HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
He has a history of arterial hypertension, type II diabetes without target organ involvement and dyslipidaemia.
Cardiologically, he had ischaemic dilated cardiomyopathy with very severe ventricular dysfunction (LVEF 8%), secondary to coronary artery disease of the trunk and 3 vessels revascularised percutaneously on several occasions with severe diffuse distal disease. A cavo-tricuspid isthmus ablation was performed for common flutter in 2008, presenting permanent atrial fibrillation since February 2014. Valvularly, he had moderate aortic stenosis with a maximum gradient of 36 mmHg and an average gradient of 18 mmHg, and an area per continuity equation of 1.2 cm2.
He has an ICD in primary prevention.
He presented hyperthyroidism due to type 2 thyroiditis induced by amiodarone.
Since device implantation, he has had no thrombotic or embolic complications, with stable flow parameters and pulsatility indices. Subsequent reviews showed a tendency to hypertension, with deterioration of renal function up to 2 mg/dl after increasing hypotensive drugs, in relation to previous renal disease.
During a routine check-up at the Cardiology day hospital, the patient reported worsening dyspnoea until it became moderate exertion over 15 days of evolution, accompanied by chest pain related to inspiratory movements in the left hemithorax.
Physical examination showed a mean blood pressure of 100 mmHg measured with the aid of a portable vascular Doppler. Weight was stable with respect to previous examinations, with normal O2 saturation (95 %). Of note was the presence of jugular venous ingurgitation of 7cm with positive hepatojugular reflux. Cardiac auscultation showed continuous flow noise of ventricular assistance and minimal systolic murmur, barely audible, with pulmonary auscultation with hypoventilation in the left hemithorax. There was no hepatomegaly, but there was bimalleolar oedema in the lower limbs. The driveline outlet was explored and found to be in perfect condition, without suppuration or erythema.
The Heart Mate II daily chart shows speeds of 9,200 rpm, flow rate 4.7-5.2 litres, pulsatility index 6.9-7.3 and power 5-5.6W. Multiple PI events in relation to suction episodes detected by the machine (previously only occasional).

COMPLEMENTARY TESTS
ECG: atrial fibrillation with controlled ventricular response, with controlled RV.
Lower QS. Wide QRS (140 ms) with BRD and negative T wave in V1-V5 (unchanged).
Chest X-ray: pleural effusion predominantly left. No increase in interstitial pattern. Cardiac silhouette unchanged with respect to previous studies. Left ventricular assistance and ICD normoimplanted.
Analysis on admission: Hb 12.5 mg/dl, leukocytes 9,450 without alteration of the formula.
Glucose 97, ALT 15; GGT 98; FA 112; Cr 1.92; Na 135; K+ 4.0; NTproBNP 4714; TSH 2.31; T4 1.6. CBC at discharge: Hb 12.2, creatinine 2.1; Na 137, K 3.9, NTProBNP 1643.
Transthoracic echocardiogram on admission: very limited study due to the poor window.
Left ventricle with dyskinetic movement of the septum. Global function appears severely depressed. Segmental contraction cannot be assessed.
Right ventricle not dilated, with apparently normal systolic function.
Transesophageal echocardiogram on admission: outflow tract at the level of the LV apex positioned close to the anterior interventricular septum, without clear obstruction. Predominantly systolic flow with a high peak end-systolic flow of 54 mHg (3.6 m/s). No evidence of intraventricular thrombus. Entrance cannula in ascending aorta with laminar flow, systolic peak 1.1 m/s, diastolic peak 0.24 m/s. No thrombus in LVOT or aortic root. Left aortic valve free of thrombus with a velocity of around 20 cm/s. Sclerocalcified aortic valve, opening is observed in all beats. Mild (I) commissural insufficiency. Left ventricle not dilated, moderately depressed global systolic function. Long axis DTD of 48.5 mm. Short-axis fractional area change (transgastric) of 48%. Non-dilated right ventricle with slightly reduced global function (although larger compared to the left), acceptable global function.
Interventricular septum with slight bulging towards the LV. Atrial septum intact, slightly bulging to the left. No pericardial effusion.
Transesophageal echocardiogram after reduction of the assist revolutions: inflow cannula at the level of the LV apex positioned close to the anterior interventricular septum, without obstruction. Continuous flow with a maximum end-systolic peak of 18 mHg and peak velocity of 2.1 m/s (decrease from previous TEE). Adequate centration of the IVS, without ballooning to the right or left cavities. The rest was unchanged with respect to the previous study.
Haemodynamic study on admission: AD 16. VD 41/22. PCP 17. AP 32/ 16 mean 24. GTP 7. Cardiac output Fick 7.7; thermodilution 6.9.
Haemodynamic study at discharge: CVP 8 mmHg; BP 32/11/18 mmHg; PCP 14 mmHg; thermodilution CO 4.9 (CI 2.5 l/min); Fick CO 5.3 l/min (CI 2.8). SVR 947 dynes.

EVOLUTION
After admission to Cardiology, a haemodynamic study was initially performed, which showed increased right and left pressures with high cardiac output (CO 7 l/min, PCP 18, DBP 16 mmHg). In view of this result, treatment was adjusted with an increase in diuretics, which was not tolerated due to worsening renal function.
A transesophageal echocardiogram was performed with recovery of partial LVEF (shortening faction 48%) with interventricular septum slightly deviated to the left and suction events in the systoles due to increased contractility.
The right ventricle persists with good radial function and no cavity dilatation. Aortic valve opening was observed in all beats (previously closed), with no intracavitary thrombi. To rule out extracardiac causes, a study of pleural fluid compatible with transudate and a chest CT scan was performed, showing no tumour lesion or infectious consolidation, with passive atelectasis of the left lung due to the effusion.
Given the absence of thrombosis data and the recovery of contractility and myocardial function, a diagnosis of high output heart failure with high right and left filling pressures was made, so the assist speed was reduced to 8,800 rpm (parameters after lowering: speed 8,800 rpm, output 4.2-4.5 l/min, pulsatility index 6.5-7, power 4.8 W). After this, the clinical symptoms of dyspnoea and chest pain resolved and the eventual disappearance of the PI on the alarms. Right catheterisation and TEE showed a normal haemodynamic situation and disappearance of suction events, with pulsatile flow through the assistance but with peak velocities of around 2-2.4 m/s. In a stable situation, with vasodilators and low doses of diuretic, the patient was discharged.

DIAGNOSIS
Heart failure due to high cardiac output. Secondary pleural effusion.
HeartMate II type circulatory assist device, normofunctioning.
Severe ventricular dysfunction partially recovered after a long period of assistance.
Ischaemic dilated cardiomyopathy. 3-vessel coronary artery disease revascularised with stents.
