Case: 67-years-old woman, with familiarity for ischemic cardiopathy, affected by dyslipidaemia and depression treated with antidepressant tricyclic drugs (TCA). Admitted to our ED for dyspnoea, palpitations and orthopnoea. Both clinical and instrumental examinations were suggestive of acute decompensated heart failure (HF): clinically, we objectivated jugular veins turgidity, S3 tone with gallop rhythm, olosystolic murmur at cardiac auscultation, bilateral rales at lung auscultations and peripheral oedema. Blood pressure was 120/80 mmHg with a cardiac frequency of 120 bpm and oxygen saturation of 96% in oxygen (2 l/min). Lung radiography showed left pleural effusion and diffuse interstitial oedema. BNP was 818 pg/ml, ECG showed left bundle branch block. Cardiac ultrasound showed severe left ventricle (LV) dysfunction, with reduced ejection fraction (22%), left chamber dilatation, diffuse LV hypokinesis, increased filling pressures, restrictive pattern, severe functional mitral insufficiency (vena contracta 0.81 cm) and moderate tricuspidalic insufficiency with increased pulmonary pressure (66 mmHg). Lung ultrasound confirmed left pleural effusion and interstitial syndrome. Admitted to our Internal Medicine department with diagnosis of acute HF with reduced ejection fraction (HFrEF), NYHA class IV, AHA class C. She underwent 24-h saturation and ECG monitoring and submitted to high-dose furosemide, spironolactone, low-dose bisoprolol and ivabradine with symptoms recovery. Coronary angiography, performed in the 3rd day, did not show any significant stenosis. In the 7th day echocardiography confirmed the EF (25%), a reduction of filling pressures, disappearance of the restrictive pattern with a residual type 1 diastolic dysfunction and reduction of mitral insufficiency (vena contracta 5.0 mm). At discharge, she was in good general conditions, without evidence of oedema or pleural effusion at lung ultrasound. Blood pressure was 120/50 mmHg, cardiac frequency was 68 bpm, SpO2 96% in room air. We decided to withdraw TCA, following the hypothesis of a potentially causative role of this class of drugs in the pathogenesis of HF. 25 days after discharge we underlined a net improvement of both clinical conditions and EF (34%), with reduction of BNP (466 pg/ml). We then started titrating bisoprolol (from 2.5 to 5 mg/day) and ivabradine (from 5 to 7.5 mg bid), obtaining a cardiac frequency of 55 bpm and started ACE-inhibitor (ramipril, 2.5 mg bid titrated to 5 mg bid). In the next control we observed further clinical improvement, with amelioration of exercise tolerance (NYHA I-II) and a further reduction of BNP (196 pg/ml, 60th day). Ramipril was switched to valsartan for ACE-inhibitors-related cough. At 90th day after discharge, echocardiography underlined a normalization of EF to 55% and the other previously underlined alterations. At 120th day patient was in NYHA class I, AHA class A. After excluding other common causes, we last hypothesized that TCA have been the cause of the observed clinical picture, which completely reversed after drug withdrawal. TCA-related dilated cardiomyopathy is a rare but reversible cause of HFrEF(1), which can improve after medication removal(2) but can often recur after reintroduction of the causative drug(3). This case underlines the importance of an internistic clinical reasoning even when managing a common pathology such as HF. References: (1) Montastruc G, Favreliere S, Sommet A, Pathak A, Lapeyre-Mestre M, Perault-Pochat MC, Montastruc JL; French Association of Regional PharmacoVigilance Centres. Drugs and dilated cardiomyopathies: A case/noncase study in the French PharmacoVigilance Database. Br J Clin Pharmacol. 2010 Mar;69(3):287-94. (2) Martí V, Ballester M, Obrador D, Udina C, Moya C, Pons-Lladó G. Reversal of dilated cardiomyopathy after chronic tricyclic antidepressant drug withdrawal. Int J Cardiol. 1995 Feb;48(2):192-4. (3) Briec F, Delaire C, Bouhour JB, Trochu JN. Recurrence of dilated cardiomyopathy after re-introduction of a tricyclic antidepressant. Arch Mal Coeur Vaiss. 2006 Oct;99(10):933-5.
Capeci William, T.N. (2016). Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report. Springer.
Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
Falsetti LorenzoWriting – Review & Editing
;
2016
Abstract
Case: 67-years-old woman, with familiarity for ischemic cardiopathy, affected by dyslipidaemia and depression treated with antidepressant tricyclic drugs (TCA). Admitted to our ED for dyspnoea, palpitations and orthopnoea. Both clinical and instrumental examinations were suggestive of acute decompensated heart failure (HF): clinically, we objectivated jugular veins turgidity, S3 tone with gallop rhythm, olosystolic murmur at cardiac auscultation, bilateral rales at lung auscultations and peripheral oedema. Blood pressure was 120/80 mmHg with a cardiac frequency of 120 bpm and oxygen saturation of 96% in oxygen (2 l/min). Lung radiography showed left pleural effusion and diffuse interstitial oedema. BNP was 818 pg/ml, ECG showed left bundle branch block. Cardiac ultrasound showed severe left ventricle (LV) dysfunction, with reduced ejection fraction (22%), left chamber dilatation, diffuse LV hypokinesis, increased filling pressures, restrictive pattern, severe functional mitral insufficiency (vena contracta 0.81 cm) and moderate tricuspidalic insufficiency with increased pulmonary pressure (66 mmHg). Lung ultrasound confirmed left pleural effusion and interstitial syndrome. Admitted to our Internal Medicine department with diagnosis of acute HF with reduced ejection fraction (HFrEF), NYHA class IV, AHA class C. She underwent 24-h saturation and ECG monitoring and submitted to high-dose furosemide, spironolactone, low-dose bisoprolol and ivabradine with symptoms recovery. Coronary angiography, performed in the 3rd day, did not show any significant stenosis. In the 7th day echocardiography confirmed the EF (25%), a reduction of filling pressures, disappearance of the restrictive pattern with a residual type 1 diastolic dysfunction and reduction of mitral insufficiency (vena contracta 5.0 mm). At discharge, she was in good general conditions, without evidence of oedema or pleural effusion at lung ultrasound. Blood pressure was 120/50 mmHg, cardiac frequency was 68 bpm, SpO2 96% in room air. We decided to withdraw TCA, following the hypothesis of a potentially causative role of this class of drugs in the pathogenesis of HF. 25 days after discharge we underlined a net improvement of both clinical conditions and EF (34%), with reduction of BNP (466 pg/ml). We then started titrating bisoprolol (from 2.5 to 5 mg/day) and ivabradine (from 5 to 7.5 mg bid), obtaining a cardiac frequency of 55 bpm and started ACE-inhibitor (ramipril, 2.5 mg bid titrated to 5 mg bid). In the next control we observed further clinical improvement, with amelioration of exercise tolerance (NYHA I-II) and a further reduction of BNP (196 pg/ml, 60th day). Ramipril was switched to valsartan for ACE-inhibitors-related cough. At 90th day after discharge, echocardiography underlined a normalization of EF to 55% and the other previously underlined alterations. At 120th day patient was in NYHA class I, AHA class A. After excluding other common causes, we last hypothesized that TCA have been the cause of the observed clinical picture, which completely reversed after drug withdrawal. TCA-related dilated cardiomyopathy is a rare but reversible cause of HFrEF(1), which can improve after medication removal(2) but can often recur after reintroduction of the causative drug(3). This case underlines the importance of an internistic clinical reasoning even when managing a common pathology such as HF. References: (1) Montastruc G, Favreliere S, Sommet A, Pathak A, Lapeyre-Mestre M, Perault-Pochat MC, Montastruc JL; French Association of Regional PharmacoVigilance Centres. Drugs and dilated cardiomyopathies: A case/noncase study in the French PharmacoVigilance Database. Br J Clin Pharmacol. 2010 Mar;69(3):287-94. (2) Martí V, Ballester M, Obrador D, Udina C, Moya C, Pons-Lladó G. Reversal of dilated cardiomyopathy after chronic tricyclic antidepressant drug withdrawal. Int J Cardiol. 1995 Feb;48(2):192-4. (3) Briec F, Delaire C, Bouhour JB, Trochu JN. Recurrence of dilated cardiomyopathy after re-introduction of a tricyclic antidepressant. Arch Mal Coeur Vaiss. 2006 Oct;99(10):933-5.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
