaging: Stress TTE (to assess for increased LVOT gradient in the setting of increased cardiac output), Perfusion scan, Cardiac MRI

MINOCA or Myocardial infarction with nonobstructive coronary arteries

Definition: Presence of acute myocardial infarction in the absence of CAD > 50%

Prevalence: A recent systemic review of the published literature using a < 50% stenosis threshold for MINOCA reported a prevalence of 6% (Pasupathy S, Air T, Dreyer RP, et al. Systematic review of patients presenting with suspected myocardial infarction and nonobstructive coronary arteries. Circulation 2015;131:861–70.)

Although there are diagnostic criteria, this should NOT be considered a final diagnosis, but a ‘working’ diagnosis that incudes the following aetiologies:


Further Evaluation: Cardiac MRI should be the initial diagnostic study to identify the underlying cause of MINOCA. In as many as 87% of patients with MINOCA a diagnosis is made with cardiac MR.

European Cardiology Article outlining MINOCA:


Moffitt Pearls 6.6.17 – Chest Pain s/p CABG

Thank you to Satvik for sharing a great case of an elderly man w/ multiple co-morbities s/p CABG (several years prior) presenting with chest pain and hypertensive emergency. We discussed the management of HTN emergency and how to approach chest pain in a patient s/p CABG. We loved the lively discussion so thank you everyone for your participation!

Key Learning Points

Causes of chest pain in pt w/ hx of CABG vary by time

  • Recurrent angina during the early postoperative period is usually due to a technical problem with a graft or with early graft closure. This is indication for prompt coronary angiography with percutaneous coronary intervention (PCI), if feasible.
  • Recurrent angina after the first few months and beyond, called late recurrent angina, can occur with the development of stenosis in a bypass graft (either saphenous vein or arterial) or with progression of atherosclerosis in non-bypassed vessels.

Ashman’s Phenomenon

  • Functional right bundle branch block (RBBB) in atrial fibrillation occurring in the short cycle following a preceding long cycle that lengthened the refractory period in the right bundle branch (the Ashman phenomenon).




Moffitt Morning Report Pearls 6/2/17 – PEA + ARDS

Hello Moffitt!

Thanks for welcoming us to our first Morning Report! And a special thanks to Salman for presenting a great case of an older woman found down at home with asystole who developed shock and refractory hypoxemia.


Top Pearls:

  1. Causes of PEA include both cardiac and non-cardiac etiologies. In women and non-whites, the non-cardiac etiologies, such as SAH and massive PE, are more common! (see more below)
  2. Some centers are using esophageal balloon catheters to estimate pleural pressures and guide PEEP therapy (see attached NEJM reference)!
  3. Therapeutic strategies with treating refractory hypoxemia include the 6 Ps:
  • Higher PEEP
  • lung Protective ventilation
  • Paralytics
  • Prostacylcins
  • Proning
  • P-ECMO (A-V)


For those who want more info:

  1. Satvik Ramakrishna presented a fantastic R3 Talk on Thursday about redefining sudden cardiac death (SCD) using insights from the San Francisco POST SCD Study. Working with Dr. Zian Tseng, UCSF researchers used comprehensive autopsy data to determine the cause of death of nearly all out of hospital “sudden deaths” in San Francisco during a 3 year period. The group found that while under previous definitions, 80% of the nearly 5000 deaths would have been classified as SCD, including autopsy information reduced this proportion to 56%! They also found important disparities based on gender and race. Publication soon to come!
  2. Esophageal pressures to manage PEEP: NEJM RCT comparing MV directed by esophageal-pressure measurements with that according to ARDSNet recommendations. This study demonstrated the feasibility of using repeated measurements of esophageal pressures to determine the transpulmonary pressures and make timely adjustments to PEEP. Patients with ARDS in the esophageal pressure arm had improved oxygenation based on the P:F ratio and improved respiratory-system compliance. The researchers found that the 28 day mortality was lower among the patients with esophageal-pressure-guided MV, however, mortality at 180 days was the not different between the two groups.
  3. The supportive strategies that have shown mortality benefits for patients with ARDS include lung protective ventilation (pioneered here at UCSF!), early neuromuscular blockade and prone positioning. Prostacyclines, recruitment maneuvers, and ECMO are all used and can improve oxygenation, but a mortality benefit has not been shown. Each of the ground-breaking papers that showed mortality benefits for ARDS supportive therapies are below!


Talmor et al. Mechanical ventilation guided by esophageal pressure in acute lung injury.

ARDS-net. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.

Papazian L, et al. Neuromuscular blockers in early acute respiratory distress syndrome.


Guerin et al. Prone positioning in severe acute respiratory distress syndrome.



Have a great weekend!

Your super sweet Moffitt chiefs – DKA

MOFFITT CARDIOLOGY REPORT PEARLS 5/30/17: Non-Cardiac Surgery after DES-PCI!

Hey Everyone! Thanks to James for sharing the case of a middle-aged man on DAPT after an NSTEMI who required amputation for chronic osteomyelitis. We discussed several issues around DAPT and surgery. Pearls below!


Top Pearls:

  1. Up to 34% of patients undergoing DES-PCI will need non-cardiac surgery within 12 months after stent placement!
  2. Current guidelines strongly advise against performing non-cardiac surgery < 3 months after DES-PCI and recommending delaying past 6-12 months if possible.
  3. In a recent observational study, the increased risk of cardiac and all-cause mortality after surgery only held true if surgery was performed <1 month after DES-PCI, suggesting that non-cardiac surgery might be safe as soon as 1 month after DES-PCI.


For those who want more info:

5-34% of patients undergoing DES-PCI will need non-cardiac surgery within 12 months after stent placement. (JACC 2016;68:2633-6).

Current U.S. guidelines recommend delaying non-cardiac surgery for 12 months after DES-PCI, but state surgery may be considered within 3-6 months (with discontinuation of DAPT) if the risk of surgical delay exceeds that of stent thrombosis. The guidelines strongly advise against surgery < 3 months after DES-PCI (ACC/AHA guidelines, JACC 2016;68:1082-115).

Here’s a recent study arguing that surgery could be considered sooner than current guidelines recommend:

*Ergholm G et al, Risk associated with surgery within 12 months after coronary DES implantation, JACC 2016;68:2622-32.

Summary: Observational study of 4,303 Danish patients who underwent DES-PCI followed by surgery within 12 months, compared to 20,232 controls undergoing similar surgical procedures. Patients requiring surgery after DES-PCI had increased risk of MI, cardiac death, and all-cause mortality compared to controls, but the increased risk in this study was only present within the first month after DES-PCI, suggesting that surgery might be undertaken earlier than currently recommended.

Central figure from article: Only patients who had a time from PCI to surgery of < 1 month had significantly increased MI, cardiac death, and all-cause mortality at 30 days after surgery compared to controls.


Conclusion: The authors conclude that non-cardiac surgery could be considered as soon as 1 month after DES-PCI. An accompanying article ( notes that data from a single registry may not be sufficient to change guidelines, but this study does provide data to support the safety of truly necessary non-cardiac surgery performed earlier than current guidelines recommend.



Egholm G et al, Risk associated with surgery within 12 months after coronary drug-eluting stent implantation. JACC 2016;68:2622-32.

Spaulding C and Mennuni MG, Surgery after DES implantation: to operate or not to operate: is it still a question? JACC 2016;68:2633-6.

Levine GN et al, 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. JACC 2016;68:1082-115.




Have a great day everyone!


MOFFITT CARDIOLOGY REPORT PEARLS 5/23/17: Digoxin Toxicity and DigiFab!

Hey Everyone! Thanks to Jesse and YY for discussing the case of an elderly man with bradycardia due to possible digoxin toxicity! We also discussed a second case of possible Heyde syndrome and looked at an echo with aortic valve endocarditis. Pearls below focusing on digoxin toxicity:


Top Pearls:

  1. In a patient with a-fib, regularization of a-fib is a sign of digoxin toxicity!
  2. An elevated digoxin level is helpful, but a normal level does not rule out digoxin toxicity!
  3. Digoxin-specific Fab fragments (DigiFab) indicated for unstable arrhythmias, among other indications (see below). Digibind was discontinued in the U.S.


For those who want more info:

Check out Myung’s previous pearls on bradycardia and digoxin toxicity:

A few additional pearls from today’s discussion:

  • In a patient with a-fib, regularization of a-fib is a sign of digoxin toxicity!
  • An elevated digoxin level is helpful, but a normal level does not rule out digoxin toxicity!

Management of digoxin toxicity:

  • CABs, tele, IV access, ECG, finger stick glucose if AMS
  • Digoxin-specific antibody (Fab) fragments (Digibind was discontinued in the U.S. The newer model is called DigiFab! LOVE that name.)
    • See below for recommended indications
  • Atropine can temporize bradyarrhythmias
  • IV fluid can temporize hypotension (caution heart failure)
  • ACLS for life-threatening ventricular arrhythmias

Indications for DigiFab:

  • Life-threatening or hemodynamically unstable arrhythmia
    • VT, VF, asystole, complete heart block, Mobitz II heart block, symptomatic bradycardia
  • Hypotension
  • Hyperkalemia (K>5)
  • End-organ dysfunction (renal failure, AMS)
  • Some advocate treating based on dig level or amount ingested, controversial

More info on DigiFab:

  • Each vial (40 mg) of Fab binds approximately 0.5 mg of digoxin. Dosing is complicated- look it up or discuss with pharmacy! 10 vials initially for ingestion of unknown amount.
  • Side effects = hypotension, phlebitis, hypokalemia, hypersensitivity reaction, serum sickness, and digoxin withdrawal effect can lead to VT or decompensated heart failure.




