<?xml version="1.0" encoding="UTF-8"?>
<records>
<record>
<language>eng</language>
<publisher>Science and Education Publishing</publisher>
<journalTitle>American Journal of Medical Case Reports</journalTitle>
<eissn>2374-216X</eissn>
<publicationDate>2019-08-14</publicationDate>
<volume>7</volume>
<issue>11</issue>
<startPage>271</startPage>
<endPage>273</endPage>
<doi>10.12691/ajmcr-7-11-2</doi>
<publisherRecordId>AJMCR20197112</publisherRecordId>
<documentType>article</documentType>
<title language="eng">Yohimbine Induced Type II Myocardial Injury: An Underrecognized and Dangerous Adverse Effect</title>
<authors>
<author>
<name>Jeffrey Song</name>
<email>j_song11@hotmail.com</email>
<affiliationId>1</affiliationId>
</author>
<author>
<name>Tariq Sharman</name>
<affiliationId>1</affiliationId>
</author>

</authors>
<affiliationsList>
<affiliationName affiliationId="1">Department of Medicine, Heritage College of Osteopathic Medicine at Ohio University, Southern Ohio Medical Center, Portsmouth, Ohio, U.S.A.</affiliationName>

</affiliationsList>
<abstract language="eng">Yohimbine is an Indoloquinolizidine alkaloid derived from the bark of the African tree Pausinystalia johimbe, as well as from the bark of the unrelated South American tree Aspidosperma quebracho-blanco. It is commonly sold as a dietary supplement for the purpose of enhancing libido, weight loss and natural bodybuilding aids. Yohimbine has high affinity for the α2-adrenergic receptor, moderate affinity for the α1 receptor, dopamine D2 receptor, and weak affinity for the dopamine D3 receptors and some of the serotonin receptors. Depending on dosage, Yohimbine can either increase or decrease systemic blood pressure (through vasoconstriction or vasodilation, respectively). We present a 51-year-old male who presented with substernal chest pressure and the sensation of a “pounding heart” after starting Yohimbine as a dietary supplement. He was found to have type II myocardial injury characterized by elevated troponin levels. We propose that the mechanism for this was 1) elevation of blood pressure and sinus tachycardia causing myocardial ischemia due to increased myocardial oxygen demand and supply mismatch, 2) cardiac norepinephrine release causing direct non-ischemic norepinephrine mediated myocardial injury and 3) increased sympathetic outflow mediated coronary vasoconstriction and spasm causing ischemia.</abstract>
<fullTextUrl format="pdf">http://pubs.sciepub.com/ajmcr/7/11/2/ajmcr-7-11-2.pdf</fullTextUrl>
<keywords language="eng"><keyword>Yohimbine</keyword>
<keyword>Hypertension</keyword>
<keyword>Norepinephrine</keyword>
<keyword>α2 receptor</keyword>
<keyword>Type II NSTEMI</keyword>
<keyword>Tachycardia</keyword>
<keyword>Erectile Dysfunction</keyword>
</keywords>
</record>
</records>
