Is there a connection between my patient’s blood type and risk of thromboembolic events?

There seems to be, given the weight of the evidence to date suggesting that non-blood group O may be associated with non-valvular atrial fibrillation (NVAF)-related peripheral cardioembolic complications, myocardial infarction (MI) and ischemic stroke. 1-4

A 2015 retrospective Mayo Clinic study involving patients with NVAF adjusted for CHADS2 score found significantly lower rate of peripheral embolization in those with blood group O compared to those with other blood groups combined (3% vs 2%, O.R. 0.66, 95% CI, 0.5-0.8); rates of cerebral thromboembolic events were not significantly different between the 2 groups, however. 1

A 2008 systematic review and meta-analysis of studies spanning over 45 years reported a significant association between non-O blood group and MI, peripheral vascular disease, cerebral ischemia of arterial origin, and venous thromboembolism.2 Interestingly, the association was not significant for angina pectoris or for MI when only prospective studies were included.  Some studies have reported that the association between VWF and the risk of cardiovascular mortality may be independent of blood group. 5,6

Although the apparent lower risk of thromboembolic conditions in O blood group patients may be due to lower levels of von Willebrand factor (VWF) and factor VIII in this population 1,4, other pathways likely  play a role.7  

As for why the rate of peripheral (but not cerebral) thromboembolic events in NVAP is affected by blood group, it is suggested that, because of their size, larger clots (facilitated by lower VWF levels) may bypass the carotid and vertebral orifices in favor of their continuation downstream to the “peripheral bed”.1

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References

  1. Blustin JM, McBane RD, Mazur M, et al. The association between thromboembolic complications and blood group in patients with atrial fibrillation. Mayo Clin Proc 2015;90;216-23. https://www.sciencedirect.com/science/article/abs/pii/S002561961401043X
  2. Wu O, Bayoumi N, Vickers MA, et al. ABO (H) groups and vascular disease: a systematic review and meta-analysis. J Thromb Haemostasis 2008;6:62-9. https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1538-7836.2007.02818.x
  3. Medalie JH, Levene C, Papier C, et al. Blood groups, myocardial infarction, and angina pectoris among 10,000 adult males. N Engl J Med 1971;285:1348-53. https://www.nejm.org/doi/pdf/10.1056/NEJM197112092852404
  4. Franchini M, Capra F, Targher G, et al. Relationship between ABO blood group and von Willebrand factor levels: from biology to clinical implications. Thrombosis Journal 2007, 5:14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042969/
  5. Meade TW, Cooper JA, Stirling Y, et al. Factor VIII, ABO blood group and the incidence of ischaemic heart disease. Br J Haematol 1994;88:601-7. https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2141.1994.tb05079.x
  6. Jager A, van Hinsbergh VW, Kostense PJ, et al. von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. Arterioscl Thromb Vasc Biol 1999;19:3071-78. https://www.researchgate.net/publication/12709043_von_Willebrand_Factor_C-Reactive_Protein_and_5-Year_Mortality_in_Diabetic_and_Nondiabetic_Subjects_The_Hoorn_Study
  7. Sode BF, Allin KH, Dahl M, et al. Risk of venous thromboembolism and myocardial infarction associated with factor V Leiden and prothrombin mutations and blood type. CMAJ 2013.DOI:10.1503/cmaj.121636. https://www.ncbi.nlm.nih.gov/pubmed/23382263
Is there a connection between my patient’s blood type and risk of thromboembolic events?

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?

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?

My patient with brain tumor suffered a myocardial infarction (MI) just before having a diagnostic brain surgery. Could the tumor have placed him at higher risk of a coronary event?

Yes! Arterial thromboembolism—just as venous thromboembolism— is more common in patients with cancer.

