Hyperlipidemia;

“Should I consider cardiac CT angiography in my 76-year-old male patient with chest pain of unclear origin?”  

FA Manian MD, MPH, , , , , , , , , , , , , , Leave a comment

Probably not!1-4 Although the 2021 AHA/ACC Chest Pain Guidelines have generally widened the scope of indications for cardiac CT angiography (CCTA) to patients at low to intermediate risk of coronary artery disease (CAD) presenting with acute coronary syndrome (ACS)1 (with or without known CAD), several caveats should be considered before ordering this test. In general preference is given to patients with the following characteristics: 

  • Age sixty-five years of age or younger.  Elderly are not ideal candidates for CCTA as the calcium burden may be too high, rendering the test non-diagnostic due to the interference with proper coronary artery lumen assessment. Women tend not to accumulate as much calcium and their age threshold may be increased to 70 years. Some studies like the ROMICAT II Trial extended the age up to 74 years.4 
  • BMI <40.2
  • Sinus rhythm. Atrial fibrillation can be circumvented with expanded padding techniques, albeit at higher radiation exposure.2
  • Without coronary stents, unless their stents are > 3.0 mm in diameter (eg, in left main, very proximal left anterior descending, circumflex or right coronary stents).2
  • Without high coronary calcium burden, or without multiple risk factors for CAD (eg, type 2 diabetes, hypertension, hyperlipidemia) in the setting of typical anginal chest pain.1
  • Other technical requirements: must be able to hold breath during procedure, not have contraindications to beta blockers (ideal heart rate <60 bpm), not have an iodinated contrast allergy, and have stable kidney function.2

Despite these caveats, many patients may still be able to undergo CCTA to help exclude coronary causes of their chest pain.  For example, a 49-year-old patient at low to intermediate risk of CAD presenting with atypical chest pain can potentially undergo CCTA and, if negative, be discharged the same day!4  

In our patient, however, given his older age, CCTA is likely to be non-diagnostic and proceeding to an alternative test, such as stress test or invasive coronary angiography (depending on circumstances and pre-test probability), may be a better option.  

Bonus Pearl: Did you know that, as a “bonus”,  CCTA provides a “free” look at the lungs, calcium score (used largely in asymptomatic patients to help weigh pros and cons of starting a statin)3, and other cardiopulmonary structures that may hint at alternative diagnoses for the cause of chest discomfort and/or dyspnea?

Contributed by Eldin Duderija MD, Cardiologist, Mercy Clinic, St. Louis, Missouri

 

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References:

  1. Gulati M, Levy P, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. J Am Coll Cardiol. 2021;78:e187–e285. https://pubmed.ncbi.nlm.nih.gov/34709879/
  2. Raff GL, Chinnaiyan KM, Cury RC, Garcia MT, Hecht HS, Hollander JE, O’Neil B, Taylor AJ, Hoffmann U; Society of Cardiovascular Computed Tomography Guidelines Committee. SCCT guidelines on the use of coronary computed tomographic angiography for patients presenting with acute chest pain to the emergency department: a report of the Society of Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc Comput Tomogr 2014;8:254-71. doi: 10.1016/j.jcct.2014.06.002. Epub 2014 Jun 12. PMID: 25151918. https://pubmed.ncbi.nlm.nih.gov/25151918/
  3. Hecht H, Blaha MJ, Berman DS, Nasir K, Budoff M, Leipsic J, Blankstein R, Narula J, Rumberger J, Shaw LJ. Clinical indications for coronary artery calcium scoring in asymptomatic patients: Expert consensus statement from the Society of Cardiovascular Computed Tomography. J Cardiovasc Comput Tomogr 2017;11:157-168. doi: 10.1016/j.jcct.2017.02.010. Epub 2017 Feb 24. PMID: 28283309. https://pubmed.ncbi.nlm.nih.gov/28283309/
  4. Hoffmann, Udo, et al. “Coronary CT angiography versus standard evaluation in acute chest pain.” N Engl J Med 2012;367:299-308. https://www.nejm.org/doi/full/10.1056/nejmoa1201161

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

“Should I consider cardiac CT angiography in my 76-year-old male patient with chest pain of unclear origin?”  

