Cardiac disease

Why do patients with anorexia nervosa often experience bradycardia?

FA Manian MD, MPH, , Leave a comment

Cardiac complications are common in anorexia nervosa (AN), with sinus bradycardia occurring in up to 95% of patients1,2. The mechanism of bradycardia in AN has yet to be clearly elucidated.

The predominant hypothesis posits that bradycardia is due to an increased cardiac vagal tone3,4, with a direct relationship observed between vagal tone and percent weight loss4. Additionally, sympathetic response may be altered through down-regulation of cardiac beta-adrenoceptors5. The physiologic response of lowering the resting heart rate through an increase in parasympathetic activity and sympathetic down-regulation leads to energy conservation in the fasting state of AN.

Current guidelines recommend that patients with AN and “severe” sinus bradycardia—defined as heart rate <50 beats/min during the day or <45 beats/min at night—should be admitted to the hospital for cardiac monitoring and gradual weight gain6. Fortunately, bradycardia associated with AN is reversible with weight gain7,8.

 

References

  1. Portilla MG. Bradycardia: an important physical finding in anorexia nervosa. J Ark Med Soc 2011;107:206-208. https://www.ncbi.nlm.nih.gov/pubmed/21739848
  2. Katzman DK. Medical complications in adolescents with anorexia nervosa: a review of the literature. Int J Eat Dis 2005; 37:S52-S59. https://onlinelibrary.wiley.com/doi/full/10.1002/eat.20118
  3. Petretta M, et al. Heart rate variability as a measure of autonomic nervous system function in anorexia nervosa. Clin Card 1997; 20: 219-224. https://www.ncbi.nlm.nih.gov/pubmed/9068906
  4. Kollai M., et al. Cardiac vagal hyperactivity in adolescent anorexia nervosa. Eur Heart J 1994;15:1113-1118. https://www.ncbi.nlm.nih.gov/pubmed/7988604
  5. Kaye WH, et al. Isoproterenol infusion test in anorexia nervosa: Assessment of pre-and post-beta-noradrenergic receptor activity. Psychopharm Bull 1990.
  6. Golden NH, et al. Eating disorders in adolescents. J Adolesc Health 2003;33: 496-503. https://www.ncbi.nlm.nih.gov/pubmed/14642712
  7. Gottdiener JS, et al. Effects of self-induced starvation on cardiac size and function in anorexia nervosa. Circulation 1978;58: 425-433. https://www.ncbi.nlm.nih.gov/pubmed/679432
  8. Olivares JL, et al. Cardiac findings in adolescents with anorexia nervosa at diagnosis and after weight restoration. Eur J Pediatrics 2005;164:383-386. https://www.ncbi.nlm.nih.gov/pubmed/15909184

 

Contributed by Marissa K Shoji, Medical Student, Harvard Medical School

Why do patients with anorexia nervosa often experience bradycardia?

The serum creatinine of my patient originally admitted for management of tense ascites is slowly rising. How concerned should I be?

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

Although the causes of increasing serum creatinine (SCr) in patients with cirrhosis are legion (eg, sepsis, acute tubular injury, and intravascular volume depletion due to over-diuresis, gastrointestinal bleed, or other causes), the most feared cause is often hepatorenal syndrome (HRS). HRS is a functional renal impairment that reflects the final pathophysiological stages of systemic circulatory impairment1, and significantly contributes to a worsening prognosis in patients with cirrhosis2. For example, without treatment, in patients whose SCr doubles in less than 2 weeks (type I HRS) the median survival is less than 2 weeks , while in those who develop a more gradual renal impairment (type II HRS) the median survival is 6 months3.

Physiologically, HRS is a culmination of significant vasodilation in the splanchnic arteries which, in time, leads to reduced organ perfusion due to a drop in the cardiac output. The associated increase in the activity of the renin-angiotensin-aldosterone and the sympathetic nervous systems contributes to sodium and water retention, and further exacerbates intra-renal vasoconstriction and ascites3.

The primary goal in the medical management of HRS is to increase splanchnic vascular resistance4, often by administering a combination of IV albumin, octreotide and other vasoconstricting agents (eg, midodrine, norepinephrine, or terlipressin [unavailable in US and Canada]).  Of interest, in addition to expanding the circulating plasma volume, albumin may have a vasoconstricting effect by binding to endotoxins, nitric oxide, bilirubin and fatty acids4!

