HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
81-year-old female patient, with the following history of interest:
Baseline situation: lives alone. Independent. Active life for her age. Unborn children.
She worked as an assistant.
Cardiovascular risk factors: high blood pressure of long evolution.
Obesity.
Cardiological history:
Paroxysmal paroxysmal atrial fibrillation (AF) anticoagulated with aldocumar with good INR control.
She had been assessed 1-2 years previously in outpatient cardiology consultations and bisoprolol was withdrawn due to first-degree atrioventricular block. An exercise test was performed to assess chest pain, which was clinically and electrically negative.
Transthoracic echocardiography (TTE) (November 2016): non-dilated left ventricle (LV) with mild concentric hypertrophy, unaltered contractility with normal left ventricular ejection fraction (LVEF), pseudonormal diastolic pattern with data suggestive of elevated pressures. No significant aortic valvular heart disease. Right ventricle (RV) not dilated with normal systolic function.
Moderate left atrial (LA) dilatation. Mild mitral insufficiency.
Mild tricuspid insufficiency. Estimated normal pulmonary arterial systolic pressure (PSAP).


Other history:
Studied by pulmonology for dyspnoea without specific diagnosis. Normal respiratory function tests; chronically on a bronchodilator.
Arthrosis.
Depressive syndrome.
She denies surgical interventions of interest.
Previous medication: aldocumar 1 mg (1 tablet every day except Thursday and Sunday when he takes 1 and a half), furosemide 40 mg (half a tablet every 48 hours), paroxetine 20 mg (1 tablet at breakfast and half at lunch), omeprazole 20 mg (1 tablet at breakfast), quetiapine 25 mg (1 tablet at dinner), umeclidinium/vilanterol (55/22 mcg) inh every 24 hours, paracetamol 1 g (if required), hydroferol 0.266 mg (every 15 days).

CURRENT ILLNESS
An 81-year-old woman, with the history described above, attended the emergency department due to worsening of dyspnoea in previous days until she became resting with associated tachypnoea and significant respiratory distress.
The patient and family were told of progressive dyspnoea that had started as moderate exertion in previous weeks with wheezing. On the day of admission, her daughter went home and found her with dyspnoea and respiratory work complaining of epigastralgia that the patient could not define. She also reported cough and rhinorrhoea in recent weeks without fever.
She denies chest pain (only occasionally with coughing) or palpitations. No orthopnoea or paroxysmal nocturnal dyspnoea, although the family reports that she has been sleeping badly for the last few days. She did not report decreased diuresis or oedema in the lower limbs.
In the initial emergency department assessment, the patient was diagnosed with acute pulmonary oedema and treatment was started with parenteral bolus amiodarone, given that he was in rapid atrial fibrillation, which was poorly tolerated clinically.

PHYSICAL EXAMINATION
Arrival: afebrile (36.7 ̊C), heart rate (HR) 120-145 bpm, blood pressure (BP) 114/96 mmHg, RF 31 rpm, baseline SatO2 90%. After amiodarone bolus: HR 120 bpm, BP 65-57/30-37 mmHg, SatO2 100% with NIV.
Global inspection: conscious, oriented in the three spheres and cooperative. With regular general condition. Tachyonic with tugging.
Cardiac auscultation: arrhythmic. No murmurs or extratonos were heard. Artefactual respiratory sounds.
Pulmonary auscultation: preserved vesicular murmur (CVM) bilaterally with crackles up to midfields and scattered wheezing.
Abdomen: hydro-aerial sounds present. Slightly distended, diffusely tender on palpation. No signs of peritoneal irritation. No masses or visceromegaly.
Extremities: no oedema or signs of phlogosis.

COMPLEMENTARY TESTS
On admission
Blood count: haemoglobin 12.6 g/dl. Red cells 4.38 x10E6/μl. MCV 85.6 fl. MCH 28.8 pg.
Leukocytes 8.09 x10E3/μl. Neutrophils (blood-%) 89.6%, 7.25 x10E3/μl. Lymphocytes (%) 5.4%. Lymphocytes 0.44 x10E3/μl. UPLAQ platelets 313 x10E3/μl. Haematocrit 37.5%.
Biochemistry: glucose 155 mg/dl. Urea 53 mg/dl. Creatinine 1.49 mg/dl. Sodium ion 136 mmol/l. Plasma potassium ion 4.5 mmol/l.
Cardiac markers: creatine kinase: 254-->304 U/l. Troponin T 328-->382 ng/l. NTproBNP 3531.
Coagulation: partial thromboplastin R 1.05. Prothrombin T. (ratio) 2.28. INR 2.22. T. partial thromboplastin 30.40 sec. T. prothrombin 25.50 sec. Fibrinogen derivative 478. Ddimer 482.00 ng/ml. FEU T. prothrombin (%) 34.0%.
Blood gas: pH (arterial blood gas) 7.39, pO2 (arterial blood gas) 68 mmHg, pCO2 (arterial blood gas) 30 mmHg, total CO2 (arterial blood gas) 19.1 mmol/l. Bicarbonate (arterial gas) 19.7 mmol/l.
Excess bases (arterial gas) -6.9 mmol/l. Oxyhaemoglobin saturation (arterial gas) 94%.
Electrocardiogram (ECG): AF at 160 bpm, with Q wave in III and R wave amputation up to V5 not present in previous ECGs. Diffuse flattening of repolarisation. After CVE (1 shock 150 J): sinus rhythm at 90 bpm, Q wave in III and aVF as well as V1-V3.
Chest X-ray: decubitus study of poor quality but with signs of water overload and interstitial pattern. Probable cardiomegaly although oversized by the projection.
Transthoracic echocardiography (TTE) in HED (in patient in RS at 80 bpm in sedentary position): suboptimal window. Moderately dilated LV with severe LV dysfunction (LVEF visu: 20-25%). Better basal segment contractility, but difficult to assess segmental alterations. Prolonged relaxation Doppler pattern. RV with mild systolic dysfunction.
TAPSE 15 mm. Mild-moderate mitral insufficiency of mixed degenerative origin and secondary to LV dilatation. Trivalve aortic valve with slight calcification of the free edge of the leaflets. No significant gradients. Minimal aortic insufficiency (AIo).
Moderate tricuspid insufficiency, with A-V gradient of 25-30 mmHg. Vena cava not visualised.


