HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

We present the case of an 89 year old male with a history of: Arterial hypertension under treatment with good control. Common flutter treated with cavotricuspid isthmus ablation. Implantation of a VDD pacemaker in 2007 after cardiogenic syncope (no reports). Non-ST-elevation acute coronary syndrome in 2013 with coronary angiography showing no significant lesions. Usual treatment: ramipril 2.5 mg at breakfast, omeprazole 20 mg at breakfast, atorvastatin 40 mg at dinner, tamsulosin/dutasteride 0.4/0.5 mg at breakfast, bisoprolol 5 mg at lunch, acenocoumarol as prescribed, calcifediol 0.266 mg monthly. Baseline condition: physically active, no cognitive deterioration. The patient was under cardiological follow-up for aortic stenosis, of degenerative origin, progressing to severe, the patient being asymptomatic. Last echocardiographic control in October/19, where preserved LVEF and severe aortic stenosis were found: aortic valve area (AVA) by continuity equation of 0.72 cm2 (0.38 cm2/m2), maximum/average gradients of 79/44 mmHg, a maximum velocity of 4.5 m/s and an integral LVOT/aorta ratio of 0.21. In January 2021, a telephone consultation was made in which the patient reported that he continued to carry out his daily activities without difficulty and was asymptomatic, in class I of the New York Heart Association (NYHA). Two months after this consultation, the patient needed to be hospitalised in another centre for acute heart failure in the context of SARS-CoV-2 pneumonia. The patient made good progress on the ward with diuretic oxygen therapy. His doctors contacted our clinic, and the patient was discharged without congestive data and with an appointment for preferential assessment in the week following hospital discharge. However, a few days after discharge, the patient needed to visit the emergency department of our centre due to the appearance of oppressive chest pain triggered by slight exertion, which subsided with rest and which was self-limiting, with none of the episodes lasting more than 5 minutes. In addition, she reports a feeling of dizziness that makes it difficult for her to walk. All this has occurred since the last hospital admission. Physical examination revealed a blood pressure of 160/83 mmHg at 64 beats per minute, saturation of 98% of ambient air and normothermia. There was also an ejection murmur in aortic focus III/VI, radiating to the suprasternal and carotid cavities with effacement of the second tone. Pulmonary auscultation showed bibasal crackles. Oedema with pretibial fovea in both lower limbs.

COMPLEMENTARY TESTS
Last outpatient echocardiogram: severe aortic stenosis with the following additional data: aortic valve area (AVA) by continuity equation of 0.72 cm2 (0.38 cm2/m2), maximum/average gradients of 79/44 mmHg, a maximum velocity of 4.5 m/s and an integral ratio of 0.21. ED electrocardiogram (digitised recording not available): alternating sinus rhythm around 70 bpm with electro-stimulated tachycardia 130 bpm. Chest X-ray in the ED: study limited by technique. Increased cardiothoracic index, without clear parenchymal consolidation. Impression of absence of pleural effusion. Normopositioned pacemaker electrocatheter. Emergency blood tests: CBC: red cells 4.77 xmill/μl, haemoglobin 13.2 g/dl, haematocrit 39.1%, MCV 82.1 fl, MCH 27.7 pg, MCHC 33.8 g/dl, RDW 17.0%, platelets 216 x1000/μl, MPV 9.2 fl, leukocytes 8.3 x1000/μl, neutrophils 5.9 x1000/μl, neutrophils % 71.3%, lymphocytes 1.3 x1000/μl, lymphocytes % 15.8%, monocytes 1.0 x1000/μl, monocytes % 12.0%, eosinophils 0.0 x1000/μl, eosinophils % 0.6%, basophils 0.0 x1000/μl, basophils % 0.3%. Biochemistry: glucose 120 mg/dl, creatinine 1.85 mg/dl, sodium 128 mEq/l, potassium 4.21 mEq/l, chlorine 83 mEq/l, ALT (GPT) 33 U/l, AST (GOT) 36 U/l, gamma-GT 41 U/l, alkaline phosphatase 89 U/l, LDH 290 U/l, bilirubin 0.6 mg/dl, CK 87 U/l, troponin T hs 852.6 ng/l, NTproBNP 14,106 pg/ml, C-reactive protein 0.84 mg/dl. Haemostasis: prothrombin activity 9%, prothrombin time 79.5 s, INR (lab) 7.76, TTPa 51 s, fibrinogen (derivative) 405 mg/dl, D-dimer 243 ng/ml. Blood tests during admission: enzyme serology with peak troponin T hs of 1,440 ng/l. Echocardiogram during admission: non-dilated left ventricle with moderate hypertrophy. Segmental contractility alterations: global hypokinesia and apical, inferior and inferolateral inferoseptal akinesia with severe systolic dysfunction (LVEF 33%). The aortic valve was severely calcified and unstructured with marked restriction of leaflet mobility: AVA 0.48 cm2 (0.26 cm2/m2), peak/average gradients of 87/52 mmHg, peak velocity of 4.7 m/s and an integral ratio of 0.12, all compatible with severe-critical aortic stenosis. In addition, the tricuspid valve exhibited mild insufficiency allowing an estimated pulmonary arterial systolic pressure of 63 mmHg. Coronary angiography: significant calcification of the coronary tree. Left main coronary artery of good calibre, with mild atheromatosis. Anterior descending artery (LAD) of good calibre and development. Proximal LAD with mild atheromatosis. Mid LAD with moderate focal lesion at the level of the bifurcation with the 2nd dominant diagonal without lesions. Distal LAD without lesions. Non-dominant circumflex with moderate ostial atheromatosis. Dominant right coronary artery with diffuse mild atheromatosis. Study superimposable to the previous one in 2013.


CLINICAL EVOLUTION
Given the chest pain with elevated troponin T hs and semiological data compatible with decompensation of heart failure, depletive treatment with intravenous furosemide was started in the emergency department, obtaining a favourable response and subsequently allowing the patient to be started on drugs for ventricular dysfunction. On the other hand, in view of the patient's tachycardia, the pacemaker was interrogated, confirming a pacemaker-mediated tachycardia, which was resolved after extending the post-ventricular atrial refractory period. A new transthoracic echocardiogram showed a non-dilated left ventricle with moderate hypertrophy, alterations of segmental contractility: global hypokinesia and apical, inferior and inferolateral inferoseptal akinesia with severely depressed systolic function (LVEF 33%). The aortic valve was severely calcified, with the following additional data: AVA 0.48 cm2 (0.26 cm2/m2), peak/average gradients of 87/52 mmHg, peak velocity of 4.7 m/s and an integral ratio of 0.12, all compatible with severe-critical aortic stenosis. In addition, the tricuspid valve exhibited mild insufficiency allowing an estimated pulmonary arterial systolic pressure of 63 mmHg. Given the previous findings, coronary angiography was performed and showed non-significant coronary lesions. The case was discussed in a medical-surgical session and transcatheter valve implantation via the femoral artery (TAVI) was chosen. In addition, the possibility of urgent percutaneous valvotomy was considered if the patient's situation required it at some point during admission. However, the patient evolved favourably and was discharged pending completion of the outpatient TAVI study.


DIAGNOSIS
Severe symptomatic aortic stenosis.
Pacemaker-mediated tachycardia.
Decompensation of heart failure secondary to previous.
Acute myocardial infarction without type II ST elevation within the prior.
Severe left ventricular systolic dysfunction.
Severe pulmonary hypertension.
Acute renal failure.
Mild hyponatraemia.
Acenocoumarol overdosage.
