ABC | Volume 112, Nº4, April 2019

Anatomopathological Correlation Pereira et al Arrhythmia and heart failure Arq Bras Cardiol. 2019; 112(4):466-472 Regarding the less probable diagnostic hypothesis, one must consider coronary artery disease. Despite presenting segmental dysfunction at the MRI, we have here a young patient with no clinical features or risk factors for this etiology. Additionally, the thickening of the septum and posterior wall have systemic arterial hypertension and hypertrophic cardiomyopathy as important differential diagnoses. However, the patient did not suffer from arterial hypertension and the echocardiography, as well as the magnetic resonance imaging, did not show any characteristic findings of hypertrophic cardiomyopathy: asymmetric septal hypertrophy, left ventricular outflow tract obstruction and septum/wall ratio >1.3. Valvular disease can also be ruled out, since the patient did not show it initially, either at the physical examination or imaging test, and the patient only developed mitral regurgitation after heart failure progression. Finally, idiopathic dilated cardiomyopathy cannot be ruled out as a diagnostic possibility for this case. It typically affects men between the ages of 18 and 50 and at least 25% of the cases show genetic transmission of the disease. It is believed that genetic factors associated with changes in immune response and infectious factors could act synergistically in the development of structural changes and consequent onset of clinical manifestations. It is estimated that between 10%-20% of cases of idiopathic cardiomyopathy are caused by a previous viral infection sequela. 8,9 The patient rapidly evolved to functional class IV, showing marked ejection fraction reduction and underwent successive hospital admissions due to the decompensations. There are many factors that exacerbate heart failure and taking into account the patient’s history, one cannot infer a specific precipitating factor for the case described herein. Among the possible hypotheses is the natural evolution of the underlying disease, of which etiology was not clarified, and this fact may have prevented the implementation of specific treatment strategies. The following are other possible precipitating factors of the acute decompensation observed in the patient: 3,5,10,11 absence of health education performed by the professionals and/or the patient's poor adherence to non-pharmacological measures for heart failure management; inadequate diet and water intake, as well as the abuse of alcohol and other drugs, are frequent factors for decompensation. Moreover, all patients with heart failure should be vaccinated against influenza and pneumococcus, considering that respiratory infections are common etiologies for decompensation; however, in this case, the patient showed no signs of infection leading to hospitalization or leukogram alterations. As for pharmacological measures, the use of beta-blockers (carvedilol, nebivolol, bisoprolol and metoprolol succinate) in patients with reduced ejection fraction associated with angiotensin-converting enzyme inhibitor is the effective treatment for patients with New York Heart Association functional class I to IV, because they reduce morbimortality by acting on cardiac reverse remodeling . There are contraindications for the use of these classes of drugs; however, there are no records in the clinical case of reasons justifying the absence of introduction of these classes of drugs after the development of systolic heart failure. Furthermore, systolic insufficiency refractory to optimized clinical treatment and ejection fraction ≤35%, also requires the use of aldosterone antagonists, a medication that also has an effect on reverse remodeling, if the patient does not have contraindications to its use. There is information about the introduction of this drug only after the third decompensation event. Arrhythmia, in turn, is an important decompensatory factor, such as the atrial fibrillation developed by this patient during one of the hospitalizations. Its onset is associated with several adverse hemodynamic effects, such as loss of atrioventricular synchrony and loss of atrial contraction, leading to cardiac output reduction in a heart with an already impaired ventricular function. Other possible etiologies for decompensation detected in this patient were the concomitant presence of anemia and kidney dysfunction, which are conditions that considerably increase mortality in heart failure. The patient’s hemoglobin level was 11.1 g/dL. Being an important precipitating factor, anemia becomes important due to its deleterious effects on the heart. The erythrocytes, in addition to providing oxygen to myocardial cells, favor the exchange of antioxidants that prevent oxidative stress and programmed cell death, but the impairment of these mechanisms favor myocardial dysfunction. Additionally, in response to hypoxemia resulting from anemia, the sympathetic system is stimulated, leading to tachycardia, increased inotropism and vasoconstriction, further compromising myocyte function and leading to hypervolemia in parallel. Specifically, hypoxemia of anemia and kidney vasoconstriction generate renal ischemia, with the release of inflammatory factors related to myocardial injury and hypervolemia due to the activation of the renin-angiotensin-aldosterone system. Proteinuria was observed in a urinalysis result, despite normal values of creatinine and urea. Like anemia, nephropathy may be a factor of decompensation, etiology and/or consequence of heart failure. As a precipitating factor, one can point to salt and water retention; alterations in the cardiomyocyte structure and function due to inflammatory activation and calcium and phosphorus metabolism abnormalities; and due to the anemia itself, generated by kidney dysfunction, leading to reduced erythropoietin production. One should consider that nephropathy can also be a consequence of amyloidosis, as it leads to amyloid deposition in the kidneys, impairing their function, and 80% of patients with this disease have proteinuria. Due to increased pulmonary artery and right ventricular systolic pressure, pulmonary embolism could be a cause for decompensation. However, in this clinical setting, these cardiopulmonary alterations are possibly due to heart failure progression. Hypothyroidism is a potential cause of heart failure due to bradycardia, systolic and diastolic dysfunction, increased systemic vascular resistance, diastolic hypertension, increased arterial stiffness and endothelial dysfunction. 12 Laboratory examination showed the patient had TSH of 88 um/L and the introduction of levothyroxine was not reported. The patient may also have decompensated due to marked mitral regurgitation caused by left ventricular 468