Month: December 2015

How does obesity lower serum brain natriuretic peptide (BNP) levels in patients with heart failure?

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

The association between high body mass index (BMI) and low serum BNP levels  has been reported in heart failure patients with diminished or preserved left ventricular systolic function (1).  

However, The exact mechanism underlying the inverse relationship of BNP levels with BMI is unclear.  Decreased production of BNP by myocytes, increased clearance of BNP and decreased sensitivity of the myocytes to stretch have been proposed (1). 

Of interest, in obese patients who undergo gastric bypass surgery, serum BNP levels increases significantly postoperatively and correlates with weight loss  (2).  

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References 

  1. Stavrakis S, Pakala A, Thomas J et al. Obesity, brain natriuretic peptide levels and mortality in patients hospitalized with heart failure and preserved left ventricular systolic function. Am J Med Sci 2013;345:211-217. https://www.ncbi.nlm.nih.gov/pubmed/23422653
  2. Changchien EM, Shushmita A, Betti F, et al. B-type natriuretic peptide increases after gastric bypass surgery and correlates with weight loss. Surg Endosc 2011;25:2338-2343. https://www.ncbi.nlm.nih.gov/pubmed/21424205
How does obesity lower serum brain natriuretic peptide (BNP) levels in patients with heart failure?

Is there a seasonal variation in the incidence of cardiovascular (CV) events or venous thromboembolism (VTE)?

FA Manian MD, MPH, , , , , , , , , , 1 Comment

Seasonal variation, primarily characterized by a winter peak, has been reported for acute CV events, such as acute myocardial infarction (AMI) and sudden death, aortic rupture or dissection, and ischemic or hemorrhagic stroke, and VTE (1). A meta-analysis involving patients with VTE, primarily with a diagnosis of pulmonary embolism, revealed a 20% absolute increase in the incidence of VTE during January (1).  

Potential physiological mechanisms for these observations include increased sympathetic activity, decreased loss of fluids and sodium, increase in LDL cholesterol, increase in serum fibrinogen levels and other coagulation markers and C-reactive protein, and lower vitamin D levels due to shorter daylight hours during winter months (1,2).  At least in the case of AMI in the U.S., the higher incidence in winter is not affected by climate (2).  

Respiratory virus infections as a cause of acute inflammation leading to  CV or VTE events is another intriguing explanation (3). Indeed, influenza vaccination has been associated with reduction in hospitalization for cardiac disease and stroke among the elderly (4) and, in patients with cardiovascular disease, a reduction in death due to combined cardiovascular disease events such as heart attacks and strokes (5).

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References

  1. Dentali F, Ageno W, Rancan E, et al. Seasonal and monthly variability in the incidence of venous thromboembolism. A systematic review and a meta-analysis of the literature. Thromb Haemost 2011;106:439-447. https://www.ncbi.nlm.nih.gov/pubmed/21725580
  2. Spencer FA, Goldberg RJ, Becker RC, et al. Seasonal distribution of acute myocardial infarction in the Second National Registry of Myocardial Infarction. J Am Coll Cardiol 1998;31:1226-33.h ttps://www.ncbi.nlm.nih.gov/pubmed/9581712
  3. Woodhouse PR, Khaw KT, Plummer M, et al. Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease. Lancet 1994;343:435-39.  https://www.ncbi.nlm.nih.gov/pubmed/7508540
  4. Nichol KL, Nordin J, Mulloly J, et al. Influenza vaccination and reduction in hospitalization for cardiac disease and stroke among the elderly. N Engl J Med 2003; 348:1322-1332. http://www.nejm.org/doi/full/10.1056/NEJMoa025028
  5. Clar C, Oseni Z, Flowers N, et al. Cochrane Database of Systematic Reviews 2015. DOI: 10.1002/14651858.CD005050.pub3h ttp://www.cochrane.org/CD005050/VASC_flu-vaccines-for-preventing-cardiovascular-disease  

 

 

 

 

Is there a seasonal variation in the incidence of cardiovascular (CV) events or venous thromboembolism (VTE)?

Which patients outside of ICU setting should be placed on telemetry monitoring in the hospital?

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

Telemetry monitoring should be used in patients at increased risk of arrhythmias during hospitalization (1). While the American Heart Association provides expert opinion on telemetry for a variety of cardiac conditions (1), a more recent review (2) makes suggestions for common cardiac and non-cardiac diagnoses based on arrhythmia risk.

Telemetry is recommended for patients admitted for implantable cardioverter- defibrillator firing, second or third degree AV block, prolonged QT interval with ventricular arrhythmia, acute heart failure, acute cerebrovascular event,  acute coronary syndrome and massive blood transfusion.

Telemetry may be beneficial in syncope with arrhythmia as a suspected cause, gastrointestinal hemorrhage after endoscopy, atrial arrhythmias on rate or rhythm control therapy, electrolyte imbalance and subacute congestive heart failure.

Telemetry is not generally indicated in chest pain with normal EKG and cardiac markers, COPD exacerbation, PE if the patient is stable and on anticoagulation, and cases requiring minor blood transfusion. 

Contributed by Joome Suh, MD, Boston, MA

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References 

(1) Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care Nurses. Circulation 2004;110:2721–46. 

(2) Chen EH and Hollander JE. When do patients need admission to a telemetry bed? The Journal of Emergency Medicine 2007:33(1):53-60.

 

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, Mass General Hospital, Harvard Medical School or its affiliated institutions. 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!

Which patients outside of ICU setting should be placed on telemetry monitoring in the hospital?

Are GI symptoms such as nausea, vomiting, and diarrhea common in patients with influenza?

