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Our mission is to reduce the burden of cardiovascular disease through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
A 71- year old woman with type 2 diabetes mellitus, previous herniated disk surgery, and a patient-controlled epidural morphine infusion pump for neurogenic pain (L5-S1) was admitted to the local hospital for fever. A bronchopulmonary infection was diagnosed and treated with antibiotics.
After 4 months she underwent a routine cardiological assessment and on ECG lateral subepicardial ischemia was noted. After 1 month she was readmitted to the local hospital for suspected non ST elevation acute coronary syndrome; coronary angiography showed normal coronary arteries, left ventriculography showed ejection fraction at the lower limit of normality with inferior wall hypokinesia.
After 2 weeks from discharge she was readmitted to the same hospital because of dyspnea at rest, pedal edema, no chest pain or palpitation. ECG showed: sinus rhythm, HR 95 bpm, low voltages, diffuse unspecific repolarization changes. On Chest-X ray there were increased hilar-perihilar vascular markings, mild cardiomegaly, no pleural effusion. An echocardiogram showed a mild left ventricular dilation, mild left ventricular hypertrophy, severely depressed global left ventricular ejection fraction (EF 27%) with hypo-akinesia at the apex, mid septum, lateral and anterior walls,mild hypokinesis of the posterior and inferior walls. The right ventricle was mildly dilated and diffusely hypo-akinetic. There was moderate mitral and tricuspid regurgitation, mild pulmonary hypertension, no pericardial effusion. On telemetry no significant arrhythmias or ST-T abnormalities were present. At hospital admission BNP was high (3090 pg/mL), no other biochemical abnormalities were present, troponin I was not tested, ESR was normal, viral serology (IgM for adenovirus, coxsackievirus, parvovirus, CMV, EBV) was negative, as well as anti-mycoplasma antibodies and Lyme test. Since the epidural infusion pump was a contraindication to perform cardiovascular MRI, the patient was transferred to a tertiary referral centre to perform endomyocardial biopsy (EMB). The patient underwent EMB without any complication and was retransferred to the local hospital where she was put on ACE-inhibitors, diuretics and betablockers, recompensated, and subsequently transferred to our centre in NYHA class I for further diagnostic work-up.
Upon admission at our cardiology ward the patient was haemodynamically stable, asymptomatic, apyretic, with blood pressure of 110/70 mmHg and a heart rate of 80 beats/min. On physical examination she had no jugular venous distention at 45 degrees, had an audible S4 sound, 2/6 soft systolic murmur at the apex, rare crackles at both lung bases, mild bilateral poedal oedema. Her ECG on admission is shown in Figure 1.
High sensitivity cardiac troponin I was only slightly elevated with fluctuation and a peak of 0.154 microg/L (normal range 0.000 to 0.045), erythrocyte sedimentation rate, CRP, urea, creatinine, and thyroid hormones, liver enzymes, tumour markers, serum protein profile, Quantiferon test, were normal. Blood count revealed sideropenic hypocromic anemia (Hemoglobin 8.6 g/dL), NTpro BNP was high (10122 ng/L, normal range 0-900).
In the first days following admission to our ward the patient developed an isolated episode of paroxysmal nocturnal dyspnea, without ECG changes from basal, which responded to Oxigen administration
Fig. 1. ECG on admission showed sinus rhythm, 80 bpm, low voltage in limb leads, reduced progression of the R wave in leads V1-V3, isodiphasic/negative T waves in leads V1 to V6, D1 and aVL, prolonged QT (QTc 490 msec)Pa
Fig. 2. On telemetry documentation of a short run (7 beats) of asymptomatic supraventricular paroxysmal tachycardia, with minimum RR 0,37 sec (top strip) and of NSVT (4 beats) with minimum RR 0,31 sec (middle strip): Telemetry (shown in Figure 2) was unremarkable, except for short runs of PSVT and NSVT. Since anemia was refractory to iron administration, following hematology specialist consultation, the patient received blood transfusion with improved hemoglobin content (10.8 g/dL). A repeat echocardiogram showed: a mildly dilated left ventricle (EDV 75 ml/mq), moderately reduced global left ventricular ejection fraction (LVEF=39%) with normal kinesis of basal inferior, posterior, lateral and anterior wall segments and ipo-akinesis of the remaining segments, normal right ventricular dimension with moderate reduction of ejection fraction (RVEF=34%, FAC=24%, TAPSE=16). There was moderate tricuspid regurgitation and pulmonary hypertension (systolic pulmonary artery pressure 44 mmHg).
1) Can we make the final diagnosis based on the above cited results and what are the possible etiologies of this non-ischemic biventricular failure?2) If not, which additional examination would you recommend?3) What do you predict will be the clinical outcome in this patient?
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