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Letters to the Editor

Prosthetic mitral valve tamponade alternans Pankaj Garg, Ian R. Hall, Abdallah Al-Mohammad ⁎ Cardiothoracic Unit, Chesterman Wing, Northern General Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Herries Road, S5 7AU England, UK

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Article history: Received 8 May 2014 Accepted 29 June 2014 Available online 6 July 2014 Keywords: Pulmonary hypertension Mitral valve prosthesis Tamponade alternans

Dear Professor Coats, We wish to report an important clinical observation that combined several forms of imaging followed by pharmacological intervention that saved a patient from a potentially unnecessary surgical intervention. This was in a 65-year-old lady with previous Ultracor single tilting disc mitral valve replacement in 1996, systemic hypertension, chronic atrial fibrillation and epilepsy; who complained of worsening breathlessness. Clinically, she had physical signs of right heart failure. Trans-thoracic echocardiogram (TTE) showed mild left ventricular systolic impairment, dilated left atrium, significantly dilated right ventricle, moderate right ventricular systolic impairment, moderate rise of the systolic pulmonary artery pressure (55 mm Hg), and a well-seated mechanical mitral valve prosthesis with no para-valvular leak. However, the Ultracor single-tilting-disc mechanical MV prosthesis was not opening on alternate cardiac cycles, Fig. 1.

We did not agree with those who suspected a catastrophic malfunctioning of mechanical MV prosthesis and proposed a re-do operation. We noted that the function of the MV prosthesis was normal on alternate beats. We postulated that the intermittent malfunction indicated a dynamic intermittent problem most likely related to the impact of the high right sided pressure on the diastolic pressure of the left ventricle which is preventing the mechanical MV prosthesis from opening every other beat. This is similar, though intermittent, to tamponade. We called that tamponade alternans of the MV prosthesis. We went on to confirm our hypothesis and performed fluoroscopy and an invasive simultaneous left and right heart catheter study [1]. Fluoroscopy confirmed the intermittent opening of the Ultracor singletilting-disc mechanical MV prosthesis every other beat (Fig. 2). The invasive studies showed severe pulsus alternans. The beats with the lower cardiac output were preceded by equalisation of right and left ventricular diastolic pressures (Fig. 2). The beats with the higher left ventricular output were preceded by a left ventricular end diastolic pressure higher than the right ventricular end diastolic pressure. The pulmonary artery pressure was 50/23 mm Hg with a mean of 38 mm Hg. The pulmonary capillary wedge pressure was high at 34/28 mm Hg. We had thus confirmed our hypothesis that the pulmonary hypertension is pushing the inter-ventricular septum paradoxically to the left (Fig. 2), and raising the left ventricular diastolic pressure to a level higher than the left atrial pressure as shown by changes in the diastolic left ventricular pressure curves (Fig. 2). This is preventing the opening of the mitral valve. However, by the following cardiac cycle, the

Fig. 1. Pre-sildenafil treatment pulse-wave echocardiographic Doppler in alignment with mitral valve inflow clearly showing missed alternate mitral valve prosthesis opening resulting in no forward flow signal for the respective electrocardiographic QRS.

⁎ Corresponding author at: Department of Cardiology and Cardio-thoracic Surgery, Chesterman Wing, Northern General Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Herries Road, Sheffield S5 7AU, UK. Tel.: + 44 1142266115; fax: +44 1142610350. E-mail address: [email protected] (A. Al-Mohammad).

Letters to the Editor

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pressure in the left atrium that had not been emptied during the previous cycle would have risen significantly (because it is made up of the volume produced by the pulmonary venous return from two cycles) to levels beyond the raised left ventricular diastolic pressure. The gradient, thus created, would force the MV prosthesis to open and the left atrium would be emptied raising the left ventricular end diastolic pressure and the cardiac output of the beat that follows. In other words, the lady was intermittently not filling her left ventricle. After the invasive study, the patient was started on standard dose of cyclic guanosine monophosphate-specific phosphodiesterase-5 inhibitor — sildenafil 20 mg three times a day. A repeat transthoracic echocardiographic study was carried out after 2 months to re-assess the mitral inflow pattern on Doppler study and the right heart function. The right heart function and dimensions improved. The pulmonary artery pressure dropped from 50–55 mm Hg to 30–35 mm Hg. The tricuspid regurgitation had become mild. Most importantly, these changes were also associated with complete resolution of the paradoxical inter-ventricular septal motion and also of the tamponade alternans of the mitral valve prosthesis (Fig. 3). We have therefore been able to confirm the pathophysiological basis of the phenomenon noted non-invasively, and based on prior observations of the impact of pulmonary hypertension on left ventricular filling [2–5], by invasive simultaneous cardiac catheterisation and this was followed by correction of the pathological process responsible for the abnormality by pharmacological means saving the patient from what would have been un-necessary and potentially dangerous surgical intervention.