 

References

  1. Arroyo V, Fernandez J, Gines P. Pathogenesis and treatment of hepatorenal syndrome. Semin Liver Dis 2008;28:81-95.
  2. Salerno F, Gerbes A, Ginès P, et al. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut. 2007 Sep;56(9):1310-8.
  3. Cardenas A, Gines P. A Patient with cirrhosis and increasing creatinine Level: What Is It and what to do? Clin Gatroenterol Hepatol 2009;7:1287–1291. 
  4. Baraldi O, Valentini C, Donati G, et al. Hepatorenal syndrome: Update on diagnosis and treatment. World J Nephrol. 2015;4:511-20.

Contributed by Alireza Sameie, Medical Student, Harvard Medical School

The serum creatinine of my patient originally admitted for management of tense ascites is slowly rising. How concerned should I be?

Why is there a predilection for the tricuspid valve (TV) infection among injection drug users (IDUs) with infective endocarditis (IE)?

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

Although right-sided IE accounts for only 9% of IE cases among non IDUs, in IDUs it accounts for over three-quarters of IE cases1.  

Several potential mechanisms have been posited to explain susceptibility of TV to infection in IDUs, including endothelial damage due to repeated inoculation of small bacterial loads, specific substances (eg talc) injected with drugs,  cocaine-induced vasospasm and thrombus formation, and drug-induced pulmonary hypertension associated with increased pressure gradients and turbulence.  In addition, facilitation of bacterial adhesion due to the deposition of immune complexes (eg antibody vs antigens in injected drugs) on the TV and coating of the injected particulate matter with bacterial adherence matrix molecules on valve surfaces may also play an important role1,2.

Add to these potential factors a higher risk nasal and cutaneous colonization with Staphylococcus aureus (a common cause of IE) among IDUs, and we have a perfect storm!

References

  1. Frontera JA, Gradon JD. Right-sided endocarditis in injection drug users: review of proposed mechanisms of pathogenesis. Clin Infect Dis 2000;30:374-9.
  2. Chahood J, Yakan AS, Saad H, et al. Right-sided infective endocarditis and pulmonary infiltrates: An update. Cardiol Rev 2016;24:230-37.
Why is there a predilection for the tricuspid valve (TV) infection among injection drug users (IDUs) with infective endocarditis (IE)?

How accurate is EKG when evaluating for left ventricular hypertrophy (LVH)?

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

A systematic review comparing 6 EKG criteria for LVH (including commonly used Sokolow-Lyon [defined below], Cornell voltage index or product, Gubner, and Romhilt-Estes scores 4 or 5) with echocardiography reported very low median sensitivities; “highest” sensitivity was found using the Sokolow-Lyon criteria (median 21%, 4-52%). Median specificities were  89% (53-100%) and 99% (71-100%) for Sokolow-Lyon and Romhilt-Estes criteria (5 points) (1).

LVH definition of selected EKG indexes

Sokolow-Lyon index: SV1+(RV5 or V6)>35 mm 

Cornell voltage index: men, RaVL+SV3>28 mm; women, RaVL+SV3>20 mm

Modified Cornell: RaVL>11mm (>10 mm, ref. 3)

Gubner: RI+SIII>24mm

More recently, MRI has become the gold standard for in-vivo LV mass measurement. In a study involving patients with aortic stenosis undergoing MRI, EKG generally had poor negative predictive value (NPV) (<70% by most criteria), but high positive predictive value (PPV) (>90% by most criteria) for LVH; for Sokolow-Lyon criteria, the NPV and PPV were 46% and 90%, respectively (2). 

In another MRI study involving patients with various cardiovascular conditions (eg hypertension, CAD), RaVL alone (>10mm) performed better than Sokolow-Lyon (AUC 0.78, specificity 95.5%) but its sensitivity was still nothing to brag about (36.5%) (3).

So, EKGs are better at ruling in than ruling out LVH!

