Category Archives: Cardiovascular Medicine

Moffitt Cardiology Pearls 10/10/17 – Congenital Heart Disease and SVC Syndrome

Thank you so much to Nick and Matt for presenting the case of a young man with a history of congenital pulmonary atresia and hypoplastic RV decades status post a bidirectional Glenn procedure coming in with shortness of breath and chest pain. The patient was found to have a severely dilated aortic root with resultant aortic insufficiency and severe pulmonary hypertension.

 

KEY PEARLS:

  1. When assessing a patient with congenital heart disease, it is VITAL to obtain records outlining the pathophysiology and previous procedures in order to understand their current physiology and what might go wrong.
  2. As Anne Thorson shared with us, in a patient with congenital heart disease who was previously doing well and then decompensates, ALWAYS consider the possibility of infection (particularly endocarditis) as the cause.
  3. SVC syndrome is a clinical diagnosis – see some physical exam features below.

    Cyanotic Congenital Heart Lesions: There are 5 main lesions, often called the “5 Ts”, of congenital heart defects that can result in cyanosis at birth or in the neonatal period. Most of these conditions will require intervention within the first months of life.

     

    Here’s a review on cyanotic congenital heart disease in adults. Of note, it’s from 1975… my guess is many things have changed since then and we see significantly more adult survivors of congenital disease.

Pulmonary atresia and hypoplastic RV is NOT typically a cyanotic heart lesion. However, the small RV + atretic pulmonic valve can lead to a volume and pressure overloaded state on the right side the heart. The Bidirectional Glenn Procedure reduces blood flow to the hypoplastic RV (thus offloading the pressures) by diverting the SVC directly into the pulmonary arteries. Blood return from the IVC continues to enter into the RA.

 


While we most commonly see SVC Syndrome in the setting of extrinsic compression or internal invasion of the SVC in malignancy, remember that there are multiple other risk factors as well!

Risk factors for SVC syndrome:

  • Thoracic mass – lung cancer, lymphadenopathy, lymphoma, teratoma, thymoma
  • Vascular disease – aortic aneurysm, vasculitis, AV fistula
  • Scarring or Fibrosis – related to chronic infection (like histo as Harry mentioned or tuberculous mediastinitis as described by Schechter in 1954), radiation, or instrumentation
  • Cardiac causes – pericarditis, atrial myxoma OR, as in this case, severe pulmonary hypertension in patient whose SVC connects directly to the pulmonary veins!
  • Clot – with or without underlying malignancy or central venous catheter

Here’s another, more recent, review of SVC syndrome, describing the pathology, risk factors, diagnosis, and management.

Harry mentioned Pemberton’s sign, described in the linked NEJM images in Clinical Medicine article. Below are 2 YouTube videos showing the classic finding:  signs of SVC syndrome brought on by extending the arms over the head. The second is quite dramatic.

1) https://www.youtube.com/watch?v=r1dkasbE7v8

2) https://www.youtube.com/watch?v=m_ZecWGnb2A

 

Evernote: https://www.evernote.com/shard/s462/sh/d5befae6-e090-4f3e-ab15-7dfa8ed3e73a/6e88cb495f580e320334ed1c2932afb5

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Moffitt Pearls 10.03.17 – Chest Pain in the Young , FFR & Myocardial Bridging

Thank you to Vaibhav for presenting the fascinating case of a young woman with a hx of myocardial bridging s/p unroofing p/w recurrent chest pain and elevated troponin to 1.8 of unknown cause. She has had an extensive prior work-up that has included abnormal MRI (initially thought to be Sarcoid, then reviewed normal), mild diastolic dysfunction and reduction in voltage c/f infiltrative disorder. She will get a repeated cardiac MRI (possibly PET), ANA, serum free light chains and ESR/CRP to help determine the cause.

Key Pearls

  1. Low voltage on the ECG is defined by < 5mm in limb leads and < 10mm in the precordial leads. Amyloid is the predominate infiltrative disease to consider with this finding as other diseases such as Sarcoid often does not present with low voltages.
  2. Myocardial bridging is present in up to 25% of people per autopsy/imaging reports AND it can be very difficult to determine if this is driving symptoms. 
  3. Medical management for myocardial bridging includes beta-blockers and calcium channel blockers to decrease inotropy. Nitrites are contraindicated as they increase contractility.

