This month’s Emergency Medicine Practice issue on SVT emergencies, written by Drs. Amandeep Singh and Jennifer Carnell of Highland General Hospital, is really a tremendous resource. From pathophysiology to therapy, this issue reflects the latest literature and evidence-based recommendations, and is chock full of figures, tables, and tracings to illustrate the concepts. I frequently gravitate toward EM Practice’s sections on Risk Management and Cost-Effective Strategies, and this month’s issue has some gems, a few of which are excerpted below:
While certain forms of SVT (e.g., NPJT) may be associated with ACS/MI, most patients with SVT do not require evaluation for cardiac ischemia. In fact, ordering cardiac enzymes in all patients with SVT can be a dangerous approach that leads to unnecessary anti-anginal therapy and invasive testing. Several studies have shown that markers of cardiac ischemia (troponin I) can be elevated but that patients do not have significant coronary artery disease on further evaluation. Of course, in patients in whom you suspect cardiac ischemia or who have significant risk factors, appropriate evaluation is indicated and may include serial cardiac enzymes and admission.
While hyperthyroidism, electrolyte abnormalities, anemia, and drug/alcohol use have all been associated with SVT, it is unlikely that all of these etiologies need to be investigated in every single patient. A focused history and physical examination will help guide which, if any, laboratory testing is appropriate. Additionally, if a patient discloses that he/she abuses drugs or alcohol, a confirmatory test is likely unnecessary. I remember a conversation on shift with one of my mentors (and prior EM Practice contributor – Scott Weingart, MD – see the July 2007 EM Practice article) about EKG signs of demand ischemia in SVT, and the relevancy of troponin levels. I was pleased to see this edition cite some relevant literature on this vexing issue (references 62 & 63: Redfearn DP, Ratib K, Marshall HJ, et al. Supraventricular tachycardia promotes release of troponin I in patients with normal coronary arteries. Int J Cardiol. Jul 2005;102(3):521-522. [Retrospective case series; 7 patients] Zellweger MF, Schaer BA, Cron TA, et al. Elevated troponin levels in the absence of coronary artery disease after supraventricular tachycardia. Swiss Med Wkly. Aug 2003;133(31-32):439-441. [Case series; 4 patients]).
To elaborate on this topic, Zellweger et al wrote:
“Generally speaking, elevated troponin levels are consistent with the diagnosis of acute coronary syndrome and haemodynamically significant coronary artery stenosis. However, it must be borne in mind that troponin results (as also other easily available laboratory variables) need to be interpreted in the context of the patient’s clinical presentation. The TIMI risk score provides a useful tool in the clinical evaluation of patients with elevated troponin levels. In the absence of clinical coronary artery disease, troponin levels may point to minor myocardial injury, as shown by this report on four cases of supraventricular tachycardia (AVNRT).”
This earlier, small prospective study in a Turkish hospital (Am J Emerg Med. 2001 Jan;19(1):40-2. PMID: 11146016 ) looked explicitly at ST depression in older (45 years and up) patients with paroxysmal SVT. They, too, found the risk of coronary artery disease related to cardiac risk factors:
“In this study, we detected CAD in 7 of 21 patients (33%) .45 years old who had ST-segment depression during paroxysmal SVT. All patients with significant coronary artery stenosis had evidence of myocardial ischemia on exercise thallium scintigraphy, whereas 6 had had .1-mm ST-segment depression during exercise testing. One patient with isolated left circumflex coronary artery stenosis who developed a thallium defect with redistribution had normal exercise testing. … We failed to identify any electrocardiographic parameter indicative of CAD in patients with ST-segment depression during paroxysmal SVT. The only difference between patients with and without CAD in group I was the coronary risk score, which was higher in those with CAD.”