In a large 2017 epidemiologic study involving patients 66 years of age or older, the 6-month cumulative incidence of MI was nearly 3-fold higher in newly-diagnosed cancer patients compared to controls, with the excess risk resolving by 1 year. 1 These findings were similar to a previous report involving patients with newly-diagnosed cancer, although in that study the overall coronary heart disease risk remained slightly elevated even after 10 years. 2

In addition, the incidence of coronary events and unstable ischemic heart disease during the 2 year period prior to the diagnosis of cancer is 2-fold higher among cancer patients suggesting that ischemic heart disease may be precipitated by occult cancer. 3

The association of cancer and thromboembolic coronary events may be explained through several mechanisms, including development of a prothrombotic or hypercoagulable state through acute phase reactants, abnormal fibrinolytic activity and increased activation of platelets which are also significantly involved in the pathophysiology of acute coronary syndrome (ACS). 4 Coronary artery embolism from cancer-related marantic endocarditis may also occur.5

More specific to our case, primary brain tumors may be associated with a hypercoagulable state through expression of potent procoagulants such as tissue factor and tissue factor containing microparticles, with a subset producing carbon monoxide, another procoagulant. 6

So our patient’s MI prior to his surgery for brain tumor diagnosis might have been more than a pure coincidence!

Bonus Pearl: Did you know that cancer-related prothrombotic state, also known as  “Trousseau’s syndrome” was first described in 1865 by Armand Trousseau, a French physician who diagnosed the same in himself and died of gastric cancer with thrombotic complications just 2 years later? 7,8

References

  1. Navi BB, Reinder AS, Kamel H, et al. Risk of arterial thromboembolism in patients with cancer. JACC 2017;70:926-38. https://www.ncbi.nlm.nih.gov/pubmed/28818202
  2. Zoller B, Ji Jianguang, Sundquist J, et al. Risk of coronary heart disease in patients with cancer: A nationwide follow-up study from Sweden. Eur J Cancer 2012;48:121-128. https://www.ncbi.nlm.nih.gov/pubmed/22023886
  3. Naschitz JE, Yeshurun D, Abrahamson J, et al. Ischemic heart disease precipitated by occult cancer. Cancer 1992;69:2712-20. https://www.ncbi.nlm.nih.gov/pubmed/1571902
  4. Lee EC, Cameron SJ. Cancer and thrombotic risk: the platelet paradigm. Frontiers in Cardiovascular Medicine 2017;4:1-6. https://www.ncbi.nlm.nih.gov/pubmed/29164134
  5. Lee V, Gilbert JD, Byard RW. Marantic endocarditis-A not so benign entity. Journal of Forensic and Legal Medicine 2012;19:312-15. https://www.ncbi.nlm.nih.gov/pubmed/22847046
  6. Nielsen VG, Lemole GM, Matika RW, et al. Brain tumors enhance plasmatic coagulation: the role of hemeoxygenase-1. Anesth Analg 2014;118919-24. https://www.ncbi.nlm.nih.gov/pubmed/24413553
  7. Thalin C, Blomgren B, Mobarrez F, et al. Trousseau’s syndrome, a previously unrecognized condition in acute ischemic stroke associated with myocardial injury. Journal of Investigative Medicine High Impact Case Reports.2014. DOI:10.1177/2324709614539283. https://www.ncbi.nlm.nih.gov/pubmed/26425612
  8. Samuels MA, King MA, Balis U. CPC, Case 31-2002. N Engl J Med 2002;347:1187-94. https://www.nejm.org/doi/pdf/10.1056/NEJMcpc020117?articleTools=true

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My patient with brain tumor suffered a myocardial infarction (MI) just before having a diagnostic brain surgery. Could the tumor have placed him at higher risk of a coronary event?

Why was the myocardial infarction in my postop patient silent?

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?

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 is asking about the benefits of smoking cessation. How soon should she realize the health benefits of quitting her habit?

She should realize the health benefits of smoking cessation (SC) almost immediately! As the effect of nicotine wears off, just 15-20 minutes after her last cigarette, her heart rate and blood pressure should begin to fall.1,2Other health benefits, some within a year others longer, soon follow. 3,4 Between 2-12 weeks after SC, your patient may notice an improvement in her breathing and pulmonary function tests.

