Cardiovascular disease

Can I estimate the central venous pressure (CVP) of my patient with dyspnea at the bedside by using point of care ultrasound (POCUS)?

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

Absolutely! Not only can POCUS be used to estimate the CVP by measuring the jugular venous pressure (JVP), it may also be more reliable than the traditional—often challenging—visual method of looking for internal jugular (IJ) waveforms in the neck.1

To estimate the CVP by POCUS, first position the patient in a comfortable (usually semi-recumbent) position.   Select “vascular” (ie, high frequency) setting on your device (linear array probe for traditional ultrasound devices).  With the probe in the transverse plane (ie,  perpendicular to the IJ) and the orientation marker pointing to the right of the patient, slowly slide the probe cranially until the IJ appears to collapse during end-expiration, a point commonly referred to as the “meniscus” (CLIP 1 below). Measure the vertical distance between the meniscus and the sternal angle and, just as you would using the traditional method, add 5 cm (see limitation below) to calculate the height of the JVP, with values > 8 cm considered elevated (Figure 1 below).1,2,3

You can also look for the point of JVP collapse in the longitudinal axis by rotating the transducer 90° clockwise (CLIP 2 below).  Here, the shape of the IJ resembles a wine bottle with the collapsed portion or the tip of the tapered portion or triangle, representing the meniscus.3

A major limitation of estimating the CVP by visualization of JVP or by POCUS is the assumption that the distance between the right atrium and the sternal angle is constant at 5 cm.  It turns out that this distance may potentially vary among patients depending on their body habitus and position.4    A cool study from 2015, however, more accurately determined this distance by adjusted ultrasound views of the center of the right atrium. 5    Clearly, bedside estimation of CVP by POCUS will continue to be refined in the future. 

Bonus Pearl: Did you know that the traditional non-invasive method of estimating CVP by examining neck veins was first proposed in 1930 by Sir Thomas Lewis, a British cardiologist, who has been called the “father of clinical cardiac electrophysiology” and coined the terms “pacemaker,” “premature contractions,” and “auricular fibrillation”?6,7

 

Clip 1. Transverse visualization of the internal jugular vein (IJV) by using POCUS. The meniscus is the point of IJV collapse during end-expiration. 

 

Figure 1. Measurement of the jugular venous pressure (JVP) by POCUS. Add 5 cm (green arrow) to the distance between the meniscus (internal jugular collapse on the transverse view or tip of the tapering zone on the longitudinal view) and the sternal angle (red arrow).

Clip 2. Longitudinal visualization of the internal jugular vein (IJV) by using POCUS. The meniscus is the tip of the tapering zone or triangle of the IJV. 

 

 

 

Contributed by Woo Moon D.O., Mercy Hospital, St. Louis, Missouri

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References

1. Wang L, Harrison J, Dranow E, Aliyev N, Khor L. Accuracy of ultrasound jugular venous pressure height in predicting central venous congestion. Ann Intern Med 2021; 175:344-51.

2. McGee MD S. Evidence-Based Physical Diagnosis. 5th ed. Philadelphia: Elsevier; 2021.

3. Lipton B. Estimation of central venous pressure by ultrasound of the internal jugular vein. Am J Emerg Med 2000;18(4):432–4.

4. Istrail, L. POCUS and the jugular venous pressure: A deep dive. POCUS Med Ed, November 12. 2021. POCUS and the Jugular Venous Pressure: A Deep Dive (pocusmeded.com)

5. Xing C-Y, Liu Y-L, Zhao M-L, et al. New method for nonivasive quantification of central venous pressure by ultrasound. Circulation: Cardiovascular Imaging 2015;8/ https://doi.org/10.116/CIRCIMAGING.114.003085. New Method for Noninvasive Quantification of Central Venous Pressure by Ultrasound (ahajournals.org)

6. Sir Thomas Lewis – the Father of clinical cardiac electrophysiology | SciHi Blog [Internet]. [cited 2023 Feb 2]; Available from: http://scihi.org/thomas-lewis-cardiac-electrophysiology/

7. Lewis T. Remarks on early signs of cardiac failure of the congestive type. Br Med J 1930;1(3618):849–52.

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!

