Profound left ventricular systolic deterioration during dobutamine stress echocardiography despite normal resting speckle-tracking imaging revealing subclinical dilated cardiomyopathy and reversal under treatment

Abstract

Profound left ventricular systolic deterioration during dobutamine stress echocardiography despite normal resting speckle-tracking imaging revealing subclinical dilated cardiomyopathy and reversal under treatment The two-dimensional speckle tracking echocardiography (2D-STE) method has recently emerged as a more sensitive modality than conventional echocardiography in detecting subclinical ventricular dysfunction in various clinical disorders [1]; in contrast, dobutamine stress echocar-diography (DSE) is increasingly considered as an old less fashionable technique and rather unsuitable for the detection of subclinical myocar-dial dysfunction and early stages of idiopathic dilated cardiomyopathy. We report the case of a 55 year-old man who underwent a preoper-ative cardiac evaluation; he had normal left ventricular ejection fraction, diastolic function and resting global strain and no wall motion abnormalities. At peak dobutamine infusion, a spectacular global dysfunction was shown in the absence of coronary artery disease. Control DSE after a 4 month-treatment with an angiotensin-converting enzyme (ACE) in-hibitor was normalized. Mr AE, a 55 year-old man was addressed to our department for a preoperative cardiac assessment prior to a lung biopsy in the setting of a recently discovered nodular mass in his right lung. He had neither hypertension nor diabetes mellitus but had a documented peripheral artery disease as he underwent an angioplasty of his iliac arteries several years ago and had an occluded left tibial artery. Clinically, the patient reported a mild effort dyspnea NYHA classes I– II but no chest pain, his resting ECG was normal. His treatment only consisted in aspirin (75 mg daily) and low dose atorvastatin (10 mg daily). Echocardiography at rest was unremarkable with normal cavity dimensions, left ventricular ejection fraction at 66%, no wall motion abnormalities and normal diastolic function (E wave = 90 cm/s, A wave = 61 cm/s, E = 10 cm/s and E/E = 9.1). Global longitudinal strain was also normal at − 20.2%. DSE with a standard protocol was performed , at peak dobutamine infusion, a spectacular and profound global ventricular dysfunction was observed with dilatation of the left ventri-cle and an estimated ejection fraction at 30% (Fig. 1; Video loop 1); meanwhile, the patient reported no chest pain, ECG didn't show any specific changes and arterial pressure profile was normal. A severe coronary artery disease was strongly suspected but coronary angiography was normal. Given these parameters, the diagnosis of an early subclinical form of idiopathic dilated cardiomyopathy was considered. We initiated a treatment with an ACE inhibitor (5 then 10 mg perindopril daily) associated with a high dose atorvastatin (80 mg daily) and we planned re-evaluation. A control DSE was carried out 4 months later, and showed a complete reversal of the dobutamine-induced ventricular dysfunction (Fig. 2, Video loop 2), an effort echocardiography was also performed and was normal. The presumptive diagnosis of a subclinical cardiomyop-athy was hence comforted as we've been able to document a treatment-induced reversal of the stress-provoked dysfunction. For a definitive confirmation, we opted for an additional DSE testing after 3 months of ACE-I withdrawal. At rest, 2D-echocardiography and global longitudinal strain were still normal (− 18.4%). However, during dobutamine infusion, a progressive deterioration of the global strain was noted with − 11.9% at 115 beats/min (Fig. 3) and −9% at maximal rate; ejection fraction was only mildly deteriorated (Fig. 4, Video 3). The final diagnosis of a subclinical dilated cardiomyopathy undiag-nosed by the different resting imaging modalities including speckle tracking but spectacularly unmasked with dobutamine infusion was definitely made and the patient was prescribed long-term ACE inhibitor and beta-blockers.