Category Archives: Cardiovascular Medicine

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.

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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

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).

 

ffoashman

 

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.

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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)

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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!

References:

Talmor et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. http://www.nejm.org/doi/full/10.1056/NEJMoa0708638#t=article

ARDS-net. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. http://www.nejm.org/doi/full/10.1056/NEJM200005043421801#t=abstract

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

http://www.nejm.org/doi/full/10.1056/NEJMoa1005372

 

Guerin et al. Prone positioning in severe acute respiratory distress syndrome. http://www.nejm.org/doi/full/10.1056/NEJMoa1214103#t=article

Blog:

Evernote: https://www.evernote.com/shard/s462/sh/7b428e2c-0771-49cf-ab44-2a8262dee775/ce84685da30f0cc865557bc94ee80226

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!

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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.

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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. https://doi.org/10.1016/j.jacc.2016.09.967

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.

Figure

Conclusion: The authors conclude that non-cardiac surgery could be considered as soon as 1 month after DES-PCI. An accompanying article (https://doi.org/10.1016/j.jacc.2016.09.960) 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.

 

References:

Egholm G et al, Risk associated with surgery within 12 months after coronary drug-eluting stent implantation. JACC 2016;68:2622-32. https://doi.org/10.1016/j.jacc.2016.09.967

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. https://doi.org/10.1016/j.jacc.2016.09.960

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. https://doi.org/10.1016/j.jacc.2016.03.513

 

Evernote: https://www.evernote.com/shard/s272/sh/3c0246a4-b66c-4583-913a-b386010007e3/b3aec87d5783d83600177504adebc172

 

Have a great day everyone!

SamMy