Can I estimate the central venous pressure (CVP) of my patient with dyspnea at the bedside by using point of care ultrasound (POCUS)?

“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?”  

Is it safe to use diltiazem or verapamil for treatment of my hospitalized patient with heart failure with reduced ejection fraction (HFrEF) and atrial fibrillation?

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

Short answer, no! It is generally recommended to avoid the use of diltiazem or verapamil, both a non-dihydropyridine calcium channel blocker (CCB), in patients with HFrEF.  Multiple randomized controlled trials involving patients with HFrEF have shown that use of diltiazem [1] or verapamil [2] is associated with increased cardiovascular mortality and morbidity, especially congestive heart failure (CHF) exacerbations.

Although you might argue that most studies [1,2] on HFrEF on CCBs have been based on patients on chronic (weeks to months) therapy, these agents are also sometimes used in the acute inpatient setting for rate control in atrial fibrillation and even blood pressure control. Even in acute settings, avoidance of these agents–or at least using them with great caution— in patients with HFrEF is prudent. Fortunately, for blood pressure control, another CCB, amlodipine [3] has been deemed safe to use in patients with HFrEF.

Adverse effects of diltiazem and verapamil are often attributed to their negative inotropic effects. As a result, patients with preexisting left ventricular dysfunction may be expected to have worse outcomes. In contrast, amlodipine primarily acts on the peripheral vasculature without significant negative inotropic effect. [4]

What about the use of these agents in patients with heart failure and preserved ejection fraction? Studies to date have found that CCBs are safe in this setting, although no mortality benefit has been shown with their use either [1]. 

Bonus Pearl: Did you know that use of another CCB, nifedipine, a close cousin of amlodipine (both 1,4- dihydropyridines), has been associated with increased cardiovascular morbidity (worsening CHF and increased hospitalizations) in patients with HFrEF? [5]

Contributed by Fahad Tahir, MD, Mercy Hospital-St. Louis, St. Louis, Missouri

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References:

  1. Goldstein RE, Boccuzzi SJ, Cruess D, Nattel S. Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in ejection fraction. The Adverse Experience Committee; and the Multicenter Diltiazem Postinfarction Research Group. Circulation. 1991 Jan;83(1):52-60. doi: 10.1161/01.cir.83.1.52. PMID: 1984898.https://www.ahajournals.org/doi/epdf/10.1161/01.CIR.83.1.52
  2. Effect of verapamil on mortality and major events after acute myocardial infarction (the Danish Verapamil Infarction Trial II–DAVIT II). Am J Cardiol. 1990 Oct 1;66(10):779-85. doi: 10.1016/0002-9149(90)90351-z. PMID: 2220572.https://www.ajconline.org/article/0002-9149(90)90351-Z/pdf
  3. Packer M, Carson P, Elkayam U, Konstam MA, Moe G, O’Connor C, Rouleau JL, Schocken D, Anderson SA, DeMets DL; PRAISE-2 Study Group. Effect of amlodipine on the survival of patients with severe chronic heart failure due to a nonischemic cardiomyopathy: results of the PRAISE-2 study (prospective randomized amlodipine survival evaluation 2). JACC Heart Fail. 2013 Aug;1(4):308-314. doi: 10.1016/j.jchf.2013.04.004. Epub 2013 Aug 5. PMID: 24621933.https://reader.elsevier.com/reader/sd/pii/S2213177913001844?token=510153852A5AEBBDF5CA9F8B16C671C4E2F4B511B6F723227BA1D2180CDAA4726EC329D5ABC4118738CB1D8B67A3CF6B&originRegion=us-east-1&originCreation=20220316135803
  4. Zamponi, G. W., Striessnig, J., Koschak, A., & Dolphin, A. C. (2015). The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential. Pharmacological reviews, 67(4), 821–870.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4630564/
  5. Elkayam U, Amin J, Mehra A, Vasquez J, Weber L, Rahimtoola SH. A prospective, randomized, double-blind, crossover study to compare the efficacy and safety of chronic nifedipine therapy with that of isosorbide dinitrate and their combination in the treatment of chronic congestive heart failure. Circulation. 1990 Dec;82(6):1954-61. doi: 10.1161/01.cir.82.6.1954. PMID: 2242521.https://www.ahajournals.org/doi/epdf/10.1161/01.CIR.82.6.1954

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!

