Case report: We present a case of an 87-year-old normally active woman who presented in cardiogenic shock following a three-week history of breathlessness and intermittent chest pain. On examination she was afebrile, with a HR 135/min, BP 96/48mmHg, SO2 78%, respiratory rate 30/min, mottled skin, bilateral lung crepitations, irregular cardiac sounds without murmurs and cold extremities. Arterial blood gas showed hypoxaemia with mixed respiratory and metabolic acidosis and increased lactate. ECG showed atrial fibrillation and new left bundle branch block. A point-of-care echocardiogram showed severe left ventricular systolic dysfunction with global hypokinesia and chest X-ray revealed pulmonary oedema, right basal/mid consolidation and bilateral pleural effusions. Initial investigation showed elevated Troponin-T levels and white cell count. Non-invasive mechanical ventilation, inotropic support with dobutamine and noradrenaline, dual antiplatelet therapy and antibiotics were initiated. A coronary angiogram was not undertaken due to haemodynamic instability and infection.
Patient responded well to respiratory and inotropic support. Transthoracic echocardiogram showed severe systolic impairment, akinetic apex and all mid to apical segments with preserved contractility of basal segments. Heart failure treatment was commenced. Differential diagnosis included LAD infarct, Takotsubo cardiomyopathy, sepsis complicated with acute heart failure and myocarditis, however myocarditis screen was negative.
On day 7, following clinical improvement, a dobutamine stress echocardiogram was performed to assess viability to guide need for coronary angiography. Improvement of overall left ventricular function was noted at rest, however during stress akinetic segments did not improve, suggesting no benefit from potential revascularization. Patient was discharged on dual antiplatelet treatment, bisoprolol, ramipril and eplerenone.
Six weeks later a cardiac MRI was performed, which revealed complete improvement of systolic function and transmural LGE in mid inferior, inferoseptal and inferolateral segments suggesting a localised RCA infarct.
Discussion: This is a case of a stress cardiomyopathy presenting with cardiogenic shock. Initial presentation suggested possible LAD infarct or septic cardiomyopathy, however the quick improvement of systolic function and the absence of apical scar in CMR set the diagnosis. Potential stress trigger includes sepsis or inferior infarct. Alternative hypothesis of inferior infarct caused by embolization of thrombus created in akinetic apex is also possible. Coronary angiogram, which was not performed early due to critical clinical presentation, would have provided information regarding the diagnosis and the nature of inferior infarct.