Between 1-9 months, the cilia in the lungs should begin to regenerate and regain normal function, allowing her to adequately clear mucus and bacteria with a decrease in cough and shortness of breath.

At 1 year, the risk of cardiovascular disease (eg, myocardial infarction, stroke) falls by one-half.

At 5 years, the risk of mouth, throat, esophagus, and bladder cancer also drops by one-half.

It takes 10 years for the risk of lung cancer to drop by one-half, and 15 years for it to approach that of non-smokers asymptotically. 4

 

Fun fact: Did you know that in hypertensive patients who smoke, the blood pressure lowering effect of beta-blockers may be partly abolished by tobacco smoking,  whereas alpha-blockers may maintain their antihypertensive effects? 5

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References

  1. Omvik P. How smoking affects blood pressure. Blood Press. 1996;5:71–77. https://www.ncbi.nlm.nih.gov/pubmed/9162447
  2. Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension. 2003;41(1):183-187. https://www.ncbi.nlm.nih.gov/pubmed/12511550
  3. US Surgeon General’s Report, 1990, pp. 193, 194, 196, 285, 323
  4. US Surgeon General’s Report, 2010 and World Health Organization. Tobacco Control: Reversal of Risk After Quitting Smoking. IARC Handbooks of Cancer Prevention, Vol. 11. 2007, p. 341.
  5. Trap-Jensen. Effects of smoking on the heart and peripheral circulation. Am Heart J 1988;115:263-7.   https://www.ncbi.nlm.nih.gov/pubmed/3276115

Contributed by Felicia Hsu, Medical Student, Harvard Medical School

My patient is asking about the benefits of smoking cessation. How soon should she realize the health benefits of quitting her habit?

How does hyperventilation cause coronary vasospasm?

Hyperventilation may be an important cause of coronary vasospasm and chest pain. 1 The mechanism likely revolves around the competition between the effects of hydrogen and calcium ions on the smooth muscle of coronary arteries. 2

Respiratory alkalosis induced by hyperventilation causes a reduction of hydrogen ions which, under physiologic conditions, compete with calcium ion, an important trigger for arterial smooth muscle contraction. Lower hydrogen ion concentrations tips the balance in favor of calcium’s effects on transmembrane channels and myofibrillar ATP-ase of the smooth muscle and causes vasoconstriction.2

In fact, hyperventilation has been used to reproduce coronary spasm during angiography in patients with non-obstructive coronary artery disease and angina symptoms.The efficacy of hyperventilation in inducing an alkalotic state during this test is verified by obtaining an arterial blood gas after 6-minutes of hyperventilation.  A basic Tris-buffer to enhance alkalotic provocation was also used in earlier studies. 2

In addition to producing spasm and angina, hyperventilation-induced alkalosis has been associated with frank transmural myocardial infarction and ischemia-related arrhythmias such as ventricular tachycardia. 2,4,5

So in the appropriate context, hyperventilation may not be so benign!

References:

  1. Freeman LJ, Nixon PGF. Chest pain and the hyperventilation syndrome-some aetiologic considerations. Postgrad Med J 1985;61:957-61. http://pmj.bmj.com/content/postgradmedj/61/721/957.full.pdf
  2. Yasue HM, Nagao S, Omote A, et al. Coronary arterial spasm and Prinzmetal’s variant form of angina induced by hyperventilation and Tris-buffer infusion. Circulation 1978;58:56-62. https://www.ncbi.nlm.nih.gov/pubmed/25720
  3. Zaya M, Mehta PK, Merz NB, etal. Provocative testing for coronary reactivity and spasm. J Am Coll Cardiol 2014; 63:103-9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3914306/pdf/nihms549572.pdf
  4. Magarian GJ, Jones S, Calverley T. Hyperventilation testing for coronary vasospasm: induction of spontaneous ventricular tachycardia in association with transmural ischemia without obstructive coronary disease. 1990; 120:1447-49. http://journal.chestnet.org/article/S0012-3692(16)52837-2/pdf
  5. Chelmowski MK, Keelan MH. Hyperventilation and myocardial infarction. Chest 1988;93:1095-96. https://www.ncbi.nlm.nih.gov/pubmed/3359829

Contributed by Ramya Chitra Mosarla, Medical Student, Harvard Medical School

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How does hyperventilation cause coronary vasospasm?