Is it safe to use diltiazem or verapamil for treatment of my hospitalized patient with heart failure with reduced ejection fraction (HFrEF) and atrial fibrillation?

Is compression therapy for leg edema harmful in patients with congestive heart failure?

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

The evidence to date, albeit based on small non-randomized studies, suggests that compression therapy of lower extremities in stable patients with congestive heart failure (CHF) is not associated with clinical deterioration, while more studies are needed to evaluate its safety in advanced classes of CHF (NYHA III and IV). The theoretical concern is that by mobilizing fluid from lower extremities, compressive therapy could lead to worsening pulmonary edema in patients with less stable CHF. 1,2

A study of subjects with NYHA II CHF wearing compression stockings found a significant increase in human atrial natriuretic peptide (hANP) in patients with known heart disease but the rise was only transient and not accompanied by hemodynamic changes or clinical deterioration.3 Similar findings have been reported by studies involving patients with NYHA III and IV CHF involving compressive therapy which demonstrated no clinically significant deleterious effects. 4-5

Nevertheless, isolated reports of acute pulmonary edema following compressive therapy in the literature, 6,7 and the theoretical concern raised above have often led to recommendations against the use of CT in patients with advanced CHF. 1,2 We clearly need more studies to evaluate the risks vs benefits of CT in patients with CHF.

Bonus Pearl: Did you know that compressing the legs with pressures of 25 mm Hg and 50 mm Hg can reduce the blood volume in legs by 33% and 38%, respectively? 2

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References

  1. Urbanek T, Jusko M, Kuczmik WB. Compression therapy for leg oedema in patients with heart failure. ESC Heart Failure 2020;7:2012-20. https://onlinelibrary.wiley.com/doi/10.1002/ehf2.12848
  2. Hirsch T. Oedema drainage and cardiac insufficiency—When is there a contraindication for compression and manual lymphatic drainage? Phlebologie 2018;47:115-19. https://www.thieme-connect.de/products/ejournals/pdf/10.12687/phleb2420-3-2018.pdf?articleLanguage=en
  3. Galm O, Jansen-Genzel W, von Helden J, et al. Plasma human atrial natriuretic peptide under compression therapy in patients with chronic venous insufficiency with or without cardiac insufficiency. Vasa 1996;25:48-53. https://pubmed.ncbi.nlm.nih.gov/8851264/
  4. Wilputte F, Renard M, Venner J, et al. Hemodynamic response to multilayered bandages dressed on a lower limb of patients with heart failure. Eur J Lymphology 2005;15:1-4. https://www.researchgate.net/profile/Olivier_Leduc/publication/287602727_Hemodynamic_response_to_multilayered_bandages_dressed_on_a_lower_limb_of_patients_with_heart_failure/links/5704dff008ae44d70ee12eb5/Hemodynamic-response-to-multilayered-bandages-dressed-on-a-lower-limb-of-patients-with-heart-failure.pdf?origin=publication_detail
  5. Leduc O, Crasset V, Leleu C, et al. Impact of manual lymphatic drainage on hemodynamic parameters in patients with heart failure and lower limb edema. Lymphology 2011;44:13-20. https://pubmed.ncbi.nlm.nih.gov/21667818/
  6. Vaassen MM. Manual lymph drainage in a patient with congestive heart failure: a case study. Ostomy Wound Management 2015;61:38-45. https://www.o-wm.com/article/manual-lymph-drainage-patient-congestive-heart-failure-case-study
  7. McCardell CS, Berge KH, Ijaz M, et al. Acute pulmonary edema associated with placement of waist-high, custom fit compression stockings. Mayo Clin Proc 1999;74:478-480. https://www.mayoclinicproceedings.org/article/S0025-6196(11)64822-2/fulltext

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 or its affiliate healthcare centers. 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!

