Letter to the Editor Reversible left ventricular apical ballooning after heavy alcohol consumption in a patient with hypertrophic cardiomyopathy A.P. Patrianakos ⁎, E. Nyktari, F.I. Parthenakis, P.E. Vardas Cardiology Department, Heraklion University Hospital, Crete, Greece article info Article history: Received 2 September 2012 Accepted 25 September 2012 Available online 17 November 2012 Keywords: Takotsubo Hypertrophic Cardiomyopathy Alcohol A 49-year-old man was admitted to our hospital with a 1-hour acute chest pain. The patient had a known history of hypertrophic cardiomyopathy with mild midventricular obstruction (HOCM) but was otherwise asymptomatic and medication free. In search of ante- cedent emotional or physical stressors, heavy alcohol consumption was reported. A grade II/VI systolic murmur at the left parasternal border was audible and his electrocardiogram on presentation revealed new ST-T segment elevation in leads V3–6 and laboratory work up demon- strated mild troponin I elevation (2.5 ng/ml). The patient was rushed to the coronary catheterization laborato- ry but the coronary angiography revealed no abnormalities while ventriculography showed apical ballooning with basal hyperkinesis and low ejection fraction (EF) (Fig. 1, Video 1). Bedside echocardiography demonstrated asymmetric basal septal wall hypertrophy of 18 mm, left ventricular (LV) mid-apical dyskine- sia with compensatory basal hyperkinesis, systolic anterior motion (SAM) of the mitral valve with outflow tract (LVOT) obstruction and recorded velocities up to 4.5 m/s. Spontaneous echo contrast was noted inside the LV cavity and the overall EF was severely reduced (LVEF 30%) (Fig. 2, Videos 2 and 3). The patient was admitted to the ICU and treated with i.v. fluid ad- ministration and metoprolol 100 mg twice per day. His course was uncomplicated while repeat ECGs demonstrated resolution of ST-T segment elevation and the appearance of giant negative T waves throughout the precordial leads. A repeat echocardiogram after 2 days, revealed normalisation of wall motion and LVEF, resolution of SAM and LVOT obstruction and reappearance of the midventricular obstruction at the level of papil- lary muscles with velocities up to 2.5 m/s (Fig. 2, Videos 2 and 3). Cardiac MRI performed at the 5th day showed no oedema or early/ late gadolinium enhancement in the previously affected segments thus making the diagnosis of myocarditis unlikely. The diagnosis of Takotsubo cardiomyopathy (TC) was consid- ered based on the clinical presentation, ECG changes, mild troponin elevation, reversible mid-apical dyskinesia that extended beyond a single epicardial vascular distribution [1], and the rapid full LV re- covery. Even though no clear preceding stressor was documented the acute effects of alcohol consumption were suggested as the stressor of TC. According to the modified Mayo clinic proposed diagnostic criteria for TC [1] our patient fulfilled all four of them. Furthermore, at present two more cases of TC have been reported in patients with HOCM and no identifiable stressor with rapid recov- ery of LV [2,3]. Recently, Merli et al. [4] has proposed the development of an intracavitary pressure gradient such as a severe transient LVOT or midcavitary obstruction as an important contributor to the genesis of TC. The presence of a geometric abnormality such as the localised septal thickening found in HCM, when combined with dehydration and/or adrenergic surge, leads to intracavitary obstruction with a marked increase in wall stress in the high pressure distal apical com- partment, diffuse subendocardial ischemia and myocardial stunning [4]. In our case heavy alcohol consumption through venous and arteri- al dilatation led to a decrease in both pre- and after-load. It is possible that the resultant reduction of size in a structurally predisposed LV and the fall of peripheral resistance precipitated an aggravated dy- namic obstruction which in turn led to a sympathetic surge and in- creased wall stress [5]. It is interesting that in our case the site of obstruction has changed from midventricular to LVOT level with a remarkable increase of reg- istered velocities (from 2.3 m/s to 4.5 m/s) (Fig. 2). In conclusion, heavy alcohol consumption in HOCM can promote TC and thus caution should be advised. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. Supplementary data to this article can be found online at http:// dx.doi.org/10.1016/j.ijcard.2012.09.163. International Journal of Cardiology 164 (2013) e29–e31 ⁎ Corresponding author. Tel.: +30 2810392706; fax: +302810542055. E-mail address: alpat@otenet.gr (A.P. Patrianakos). 0167-5273/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2012.09.163 Contents lists available at SciVerse ScienceDirect International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard