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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 Renal Report Pearls 6.16.17

Thank you to Kenny for his sense of humor AND for presenting an elderly patient with h/o BPH, recent acute prostatitis, now presenting with altered mental status and acute renal failure w/ hyponatremia 2/2 multiple mechanisms including obstruction with concurrent use of NSAIDs and an ACEi. We discussed the management of post-obstructive diuresis, hyponatremia, and volume overload.


Key Pearls:

  1. The old rule of thumb that you get an elevation in creatinine of 1 for each day of renal injury turns out NOT to be totally accurate. [20mg/kg/day with volume distribution of 0.6 allows for increases in Cr by as much as 3mg/dL per day!!]
  2. Approach to AKI anatomically: Pre, Intrinsic and Post-renal (more below)
  3. Postobstructive diuresis is primarily a problem with CHRONIC, not ACUTE, urinary retention with management details outlined below.


More Review on AKI

– Definition: < 48 hours (abrupt) time course with 1 or more of the following:

  1. Increase in serum Cr > 0.3 mg/dL
  2. Greater than 50% increase in serum creatinine from baseline
  3. Reduction in urine output of < 0.5 mL/kg/hr for > 6 hours

– Oliguria is defined as UOP < 400 mL/day, while anuria is < 100 mL/day

Approach to AKI based on anatomy

  • Pre-renal – 70% of community acquired and 40% of hospital acquired AKI
    • Hypovolemia: vomiting, diarrhea, diuretics, hemorrhage, burns
    • Decreased effective circulation volume: Cardiorenal, hepatorenal
    • Change in renal vascular tone: ACEi, NSAIDs
  • Intrinsic Renal – urinalysis is the key here!
    1. Glomerular – RBCs; Anti0GBM, Pauci-immune, Immune complex
    2. ATN – muddy brown casts; prolonged pre-renal -> ischemic, toxic, septic shock (most common)
    3. AIN – WBCs; drug-induced, Infectious (fevers, rash and eosinophilia ~ 15% of pt)
    4. Vascular – micro: HUS/TTP or macro: renal artery stenosis, thrombosis
  • Post-renal – important to exclude early
    1. Obstruction from BPH, acute prostatitis, constipation, pelvic masses, neuogenic bladder


 Post-obstructive diuresis

  • A postobstructive diuresis is primarily a problem with CHRONIC, not ACUTE, urinary retention and usually represents an appropriate attempt to excrete excess fluid retained during the period of obstruction


  • Management of post-renal obstruction:
    1. Relieve the obstruction
    2. Anticipate a post-obstructive diuresis if chronic (more below)
    3. Frequent monitoring of I/Os and electrolytes (q6-q8)
    4. If going to give fluid, caution with chloride-containing fluids: Loss of hypotonic urine, may need replacement fluid, usually in a 2:1 ratio (replace approximately half the volume the patient is putting out).
    5. Fluid replacement is usually with one-half isotonic solution
    6. Remember that “The kidney is a better judge of the volume status than the doctor!” per Dr. Chi Hsu – In most patients, things will correct themselves.

Altered Mental Status (AMS)

Remember the MISTO mnemonic for AMS:

    1. Metabolic (electrolytes, esp Na and Ca; endo, esp thyroid and glucose; liver; kidney)
    2. Infectious
    3. Structural (stroke, mass, bleed)
    4. Toxin
    5. Oxygen/Other
    6. As Jen O mentioned in report “AMS” can be a very nonspecific description – it’s helpful to break this down into more specific characteristics, such as decreased level of consciousness, agitation, confusion, disorientation, etc. This helps one to narrow your differential – also remember MISTO!!

Evernote Blog:

Moffitt Cardiology Pearls 6.13.17

Thank you, Salman, for presenting a case of a middle-aged man with HIV presenting with repeated “ICD zaps,” fevers, back pain, and night sweats over the last several months. This patient was ultimately found to have a dual-chamber pacemaker with right ventricular under-sensing and spine imaging with evidence of septic emboli and discitis! His unifying diagnosis was enterococcus device infection complicated by endocarditis and discitis.

Key Pearls:

  1. Chest imaging can provide important information about the type of cardiac conduction device and can be used to assess lead placement for pacemakers and ICDs.
  2. MRIs and Pacemakers – almost all newer pacemakers are compatible with MRIs (see below for more details).
  3. You can breakdown the likely bacterial organisms to cause infection of cardiac conduction devices into early and late device infections, similar to how we classify other prosthetic hardware infections.



What can a chest radiograph tell you about a cardiac conduction device?

  1. ICD vs. Pacemaker – can differentiate based on size of generator, presence or absence of a “coil” – the thicker wire that is present in ICDs
  2. Lead placement – can assess for presence of leads in the right atrium, right ventricle, and coronary sinusCheck out this radiology pictorial review of pacemakers and ICDs:

Approach to Pacemaker Malfunction:

  • Under-sensing – inability for PM to detect native beats, often resulting in inappropriate pacing.
    • Lead failure: fracture, misplacement/migration, infection
    • Program failure: not sensitive enough
    • Change in patient’s intrinsic amplitude (infiltrative cardiomyopathy, scar)
  • Over-sensing – PM detecting electricity other than native heart beats, resulting in a failure to pace when it should.
    • Lead misplacement/migration, inappropriate programming (too sensitive)
    • Interference from alternative electronic device
  • Loss of Capture – inability for PM to capture the heart and cause contraction when it delivers a paced beat.
    • Lead failure: fracture, misplacement, infection
    • Metabolic derangements: electrolytes, acidosis

My patient has a pacemaker. Can she get an MRI?