References [1] Grossman W, Barry W. Cardiac catheterization. In: Braunwald E, editor. Heart disease: a textbook of cardiovascular medicine. Philadelphia, Pa: WB Saunders; 1988. p. 247–52. [2] Gurudevan SV, Malouf PJ, Auger WR, et al. Abnormal left ventricular diastolic filling in chronic thromboembolic pulmonary hypertension: true diastolic dysfunction or left ventricular underfilling? J Am Coll Cardiol Mar 27 2007;49(12):1334–9. [3] Mahmud E, Raisinghani A, Hassankhani A, et al. Correlation of left ventricular diastolic filling characteristics with right ventricular overload and pulmonary artery pressure in chronic thromboembolic pulmonary hypertension. J Am Coll Cardiol 2002;40:318–24. [4] Hardegree EL, Sachdev A, Fenstad ER, et al. Impaired left ventricular mechanics in pulmonary arterial hypertension: identification of a cohort at high risk. Circ Heart Fail Jul 2013;6(4):748–55. [5] Stojnic BB, Brecker SJ, Xiao HB, et al. Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction. Br Heart J Jul 1992;68(1):16–20.

Fig. 2. Combined pressure–waveform of left and right ventricle with synchronized Doppler study of mitral inflow, fluoroscopy of mitral valve and 2-dimensional parasternal long-axis view of mitral valve on echocardiography. (Red arrow—diastole where LV early diastole pressure is higher than LV filling pressure from LA; Green arrow — diastole where LV early diastole pressure is lower and hence the mitral valve opens).

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Letters to the Editor

Fig. 3. Post-sildenafil treatment pulse-wave echocardiographic Doppler in alignment with mitral valve inflow showing complete resolution of the tamponade alternans of the mitral valve prosthesis.

0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.06.100

Takotsubo syndrome as a complication of Pickering syndrome, and perhaps hypertensive emergencies John E. Madias ⁎ Icahn School of Medicine at Mount Sinai, New York, NY, United States Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, United States

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Article history: Received 7 May 2014 Accepted 29 June 2014 Available online 5 July 2014 Keywords: Takotsubo syndrome Pickering syndrome Hypertensive emergency Malignant hypertension Renal artery stenosis Flash pulmonary edema

To the Editor: For some time now, I have been suspecting that Takotsubo syndrome (TTS) could be conceivably occurring in association with hypertensive emergencies (HE), presenting in a picture of heart failure (HF) with or without flash pulmonary edema. I have sought evidence for this hypothesis in patients admitted with HE (previously known as malignant

⁎ Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, United States. Tel.: + 1 718 334 5005; fax: +1 718 334 5990. E-mail address: [email protected].

hypertension) and HF, without success since an echocardiographic (ECHO) evaluation of such patients usually follows management of elevated blood pressure and HF, which have precedence. The baseline (prior to the admission with HE, and prior, or after hospital discharge) ECHO findings run the gamut from low, to normal, and sometimes hyperdynamic, left ventricular (LV) ejection fraction [1]. What is needed is ECHO evaluation(s) during the acute phase of the illness in patients admitted with HE and HF, in order to ascertain whether typical, or variant (like in the present case) [2] phenotypes of TTS, or even “formes frustes” TTS cases, (characterized by regional wall motion abnormalities [RWMAs]) [3] are encountered. Repeated ECHO evaluations may be needed over the course of weeks to months in such patients with HE to ascertain whether full return of the baseline LV function has taken place. The essence of this hypothesis is the thought that the LV in conditions like Pickering syndrome (PS) [2] or HE, and the right ventricle in acute pulmonary embolism [4], characterized by abrupt intense increase of their afterload, may be subject to transient ventricular dysfunction [5], which may even have a cardioprotective effect on the eventual integrity of the ventricles [6]. A relevant article has been just published [2], about a patient who suffered a case of midventricular (TTS) in the setting of an admission with flash pulmonary edema with an underlying renal artery stenosis with subsequent subacute occlusion of a solitary right kidney PS. In terms of pathophysiology PS and HE are very close, and indeed PE often presents not only with severe, difficult to treat hypertension, but with HE, which implies organ (often the heart) damage. It would be of value for clinicians and investigators to explore with frequent ECHOs the probable

Prosthetic mitral valve tamponade alternans.

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