Is compression therapy for leg edema harmful in patients with congestive heart failure?

Is intermittent pneumatic compression effective in reducing the risk of deep vein thrombosis in non-surgical hospitalized patients at high risk of major bleed?

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

The weight of the evidence to date suggests that intermittent pneumatic compression (IPC) is effective in reducing the risk of deep venous thrombosis (DVT) in hospitalized patients with stroke. 1,2 Whether IPC is also effective in non-surgical hospitalized patients without stroke at high risk of DVT and major bleed needs further studies.

A 2013 multicenter randomized trial (CLOTS 3) involving over 2,000 immobile hospitalized patients post-stroke found a significantly lower risk of DVT in proximal veins or any symptomatic DVT in the proximal veins within 30 days of randomization (8.5% vs 12.1%; absolute reduction risk 3.6%, 95% C.I. 1.4-5.8). Of note, the rate of concurrent heparin or low molecular weight heparin (LMWH) prophylaxis was similar between the 2 groups (17%). 1

A meta-analysis including the CLOTS 3 study and 2 other smaller trials 2 in patients with stroke found a risk reduction for proximal DVT (O.R. 0.66, 95% C.I 0.52-0.84) with nearly significant reduction in deaths by the end of the treatment period (O.R. 0.81, 95% 0.65-1.01).1

Although IPC may also be effective in non-surgical hospitalized patients without stroke but at high risk of DVT and bleed, proper trials in this patient population is lacking. In fact, the 2012 American College of Chest Physicians guidelines on antithrombotic therapy and prevention of thrombosis classifies use of IPC in preventing DVT’s in non-surgical acutely ill hospitalized patients as category 2C recommendation (weak, low quality evidence). 3

The patient population and methodology of above studies should be distinguished from those of a 2019 published trial involving only critically ill patients—all receiving pharmacologic thromboprophylaxis—which reported no reduction in the incidence of proximal lower-limb DVT with the addition of IPC. 4

 

Bonus Pearl: Did you know that venous thromboembolism has been reported in up to 42% of hospitalized patients who have had a stroke? 1

 

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References

  1. Dennis M, Sandercock P, Reid J, et al. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicenter randomized controlled trial. Lancet 2013;382:516-24. https://www.thelancet.com/cms/10.1016/S0140-6736(13)61050-8/attachment/1a0438d2-86eb-4da1-8bdb-92c0aec18b8d/mmc1.pdf
  2. Naccarato M, Chiodo Grandi F, Dennis M, et al. Physical methods for preventing deep vein thrombosis in stroke. Cochrance Database Syst Rev 2010;8:CD001922. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD001922.pub3/full
  3. Guyatt GH, Akl EA, Crowther M, et al. Executive summary: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. CHEST 2012;141 (suppl):7S-47S. http://www.sphcs.org/workfiles/CardiacVascular/7S-full.pdf
  4. Arabi YM, Al-Hameed F, Burns KEA, et al. Adjunctive intermittent pneumatic compression for venous thromboprophylaxis. N Engl J Med 2019;380:1305-15. https://pubmed.ncbi.nlm.nih.gov/30779530/

 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its 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!

Is intermittent pneumatic compression effective in reducing the risk of deep vein thrombosis in non-surgical hospitalized patients at high risk of major bleed?

Should I consider acute acalculous cholecystitis in my elderly ambulatory patient admitted with right upper quadrant pain?

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

Short answer: Yes! Although we usually associate acute acalculous cholecystitis (AAC) with critically ill patients (eg, with sepsis, trauma, shock, major burns) in ICUs, AAC is not as rare as we might think in ambulatory patients. In fact, a 7 year study of AAC involving multiple centers reported that AAC among outpatients was increasing in prevalence and accounted for 77% of all cases (1)!