Have a great day everyone!


ZSFG can’t be MIF’d by penile lesion ddx & indications for sgy in endocarditis

At the General, we give you a little bit of this and a little bit of that in report. And same thing goes for the chiefs’ blog. This is a quick run-through of a few recent legendary reports!


In Neuro Report today, we crushed, I mean discussed, hypercarbic respiratory failure and the role of neuromuscular causes for it. We were joined by neurology guru, Andy Romeo, and here are a few of his pearls:

-Whenever you come across someone reporting dysphagia, make sure to ask about other bulbar sx’s
-In a patient with increased work of breathing in whom you’re considering if diaphragmatic weakness is playing a role, check neck flexor strength to assess if a new neuromuscular weakness is present
MIF & VC are the confrontational tests for the diaphragm. To remind ourselves about those two entities:

  • For Vital capacity (VC) and Mean inspiratory force (MIF), there is the 20-30 rule
  • VC: deep breath and exhalation maximally into spirometer; goal is at least 20cc/kg
  • MIF: inhalation against a closed valve with negative force recorded; goal is “more negative” than -30 cmH20. -60cmH20 is expected or what is associated with weak cough in NL person


In a recent ID report, we discussed the well-known penile lesion ddx and added in a lesser known branch point of the *PRURITIC* penile lesion. The following is a non-exhaustive (and likely with much overlap) summary of what we came up with:

PAINFUL penile lesion

  • Chancroid/H. ducreyi
  • SJS/TEN drug lesion
  • SCC
  • Traumatic lesion/entrapment injury
  • Ulcers in s/o foley
  • HSV
  • Paraphimosis

 PAINLESS penile lesion

  • Syphilis
  • LGV (Of note, the lymphadenopathy *IS* painful in Lymphogranuloma venereum; LGV caused by L1, L2, L3 serovars of Chlamydia trachomatis)
  • Granuloma Inguinale (uncommon infection caused by K. granulomatis)
  • HIV
  • HPV
  • Pearly penile papule

*PRURITIC* penile lesion

  • Fixed drug reaction, DRESS/DHR
  • Yeast
  • Infestation-scabies/pubic lice
  • HSV
  • Behcet’s

 So how do we diagnosis LGV? Does our usual urine test work??????
Lisa Winston teaches us:

Turns out the usual Chalmydia culture or the more commonly ordered/sensitive NAAT test will be positive in LGV as the serovars will be picked up—it just won’t specify that it detected the L1-3 serovars. Usually when the sx’s are classic, empiric tx (longer course) is initiated. If you want a definitive dx, you can talk to colleagues at communicable dz and public health to see if need to send serology or special PCR to the SF public health lab (and then potentially to state’s public health lab or CDC).


Lastly, Mike and Carine presented a patient in intern report with MV endocarditis 2/2 MSSA where we discussed the role of early surgical intervention in infective endocarditis.

There is a fantastic 2013 NEJM Infective Endocarditis review article by Hoen and Duval that breaks down the indications for surgery into three big categories: heart failure, uncontrolled infection, and prevention of embolic events. Or in image form:

indications for sgy

For those of you who want more…

Punag, one of the cardiology fellows, passes on the following for the ACC/AHA class indications for surgical intervention:

Early surgery is recommended for patients with complicated infective endocarditis (IE), but data from randomized trials are scarce. The following are points to remember about the timing of surgery among patients with IE:

  1. The main indications for early surgery in IE are heart failure, uncontrolled infection, and prevention of embolization. The reduction in mortality with surgery is greatest among patients with IE and moderate to severe heart failure.
  2. Heart failure. The European Society of Cardiology (ESC) guideline (2009) recommends emergent surgery for heart failure with refractory pulmonary edema or cardiogenic shock (Class I), or urgent surgery for persistent heart failure with signs of poor hemodynamic tolerance (Class IIa). The American Heart Association (AHA)/American College of Cardiology (ACC) guideline (2014) recommends early surgery for valve dysfunction causing heart failure (Class I).
  3. Uncontrolled infection. The ESC guideline recommends urgent surgery (Class I) for evidence of uncontrolled infection defined as either abscess, fistula, or pseudoaneurysm; or for an enlarging vegetation, persistent fever, or positive blood cultures after 7-10 days of appropriate therapy. The AHA/ACC guideline recommends early surgery (Class I) for evidence of persistent infection, heart block or abscess, or a resistant organism ( aureus, fungi).
  4. Prevention of embolization. The ESC guideline recommends urgent surgery for a vegetation >10 mm with previous embolization or other surgical indication (Class I), or for isolated vegetation >15 mm and feasible valve repair (Class IIb). The AHA/ACC guideline recommends early surgery for recurrent emboli and persistent vegetations despite appropriate antibiotic therapy (Class IIa); or a large mobile vegetation on a native valve (Class IIb).
  5. Neurological complications. Patients with a neurological complication may have other indications for early surgery. However, early surgery may pose a significant risk for perioperative neurological deterioration (related to anticoagulation potentiating the risk of intracerebral bleeding, and to hypotension during cardiopulmonary bypass aggravating neurological ischemia and edema).
  6. Prosthetic valve IE. Prosthetic valve endocarditis is the most serious form of IE, and more difficult to treat using antibiotics alone. In general, current guidelines support consideration of a surgical strategy for high-risk subgroups with prosthetic valve IE, including patients with heart failure, abscess, or persistent fever.
  7. Definitions of early surgery. There is no consensus as to the optimal timing of early surgery. The ESC guideline classifies surgical indications in IE as emergent (within 24 hours), urgent (within a few days), and elective (after 1-2 weeks of antibiotic therapy). The AHA/ACC guideline defines early surgery as occurring during the initial hospitalization and before completion of a full therapeutic course of antibiotics.


Evernote link:


Hoen B, Duval X. Infective Endocarditis. N Engl J Med 2013; 368:1425-1433April 11, 2013DOI: 10.1056/NEJMcp1206782

MOFFITT CARDIOLOGY REPORT PEARLS 5/2/17: Kawasaki Disease and Coronary Aneurysms!

Hey Everyone! Thanks to Jin and Alayn for presenting the case of a young man with childhood Kawasaki disease coming in with progressive chest pain and dyspnea, and found to have a coronary aneurysm! He will undergo a cardiac stress test to figure out whether the symptoms are related to the aneurysm. Pearls below!


Top Pearls:

  1. Kawasaki disease is usually self-limited, but cardiac complications are common.
  2. Coronary aneurysms are the most common complication.
  3. Treat early with IVIG and aspirin to prevent these complications.


For those who want more info:

Kawasaki disease (KD) is rare in adults and is typically self-limited with an acute course of (average) 12 days. There DOES seem to be a genetic component to Kawasaki disease (increased frequency among family members of an index case and increased frequency in Asian and Asian-American patients).

*Cardiovascular complications include:

  • Coronary aneurysms (this is the major one, see below for more info!)
  • Heart failure
  • MI
  • Arrhythmias
  • PAD

*Diagnostic criteria: Fever lasting at least 5 days without other explanation, AND at least 4 of:

  • Bilateral conjunctivitis [>75%]
  • Oral mucous membrane changes (fissures, injection, strawberry tongue) [90%]
  • Cervical lymphadenopathy [25-70%]
  • Peripheral erythema or edema (palms/soles) [50-85%]
  • Polymorphous rash [70-90%]

*Treatment: IVIG (single dose), ASA during acute phase until inflammatory markers resolve. ASA is continued if aneurysms persist.

*Coronary artery aneurysms:

  • 30-40% of patients with acute Kawasaki disease!


  • 10-20% persist beyond one month (highest mortality is 15-45 days after disease onset)
  • May cause late ischemic heart disease
  • ECG and TTE for all patients with KD (CTA or MRA if TTE cannot image arteries)
  • Aneurysms most commonly found in proximal LAD, often at arterial branch points
  • “Giant” aneurysms >8 mm have high risk of morbidity/mortality (up to 50%), often anticoagulated in addition to aspirin
  • Who gets PCI? Ischemic symptoms + reversible ischemia on stress testing + >75% stenosis. CABG recommended if severe LV dysfunction or stenosis not amenable to PCI.

IN SUMMARY: If someone has suspected KD, treat early with IVIG and aspirin to prevent cardiac complications. Do ECG and TTE (and possibly CTA/MRA) in the acute phase looking for coronary aneurysms.

*Pearl: KD is not the only disease associated with coronary aneurysms. Other associations include PAN, Ehlers-Danlos, Loeys-Dietz, and other familial syndromes.




Have a great day everyone!