  • Most modern pacemakers are “MRI compatible” and should be safe (though not all radiology departments are comfortable). Interestingly, even older devices are likely safer than previously thought. In this 2017 NEJM study of 1500 patients with non-MRI-conditional pacemakers or ICDs, there were no deaths, lead failures, losses of capture, or ventricular arrhythmias during non-thoracic MRI!
  • Institutions have varying levels of comfort with pacemakers. If the imaging is of high clinical importance, consider involving your EP colleagues to assess safety and facilitate the imaging.

Approach Cardiac Conduction Device Infections (from NEJM link below)



Moffitt Pearls 6.7.17 – Hypercalcemia and Indications for BiPAP

Thank you to Geoffrey for presenting 2 mini cases today in report. In the first case we discussed an elderly woman presenting from an OSH with hypercalcemia who was found to have a retroperitoneal mass w/ histology c/f B-cell lymphoma! We broadly discussed the differential and diagnostic approach to hypercalcemia. In the next case, we discussed a middle aged man presenting with severe hypoxemic and hypercapnic respiratory failure from unknown trigger c/f COPD exacerbation and the indications for BiPAP and ICU admission. There are never bad cases!!


Key Learning Pearls

  1. Approach hypercalcemia by looking at PTH (see image below)
  2. Indications for BiPAP include the following:
    1. Cardiogenic pulmonary edema
    2. Moderate to severe COPD exacerbation
    3. Hypoxemic respiratory failure
    4. Post-extubation
    5. Immunocompromised patient with acute respiratory failure
    6. Those with neuromuscular or chest wall disease
  1. Consider intubation with pH < 7.2 or RR >35  For those who would like more information


For those who would like more information. 🙂


  1. Clinical Indications for NIPPV:
  • Moderate-severe COPD exacerbation (PaCO2 >45 mmHg or pH <7.3): BiPAP is first-line treatment.
  • Decreased mortality, intubation rate, treatment failure, hospital length of stay and complications related to treatment.
  • Cardiogenic pulmonary edema: CPAP and BiPAP decrease afterload, decrease wall stress, improve oxygenation, and improve dyspnea.
  • Shown to lower in-hospital mortality.
  • Hypoxemic respiratory failure:
  • Decreased ICU mortality and intubation in patients with community-acquired pneumonia WITHOUT significant secretions
  • Decreased ICU mortality, intubation rate, and ICU length of stay in immunosuppressed patients with pulmonary infiltrates and fever (likely due to decreased ventilator-associated pneumonia in these vulnerable patients).


  • Immediately post-extubation (planned NIPPV)
  • Decreased all-cause mortality, ICU length of stay, hospital length of stay, and rates of VAP. No increased rate of extubation failure or reintubation. Benefits greatest in COPD patients.
  • Severe asthma exacerbation:
  • Data inconclusive, though suggest decreased rate of hospitalization


Diagnostic Approach and Differential Diagnosis for Hypercalcemia


Moffitt Pearls 6.5.17 – Palpable Purpura

Thank you to Kenny for presenting a fascinating case of an elderly woman with a remote history of breast cancer presenting with SOB and weight loss found to have lower extremity edema, a diastolic murmur and finally skin findings that included palpable purpura and splinter hemorrhages!!!


Key Learning Points

  • Diastolic murmurs are graded from 1-4 (thank you Arvind!)
  • Photos such as those presented in report can be uploaded via the Haiku app
  • Here is diagnostic pathway for palpable purpura Palpable Purpura


As we discussed palpable purpura has an exhaustive list of etiologies – think big categories – Malignancy, Infectious and noninfectious endocarditis and primary rheum. In this patient in particular we had a discussion around sub-acute bacterial endocarditis given her diastolic murmur, splinter hemorrhages and palpable purpura.

Palpable Purpura

  •  A sign of vascular inflammation or damage, usually a small or medium vessel vasculitis
  • Palpable purpura is the hallmark of a leukocytoclastic vasculitis, but LCV is a histopathologic diagnosis


  •  Primary rheum
    • ANCA-associated
    •  Cryoglobuinemic vasculitis
    • Polyarteritis nodosa
    • Henoch-schonlein purpura (rare in adults)
    •      Urticarial vasculitiS
    •  SLE
  •   Infection
    •          HBV-associated PAN
    •          HCV associated cryoglobulinemia
    •          Purpura fulminans associated with DIC
  •   Malignancy-related
  •   Medication effect (meds can cause an LCV on their own!)

Recommendation for first line w/u of palpable purpura

  •          CBC w platelets
  •          ESR/CRP
  •          ANA
  •          ANCAs
  •          Complements
  •          UA
  •          Infectious w/u including Blood Cx, HIV, HCV, HBV, +/- ASo or strep throat culture and cryos