 
Although the pathophysiology of ACC is not fully understood, bile stasis and ischemia of the gallbladder either due to microvascular or macrovascular pathology have been implicated as potential causes (2). One study found that 72% of outpatients who developed ACC had atherosclerotic disease associated with hypertension, coronary, peripheral or cerebral vascular disease, diabetes or congestive heart failure (1). Interestingly, in contrast to calculous cholecystitis, “multiple arterial occlusions” have been observed on pathological examination of the gallbladder in at least some patients with ACC and accordingly a name change to “acute ischemic cholecystitis” has been proposed (3).

 
AAC can also complicate acute mesenteric ischemia and may herald critical ischemia and mesenteric infarction (3). The fact that cystic artery is a terminal branch artery probably doesn’t help and leaves the gallbladder more vulnerable to ischemia when arterial blood flow is compromised irrespective of the cause (4).

 
Of course, besides vascular ischemia there are numerous other causes of ACC, including infectious (eg, viral hepatitis, cytomegalovirus, Epstein-Barr virus, Salmonella, brucellosis, malaria, Rickettsia and enteroviruses), as well as many non-infectious causes such as vasculitides and, more recently, check-point inhibitor toxicity (1,5-8).

 
Bonus Pearl: Did you know that in contrast to cholecystitis associated with gallstones (where females and 4th and 5th decade age groups predominate), ACC in ambulatory patients is generally more common among males and older age groups (mean age 65 y) (1)?

 

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References
1. Savoca PE, Longo WE, Zucker KA, et al. The increasing prevalence of acalculous cholecystitis in outpatients: Result of a 7-year study. Ann Surg 1990;211: 433-37. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1358029/pdf/annsurg00170-0061.pdf
2. Huffman JL, Schenker S. Acute acalculous cholecystitis: A review. Clin Gastroenterol Hepatol 2010;8:15-22. https://www.cghjournal.org/article/S1542-3565(09)00880-5/pdf
3. Hakala T, Nuutinene PJO, Ruokonen ET, et al. Microangiopathy in acute acalculous cholecystitis Br J Surg 1997;84:1249-52. https://bjssjournals.onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2168.1997.02775.x?sid=nlm%3Apubmed
4. Melo R, Pedro LM, Silvestre L, et al. Acute acalculous cholecystitis as a rare manifestation of chronic mesenteric ischemia. A case report. Int J Surg Case Rep 2016;25:207-11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4941110/
5. Aguilera-Alonso D, Median EVL, Del Rosal T, et al. Acalculous cholecystitis in a pediatric patient with Plasmodium falciparum infection: A case report and literature review. Ped Infect Dis J 2018;37: e43-e45. https://journals.lww.com/pidj/pages/articleviewer.aspx?year=2018&issue=02000&article=00020&type=Fulltext  
6. Kaya S, Eskazan AE, Ay N, et al. Acute acalculous cholecystitis due to viral hepatitis A. Case Rep Infect Dis 2013;Article ID 407182. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784234/pdf/CRIM.ID2013-407182.pdf
7. Simoes AS, Marinhas A, Coelho P, et al. Acalculous acute cholecystitis during the course of an enteroviral infection. BMJ Case Rep 2013;12. https://casereports.bmj.com/content/12/4/e228306
8. Abu-Sbeih H, Tran CN, Ge PS, et al. Case series of cancer patients who developed cholecystitis related to immune checkpoint inhibitor treatment. J ImmunoTherapy of Cancer 2019;7:118. https://jitc.biomedcentral.com/articles/10.1186/s40425-019-0604-2

 

 

Should I consider acute acalculous cholecystitis in my elderly ambulatory patient admitted with right upper quadrant pain?

My patient with inferior myocardial infarction with Q-waves 2 years ago now has no evidence of Q waves on his EKG. Can Q-waves from myocardial infarction really regress over time?

FA Manian MD, MPH, , , Leave a comment

Short answer: Yes! Q-waves may regress following transmural myocardial infarction (ATMI) and in fact this phenomenon may not be as unusual as once thought, occurring in 7-15% of patients (1,2).