More on Myocardial Bridging

  • The major coronary arteries occasionally have a segmental intramyocardial course. During systole, this segment of the vessel is compressed, a condition referred to as milking or systolic “myocardial bridging.” On angiography, bridging is recognized as compression of a segment of a coronary artery during systole, resulting in narrowing that reverses during diastole. This occurs most often in the left anterior descending coronary artery or its septal perforator branches
  • Myocardial bridging, which causes coronary artery obstruction only during systole, would not be expected to reduce total myocardial perfusion significantly since almost two-thirds of blood flow in the left coronary system occurs in diastole.  

Differential Diagnosis of a young pt w/ Cardiac Chest Pain:

Always rule out MI first!

  • Atheromatous CAD
    1. Think of RF including hyperlipidemia, hyperhomocysteinaemia, lipoprotein a
  • Non-Atheromatous Coronary Artery anomalies
    1. Myocardial bridging – artery dives through myocardium instead to the epicardium (tx: with B-blockers and nondihydropurine calcium channel blockers)
    2. Coronary Dissection (surgical)
    3. Anomalous coronary (surgical)
    4. Embolism to the coronary arteries – septic or clot  (through PFO)
    5. Prizmental Angina – vasospam (tx amlodipine, nitrates)
  • Hypercoagulable States
    1. Antiphospholipid syndrome
    2. Nephrotic syndrome
    3. Factor V Leiden and Antithrombin III
  • HCOM w/ demand (tx maintain euvolumia, beta-blockers)
  • Microvascular d/o (treat as angina – risk factor reduction, beta-blockers, nitrates)
  • Pericarditis
Fraction Flow Reserve (FFR) is traditionally used to quantify the degree of coronary artery narrowing to evaluate for stenting during a catheterization. The FAME trial re-defined flow limiting lesions as < 0.8 which is used to decide which lesions to stent. Diastolic FFR has also been used in the evaluation of myocardial bridging with a flow rate < 0.76 do determine if a lesion should be stented or not. Interestingly enough, dobutamine is used in the cath lab and NOT adenosine (which is usually used) the determine whether myocardial bridging is causing flow limitation.
FFR

Moffitt Pearls 8.29.17 – Cardiology Report

  1. Management of atrial fibrillation (AF) is broken down into rate control and rhythm control – see details on AFFRIM trial below. Use the CHaDsVasC score to determine anticoagulation.
  2. In patient’s with a reduced ejection fraction do not use calcium channel blockers for rate control (class iii, level C evidence).
  3. Amiodarone and dofedilide are two options for anti- arrhythmia therapy in patient’s with HFrEF.
  4. See below for flow sheet on cardioversion of patient’s with hemodynamically stable AF.

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The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Trial (2002)

Bottom Line:  In patient’s with nonvalvular AF, there is no survival benefit between rate and rhythm control, but rhythm contol trends towards increased mortsality.

Major Points:

Multicenter, parallel group, RCT of > 4,000 patients w/ nonvalvular AF

Rate control (HR <80 at rest) was achieved with B-blockers, Ca++ channel blockers, and/or digoxin (n=2,027)

Rhythm control strategy varied considerably but included class 1a (procainamide), 1c (propafenone, flecanidie) and III (amiodarone, sotalol, dofetilide) (n=2,033)

Median follow-up: 3.5 years

Analysis: Intention to treat

Primary Outcome: All cause mortality at 5 years 25.9% vs 26.7% (HR 1.15, CI 0.99-1.34, P=0.08)

What if my patient cannot be anticoagulated??

Among patients with nonvalvular atrial fibrillation (AF), the majority of thrombi are located within or involve the left atrial appendage (LAA). The importance of the LAA in thromboembolic risk among patients with AF provides the rationale for ligation or occlusion of the LAA in patients who are candidates for but have either absolute or relative contraindications to long-term oral anticoagulation

Percutaneous approaches, referred to as LAA occlusion procedures, that mechanically prevent embolization of LAA thrombi have been developed and shown to be effective

The left artial appendage ligation or LARIAT procedure was developed here at UCSF and is used in such patients (video below)

Cardioversion of patient’s with hemodynamically stable AF.

**Remember unstable patients should be immediately cardioverted**

Cardioversion Flow.png

https://www.evernote.com/shard/s307/sh/b32ec2f6-aab5-4c75-a9ed-58727105f371/e40f23a849ddc915e16c00e9ca9e8986Key Pearls

VA Ambulatory Report 8.2.17 – Weight loss and artificial valve endocarditis

Thanks Tim for presenting the case of a 76 yo M with a pmhx of AS s/p valve replacement presenting to clinic with subacute fatigue, fevers, and weight loss found to have endocarditis likely from one of the HACEK organisms with final culture results still pending.