Does methotrexate reduce the risk of cardiovascular events in patients with rheumatoid arthritis?

The weight of the evidence suggests that methotrexate reduces the overall risk of cardiovascular events (CVEs)—including myocardial infarction, congestive heart failure, stroke, and or major adverse cardiac events—in RA patients (RR 0.72, 95% CI 0.57-0.91)1.

Aside from its effect on controlling systemic inflammation, methotrexate has also been shown to increase HDL and reduce total cholesterol/HDL ratio in patients with RA compared with treated non-RA controls2. In vitro, methotrexate appears to activate mechanisms involved in reverse transport of cholesterol out of the cell to the circulation for eventual excretion3. Not surprisingly then, methotrexate has also been reported to decrease atherosclerotic plaque burden measured by carotid artery intima-media thickness2.

We tend to think of RA as a disease that primarily causes arthritis but its effects may extend far beyond the joints. Patients with RA have an increased risk of cardiovascular deaths compared to the general population4, likely due to a variety of factors, including accelerated atherosclerosis secondary to chronic inflammation. At baseline, RA patients also have an unfavorable lipid profile with decreased HDL and higher total cholesterol/HDL ratio.

Fun Final Fact: Did you know that methotrexate is on the WHO Model List of Essential Medicines (April 2015) not only as a cancer drug but for treatment of RA as well5?

References:

  1. Roubille C, Richer V, Starnino T, McCourt C, McFarlane A, Fleming P, Siu S, Kraft J, Lynde C, Pope J, Gulliver W, Keeling S, Dutz J, Bessette L, Bissonnette R, Haraoui B. The effects of tumour necrosis factor inhibitors, methotrexate, non-steroidal anti-inflammatory drugs and corticosteroids on cardiovascular events in rheumatoid arthritis, psoriasis and psoriatic arthritis: a systematic review and meta-analysis. Ann Rheum Dis. 2015;74:480-9. https://www.ncbi.nlm.nih.gov/pubmed/25561362
  2. Georgiadis AN, Voulgari PV, Argyropoulou MI, Alamanos Y, Elisaf M, Tselepis AD, Drosos AA. Early treatment reduces the cardiovascular risk factors in newly diagnosed rheumatoid arthritis patients. Semin Arthritis Rheum 2008;38:13-9. https://www.ncbi.nlm.nih.gov/pubmed/18191989
  3. Reiss AB, Carsons SE, Anwar K, Rao S, Edelman SD, Zhang H, Fernandez P, Cronstein BN, Chan ES. Atheroprotective effects of methotrexate on reverse cholesterol transport proteins and foam cell transformation in human THP-1 monocyte/macrophages. Arthritis Rheum 2008;58:3675-83. https://www.ncbi.nlm.nih.gov/pubmed/19035488
  4. Aviña-Zubieta JA, Choi HK, Sadatsafavi M, Etminan M, Esdaile JM, Lacaille D. Risk of cardiovascular mortality in patients with rheumatoid arthritis: a meta-analysis of observational studies. Arthritis Rheum 2008; 59:1690-7. https://www.ncbi.nlm.nih.gov/pubmed/19035419
  5. WHO Model List of Essential Medicines (April 2015). http://www.who.int/medicines/publications/essentialmedicines/en/

 

Contributed by Brian Li, Medical Student, Harvard Medical School

Does methotrexate reduce the risk of cardiovascular events in patients with rheumatoid arthritis?