 
A prospective study involving patients with ATMI evaluated by coronary angiography and followed for an average of 65 months found an 11% rate of loss of Q-waves over an average of 14 months after ATMI. Factors associated with loss of Q-waves included lower peak creatine kinase values, lower left ventricular end-diastolic pressures, higher ejection fractions, fewer ventricular aneurysms and lower rate of congestive heart failure, all leading to the authors’ conclusion that Q-wave loss may be related to a smaller infarct size (1).

 
Similar findings were reported from patients enrolled in the Aspirin Myocardial Infarction Study with a loss of a previously documented diagnostic Q-wave confirmed in 14.2% of participants over an average of 38 months. Mortality among patients who lost Q-waves was not significantly different than among those with persistent Q-waves in a single infarct location (2).

 
These observations suggest that Q-waves in the setting of ATMI may not necessarily be pathognomonic of myocardial necrosis and, at least in some instances, may be due to tissue ischemia, edema and inflammation causing reversible myocardial and electrical stunning (3). Of interest, reversible Q-waves have also been reported in acute myocarditis (4).

Bonus Pearl: Did you know that the EKG waves P and Q were likely named by Einthoven, the inventor of EKG, after the designation of the same letters by Descartes, the father of analytical geometry, in describing refraction points? (5). 

 

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References
1. Coll S, Betriu A, De Flores T, et al. Significance of Q-wave regression after transmural acute myocardial infarction. Am J Cardiol 1988;61:739-42.
2. Wasserman AG, Bren GB, Ross AM, et al. Prognostic implications of diagnostic Q waves after myocardial infarction. Circulation 1982;65:1451-55.
3. Barold SS, Falkoff MD, Ong LS, et al. Significance of transient electrocardiographic Q waves in coronary artery disease. Cardiol Clin 1987;5:367-80.
4. Dalzell JR, Jackson CE, Gardner RS. Masquerade: Fulminant viral myocarditis mimicking a Q-wave anterolateral myocardial infarction. Am J Med 2009. Doi:10.1016/j.amjmed.2009.01.015.

5. Hurst, JW.  Naming of the waves in the ECG, with a brief account of their genesis. Circulation 1998;98:1937-42. 

 

My patient with inferior myocardial infarction with Q-waves 2 years ago now has no evidence of Q waves on his EKG. Can Q-waves from myocardial infarction really regress over time?

Why was the myocardial infarction in my postop patient silent?

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

Myocardial infarction (MI) in postop patients is in fact usually silent (1,2) but what is less clear is how myocardial ischemia can occur without any symptoms.

Although use of analgesics and narcotics postop may dampen or mask chest pain or other symptoms associated with MI, other factors are also likely to play an important role, such as decreased sensitivity to painful stimuli, autonomic neuropathy (eg, in diabetes mellitus), and higher pain threshold among some patients (3).

Additional factors associated with silent MIs include cerebral cortical dysfunction since frontal cortical activation appears to be necessary to experience cardiac pain. Mental stress is also a frequent trigger for asymptomatic myocardial ischemia, infarction and sudden cardiac death (4).  High levels of beta-endorphin, an endogenous opiate, may also play a role (5).

 
Perhaps the most intriguing explanation for lack of symptoms is the observation that the levels of anti-inflammatory cytokines (interleukin-4 and -10)—which block pain transmission pathways and increase the threshold for nerve activation—seem to be increased in patients with silent myocardial ischemia (6).  Even more relevant to our postop patient is the finding that interleukin-10 production increases during and after major abdominal surgery and correlates with the amount of intraoperative blood loss (7). 

No wonder MIs in postop patients are often silent!