At discharge
Blood count: haemoglobin 12.4 g/dl. Red cells 4.30 x10E6/μl. MCV 84.0 fl. MCH 28.8 pg. MCHC 34.3 g/dl. Leukocytes 5.85 x10E3/μl. Neutrophils (blood-%) 64.4%. Neutrophils 3.77 x10E3/μl. Lymphocytes (%) 23.9%. Lymphocytes 1.40 x10E3/μl. Monocytes (blood-%) 9.6%.
UPLAQ platelets 271 x10E3/μl. VPM 10.5 fl. SR RDW coefficient of variation 17.6%.
Haematocrit 36.1%.
Biochemistry: glucose 89 mg/d. Urea 44 mg/dl. Creatinine 1.56 mg/dl. Sodium ion 134 mmol/.
Potassium ion 4.1 mmol/l. Plasma potassium ion 4.2 mmol/l. Amylase 75 U/l. Lipase 29 U/l.
Creatine kinase 15 U/l. Troponin T 50 ng/l. NT-proBNP 1213. Procalcitonin 0.06.
Total bilirubin 1.3 mg/dl. Direct bilirubin 0.4 mg/dl. Alanine aminotransferase 70 U/l.
Calcium 2.21 mmol/l. Transferrin 221 mg/dl. Phosphate 1.09 mmol/l. Lactate dehydrogenase 216 U/l. Aspartate aminotransferase 37 U/l. Transferrin saturation index 23 %. Iron 71 μg/dl. Folate 6.35. Albumin 31 g/l. C-reactive protein 0.6 mg/dl. Hours of evolution (X).
Gamma-glutamyltransferase 40 U/l. Magnesium 0.74 mmol/l. C-reactive protein 5,3 mg/dl.
Ferritin 272. HDL cholesterol 51 mg/dl. Urate 7.4 mg/dl. Total cholesterol 122 mg/dl.
Total protein 62 g/l. Vitamin B12 1482. Triglycerides 66 mg/dl. Estimated glomerular filtration 38. Calculated LDL cholesterol 57 mg/dl. Lactate 2,2 mmol/l. Ionic calcium 0.94 mmol/l.
Coagulation: T. partial thromboplastin R 0,96 T. prothrombin (ratio) 1,13. INR 1.12. T. partial thromboplastin 27.70 sec. T. prothrombin 12.60 sec. derived fibrinogen 625. Ddimer 482.00 ng/ml. FEU T. prothrombin (%) 84.0%.
Blood gas: pH (arterial blood gas) 7.39. pO2 (arterial blood gas) 68 mmHg. pCO2 (arterial blood gas) 30 mmHg. Total CO2 (arterial gas) 19.1 mmol/l. Bicarbonate (arterial gas) 19.7 mmol/l.
Excess bases (arterial gas) -6.9 mmol/l. Oxyhaemoglobin saturation (arterial gas) 94%.
Microbiology: antigenuria negative. Virology: RSV positive (7748), the rest undetectable.
ECG 1: sinus rhythm at 70 bpm. Atrioventricular block (AVB) first degree. Q inferior face and V1-V4 and R amputated V5-V6. Negative T precordial, I and aVL. QTc 670ms.
ECG 2: AF with controlled MVR at 89 bpm. Q waves in inferior face suggestive of necrosis of DIII and aVF (already in the first degree)
DIII and aVF (already observed in previous ECGs) ST underlevel in anterior and lateral face with asymmetrical negative T waves.
ECG 3: sinus rhythm at 70 bpm. Q waves in inferior face suggestive of necrosis of DIII and aVF (already seen in previous ECGs) with ST-segment elevation in anterior and lateral face with asymmetric negative T waves.
Telemetry: bouts of non-sustained polymorphic ventricular tachycardia until yesterday at approximately 22:30 hours (yesterday at 15:00 hours bout of PSVT). Since then abundant VE with some doublets/triplets.
Transthoracic echocardiography (1): Moderately dilated LV with severe LV dysfunction (LVEF visu: 20-25%). Better contractility of basal segments, but difficult to assess segmental alterations. Prolonged relaxation Doppler pattern. RV with normal systolic dysfunction TAPSE 16 mm. Mild-moderate mitral insufficiency of mixed degenerative origin and secondary to LV dilatation. Trivalve aortic valve with slight calcification of the free edge of the leaflets. No significant gradients. Minimal AIo. Slightly dilated LA. Moderate tricuspid insufficiency, difficult alignment. Vena cava not visualised.
Coronary angiography: coronary arteries without significant angiographic lesions.
Transthoracic echocardiography (2) (study performed in AF with RVR at 120x ́, alternating with bursts of RS at 80x ́): non-dilated LV with normal thickness, segmental contractility very poorly visualised but impressions of akinesia of basal and mid-lateral and lower basal segment. Moderate LV dysfunction with LVEFbp 43%. RV with normal systolic function. Mixed mild-moderate mitral insufficiency. Trivalve aortic valve with slight calcification of the free edge of the leaflets. No significant gradients. Minimal AoI. Slightly dilated LA. Tricuspid insufficiency poorly visualised. Vena cava not dilated.
Improvement of mitral function and mitral insufficiency with respect to previous study.
Cardiac MRI: LV normal size with moderate to mild systolic dysfunction.
Global hypokinesia. Severe hypokinesia in basal-mid inferolateral segment with small focus of late subendocardial enhancement of 50% in basal inferolateral segment of ischaemic profile. Assess the possibility of tachycardiomyopathy. Normal sized RV with normal systolic function. Voluminous sliding hiatal hernia. Assess the possibility of tachycardiomyopathy.