Why should I pay attention to the augmented vector right (aVR) EKG lead in my patient with chest pain?

Lead aVR is often “neglected” because of its non-adjacent location to other EKG leads (Fig 1) and poor awareness of its potential utility in detecting myocardial ischemia.

In acute coronary syndrome (ACS), ST-elevation (STE) in aVR (≥1mm) with diffuse ST depression in other leads (Fig 2) is usually a sign of severe left main coronary artery (LMCA), proximal left anterior descending (LAD), or 3-vessel coronary disease, and is associated with poor prognosis1-3.  In some patients with LMCA thrombosis, the EKG changes may be non-specific but STE in aVR should still raise suspicion for ischemia1.  Possible mechanisms for STE in aVR include diffuse anterolateral subendocardial ischemia or transmural infarction of the basal portion of the heart. 

The possibility of an anatomical variant of the Purkinje fibers leading to the absence of STE in the anterior leads in some patients with transmural anterior infarction is another reason to pay attention to aVR.

 

Fig 1. Standard EKG limb leads. Note that aVR is “in the fringes”.

ekggreatwork

Fig 2. 35 year old female with ACS due to LMCA spasm. Note STE in aVR with ST segment depression in leads V3-6, I, aVL, II, and aVF  (Courtesy National Library of Medicine)

ekgavr

 

References

  1. Kossaify A. ST segment elevation in aVR: clinical syndrome in acute coronary syndrome. Clin Med Insights: Case Reports 2013:6.
  2. Kireyev D, Arkhipov MV, Zador ST. Clinical utility of aVR-the neglected electrocardiographic lead. Ann Noninvasive Electrocardiol 2010;15:175-180.
  3. Wong –CK, Gao W, Stewart RAH, et al. aVR ST elevation: an important but neglected sign in ST elevation acute myocardial infarction. Eur Heart J 2010;31:1845-1853.
  4. De Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008;359:2071-3.

 

Why should I pay attention to the augmented vector right (aVR) EKG lead in my patient with chest pain?

My patient just had a run of ventricular tachycardia (VT) at a rate of 120 beats/min lasting 18 seconds without any symptoms. Does this arrhythmia meet the criteria for nonsustained VT (NSVT) and what is its significance?

Although NSVT is often defined as 3 (sometimes 5) or more consecutive beats arising below the atrioventricular node with a heart rate >100 beats/min lasting <30 s, this definition is not universal. Other definitions of NSVT include >120 beats/min using a duration cutoff of 15 s,  or at times no strictly defined diagnostic criteria1.  

NSVT can be observed in a variety of individuals, ranging from apparently healthy people to those with significant heart disease.  Whether NSVT provokes sustained life-threatening arrhythmias or is merely a surrogate marker of a more severe underlying cardiac pathology is unclear in most clinical settings 1

Because our patient  meets the generally observed criteria for NSVT, we should exclude an underlying occult pathology responsible for the arrhythmia and, in the case of known cardiac disease,  risk-stratify the patient for appropriate management2.  

The prognostic significance of NSVT is heavily influenced by the type and severity of underlying heart disease.  Patients with NSVT in the setting of >24 h post-acute myocardial infarction and those with chronic ischemic heart disease with left ventricular ejection fraction <40%  have a less desirable prognosis2. The management of patients with NSVT is generally aimed at treating the underlying heart disease.

References

  1. Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol 2012;60:1993-2004. http://www.onlinejacc.org/content/60/20/1993
  2. Katritisis DG, Camm AJ. Nonsustained ventricular tachycardia: where do we stand? Eur Heart J 2004;25:1093-1099. https://academic.oup.com/eurheartj/article/25/13/1093/465312
My patient just had a run of ventricular tachycardia (VT) at a rate of 120 beats/min lasting 18 seconds without any symptoms. Does this arrhythmia meet the criteria for nonsustained VT (NSVT) and what is its significance?