References
1. Devereaux PJ, Xavier D, Pogue J, et al. Characteristics nd short-term prognosis of perioperative myocardial infarction in patients undergoing noncardiac surgery: a cohort study. Ann Intern Med 2011;154:523-8. https://annals.org/aim/article-abstract/746934/characteristics-short-term-prognosis-perioperative-myocardial-infarction-patients-undergoing-noncardiac 
2. Badner NH, Knill RL, Brown JE, et al. Myocardial infarction after noncardiac surgery. Anesthesiology 1998;88:572-78. http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1948483
3. Ahmed AH, Shankar KJ, Eftekhari H, et al. Silent myocardial ischemia:current perspectives and future directions. Exp Clin Cardiol 2007;12:189-96. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2359606/ 
4. Gullette EC, Blumenthal JA, Babyak M, et al. Effects of mental stress on myocardial ischemia during daily life. JAMA 1997;277:1521-6. https://jama.jamanetwork.com/journals/jama/articlepdf/416233/jama_277_19_029.pdf
5. Hikita H, Kurita A, Takase B, et al. Re-examination of the roles of beta-endorphin and cardiac autonomic function in exercise-induced silent myocardial ischemia. Ann Noninvasive Electrocardiol 1997;2:319-25. https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1542-474X.1997.tb00195.x
6. Mazzone A, Cusa C, Mazzucchelli I, et al. Increased production of inflammatory cytokines in patients with silent myocardial ischemia. J Am Coll Cardiol 2001;38:1895-901. https://www.ncbi.nlm.nih.gov/pubmed/11738291
7. Kato M, Honda I, Suzuki H, et al. Interleukin-10 production during and after upper abdominal surgery. J Clin Anesth 1998;10:184-8. https://www.ncbi.nlm.nih.gov/pubmed/9603586 

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Why was the myocardial infarction in my postop patient silent?

My hospitalized patient with pneumonia has now suffered an acute myocardial infarction (MI). Can acute infection and MI be related?

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

Yes! Ample epidemiological studies implicate infection as an important risk factor for MI.1 The increased risk of MI has been observed during the days, weeks, months or even years following an infection.

A 2018 paper reported a several-fold risk of MI during the week after laboratory-confirmed infection caused by a variety of respiratory pathogens such as influenza virus (6-fold), respiratory syncytial virus (4-fold), and other respiratory viruses (3-fold). 2 Among patients hospitalized for pneumococcal pneumonia, 7-8% may suffer an MI.3,4 One study found a 48-fold increase in the risk of MI during the first 15 days after hospitalization for acute bacterial pneumonia.5 Similarly, an increase in the short-term risk of MI has been observed in patients with urinary tract infection and bacteremia.6

The risk of MI appears to be the highest at the onset of infection and correlates with the severity of illness, with the risk being the highest in patients with pneumonia complicated by sepsis, followed by pneumonia and upper respiratory tract infection. Among patients with pneumonia, the risk exceeds the baseline risk for up to 10 years after the event, particularly with more severe infections.1

Potential mechanisms of MI following infections include release of inflammatory cytokines (eg, interleukins 1, 6, tumor necrosis factor alpha) causing activation of inflammatory cells in atherosclerotic plaques, in turn resulting in destabilization of the plaques. In addition, the thrombogenic state of acute infections, platelet and endothelial dysfunction may increase the risk of coronary thrombosis at sites of plaque disruption beyond clinical resolution of the acute infection. 1

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References

  1. Musher DM, Abers MS, Corrales-Medina VF. Acute infection and myocardial infarction. N Engl J Med 2019;380:171-6. https://www.ncbi.nlm.nih.gov/pubmed/30625066
  2. Kwong JC, Schwartz KL, Campitelli MA, et al. Acute myocardial infarction after laboratory-confirmed influenza infection. N Engl J Med 2018;378:345-53. https://www.nejm.org/doi/full/10.1056/NEJMoa1702090
  3. Musher DM, Alexandraki I, Graviss EA, et al. Bacteremic and nonbacteremic pneumococcal pneumonia: a prospective study. Medicine (Baltimore) 2000;79:210-21. https://www.ncbi.nlm.nih.gov/pubmed/10941350
  4. Musher DM, Rueda Am, Kaka As, Mapara SM. The association between pneumococcal pneumonia and acute cardiac events. Clin Infect Dis 2007;45:158-65. https://www.ncbi.nlm.nih.gov/pubmed/17578773
  5. Corrales-Medina VF, Serpa J, Rueda AM, et al. Acute bacterial pneumonia is associated with the occurrence of acute coronary syndromes. Medicine (Baltimore) 2009;88:154-9. https://www.ncbi.nlm.nih.gov/pubmed/19440118
  6. Dalager-Pedersen M, Sogaard M, Schonheyder HC, et al. Risk for myocardial infarction and stroke after community-acquired bacteremia: a 20-year population-based cohort study. Circulation 2014;129:1387-96. https://www.ncbi.nlm.nih.gov/pubmed/24523433