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References

1.Pewsner D, Juni P, Egger M, et al. Accuracy of electrocardiography in diagnosis of left ventricular hypertrophy in arterial hypertension: systematic review. BMJ 2007. doi:10.1136/bmj.39276.636354.AE  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2001078

2.Buchner S, Debl K, Haimerl J, et al.  Electrocardiographic diagnosis of left ventricular hypertrophy in aortic valve disease: evaluation of ECG criteria by cardiovascular magnetic resonance. J Cardiovasc Magn Reson  2009; 11:18. https://jcmr-online.biomedcentral.com/articles/10.1186/1532-429X-11-18

3.Courand P-Y, Grandjean A, Charles P, et al. R wave in aVL lead is a robust index of left ventricular hypertrophy: a cardiac MRI study. Am J Hypertension 2015;28:1038-48. https://www.ncbi.nlm.nih.gov/pubmed/25588700

 

Contributed in part by Khin-Kyemon Aung, medical student, Harvard Medical School, Boston.

How accurate is EKG when evaluating for left ventricular hypertrophy (LVH)?

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

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

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

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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?

How does cold weather induce angina pectoris (AP) in some patients with coronary artery disease?

FA Manian MD, MPH, Leave a comment

Although it is well known that exposure to cold can provoke AP in some patients with coronary artery disease1, a unifying mechanism for its explanation has yet to be found.

One study involving subjects with exertional AP who inhaled cold air (-20 C°) during cardiac catheterization found no evidence of reactive constriction of large coronary arteries2, while another study involving patients with >50% coronary stenosis undergoing cold pressor test ( placing patient’s hand and forearm in ice water for 90 seconds), demonstrated a 39% decrease in coronary blood flow3.  

 Another experiment involving patients undergoing exercise treadmill testing at 6 and 25 C° found an increase in serum norepinephrine levels, increase in blood pressure and an increase in myocardial oxygen demand in all subjects on exposure to cold air3.  It concluded that compared to patients without cold-induced AP, patients with cold-induced AP may not have a reflex decrease in their heart rate, possibly due to a baroreceptor dysfunction. 

References

  1. Marchant B, Donaldson G, Mridha K. et al. Mechanisms of cold intolerance in patients with angina. J Am Coll Cardiol 1994;23:630-6.
  2. Hattenhauer M, Neill WA. The effect of cold air inhalation on angina pectoris and myocardial oxygen supply. Circulation 1975;51:1053-1058.
  3. Nabel EG, Ganz P, Gordon JB, et al. Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test. Circulation 1988;77:43-52.
How does cold weather induce angina pectoris (AP) in some patients with coronary artery disease?

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?

FA Manian MD, MPH, , , Leave a comment

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?

Should I use a hemoglobin level of 7 or 8 g/dL as a threshold for blood transfusion in my hospitalized patient?

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

Unlike its previous 2012 guidelines that recommended overlapping hemoglobin level triggers of 7 g/dL to 8 g/dL for most inpatients, the 2016 guidelines from AABB (formerly known as the American Association of Blood Banks) assigns 2 distinct tiers of hemoglobin transfusion triggers: 7 g/DL for hemodynamically stable adults, including those in intensive care units, and 8 g/dL for patients undergoing cardiac or orthopedic surgery or with preexisting cardiovascular disease1 , often defined as history of coronary artery disease, angina, myocardial infarction, stroke, congestive heart failure, or peripheral vascular disease2,3.  

These recommendations are based on an analysis of over 30 randomized trials, taking into account the potential risks of withholding transfusions, including 30-day mortality, and myocardial infarction. The new 2-tier recommendation specifically excludes those with acute coronary syndrome, severe thrombocytopenia (patients treated for hematological or oncological reasons who are at risk of bleeding), and chronic transfusion-dependent anemia.

The guidelines also emphasize that good clinical practice dictates considering not only the hemoglobin level but the overall clinical context when considering blood transfusion in patients. These factors include alternative therapies to transfusion, rate of decline in hemoglobin level, intravascular volume status, dyspnea, exercise tolerance, light-headedness, chest pain considered of cardiac origin, hypotension, tachycardia unresponsive to fluid challenge, and patient preferences.