Key Learning Points

  • If your baseline work-up (see details below) of weight loss in the elderly is normal, the likelihood of malignancy is very low.  There is no need for further testing, but you should continue with close follow-up.
  • TAVR is indicated for severe AS with symptoms and prohibitive surgical risk but also been shown to be non-inferior for high and intermediate surgical risk patients
  • Complications of artificial heart valves include: infection, thromboembolism, obstruction, regurgitation, and hemolytic anemia
  • HACEK organisms most often will grow in blood cultures but can take longer than our more common strep and staph species.

 

Weight loss in the elderly (flash back to report pearls from 6.7.17!)

  • Work-up is directed by history and physical but at a minimum should include: CBC, BMP, LFTs, TSH, CRP, ESR, LDH, UA, CXR, FOBT, maybe abdominal ultrasound
  • A prospective study demonstrated that if this baseline work-up is normal none of the patients went on to have malignancy demonstrated on additional testing. Therefore if the baseline work-up is normal, no further testing is necessary but continue with close follow-up.
  • AAFP Practice guidelines for Unexplained Weight Loss in Older Adults

 

Artifical Heart Valves

  • Types of artifical valves
    • When choosing between bioprosthesis vs. mechanical valves it should be a shared decision with the patient. Things to consider:
      • Longevity of the valve: Mechanical heart valves last 20-30 years vs. 10-15 years with bioprosthetic valves. Consider mechanical heart valves most often in patients < 60 years and bioprosthetic valves in patients > 70 years
      • Anticoagulation: Required in mechanical valves
    • Ball and cage valves: Phased out ~ 20 years ago, very durable but more complications including thromboembolism, migration of the whole valve, and the ball getting stuck in the cage
  • Methods for valve replacement: Surgical vs. TAVR
    • The PARTNER trial demonstrated non-inferiority of TAVR vs. SAVR for high surgical risk patients
    • Indications for TAVR:
      • Severe AS with symptoms and prohibitive risk for surgical replacement
      • Severe AS with symptoms and high surgical risk
        • Patients could also undergo SAVR
        • The PARTNER trial demonstrated non-inferiority of TAVR vs. SAVR for high surgical risk patients
      • TAVR is a reasonable alternative for patients at intermediate surgical risk depending on patient specific variables
        • PARTNER II trial demonstrated non-inferiority for TAVR vs. SAVR in intermediate risk patients
      • Contraindicated for bicuspid aortic valves
      • TAVR has not been studied in asymptomatic patients and therefore is not recommended.  Patients should be monitored clinically for development of symptoms.
  • Complications of artificial valves
    • Infection
    • Thrombus
      • Prosthetic valve thrombus leading to obstructive symptoms
      • Thromboembolism
    • Valve obstruction
      • Can be due to: leaflet fibrosis, Calcification, pannus formation, or thrombus
        • LT taught us about a patient he had with pannus formation which is fibrous tissue ingrowth around the valve.  This is much less common than other causes of obstruction
      • For dx: get echo to determine valve gradient and consider CT to better characterize the mass on the valve.  The patient may need surgery for diagnosis and treatment.
    • Valve regurgitation
      • Can occur both through the valve itself and paravalvular
      • Due to leaflet degeneration, calcification, endocarditis, thrombus, or pannus formation
    • Hemolytic Anemia

 

Endocarditis

  • HACEK organisms: Although historically classified as culture negative endocarditis, our current culture methods can grow these organisms but they take longer to grow (Median time is ~ 3 days).
  • Most common cause of culture negative endocarditis: fastidious organisms and strep species in patients already on antibiotics.
    • Diagnosing Q fever endocarditis
      • Phase I IgG antibody titer should be > 800
        • Duke’s criteria include microbiological evidence of infection. Major criteria: IgG Phase I titer > 6400. Minor criteria is a titer > 800
  • Shout out to Rabih’s prior morning report pearls on endocarditis breaking the differential down between culture positive and culture negative endocarditis.

ink-image

References:

PARTNER Trial: Smith, Craig R., et al. “Transcatheter versus surgical aortic-valve replacement in high-risk patients.” New England Journal of Medicine 364.23 (2011): 2187-2198. http://www.nejm.org/doi/full/10.1056/NEJMoa1103510#t=article

PARTNER II Trial: Leon, Martin B., et al. “Transcatheter or surgical aortic-valve replacement in intermediate-risk patients.” N Engl J Med 2016.374 (2016): 1609-1620.  http://www.nejm.org/doi/full/10.1056/NEJMoa1514616

AHA/ACC Guidelines for management of Valvular Heart Disease: http://circ.ahajournals.org/content/early/2017/03/14/CIR.0000000000000503

Ambulatory Report 7.19.17 – Secondary Hypertension and a Hemorrhagic Stroke in a young patient

Thanks John for presenting this great case!  We discussed the case of a 31 yo male with a pmhx of hypertension and hemorrhagic stroke who was presenting for primary care now undergoing a work-up for secondary hypertension.

