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|Year : 2013 | Volume
| Issue : 3 | Page : 240-241
Reversible acute myocardial injury following alcohol bingeing
I Mordi, N Tzemos
Department of Cardiovascular Medicine, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom
|Date of Web Publication||12-Sep-2013|
Department of Cardiovascular Medicine, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mordi I, Tzemos N. Reversible acute myocardial injury following alcohol bingeing. J Postgrad Med 2013;59:240-1
A 35-year-old man was admitted to our hospital complaining of resting dyspnea. He admitted to frequent alcohol "binges" over the previous few weeks; however, there was no history of chronic daily use. Resting electrocardiography was unremarkable but chest X-ray showed evidence of pulmonary edema. Troponin T was normal and nt-proBNP was elevated (1912 pg/ml). Echocardiography suggested a dilated left ventricle with moderately impaired global systolic function. Heart failure therapy was instituted and intravenous (IV) thiamine supplementation was given as per our unit's protocol and a cardiac magnetic resonance imaging (CMR) was arranged after 3 days.
CMR confirmed a moderately dilated left ventricle [Figure 1]a with globally moderately impaired systolic function (ejection fraction of 48.3%) and no regional wall motion abnormalities. Unexpectedly there was evidence of localized increased T2 signal affecting the basal and mid-sections of the inferolateral wall (b) without any late gadolinium enhancement (c). Alarmed by the magnetic resonance imaging appearances an ethanol level was measured which turned out to be almost 3 times the UK legal limit for driving (210 mg alcohol in 100 ml blood; limit 80 mg/100 ml).
|Figure 1: (a‑c) Cardiac magnetic resonance imaging examination while patient exposed to alcohol. (a) Cine steady state free precession showing a globally dilated LV; (b) T2‑short tau inversion recovery black blood imaging showing localized increased T2 signal (arrow) affecting the basal inferolateral wall suggestive of myocardial edema (166.9 ± 15 in area of interest vs. 94.2 ± 7.8 in remote myocardium); (c) Late gadolinium enhancement imaging showing no enhancement in the area of edema; (d‑f) Cardiac magnetic resonance imaging examination following a period of abstinence from alcohol; (d) Repeated cine SSFP showing a still globally dilated left ventricle; (e) T2‑STIR black blood revealing complete resolution of increased T2 signal at the inferolateral wall; (f) Late gadolinium enhancement imaging again revealing no enhancement in the basal inferolateral wall, confirming the absence of permanent injury (scarring)|
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Following a period of abstinence the patient returned for repeat CMR 20 days later. There was no further evidence of increased signal on T2-weighted imaging [Figure 1]d-f while blood alcohol level was now zero with a fall in nt-proBNP to 800 pg/ml.
It has been shown experimentally that the systemic inflammatory response known as a "hangover" extends to the myocardium producing a myocarditis-type picture that resolves completely following a period of abstinence.  The presence of increased T2 signal is consistent with acute myocardial injury leading to the presence of edema. During CMR examination gadolinium-based contrast agents are administered IV. Following a 10-min "wash-out" period, the contrast staining should have disappeared from healthy myocardium, thus making it appear dark. The contrast however does not wash out of permanently injured and scarred myocardium, making it appear bright on CMR. The absence of late gadolinium enhancement lends support to the theory of a reversible "toxic" effect without permanent damage. The most likely etiology in this case was of acute alcoholic cardiomyopathy, given the markedly raised alcohol level, the resolution of signs and symptoms with a period of abstinence and the lack of any other symptoms or signs of a viral infection.
One differential diagnosis is "wet beri-beri," caused by thiamine deficiency, which also causes edema to be seen on CMR.  This is less common however than acute alcoholic cardiomyopathy.  While it is possible to measure serum thiamine levels, this can be logistically difficult and is not routinely offered all units. Therefore, the two diagnoses are differentiated on clinical grounds. Wet beri-beri usually causes high-output cardiac failure, with associated tachycardia, hypotension and vasodilatation. It is also not common without other features of thiamine deficiency such as neurological damage and Wernicke-Korsakoff Syndrome More Details. Acute alcoholic cardiomyopathy on the other hand causes low-output cardiac failure and is not associated with extra-cardiac features. Wet beri-beri resolves with thiamine replacement, whereas acute alcoholic cardiomyopathy resolves with abstinence, as in this case.
| :: References|| |
|1.||Zagrosek A, Messroghli D, Schulz O, Dietz R, Schulz-Menger J. Effect of binge drinking on the heart as assessed by cardiac magnetic resonance imaging. JAMA 2010;304:1328-30. |
|2.||Essa E, Velez MR, Smith S, Giri S, Raman SV, Gumina RJ. Cardiovascular magnetic resonance in wet beriberi. J Cardiovasc Magn Reson 2011;13:41. |
|3.||Mahmoud S, Beauchesne LM, Davis DR, Glover C. Acute reversible left ventricular dysfunction secondary to alcohol. Can J Cardiol 2007;23:475-7. |