Despite taking higher doses of warfarin, my patient’s INR won’t budge. What am I missing?

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , Leave a comment

Poor compliance is probably the most common and least “exciting” explanation for low INRs despite seemingly adequate or high warfarin doses.  Otherwise, consider the following: 

Increased vitamin K intake: Since warfarin acts by inhibiting vitamin K recycling by VKORC1 (Vitamin K epOxide Reductase Complex), find out if your patient takes multivitamins or loves foods or products rich in vitamin K, ranging from leafy green vegetables to nutritional supplements( eg, Ensure) and even chewing tobacco!1 

Drug interactions: Warfarin is notorious for interacting with many drugs, although its effect is more often enhanced than counteracted. Run the patient’s med list and look for “counteractors” of warfarin,  including carbamazepine, phenobarbital, phenytoin, rifampin, and dexamethasone.2 

Hypothyroidism: Thyroid hormone seems to be necessary for efficient clearance of the vitamin K-dependent clotting factors (II, VII, IX, and X). Thus, larger doses of warfarin may be needed when patients are hypothyroid.3 

Hyperlipidemia and obesity: High lipid levels may allow for high vitamin K levels (since it’s lipid-soluble and carried in VLDL), especially at the start of therapy.4,5 

What if the INR is falsely low? This is usually not the problem although one major trial took a lot of heat for using a point of care INR device that gave low readings in anemic patients.6  When in doubt, check a chromogenic factor Xa test to confirm; 20-30% activity correlates with a true INR of 2-3.7

If none of these explanations fit the bill, consider genetic testing for warfarin resistance.8,9

Bonus Pearl: Did you know that use of warfarin (introduced in 1948 as a rodenticide) has already led to some selective pressure for VKORC1 mutations in exposed rat populations.10

References

  1. Kuykendall JR, et al. Possible warfarin failure due to interaction with smokeless tobacco. Ann Pharmacother. 2004 Apr;38(4):595-7. https://www.ncbi.nlm.nih.gov/pubmed/14766993
  2. Zhou SF, et al. Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. https://www.ncbi.nlm.nih.gov/pubmed/19515014
  3. Bucerius J, et al. Impact of short-term hypothyroidism on systemic anticoagulation in patients with thyroid cancer and coumarin therapy. Thyroid. 2006 Apr;16(4):369-74. https://www.ncbi.nlm.nih.gov/pubmed/16646683
  4. Robinson A, et al. Lipids and warfarin requirements. Thromb Haemost. 1990;63:148–149. https://www.ncbi.nlm.nih.gov/pubmed/16646683
  5. Wallace JL, et al. Comparison of initial warfarin response in obese patients versus non-obese patients. J Thromb Thrombolysis. 2013 Jul;36(1):96-101. https://www.ncbi.nlm.nih.gov/pubmed/23015280
  6. Cohen D. Rivaroxaban: can we trust the evidence? BMJ 2016;352:i575. https://www.bmj.com/content/352/bmj.i575/rapid-responses
  7. Sanfelippo MJ, et al. Use of Chromogenic Assay of Factor X to Accept or Reject INR Results in Warfarin Treated Patients. Clin Med Res. 2009 Sep; 7(3): 103–105. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757431/
  8. Rost S, et al. Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor deficiency type 2. Nature. 2004;427:537–41. https://www.ncbi.nlm.nih.gov/pubmed/14765194
  9. Schwarz UI, et al. Genetic determinants of response to warfarin during initial anticoagulation. N Engl J Med. 2008 Mar 6;358(10):999-1008. https://www.ncbi.nlm.nih.gov/pubmed/18322281
  10. Rost S, et al. Novel mutations in the VKORC1 gene of wild rats and mice–a response to 50 years of selection pressure by warfarin? BMC Genet. 2009 Feb 6;10:4. https://bmcgenet.biomedcentral.com/articles/10.1186/1471-2156-10-4

Contributed by Nicholas B Bodnar, Harvard Medical School student, Boston, MA.

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Despite taking higher doses of warfarin, my patient’s INR won’t budge. What am I missing?