 

My hospitalized patient with pneumonia has now suffered an acute myocardial infarction (MI). Can acute infection and MI be related?

My patient with angina symptoms also complains of neck pain with left arm numbness. Could they be related?

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

Short answer, yes! Anterior chest pain associated with cervical intervertebral disk disease, ossified posterior longitudinal ligament or other spinal disorders is sometimes referred to as “cervical angina” (CA) or “pseudoangina” and is an often overlooked source of non-cardiac chest pain. 1-5

Although its exact prevalence is unknown, 1.4% to 16% of patients undergoing cervical disk surgery may have symptoms of CA. 1 Conversely, 1 study reported 5% of patients with angina pectoris having cervical nerve root pathology.5 Many patients describe their chest pain as “pressure” or crushing in quality mimicking typical cardiac ischemia chest pain, often resulting in extensive cardiac workup.  To add to the confusion, some patients even respond to nitroglycerin! One-half of patients also experience autonomic symptoms such as dyspnea, vertigo, nausea, diaphoresis, pallor, fatigue, and diploplia.1

Certain clues in the patient’s presentation should help us seriously consider the possibility of CA: 1-3

  • History of cervical radiculopathy eg, subjective upper extremity weakness or sensory changes, occipital headache or neck pain
  • Pain induced by cervical range of motion or movement of upper extremity
  • History of cervical injury or recent manual labor (eg, lifting, pulling or pushing)
  • Pain lasting greater than 30 min or less than 5 seconds and not relieved by rest
  • Positive Spurling maneuver ie, reproduction of symptoms by rotating the cervical spine toward the symptomatic side while providing a downward compression through the patient’s head

CA is often attributed to cervical nerve root compression, likely mediated by compression of C4-C8 nerve roots which also supply the sensory and motor innervation of the anterior chest wall.

Bonus Pearl: Did you know that experimental stimulation of spinothalamic tract cells in the upper thoracic and lower cervical segments have been shown to reproduce angina pain? 6

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 References

 

  1. Susman WI, Makovitch SA, Merchant SHI, et al. Cervical angina: an overlooked source of noncardiac chest pain. The Neurohospitalist 2015;5:22-27. https://www.ncbi.nlm.nih.gov/pubmed/25553225
  2. Jacobs B. Cervical angina. NY State J Med 1990;90:8-11. https://www.ncbi.nlm.nih.gov/pubmed/2296405
  3. Sheps DS, Creed F, Clouse RE. Chest pain in patients with cardiac and noncardiac disease. Psychosomatic Medicine 66:861-67. https://www.ncbi.nlm.nih.gov/pubmed/15564350
  4. Wells P. Cervical angina. Am Fam Physician 1997;55:2262-4. https://www.ncbi.nlm.nih.gov/pubmed/9149653
  5. Nakajima H, Uchida K, Kobayashi S, et al. Cervical angina: a seemingly still neglected symptom of cervical spine disorder. Spinal Cord 2006;44:509-513. https://www.ncbi.nlm.nih.gov/pubmed/16331305
  6.  Cheshire WP. Spinal cord infarction mimicking angina pectoris. Mayo Clin Proc 2000;75:1197-99. https://www.ncbi.nlm.nih.gov/pubmed/11075751

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its 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!

 

My patient with angina symptoms also complains of neck pain with left arm numbness. Could they be related?