High-yield pearls

  • The most common causes of a hemorrhagic stroke in a young person are vascular malformations and hypertension
  • Consider an age-based approach to secondary hypertension work-up
  • LT pearl: If you are concerned about pheo, check orthostatics.  Untreated pheo patients will have positive orthostatics because they are chronically vasoconstricted and cannot adjust adequately to postural changes
  • Recognize lots of medications and dietary sodium will affect your renin/aldosterone ratio.  If your patient is on an ACEi or ARB, you do not need to stop the medication in your first pass you evaluation but know that a normal result does not exclude primary hyperaldosteronism.

 

Hemorrhagic CVA in the young:

  • Most frequent RISK FACTOR: tobacco use, HYPOcholesterolemia, HTN, alcohol use
  • Most frequent ETIOLOGY: vascular malformation and HTN
  • The final neurologic outcome was favorable in 60%
  • Causes overall:
    • Aneurysm/vascular malformation
    • Trauma
    • Severe HTN
    • Tumor
    • Septic/mycotic aneurysm
    • Bleeding d/o
    • CNS infection (eg HSV encephalitis)
    • Vasculitis
    • Drugs (cocaine, meth)
    • Secondary transformation from central venous thrombosis

 

Secondary Hypertension

Who should I work-up a patient for secondary hypertension?

  • 5-10% of all adults with HTN will have a secondary cause of HTN
  • Consider evaluation in patients with:
    • Resistant HTN: Defined as inadequately controlled BP when on three anti-hypertensives one of which must be a diuretic
    • Early or late onset HTN
    • Severe or accelerated course of HTN
    • Antihypertensive drug intolerance
    • Suggestive features on history or physical

When thinking about secondary hypertension consider an age-based approach to focus your differential. (Thanks for sharing Abbi and Jackie!)

afp20101215p1471-t3

Secondary Hypertension Differential and Suggestive Clues on history, physical, and basic labs

  • Renal Vascular Disease: Renal artery stenosis or fibromuscular dysplasia
    • Look for creatinine increases by >30% after starting ACEi or ARB, asymmetric size of kidneys, recurrent flash pulm edema, bruit on exam (not very sensitive)
  • Primary renal disease
    • Will see abnormal creatinine and UA
  • Endocrine causes
    • Pheochromocytoma
      • Triad; headache, palpitations, sweating,
      • LT pearl: check orthostatics!  Untreated pheo patients are chronically vasoconstricted so cannot adjust blood pressure with positional changes
    • Hyperaldosteronism
      • Unexplained hypokalemia, urine potassium wasting
      • One half of patients will have normal serum potassium
      • Typically mild HTN presenting in middle age
    • Cushing’s
      • Cushinoid features on physical exam
      • History of steroid use
    • Hypothyroid
    • Primary hyperparathyroidism
      • Hypercalcemia
  • Coarctation of the Aorta
    • Diminished or delayed femoral pulses
    • Asymetric BPs: BP in right arm > left arm or HTN in arms and low BP in legs
  • OSA
    • Obesity, daytime somnolence, snoring
  • Drugs
    • Cocaine, amphetamines
  • Medications
    • NSAIDs, OCPs, antidepressants, calcineurin inhibitors, decongestants, steroids,

 

Things that affect renin/aldo ratio: 

  • Meds
    • Mineralocorticoid receptor antagonist
    • Diuretics
    • ACEi or ARB
      • You do not need to take your patient off their ACEi or ARB in your first pass work-up because many with primary hyperaldosteronism will have an abnormal result.  However, if the result is normal you cannot exclude primary hyperaldosteronism and may need to recheck it off the medication.
    • Beta blockers
    • Clonidine
    • NSAIDs
    • SSRIs
    • OCPs
  • Hypokalemia/Hyperkalemia
  • Na restricted diet/Na loaded diet
  • Pregnancy
  • Renovascular HTN
  • Malignant HTN
  • Liddle syndrome: Liddle syndrome is a genetic disorder characterized by early, and frequently severe HTN with low plasma renin activity, metabolic alkalosis, hypokalemia, and normal to low aldosterone.

