When should I suspect spontaneous coronary artery dissection in my patient with chest pain?

Spontaneous coronary artery dissection (SCAD) is defined as the separation of the walls of the coronary artery.1 It is thought that hemorrhage into the false lumen can result in compression of the true lumen, leading to ischemia. Although its exact incidence is unknown, SCAD has been estimated to account for up to 35% of myocardial infarctions in women younger than 50 y of age.2-3

SCAD is often associated with acute chest pain with presentations ranging from acute coronary syndrome (ACS) to sudden cardiac death.1,4 Diagnosis is typically accomplished with coronary angiography and, increasingly, newer modalities such as optical coherence tomography, intravascular ultrasound, and cardiac CT angiography.1

Clinical features that should raise suspicion of SCAD are shown (Table)5. Among many risk factors, myocardial infarction in younger women and the absence of traditional cardiovascular risk factors or lack of typical atherosclerotic lesions in coronary arteries should be potential flags for the possibility of SCAD.

Although the optimal management of SCAD is unclear, conservative therapy with aspirin, clopidogel and beta-blockers has often been recommended5 .  Percutaneous coronary intervention (PCI) carries a risk of worsening the dissection or causing additional dissections in such patients1. Revascularization is often reserved for those with hemodynamic instability, persistent ischemia, sustained ventricular tachycardia or fibrillation, or left main dissection.1,5

Table. Clinical features that raise suspicion of SCAD5 ______________________________________________________________________________________________________________
Myocardial infarction in young women (especially age ≤ 50 y)
Absence of traditional cardiovascular risk factors
Little or no evidence of typical atherosclerotic lesions in coronary arteries
Peripartum state
History of fibromuscular dysplasia
History of relevant connective tissue disorder (eg, Marfan’s syndrome, Ehler Danlos syndrome)
History of relevant systemic inflammation (incl. SLE, IBD, sarcoidosis, polyarteritis nodosa)
Precipitating stress events caused by emotional or intense physical factors ______________________________________________________________________________________________________________
SLE: Systemic lupus erythematosus; IBD: Inflammatory bowel disease (eg, Crohn’s, ulcerative colitis).

References

  1. Saw J, Mancini GB, Humphries KH. Contemporary Review on Spontaneous Coronary Artery Dissection. J Am Coll Cardiol 2016;68:297-312.
  2. Rashid HN, Wong DT, Wijesekera H, et al. Incidence and characterisation of spontaneous coronary artery dissection as a cause of acute coronary syndrome – a single-centre Australian experience. Int J Cardiol 2016;202:336-8.
  3. Nakashima T, Noguchi T, Haruta S, et al. Prognostic impact of spontaneous coronary artery dissection in young female patients with acute myocardial infarction: a report from the Angina Pectoris-Myocardial Infarction Multicenter Investigators in Japan. Int J Cardiol 2016;207:341-8.
  4. Lettieri C, Zavalloni D, Rossini R, et al. Management and long-term prognosis of spontaneous coronary artery dissection. Am J Cardiol 2015;116:66-73.
  5. Yip A, Saw J. Spontaneous coronary artery dissection-A review. Cardiovasc Diagn Ther 2015;5:37-48. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4329168/pdf/cdt-05-01-037.pdf

Contributed by Mahesh Vidula, MD, Mass General Hospital, Boston, MA.

When should I suspect spontaneous coronary artery dissection in my patient with chest pain?

Why do patients with anorexia nervosa often experience bradycardia?

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.
  2. Katzman DK. Medical complications in adolescents with anorexia nervosa: a review of the literature. Int J Eat Dis 2005; 37:S52-S59.
  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.
  4. Kollai M., et al. Cardiac vagal hyperactivity in adolescent anorexia nervosa. Eur Heart J 1994;15:1113-1118.
  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.
  7. Gottdiener JS, et al. Effects of self-induced starvation on cardiac size and function in anorexia nervosa. Circulation 1978;58: 425-433.
  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.

 

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?

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)?

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)?

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, with Sokolow-Lyon having the “highest” sensitivity (median 21%, 4-52%). Median specificities were  89% (53-100%) and 99% (71-100%) for Sokolow-Lyon and Romhilt-Estes criteria (5 points) (1).

More recently, MRI has become the gold standard for in-vivo LV mass measurement. In a study of 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!

 

LVH definitions 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 in ref.3)

Gubner: RI+SIII>24mm

 

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 

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.

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.

 

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?

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?

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

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?