ABC | Volume 110, Nº4, April 2018

Anatomopathological Correlation Nunes et al. A 73 year-old man with ischemic heart disease and cachexia Arq Bras Cardiol. 2018; 110(4):388-392 Figure 1 – ECG: left atrial overload and indirect signs of right atrial overload (Peñaloza-Tranchesi), in addition to left bundle-branch block and left anterior hemiblock. failure. 3 Up to 34% of the patients with CHF being followed up on an outpatient basis are estimated to develop cardiac cachexia in the medium to long run. 4 The deleterious effects of that condition impair the cardiac and respiratory functions and decrease immunity, which leads to higher mortality. Our patient’s systemic complications that hindered the reversion of his final findings might have been aggravated by cardiac cachexia. Regarding treatment, the literature reports many simultaneous actions that fight the most critical points in cachexia, such as nutritional therapy and the use of appetite stimulants, correction of anemia and edema, use of anabolic steroids and immunomodulation. Parallel to drug therapy, physical activity is indicated to maintain skeletal musculature, 5 respecting the limits imposed by the disease and requiring strict follow-up. Another possible explanation for cachexia would be the development of malignant neoplasia in a patient previously debilitated by heart disease. New studies have recently shown a higher interaction between oncologic and cardiac diseases, no longer attributed to diagnostic coincidence, but to an interaction between their morbidities. A recent publication 6 has shown that the overlap between those two diseases results from the addition of shared risk factors, such as obesity, smoking, sedentary lifestyle and diabetes mellitus. In that context, the term cancer-related ‘cardiac cachexia’ appears. That complication is part of the natural history of neoplasms, leading to a progressive muscle mass loss (cachexia). However, many patients experience myocardial changes related to atrophy, remodeling and dysfunction, a set of findings known as cardiac cachexia. 7 Insidious infectious diseases, such as tuberculosis and infectious endocarditis, can also be accompanied by consumptive findings. Usually, the manifestation most commonly associated with those conditions is fever (70% to 90% of the cases), which, in our patient, was only reported during hospitalization, but not in the last months of his disease. In addition, other symptoms and signs, such as cough, productive expectoration, nocturnal sweating or skin lesions (petechiae and subungual hemorrhages), lack. On admission to the emergency service, the patient had signs of dehydration, arterial hypotension and systemic congestion, such as high jugular venous pressure, hepatomegaly and edema of the lower limbs. Such findings suggest a state of low cardiac output, which can correspond to an advanced stage of the underlying heart disease or decompensation associated with other contributing factors. On the admission electrocardiogram, signs of overload of the right chambers stand out, which might suggest a sudden increase in the pressures of the right atrium and ventricle, as observed in cases of acute pulmonary thromboembolism. Other factors that might contribute to acute decompensations in patients with chronic diseases and potentially immunosuppressed are bacterial infections, such as pneumonia and urinary tract infections. Despite the treatment instituted, the patient’s clinical status worsened with renal failure and metabolic acidosis. On the third day of hospitalization, he had lowering of consciousness, fever, oliguria and respiratory failure, being submitted to endotracheal intubation. These findings initially suggest infectious decompensation and a possible toxic-metabolic process, but cranial tomography revealed a right occipital low attenuation lesion compatible with acute ischemic stroke. In patients with structural heart disease, ischemic encephalic injuries are commonly secondary to cerebrovascular atherosclerotic disease or episodes of cardioembolism in the presence of atrial fibrillation or other intracardiac thrombi. Less frequently, the cardioembolic phenomenon can be related to infectious endocarditis or cardiac tumors. (Rafael Amorim Belo Nunes, MD, Jussara de Almeida Bruno, MD, and Hilda Sara Monteiro Ramirez, MD) Diagnostic hypotheses: ischemic cardiomyopathy, cardiac cachexia, acutely decompensated chronic heart failure (progression of the underlying disease? pulmonary thromboembolism? subjacent infection?), ischemic stroke (atherothrombosis? cardioembolic?). (Rafael Amorim Belo Nunes, MD, Jussara de Almeida Bruno, MD, and Hilda Sara Monteiro Ramirez, MD) 389