Intraoperative Stress Cardiomyopathy




The authors discuss and present transesophageal echocardiographic images of intraoperative tako-tsubo cardiomyopathy in a female patient under general anesthesia. Intraoperative transesophageal echocardiography was performed in an attempt to manage a sudden episode of hypotension and mild pulmonary edema coincidental with surgical incision. The suspected diagnosis of stress cardiomyopathy was confirmed by computed tomographic angiography and cardiac catheterization. The patient made a complete recovery. This case report stresses the utility of transesophageal echocardiography in the differential diagnosis of intraoperative hypotension and suspected acute coronary syndrome.


Case Report


A 43-year-old woman presented for an anterior lumbar interbody fusion at L4 to L5. Her medical history was unremarkable, and her surgical history included a prior anterior cervical discectomy with fusion as well as a lumbar L4 to L5 laminectomy. Preoperative electrocardiography showed normal sinus rhythm.


The patient remained hemodynamically stable through the induction of general anesthesia, but shortly after surgical incision, moderate hypotension, tachycardia, hypoxemia, and a decrease in end-tidal carbon dioxide ensued. Electrocardiography revealed sinus tachycardia, right atrial enlargement, and a nonspecific T-wave abnormality. A transesophageal echocardiographic probe was placed emergently to search for evidence of pulmonary embolism, but despite a mildly enlarged inferior vena cava, the right atrium and right ventricle did not appear dilated or pressure overloaded. Diffuse apical and midventricular hypokinesis, however, was noted concurrently with hyperdynamic basal left ventricular (LV) segments ( Video 1 ). Although the patient was premenopausal, these transesophageal echocardiographic images were suspicious for intraoperative tako-tsubo cardiomyopathy. Mild perihilar pulmonary edema was noted on chest x-ray and computed tomographic angiography, the latter of which was negative for pulmonary embolism but showed global severe hypokinesis involving the midventricular and apical LV walls, with sparing of the septum and base of the heart, unremarkable right ventricular function, and no focal lesions in the coronary arteries. Emergency cardiac catheterization was performed and confirmed the computed tomographic angiographic findings (normal coronary arteries with wall motion abnormalities consistent with tako-tsubo cardiomyopathy). Cardiac enzymes were mildly elevated (peak values: creatine phosphokinase, 542 U/L; creatine phosphokinase-MB, 10.9 μg/L; troponin I, 0.18 μg/L). The patient was treated with metoprolol, lisinopril, furosemide, and heparin infusion. She made a complete recovery, with normal LV function confirmed by transthoracic echocardiography 7 days after the event ( Video 2 ).




Discussion


Stress cardiomyopathy (also known as tako-tsubo cardiomyopathy, broken heart syndrome, and apical ballooning syndrome [ABS]) is a rare reversible cardiomyopathy, clinically resembling an acute coronary syndrome. The Mayo Clinic criteria used for the diagnosis of ABS—transient akinesis (or dyskinesis) of the apical and midventricular segments with regional wall motion abnormalities extending beyond a single-vessel distribution; no angiographic evidence of intracoronary plaque or thrombus formation; electrocardiographic evidence of new ST or T changes; and no evidence of recent head trauma, intracranial bleeding, pheochromocytoma, myocarditis or hypertrophic cardiomyopathy—were all satisfied in our patient.


Although usually reported in postmenopausal women subjected to significant emotional or physical stress, ABS has also been described in perioperative and intensive care unit settings. The incidence of ABS is close to 2% in all patients with suspected acute coronary syndromes and may be as high as 12% in women with suspected acute anterior wall myocardial infarctions. ABS seems to be a consequence of myocardial responsiveness to norepinephrine surge. In addition to direct myocyte injury, excessive adrenergic stimulation is thought to increase coronary vascular resistance and cause mild apical ischemia. The degree of impairment of microvascular perfusion correlates with the myocardial injury, as measured by peak enzyme levels. Regional differences in the density of adrenoreceptors may underlie the various clinical manifestations of stress cardiomyopathy (apical vs nonapical ballooning).


Another proposed hypothesis examines the role of acute dynamic intracavitary midventricular and LV outflow obstruction in the pathogenesis of ABS. Some patients may have myocardial functional architecture predisposing to LV outflow obstruction in the presence of hypovolemia and a high catecholamine load. For example, in a large French study of LV outflow tract obstruction in ABS, all patients with intraventricular pressure gradients were elderly and had morphologic patterns of septal bulge.


Clinically, the presentation of ABS is indistinguishable from an acute coronary syndrome, with chest pain, dyspnea, mild to moderate congestive heart failure, pulmonary edema, hypotension, and cardiogenic shock. The treatment is empiric and usually supportive and may include β-blockers, angiotensin-converting enzyme inhibitors, diuretics, and aspirin. The prognosis is usually good, with complete resolution within 4 to 8 weeks. Long-term survival is close to that among the age-matched population. The recurrence rate may be <10%.


In conclusion, we have discussed and presented transesophageal echocardiographic images of intraoperative stress cardiomyopathy, an important entity for anesthesiologists to recognize in the differential diagnosis of acute coronary syndromes.


Supplementary Data


Video 1


Four -chamberview, 2-chamber view, midesophageal long-axis view, and midpapillary short-axis view.



Video 2


Transthoracic echocardiographicapical 4-chamber view.



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Jun 16, 2018 | Posted by in CARDIOLOGY | Comments Off on Intraoperative Stress Cardiomyopathy

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