ABC | Volume 112, Nº2, February 2019

Anatomopathological Correlation Arq Bras Cardiol. 2019; 112(2):204-210 Favaratto & Aiello Heart failure after surgical correction of aortic dissection Figure 4 – Macroscopic aspect of the open left heart chambers, with marked left ventricular dilation (asterisk); Mi: mitral valve. We also have no clinical evidence of such changes in the present case. A more recent study showed gene panel alterations in 25% of patients with aortic aneurysms. 6 What should be taken into account is that even today the criterion for the indication of surgical treatment for rupture prevention remains the diameter of the aneurysm, 50 mm. In the present case, the patient had arterial hypertension and it must have had an important role in the development of the thoracic aneurysm and its rupture. Biomechanical studies show that for hypertension to lead an aneurysm development, there must be concomitant failure in the composition and maintenance of the extracellular matrix and membrane receptors. Consequently, there is damage to the mechanical stress transduction in the cell-signaling response. 7,8 Regarding the patient’s unfavorable evolution after the surgery, it is probably due to the long evolution of the aortic aneurysm with aortic valve regurgitation, leading to left ventricular dilation and severe dysfunction, which in the very late states do not undergo regression or relief despite valve replacement surgery and progress to progressive heart failure. The ECG disclosed left ventricular overload with strain and the echocardiogram showed large left ventricular dilation and marked dysfunction. The European Guidelines of Cardiology and Thoracic Surgery recommends valve replacement surgery in patients with aortic dilation or aortic regurgitation accentuated with symptoms. In asymptomatic patients, this recommendation appears if there is reduction in ejection fraction (<50%) or ventricular dilation (diastolic diameter >70 mm or diastolic >50 mm). 9 The patient had degrees of dilation (diastolic diameter, 87 mm and systolic diameter, 78 mm) and ventricular dysfunction (ejection fraction of 22%) well beyond those recommended for the indication of valve replacement surgery. This is the most plausible explanation for the poor evolution. (Dr. Desiderio Favarato) Diagnostic hypotheses: Aneurysm in the thoracic aorta, chronic aortic valve regurgitation, aortic dissection. Etiology: arterial hypertension and extracellular matrix disease of the aorta. Final clinical picture: cardiogenic shock due to valvular heart disease. (Dr. Desiderio Favarato) Necropsy The heart weighed 890g, withmarked increase in volume and dilation of all chambers, predominantly the ventricles (Figure 4). The atrioventricular valves showed no abnormalities. The aortic valve showed thickening of the free margins of the semilunar leaflets, with a central non-coaptation aspect, compatible with valve regurgitation (Figure 5). A corrugated tube replaced the ascending aorta andwas sutured just above the aortic sinotubular junction (Figure 6). Around the junction area between the ascending aorta and the ventricular mass, we noticed cavitation with irregular margins, partially filled by liquefied material, of a yellowish-brown color (Figure 5). There was also a concave circular lesion of the aortic intima, with 1.5 cm in diameter, just below the emergence of the renal arteries. The lungs showed 207