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Table of Contents
CASE REPORT
Year : 2018  |  Volume : 1  |  Issue : 1  |  Page : 53-55

Recurrent ST-segment elevation myocardial infarction caused by coronary slow flow


Department of Cardiology, Dr. S. N. Medical College, Jodhpur, Rajasthan, India

Date of Web Publication24-Aug-2018

Correspondence Address:
Dr. Anil Baroopal
Room No. 102, PG Hostel, MDM Hospital, Dr. S. N. Medical College, Jodhpur, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IHJI.IHJI_9_17

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  Abstract 

Coronary slow flow phenomenon is an angiographic clinical entity, characterized by delayed distal vessel opacification in the absence of significant epicardial coronary stenosis. Although it is well known to interventional cardiologists for approximately four decades, the pathogenic mechanisms are incompletely understood. Here, we present a case of typical chest pain with electrocardiographic changes suggesting recurrent ST-segment elevation myocardial infarction whose coronary angiography had normal coronaries with slow flow.

Keywords: Coronary angiography, coronary slow flow phenomenon, ST-segment elevation myocardial infarction


How to cite this article:
Sanghvi S, Baroopal A, Kumar A, Mathur R. Recurrent ST-segment elevation myocardial infarction caused by coronary slow flow. Indian Heart J Interv 2018;1:53-5

How to cite this URL:
Sanghvi S, Baroopal A, Kumar A, Mathur R. Recurrent ST-segment elevation myocardial infarction caused by coronary slow flow. Indian Heart J Interv [serial online] 2018 [cited 2018 Dec 14];1:53-5. Available from: http://www.ihji.org/text.asp?2018/1/1/53/239785




  Introduction Top


Coronary slow flow phenomenon (CSFP) is an angiographic clinical entity, characterized by delayed distal vessel opacification in the absence of significant epicardial coronary stenosis and myocardial bridge. Although it is well known to interventional cardiologists for approximately four decades, the pathogenic mechanisms are incompletely understood. CSFP was first described by Tambe et al.[1] in 1972. It has been reported that 1%–5.5% of patients who undergo coronary angiography experience CSFP.[2],[3]In CSFP recurrent chest pain, ST-segment elevation myocardial infarction (STEMI), arrhythmias and sudden cardiac death have been reported.[4],[5],[6],[7],[8],[9] In this report, we present a rare case of recurrent STEMI caused by CSFP in the index hospitalization.


  Case Report Top


A  52-year-old male presented to the emergency department of our institution with complaint of chest pain radiating to the left upper limb for 2 days. He had no previous history of chest pain. He was a smoker and known hypertensive. He had no other conventional risk factors such as family history of coronary artery disease, diabetes mellitus, and hyperlipidemia. His blood pressure was 136/80 mmHg and heart rate was 86 beats/min. On examination, cardiovascular, respiratory, and other systems were normal. His electrocardiogram (ECG) showed ST-segment elevation in lead II, III, and aVF with ST-segment depression in anterior leads as shown in [Figure 1]. Transthoracic echocardiogram was performed which revealed concentric left ventricular (LV) hypertrophy with normal LV function without regional wall motion abnormality. His troponin I was positive. Diagnosis of acute inferior wall STEMI was made and treated. No primary percutaneous coronary intervention was performed as the patient refused, due to financial constraints. Recurrent angina was persisting despite being on all conventional medicines for acute coronary syndrome, so he was planned for coronary angiography. On angiography, coronaries were normal with slow flow in the right coronary artery (RCA), left anterior descending (LAD) artery, and left circumflex (LCx) artery as shown in Movie 1. Corrected thrombolysis in MI frame count (CTFC) of LAD, RCA, and LCx was 55.3, 44, and 48, respectively. Intravascular ultrasound imaging of coronary arteries was not done as this facility was not present at our center. He was put on medical management. The patient was comfortable after coronary angiography.
Figure 1: Electrocardiogram tracing showing inferior wall myocardial infarction

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The patient again had severe chest pain and uneasiness after 36h of coronary angiography. At this time, ECG showed ST-segment elevation in lead I, aVL, and V1–V6 as shown in [Figure 2]. Repeat transthoracic echocardiogram was performed which revealed hypokinesia of distal interventricular septum and anterior wall and LV systolic dysfunction with ejection fraction of 45%. As the pain was intolerable and not relieved by sublingual nitrate, he was thrombolyzed with streptokinase. After thrombolysis, his ECG showed resolution of ST-segment elevation as shown in [Figure 3]. Due to the presence of recurrent angina after 2 days despite being on all conventional medicines for acute coronary syndrome and appearance of regional wall motion abnormality with LV systolic dysfunction, he was planned for repeat coronary angiography. On the next day, on repeat angiography, coronaries were again normal with slow flow in LAD artery, RCA, and LCx artery as shown in Movie 2. The patient was then managed conservatively with medications. Subsequent transthoracic echocardiogram showed hypokinesia of distal interventricular septum with improvement in LV systolic function with ejection fraction of 50%–55%. The patient was then discharged in stable condition, being put on conventional medicines plus oral anticoagulants.
Figure 2: Repeat electrocardiogram tracing showing anterior wall myocardial infarction