CLINICAL EVOLUTION
81-year-old patient, with the history described above, admitted to the coronary cardiology unit for acute pulmonary oedema secondary to AF with rapid ventricular response.
Initially, pharmacological cardioversion was performed with bolus administration and perfusion of amiodarone, which was ineffective, and, together with taking antidepressants at home, induced the appearance of a long QT. Secondary to QT prolongation, symptomatic polymorphic ventricular tachycardias were recorded, although without loss of pulse. After pharmacological lavage with fluid therapy and withdrawal of antidepressants, the QT interval was corrected and the ventricular arrhythmias disappeared. In this context, transthoracic echocardiography was carried out, with the following findings
LVEF severely affected.
In the admission analysis, elevated liver function tests were observed, and a referral was made to the gastroenterologist, who, in the light of the clinical evolution and abdominal ultrasound, diagnosed ischaemic hepatitis.
Subsequently, he was transferred to the hospital ward, with progressive improvement of symptoms of acute heart failure. Due to associated respiratory symptoms, viral serologies were extracted and were positive for respiratory syncytial virus. These symptoms progressively disappeared with bronchodilator treatment.
Regular transthoracic echocardiography was performed, confirming severe ventricular dysfunction, a finding that was also visualised in nuclear magnetic resonance. Due to persistent AF, electrical cardioversion was performed with reversion to sinus rhythm, remaining in sinus rhythm at the time of discharge, under treatment with amiodarone. Days after cardioversion, transthoracic echocardiography was performed, showing improvement in left ventricular dysfunction, confirming the diagnosis of tachycardiomyopathy.
During his hospital stay, he presented several episodes of oligosymptomatic coronary vasospasm, with ST elevation in the inferior face and sustained polymorphic ventricular tachycardias (maximum of 12 seconds). Diagnostic coronary angiography was performed, showing normal coronary arteries, and after starting treatment with nitrates and dihydropyridine calcium antagonists, the episodes disappeared. Magnetic resonance imaging performed during admission (previously mentioned) showed late subendocardial enhancement in the inferolateral segment with an ischaemic profile, probably in the context of these vasospastic episodes.
Due to the withdrawal of antidepressant medication, the patient began to show signs of major depression (anhedonia, abulia...) and so a consultation with psychiatry was requested, and after reintroduction of paroxetine, the condition was stabilised.
The patient being asymptomatic and stable from the cardiovascular point of view, she was discharged home.

DIAGNOSIS
Acute congestive heart failure with acute pulmonary oedema.
Persistent AF with rapid ventricular response cardioverted chemically and electrically.
Tachycardiomyopathy with moderate postcardioversion ventricular dysfunction.
Sustained polymorphic ventricular tachycardia (torsade de pointes).
Long QT (pharmacological).
Coronary vasospasm (Prinzmetal's angina) with ventricular arrhythmias.
Acute bronchitis without signs of respiratory infection.
Ischaemic hepatitis. Cholelithiasis.
Major depressive disorder with psychotic symptoms.
Intolerance to angiotensin-converting enzyme inhibitors (ACE inhibitors).
Contraindication to beta-blockers due to vasospasm.