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References

  1. Carson JL, Guyatt G, Heddle NW. Clinical practice guidelines from the AABB red blood cell transfusion thresholds and storage. JAMA. Doi:10.1001/jama.2016.9185. Published online October 12, 2016. https://www.ncbi.nlm.nih.gov/pubmed/27732721
  2. Carson JL, Duff A, Poses RM, et al. Effect of anemia and cardiovascular disease on surgical mortality and morbidity. Lancet 1996;348:1055-60. https://www.ncbi.nlm.nih.gov/pubmed/8874456
  3. Carson JL, Siever F, Cook DR, et al. Liberal versus restrictive blood transfusion strategy: 3-year survial and cause of death results from the FOCUS randomized controlled trial. Lancet 2015;385:1183-1189. https://www.ncbi.nlm.nih.gov/pubmed/25499165
Should I use a hemoglobin level of 7 or 8 g/dL as a threshold for blood transfusion in my hospitalized patient?

What is the significance of hyponatremia in my patient with acute decompensated congestive heart failure (ADCHF)?

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

Hyponatremia, defined as a serum sodium <135 meq/L, is observed in ~20% of patients hospitalized with ADCHF, and is often dilutional, not “depletional” (ie, not associated with hypovolemia) in this condition1.

In ADCHF, hyponatremia is primarily caused by the production of arginine vasopressin (AVP) (also known as anti-diuretic hormone, or ADH) as a result of decreased perfusion pressures in the aortic arch and renal afferent arterioles, and increased thirst due to the activation of the renin-angiotensin system.  Hyponatremia correlates with the severity of ADCHF and adverse clinical outcomes2.   

 A common approach to dilutional hyponatremia in ADCHF is fluid restriction. Other potential therapies include angiotension converting enzyme inhibitors (by increasing cardiac output and decreasing thirst), loop diuretics (by reducing water reabsorption in the renal distal tubule), and AVP antagonists (eg, tolvapatan, satavaptan)1,3.  Otherwise, in the absence of symptoms, no specific therapy is generally indicated for serum sodium levels ≥ 120mEq/L.

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References 

  1. Verbrugge FH, Steels P, Grieten L, Nijst P, Tang WHW, Mullens W. Hyponatremia in acute decompensated heart failure: Depletion versus dilution. J Am Coll Cardiol 2015;65:480-92. https://www.sciencedirect.com/science/article/pii/S073510971407394X?via%3Dihub
  2. Leier CV, Dei Cas L, Metra M. Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia. Am Heart J. 1994;128:564.  https://www.sciencedirect.com/science/article/pii/0002870394906335
  3. Schrier RW, Gross P, Gheorghiade M, Berl T, Verbalis JG, Czerwiec FS, Orlandi C, SALT Investigators. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355:2099. https://www.ncbi.nlm.nih.gov/pubmed/17105757

 

Contributed by Ricardo Ortiz, Medical Student, Harvard Medical School

What is the significance of hyponatremia in my patient with acute decompensated congestive heart failure (ADCHF)?

My elderly patient with acute heart failure with preserved ejection fraction (HFpEF) has a low serum albumin. Can hypoalbuminemia be associated with HFpEF?

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

Absolutely! As early as 1959, Guyton and Lindsey demonstrated the importance of serum colloid osmotic pressure in the pathogenesis of pulmonary edema1.

Specifically, they found that in dogs with normal plasma protein concentrations fluid began to transudate into the lungs when the left atrial pressure rose above an average of 24 mm Hg vs only 11 mm Hg when plasma protein concentration was reduced by about 50%.

Fast forward to 2003, Arques et al studied serum albumin and pulmonary artery wedge pressures in 4 groups of patients: acute HFpEF, heart failure with reduced ejection fraction (HFrEF), acute dyspnea from pulmonary origin and normal controls2.   Patients with HFpEF were significantly more likely to have hypoalbuminemia , compared to those with HFrEF, pulmonary disease or normal controls.  The main cause of hypoalbuminemia in the HFpEF was malnutrition in 77% and/or sepsis in 41% of patients.   Hypoalbuminemia was inversely related to age and plasma C-reactive protein.

Perhaps, we should pay more attention the nutritional status of our patients with HFpEF!

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References

  1. Guyton AC, Lindsey AW. Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pulmonary edema. Circ Res 1959;7: 649-657.
  2. Arquès S, Ambrosi P, Gélisse R et al. Hypoalbuminemia in elderly patients with acute diastolic heart failure. J Am Coll Card 2003;42:712-16. http://www.onlinejacc.org/content/42/4/71                                                                                                    
My elderly patient with acute heart failure with preserved ejection fraction (HFpEF) has a low serum albumin. Can hypoalbuminemia be associated with HFpEF?