We present the case of a 49-year-old woman, a professional climber, with episodes of transient ischaemic attacks. She never had chest pain, dyspnoea or any of the other symptoms we are accustomed to recording in our histories, but she presented a compendium of cardiac alterations that allowed us to get to the top of her pathology.

HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION

History
No drug allergies.
Toxic habits: smoker of 7 cigarettes/day.
No other known cardiovascular risk factors (CVRF). Professional climber.
No usual treatment.

Current illness
Our patient was admitted to the neurology department for an episode of hypoaesthesia and paraesthesia in the right hemibody, self-limited for 2 to 3 hours 2 months ago. One month ago, episode of paresis in the right hemisphere, which she recovered within half an hour. Last episode the day before admission, with the same characteristics but of longer duration. At no time did she report chest pain, dyspnoea or other cardiological symptoms. During the study, an electrocardiogram (ECG) and transthoracic echocardiogram were performed, which showed alterations, so an assessment was requested.

Physical examination
Good general condition, well hydrated and perfused. Blood pressure (BP) 118/71 mmHg. Heart rate (HR) 65 bpm. Afebrile. Eupneic at rest. Jugular venous pressure normal. Cardiac auscultation: rhythmic at 60 bpm, no murmurs. Pulmonary auscultation: preserved vesicular murmur. Abdomen without alterations. Lower limbs: no oedema, pulses preserved.

COMPLEMENTARY TESTS
Electrocardiogram: sinus rhythm at 65 bpm. PR 140 msg. Narrow QRS. Q wave in V1-V4, DI and aVL with isodiphasic T wave in V2-V4, flat in V5-V6, DI and aVL and inferior leads.
Chest X-ray: normal cardiothoracic index, no evidence of heart failure. Laboratory tests:
CBC: haemoglobin 14.3 g/dl, leucocytes 5,600/μl with normal formula, platelets 190,000/μl. Coagulation: INR 1, TTPa 29 s.
Biochemistry: glucose 88 mg/dl, urea 29 mg/dl, creatinine 0.68 mg/dl, FGR > 60 ml/min, Na 140 mmol/l, K 4.8 mmol/l, total cholesterol 136 mg/dl, HDL 52 mg/dl, LDL 71 mg/dl, TG 64 mg/dl, Inmonoglubulins normal. CRP < 1 mg/dl. Rheumatoid factor < 10 IU/ml. Folic acid and vitamin B12 normal.
Autoimmunity: negative. Complement normal. Thyroid hormone normal. Hb1Ac 5.3%. Factor Leiden factor and factor II 20,210 negative. Homocysteine normal. Proteinogram normal.
Serology: HIV, Herpes simplex, EBV, CMV, Brucella, Lues and Borrelia negative.
Echocardiogram: left ventricle (LV) slightly dilated with severe depression of LVEF (25-30%), with extensive apical akinesia and remodelling, extensive anterior akinesia, lower mid-apical and mid-apical septum. Grade II mitral regurgitation. Mobile thrombus in LV apex measuring 18 x 8 mm.
Haemodynamic study: right dominance. No coronary calcification. Coronary disease of 1 vessel. Left main coronary artery without significant stenosis. Anterior descending occluded at the origin, with TIMI 0 distal flow. The distal vessel is visualised by homo- and heterocoronary circulation. The appearance of the distal vessel is highly suggestive of spiroid dissection and haematoma of the anterior descending artery from its origin.
Right circumflex and coronary artery of good calibre and development, with smooth edges, without angiographically significant stenosis.
Renal angiography: rectilinear right renal artery with small deformations along its entire course, in both arterial borders. Double left arterial system.
Cardiac magnetic resonance imaging (MRI): LV of normal size with mid-apical anterior akinesia, apical lateral, apical septum, apical inferior and apex. Severe hypokinesia of medial septum, medial lateral, medial inferior. LVEF 36%. Hypoperfusion of the middle segment of the anterior wall and middle septum, middle segment of the lateral wall and all apical segments. Very extensive transmural late enhancement of the basal, mid and apical segments of the anterior wall, apical inferior, mid-apical lateral, mid anterior septum, apical septum and the entire apex. Large apical thrombus (28 x 9 mm), mobile. Right ventricle (RV) of normal size. Normal right atrium (RA). Left atrium (LA) slightly dilated.
Cranial CT: corticosubcortical hypodensity in the left parietal convexity and in the nuclei of the left base, which may correspond to ischaemic lesions. Doubtful hyperdensity at the level of the top of the basilar artery, without identifying ischaemic lesions in the posterior circulation. Normal ventricular system. Centred midline.
Echo Doppler of supra-aortic trunks: no alterations.
Ambulatory control echocardiogram: dilated LV with akinesia of the mid-apical segments of the anterior and lateral face, apical of the inferior septum and inferior face, with apical aneurysmal image. Moderate left ventricular systolic dysfunction (LVEF 35%). Normal sized RV with preserved systolic function. Mild LA dilatation. Protomesystolic mitral regurgitation located between A2-P2, mild-moderate grade (grade II). No other valvular abnormalities. Normal pericardium. Apical thrombus image measuring 14 x 7 mm, without mobile structures, resting on the area of the aneurysm. Compared to the previous study, there is a reduction in the volume of the thrombus.

CLINICAL EVOLUTION
The patient was admitted to neurology with a diagnosis of left hemispheric embolic stroke with good clinical evolution. She was assessed by cardiology with the diagnosis of extensive anterior myocardial infarction with severe depression of LVEF and mobile apical thrombus, due to spontaneous coronary dissection probably related to intense exercise. The study was completed with cardiac MRI.
During outpatient follow-up, medical treatment was titrated, limited by low BP and HR figures, up to maximum tolerated doses: Acetylsalicylic acid (ASA) 100 mg daily, acenocoumarol for INR between 2 and 3, omeprazole 20 mg daily, sacubitril/valsartan 49/51 mg every 12 hours, carvedilol 3.125 mg every 12 hours, spironolactone 25 mg daily, atorvastatin 10 mg daily.
An echocardiogram was performed 3 months after optimising medication, with an LVEF of 35% in NYHA functional class II, so it was decided to implant an implantable cardioverter defibrillator (ICD) for primary prevention.

DIAGNOSIS
Left hemispheric embolic stroke. Apical LV thrombus as a source of cardioembolism.
Ischaemic heart disease. Anterior descending coronary artery occlusion due to spiroid dissection. Established anterior myocardial infarction. Apical aneurysm with thrombus. Heart failure with reduced ejection fraction, in NYHA functional class II after optimisation of medical treatment. Implantation of ICD in primary prevention.