At the VA, endocrine clinic helps with obtaining this test and providing your patient with the appropriate instructions to avoid spurious results.

 

References:

Intracranial hemorrhage in Young People: http://stroke.ahajournals.org/content/30/3/537

Age Based Approach to Secondary Hypertension from the AAFP: http://www.aafp.org/afp/2010/1215/p1471.html

 

Moffitt Pearls 6.27.2017 – Cardiology Report – Chagas Cardiomyopathy

 

Thank you to Satvik for presenting a case of a young man with newly diagnosed bi-ventricular HF thought 2/2 meth use, c/b LV thrombus presenting with SOB + CP presenting with afib with RVR. We discussed the nuanced management of a patient with hemodynamically significant RVR with a known LV thrombus, later found to have positive Chagas antibodies!

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KEY PEARLS

  1. Acute management of supraventricular tachycardia generally depends on an assessment of hemodynamic stability. In the unstable patient, you should consider early cardioversion.
  2. Triggers for atrial fibrillation with RVR: volume overload (w/ decompensated heart failure), medication non-adherence, coronary ischemia, drug use, PE, infection.
  3. Bedside IVC ultrasound can help provide additional information for assessment of CVP and fluid responsiveness (see attached)
  4. Differential for biventricular heart failure: ischemia, long-standing LV failure, substance abuse (meth, EtOH), infiltrative disease (amyloid, hemochromatosis, sarcoid), tachycardia-mediated, infectious (Chagas).

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Differential Diagnosis of Dilated Cardiomyopathy

 

Disease Conduction Disease TTE Features Treatment
Cardiac Sarcoid

 

+++ + Perfusion defects, inflammation Corticosteroids, methotrexate, antimalarial agents
Giant cell myocarditis

 

+ Nonspecific Corticosteroids, cyclosporine
LV noncompaction

 

+ WPW ↑ Trabeculation, LV thrombi NA
AVRC (arrhythmogenic RV)

 

+++RBBB RV>>LV diltion/dysfunction, RV aneurysm of free wall NA
Chagas Disease

 

Early: +++ RBBB+ LAFB

Late: CBH + RBBB

Apical aneurysm or thrombus and infarct pattern Benznidazole early, Transplant late

 

More Details on Chagas Cardiomyopathy

  • Etiology: Protozoal parasite Trypanosoma cruziI spread by insect vector triatomine bug
  • Endemic regions: Central and South America
  • Epidemiology: Most common cause of non-ischemic cardiomyopathy in Latin America
  • Pathophysiology: Mechanism of cardiac injury is not well known, but is hypothesized to be a robust immune response to a small population of remaining protozoa.
  • Extracardiac involvement: Gastrointestinal dysmotility often a clue
  • Cardiac involvement: Acute infection is usually not recognized and is rarely life-threatening. ~ 20% of patients develop chronic Chagas disease within 10-20 years after an acute infection. Of these patients between 1/3 and 1/2 develop chronic cardiomyopathy characterized by conduction abnl RBBB, LV thrombi and regional wall motion abnormalities without obstructive CAD.
  • Diagnosis: Serological IgG and IgM and demonstration of cardiac or GU involvement
  • Treatment: Acute and indeterminate phase – guidelines recommend benznidazole; Chronic disease – paucity of data, however per guidelines treatment as per above (some evidence that tx may alter cardiac course – see article below), in addition to supportive care for heart failure, arrhythmias (ICD and medical therapies) and tx for thromboembolism. Ultimately, definitive therapy for those with global BiV heart failure is with heart transplantation.

IVC*We use both the maximum IVC diameter as well as IVC collapsibility

IVC2

More reading for those interested below:

  • Review of dilated cardiomyopathy with conduction disease and arrhythmias.
  • Long-term cardiac outcomes of treating chronic Chagas disease with benznidazole versus no treatment: a nonrandomized trial.Viotti R, Vigliano C, Lococo B, Bertocchi G, Petti M, Alvarez MG, Postan M, Armenti Ann Intern Med. 2006 May 16; 144(10):724-34.
    •  https://www.ncbi.nlm.nih.gov/pubmed/16702588
  • Another excellent article complements of HH on disease reactivation after transplant:

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)!!

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KEY PEARLS

  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
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 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:

https://www.ecrjournal.com/articles/myocardial-infarction-non-obstructive-coronary-arteries-diagnosis-and-management

Evernote: https://www.evernote.com/shard/s307/sh/a95813cd-1c7a-4a07-8eb3-0ee5427dc4e3/33c46ee2ed90438eba97c5eb5a4ad580