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Figure 3: Electrocardiogram showing resolution of ST-segment elevation after thrombolysis

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  Discussion Top


The exact pathophysiological mechanism of CSFP is not clear. Some underlying etiologies such as abnormally high microvascular resistance and widespread atherosclerosis of coronary arteries have been proposed. Recurrent chest pain is a commonly observed symptom in patients with CSFP.[4] Most (80%) of the patients experience debilitating recurrent chest pain, commonly resulting in hospital readmission. The overall incidence of CSFP was 1%–5.5% among patients undergoing coronary angiography.[2],[3]CSFP may also lead to life-threatening situations such as STEMI, ventricular arrhythmias, and sudden cardiac death.[5],[6],[7],[8],[9] CTFC method is used to evaluate coronary blood flow. CSFP is defined as CTFC >2 standard deviations from the normal range of 21.1±1.5 for LAD artery, 20.4±3 for RCA, and 22.2±4.1 for LCx artery.[10]

Different theories have been proposed regarding the cause of CSFP, but research has not been able to conclude its actual pathogenesis. In a variety of researches, small vessel disease, endothelial dysfunction, subclinical atherosclerosis, inflammation, and anatomic properties of coronary arteries have been reported as existing in association with CSFP. Among these, small vessel dysfunction is one of the most typical of the pathogenesis of CSFP.[11]

In conclusion, the exact pathology of CSFP is not clear and CSFP is not a normal variant but a pathological entity. It not only leads to myocardial ischemia but also can cause STEMI requiring coronary angiography. Our patient suffered recurrent STEMI (inferior wall MI followed by anterior wall MI) within short duration despite being on low-molecular-weight heparin and dual antiplatelet therapy. Such a presentation of recurrent STEMI is very rare. No such case has been reported till date, to the best of our knowledge.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Tambe AA, Demany MA, Zimmerman HA, Mascarenhas E. Angina pectoris and slow flow velocity of dye in coronary arteries – A new angiographic finding. Am Heart J 1972;84:66–71.  Back to cited text no. 1
    
2.
Chaudhry MA, Smith M, Hanna EB, Lazzara R. Diverse spectrum of presentation of coronary slow flow phenomenon: A concise review of the literature. Cardiol Res Pract 2012;1:383181.  Back to cited text no. 2
    
3.
Singh S, Kothari SS, Bahl VK. Coronary slow flow phenomenon: An angiographic curiosity. Indian Heart J 2004;1:613–7.  Back to cited text no. 3
    
4.
Beltrame JF, Limaye SB, Horowitz JD. The coronary slow flow phenomenon – A new coronary microvascular disorder. Cardiology 2002;1:197–202.  Back to cited text no. 4
    
5.
Celik T, Iyisoy A, Kursaklioglu H, Yuksel C, Turhan H, Isik E. ST elevation during treadmill exercise test in a young patient with slow coronary flow: A case report and review of literature. Int J Cardiol 2006;1:e1-4.  Back to cited text no. 5
    
6.
Tatli E, Yildirim T, Aktoz M. Does coronary slow flow phenomenon lead to myocardial ischemia? Int J Cardiol 2009;1:e101-2.  Back to cited text no. 6
    
7.
Kapoor A, Goel PK, Gupta S. Slow coronary flow – A cause for angina with ST segment elevation and normal coronary arteries. A case report. Int J Cardiol 1998;1:257–61.  Back to cited text no. 7
    
8.
Saya S, Hennebry TA, Lozano P, Lazzara R, Schechter E. Coronary slow flow phenomenon and risk for sudden cardiac death due to ventricular arrhythmias: A case report and review of literature. Clin Cardiol 2008;1:352–5.  Back to cited text no. 8
    
9.
Amasyali B, Turhan H, Kose S, Celik T, Iyisoy A, Kursaklioglu H, et al. Aborted sudden cardiac death in a 20-year-old man with slow coronary flow. Int J Cardiol 2006;1:427–9.  Back to cited text no. 9
    
10.
Gibson CM, Cannon CP, Daley WL, Dodge JT Jr., Alexander B Jr., Marble SJ, et al. TIMI frame count: A quantitative method of assessing coronary artery flow. Circulation 1996;1:879–88.  Back to cited text no. 10
    
11.
Mosseri M, Yarom R, Gotsman MS, Hasin Y. Histologic evidence for small-vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries. Circulation 1986;1:964–72.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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