A 48-year-old man came to the emergency department with a sudden episode of non-radiating stabbing chest pain that started suddenly while he was driving. It was not accompanied by dyspnoea, palpitations or syncope.

History, present illness and physical examination
48-year-old male, with no known allergies, with several cardiovascular risk factors including heavy smoking (2-3 packs/day), untreated hypertension and moderate obesity, with no other history of interest. By profession, Labrador. He came to the emergency department for an episode of non-radiating stabbing chest pain that started suddenly while he was driving. It was not accompanied by dyspnoea, palpitations or syncope. On arrival, he was in poor general condition, with profuse sweating and tachypnoea. Blood pressure was 200/81 mmHg, heart rate 95 beats per minute and oxygen saturation 86%. Physical examination revealed an IV/VI diastolic murmur, more noticeable on the left sternal border, generalised hypoventilation with crackles in both lung bases, tibiomalleolar oedema with fovea and peripheral pulses present and symmetrical. The rest of the physical examination was unremarkable.

Complementary tests
- ECG on admission: Sinus rhythm at 90 bpm. Normal PR. Narrow QRS. Voltage criteria for left ventricular hypertrophy. Negative T in lateral face.
- Emergency analytical: Highlights glycaemia 185 mg/dl, CRP 60 and elevated myocardial necrosis markers (maximum US TnT 180 ng/ml, without typical curve).
- Chest X-ray: Cardiomegaly. Aortic elongation. Hilar thickening.
- CT angiography: aortic root and proximal segment of ascending aorta at the upper limit of normality, with the rest of the aorta of normal calibre, without signs suggestive of aortic syndrome. Mild cardiomegaly and small pericardial effusion. At the abdominal level, there was only discrete hepatomegaly with hepatic steatosis.
- Transthoracic echocardiogram: The main finding was the presence of moderate-severe aortic insufficiency over the trivalve valve, secondary to dilatation of the aortic annulus. The left ventricle is slightly dilated (end-diastolic diameter of 60 mm) with severe concentric hypertrophy (15-16 mm) and preserved global and segmental systolic function. Both the right ventricle and the rest of the valves show no pathological findings.
- Cardiac MRI: The study was of suboptimal technical quality due to lack of cooperation from the patient to correctly perform apnoeas. The left ventricle showed moderate eccentric hypertrophy, dilatation (telediastolic volume of 124 ml/m2 and end-systolic volume of 50 ml/m2) and segmental and global systolic function within normal limits (ejection fraction of 60%). The right ventricle was normal in dimensions and systolic function. There was no evidence of oedema or alterations in perfusion or late gadolinium enhancement. Significant apparent aortic insufficiency was detected, but the poor quality of the study did not allow adequate quantification. Aortic root dilatation (sinuses of Valsalva: 50 mm, 21 mm/m2) and tubular portion of ascending aorta (48 mm, 20 mm/m2) were observed.
- Diagnostic cardiac catheterisation: The main finding is in the aortography, where there is evidence of dilatation of the ascending aorta from the root, with effacement of the sinuses of Valsalva, and grade IV aortic insufficiency. The coronary arteries showed no significant angiographic lesions.
- Transesophageal echocardiogram: This was interrupted due to poor tolerance given the patient's clinical situation (heart failure). Only a trivalve aortic valve with correct opening was visualised, without being able to assess aortic root or valvular insufficiency.
- Analysis on the hospital ward: There was moderate renal failure, with urea 78 mg/dL, creatinine 1.53 mg/dL and an estimated glomerular filtration rate of 48.82 mL/minute. Liver enzymes were slightly elevated, and glycosylated haemoglobin was 7.8%. The rest of the biochemistry, as well as the haemogram, were normal.

Clinical course
During his stay in the ED, CT angiography was performed to rule out acute aortic syndrome given the patient's presentation with hypertensive emergency, stabbing pain and troponin elevation. The CT angiography was reported as normal, so the patient was admitted to cardiology to study chest pain with elevated markers of myocardial necrosis and heart failure. On the second day of admission to cardiology, the patient presented a fever peak of 38.5o, with no apparent infectious focus (neither clinically nor in complementary tests), and with negative blood cultures. Given the presence of moderate-severe aortic insufficiency in the transthoracic echocardiogram, a transesophageal study was performed on suspicion of endocarditis as a possible aetiology of the clinical picture. The patient's clinical condition meant that he did not tolerate the procedure adequately, and although no clear signs of endocarditis were observed, the study was of poor quality and was stopped early.
In the following days, the patient does not present fever or infectious symptoms again. There were no new episodes of chest pain; however, in the serial ECGs there was a negative T-wave in the anterior face, so a stress cardiac MRI was requested to assess the presence of necrosis or inducible ischaemia. The MRI was negative, ruling out signs of myocarditis or myocardial necrosis, but aortic insufficiency of severe appearance was again observed.
However, given that the patient continued to present progressive elevation of troponin and the electrical changes persisted (deepening of the T wave on the lateral side), a diagnostic cardiac catheterisation was requested, which showed a non-significant lesion in the RCA and confirmed the severity of the aortic insufficiency. On the 5th day of admission, the patient presented a new febrile peak of 38o, and an episode of rapid atrial fibrillation with failed pharmacological and electrical cardioversion, in the context of mild decompensation of heart failure. Once again, a battery of tests was requested to rule out infection, which was ruled out, with negative blood cultures again. On the 7th day of admission to Cardiology, he presented an episode of desaturation, tachypnoea and hypotension, compatible with acute pulmonary oedema, for which he was admitted to the Coronary Unit and finally required orotracheal intubation and mechanical ventilation, as well as inotropic support with vasoactive drugs. A transesophageal echocardiogram was performed with the patient intubated, ruling out endocarditis, and finally a localised dissection of the aortic root responsible for the severe aortic insufficiency was observed, and Cardiovascular Surgery was contacted for urgent intervention. Intraoperatively, a type A dissection was observed, with circumferential intimal rupture at the level of the sinotubular junction causing sagging of all the commissures, this being the mechanism of the aortic insufficiency observed.
During his admission to the Coronary Unit after surgery, he evolved slowly but favourably, without new febrile peaks and with improvement in the clinical signs of heart failure, and was discharged on the 7th day post-surgery. One month later, the patient is clinically stable and asymptomatic from the cardiological point of view, with no aortic insufficiency in the outpatient echocardiogram.

Diagnosis
Localised aortic root dissection with acute severe aortic insufficiency.
