ABC | Volume 114, Nº2, February 2020

Update Update of the Brazilian Guideline on Nuclear Cardiology – 2020 Arq Bras Cardiol. 2020; 114(2):325-429 A recent study has shown that, following 1 year of treatment with anthracyclines, late HMR was the strongest parameter of scintigraphy with MIBG- 123 I. This index correlates with conventional echocardiography variables and global indexes of radial and longitudinal strain, in addition to doses of galectin-3 in patients with breast cancer treated with anthracyclines. Altered late HMR was a predictor of abnormality in the global radial strain index on ECG. 369 Cardiac scintigraphy with MIBG- 123 I was performed in 20 women with breast cancer and normal LVEF who had undergone treatment with anthracycline derivatives, associated and not associated with trastuzumab. It was observed that anthracycline use with trastuzumab promoted higher frequency and intensity of cardiac adrenergic hyperactivity. 367 Carrió et al. 371 identified abnormal MIBG- 123 I uptake in patients who used anthracyclines, where HMR of MIBG- 123 I decreased as the cumulative dose of this medication increased. 371 The degree of cardiac uptake of MIBG- 123 I may thus be an early marker of CTX. However, multicenter studies with higher case numbers and standardized exam protocols comparing the evaluation of cardiac sympathetic activity with MIBG- 123 I before and after treatment need to be carried out in order to clarify these findings further. 13.3.4. Cardiac Autonomic Dysfunction in Diabetes Mellitus (DM) In patients with DM, there is evidence of cardiac denervation in the absence of clinical manifestations. 372 Diabetic autonomic neuropathy has been implied to be a cause of sudden cardiac death, with or without associated myocardial ischemia. Patients with DM and reduced HMR of MIBG- 123 I have an increased risk for clinical progression of HF. 373 It is, however, not yet clear whether cardiac adrenergic imaging may improve clinical outcome in patients with diabetes. 13.3.5 Cardiac Transplant Cardiac scintigraphy with MIBG- 123 I may be useful for evaluation of reinnervation in transplanted hearts. It identifies ventricular sympathetic reinnervation, 345 which slowly develops from the cardiac base several months following surgery, and it is observed in 40% of patients 1 year following transplant. 374 Even though the clinical implications and the mechanisms of cardiac reinnervation have yet to be completely made clear, restoration of cardiac sympathetic innervation probably increases physical capacity, due to improved HR and contractile function during exercise in patients with heart transplants. 374 Evaluation of the process of cardiac reinnervation via scintigraphy with MIBG- 123 I seems to be useful for outpatient treatment of patients with heart transplants for the prescription of appropriate exercises, evaluation of the effect of physical training, and prediction of long-term survival. 13.3.6. Takotsubo Syndrome Takotsubo syndrome, also known as neurogenic cardiomyopathy, stress-induced cardiomyopathy, or broken heart syndrome, 375 is characterized by transient left ventricular dysfunction, electrocardiographic alterations similar to those present in AMI, and minimal alterations in cardiac enzymes in the absence of obstructive CAD. It was described in 1991 in Japan 375 and denominated “Takotsubo” owing to the similarity of the morphological aspect which the LV assumes to a type of trap used to capture octopuses in Japan (round in the bottom and narrow in the upper part). It has recently been recognized as a new entity within the spectrum of acute coronary syndromes. 376-378 Its real frequency is unknown, but it is estimated that it represents 1% to 2% of cases that present at the emergency room with acute coronary syndrome. 377,379-381 It generally affects post-menopausal women (95% of cases occur in women between the ages of 60 and 80), and it is rarely (< 3%) seen in women under the age of 50 or in men. In up to 80% of cases, the syndrome is associated with previous events which produced strong physical or emotional stress, such as separations, financial loss, conflicts, loss of a loved one, illness of a loved one, severe disease, surgery, etc. In some cases, however, no preceding physical or emotional stress may be identified. Several physiopathological mechanisms have been proposed as participants in generating the syndrome, such as occult atherosclerotic disease, multiple coronary spasms, endothelial dysfunction, and microvascular disease. Nevertheless, the most accepted hypothesis is an excess of sympathetic stimulation, with elevated circulating catecholamines causing dynamic obstruction of LV outflow and resulting in short periods of ischemia and ventricular “stunning.” 377,379,380,382-384 In fact, excessive sympathetic activity with pronounced plasma elevation of catecholamines has been found in almost 75% of patients with Takotsubo syndrome. 379 The reason why Takotsubo syndrome occurs much more frequently in women after menopause is unknown. Several explanations have been proposed, such as the influence of sexual hormones on the sympathetic neurohumoral axis 379,385 and coronary vasoreactivity; 379,386 higher vulnerability of women to myocardial stunning, mediated by the sympathetic system; 379,387 and alterations in endothelial function following menopause, in response to reduced estrogen levels. 388 Clinical presentation is characterized by intense, acute chest pain (similar to that of infarction), dyspnea, ischemic ST-segment alterations (ST-segment elevation and/or inversion of T waves and pathological Qwaves), mild increase in cardiac enzymes, and segmental systolic dysfunction in the apex and middle third of the LV, with base hyperkinesis, in the absence of obstructive epicardial coronary disease. The most accepted criteria for diagnosis are currently those proposed by the Mayo Clinic in 2008: 389,390 • Transient hypokinesis, akinesis, or dyskinesis in LV mid- segments, with or without apical involvement. • Regional abnormalities that extend beyond epicardial vascular distribution, often with a precipitating factor. • Absence of CAD or evidence of acute plaque rupture. • New ECG abnormalities (ST-segment elevation and/or T-wave inversion) or mild elevation in cardiac troponin (disproportional to the degree of LV dysfunction). • Absence of pheochromocytoma and myocarditis. 403