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

Typically, GI symptoms are more prominent in children with influenza than adults but during the H1N1 epidemic in 2009 (which has subsequently become endemic), up to 26% of hospitalized adults with H1N1 infection had abdominal pain or vomiting and up to 25% had diarrhea (1). 

In fact, H1N1 virus has been isolated from stool of adult hospitalized patients (2,3) and receptors of influenza virus have been identified in human GI epithelial cells, the correlation between GI symptoms and isolation of virus from stool is poorly defined (4).

Interestingly, the mechanism involved in influenza-mediated intestinal injury may have less to do with direct invasion of the intestinal mucosa by the virus and more to do with immune mediated changes  related to alterations in the intestinal microbiota induced by influenza virus infection itself (4,5)! 

Aside from direct or indirect effects of influenza virus on the GI tract, oseltamivir and non-steroidal anti-inflammatory use may also contribute to GI symptoms (4).

 

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References

  1. Writing Committee of the WHO Consultation on Clinical Aspects of Pandemic (H1N1) 2009 influenza. Clinical aspects of pandemic 2009 influenza A (H1N1) virus infection. N Engl J Med 2010;362:1708-19. https://www.ncbi.nlm.nih.gov/pubmed/20445182
  2. Yoo SJ, Moon SJ, Kuak E-Y, et al. Frequent detection of pandemic (H1N1) 2009 virus in stools of hospitalized patients. J Clin Microbiol 2010; 48:2314-2315. https://www.ncbi.nlm.nih.gov/pubmed/20375236
  3. Minodier L, Charrel RN, Ceccaldi PE, et al. Prevalence of gastrointestinal symptoms in patients with influenza, clinical significance, and pathophysiology of human influenza viruses in faecal samples: what do we know? Virol J 2015;12:215. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4676820/
  4. Shu Y, Li CK, Gao R, et al. Avian influenza A(H5N1) viruses can directly infect and replicate in human gut tissues. J Infect Dis 2010;201:1173-7. https://www.ncbi.nlm.nih.gov/pubmed/20210629
  5. Wang J, Li F, Wei H, et al. Respiratory influenza virus infection induces intestinal immune injury via microbiota mediated Th17 cell-dependent inflammation. J Exp Med 2014;211:2397-2410. http://europepmc.org/article/PMC/4235643
Are GI symptoms such as nausea, vomiting, and diarrhea common in patients with influenza?

What is medication overuse headache and how should we approach it?

FA Manian MD, MPH, Leave a comment

Medication overuse headache (MOH), also known as rebound headache, is caused by the overuse of medications for acute headaches. It affects 1-2% of the general population, often women, and should be considered in all patients presenting with chronic headaches (1).

According to the International Classification of Headache Disorders (ICHD) (2), MOH has the following characteristics: A. Present on ≥15 days/month in a patient with a pre-existing headache disorder; B. Present for > 3 months with regular use of acute headache medications (eg. ergotamines, triptans, opioids, combination analgesics) on ≥10 days/month, simple analgesics on ≥15 days/month, or any combination of the above drugs on ≥10 days/month; and C. Not readily accounted for by any other ICHD diagnosis. For treatment, experts recommend discontinuation of the offending medication(s) with a taper for medications that may cause severe withdrawal symptoms (e.g. narcotics, benzodiazepines, and barbiturates) (1).

 

References:

 (1) Munksgaard SB and Jensen RH. Medication Overuse Headache. Headache. 2014;54(7):1251-7.

 (2) Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. 2013;33:629-808.

 

Contributed by Joome Suh, MD, Boston, MA.

What is medication overuse headache and how should we approach it?

How can I be sure that my patient truly has orthostatic hypotension (OH)?

FA Manian MD, MPH, , , , , , , 1 Comment

 

OH is a sustained reduction of systolic blood pressure (SBP) of ≥ 20 mm Hg or diastolic BP ≥ 10 mm Hg within 3 min of standing or head-up tilt to at least 60° on a tilt table (1). In patients with supine hypertension, a reduction in SBP of 30 mm Hg has been suggested (1).  

The Centers for Disease Control and Prevention (CDC) recommends BP measurements when patient is supine for 5 min, and after standing for 1 and 3 min (2).  In some patients symptomatic OH occurs beyond 3 minutes of standing (1). Preference for mercury column sphygmomanometer due to its reliability and simplicity, with arm at the level of the heart has been stressed (3). 

A 2017 report involving over 11,000 middle-aged participants (Atherosclerosis Risk in Communities Study) has challenged the notion of waiting 3 minutes before OH is measured (4).  This prospective study  found a significant association between participant-reported history of dizziness on standing and OH but only at 1st measurement (mean of 28.0 seconds after standing), not at subsequent ones over a 2 minute period. It was concluded that measuring OH during the first minute “not only makes a lot of sense” but it’s more appropriate “because it’s more predictive of future falls”.

Keep in mind that OH is more common and more severe during mornings and after meals, and is exacerbated by large meals, meals high in carbohydrate, and alcohol intake (1).

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 References

 

  1. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Autonomic Neuroscience: Basic and Clinical 2011;161: 46–48. https://www.ncbi.nlm.nih.gov/pubmed/21431947
  2. http://www.cdc.gov/steadi/pdf/measuring_orthostatic_blood_pressure-a.pdf , accessed Dec 13, 2015.
  3. Naschitz J, Rosner I. Orthostatic hypotension: framework of the syndrome . Postgrad Med J 2007; 83:568-574. http://pmj.bmj.com/content/83/983/568
  4. Juraschek SP, Daya N, Rawlings AM, et al. Comparison of early versus late orthostatic hypotension assessment times in middle-age adults. JAMA Intern Med 2017;1177:1316-1323. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661881/

 

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!

How can I be sure that my patient truly has orthostatic hypotension (OH)?