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Pellegrini Francesco - One of the best experts on this subject based on the ideXlab platform.
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
Springer, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
country:ITA, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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) Mart\ued V, Ballester M, Obrador D, Udina C, Moya C, Pons-Llad\uf3 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 - One of the best experts on this subject based on the ideXlab platform.
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
Springer, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
country:ITA, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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) Mart\ued V, Ballester M, Obrador D, Udina C, Moya C, Pons-Llad\uf3 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
Rickard Claire - One of the best experts on this subject based on the ideXlab platform.
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Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage
American College of Cardiology. Published by Elsevier Inc., 2000Co-Authors: Parekh Nilesh, Venkatesh Bala, Cross David, Leditschke Anne, Atherton John, Miles William, Winning Adam, Clague Alan, Rickard ClaireAbstract:AbstractOBJECTIVESWe studied the incidence of myocardial injury in aneurysmal subarachnoid hemorrhage (SAH) using the more sensitive cardiac troponin I (cTnI) assay, correlated changes in cTnI with creatine kinase, MB fraction (CK-MB), myoglobin, and catecholamine metabolite assays, and examined the predictive value of changes in cTnI for myocardial dysfunction.BACKGROUNDMyocardial injury in aneurysmal SAH as evidenced by elevated CK-MB fraction has been reported. Little published data exist on the value of cTnI measurements in aneurysmal SAH.METHODSThirty-nine patients were studied for seven days. Clinical cardiovascular assessment, electrocardiographic (ECG), echocardiography, cTnI, CK, CK-MB and CK-MB index, myoglobin and 24-h urinary catecholamine assays were performed in all patients. The ECG abnormalities were defined by the presence of ST-T changes, prolonged QT intervals, and arRhythmias. An abnormal echocardiogram was defined by the presence of wall-motion abnormalities and a reduced ejection fraction. The severity of SAH was graded clinically and radiologically.RESULTSEight patients demonstrated elevations in cTnI (upper limit of normal is 0.1 μg/liter with the immunoenzymatic assay and 0.4 μg/liter with the sandwich immunoassay), while five had abnormal CK-MB levels (upper limit of normal is 8 μg/liter). Patients with more severe grades of SAH were more likely to develop a cTnI leak (p < 0.05). Patients with cTnI elevations were more likely to demonstrate ECG abnormalities (p < 0.01) and manifest clinical myocardial dysfunction (p < 0.01) as evidenced by the presence of a Gallop Rhythm on auscultation and clinical or radiological evidence of pulmonary edema as compared to those with CK-MB elevations. The sensitivity and specificity of cTnI to predict myocardial dysfunction were 100% and 91%, respectively, whereas the corresponding figures for CK-MB were 60% and 94%, respectively. Elevations in myoglobin levels (upper limit of normal
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Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage
'Elsevier BV', 2000Co-Authors: Parekh Nilesh, Venkatesh Bala, Cross David, Leditschke Anne, Atherton John, Miles William, Winning Adam, Clague Alan, Rickard ClaireAbstract:We studied the incidence of myocardial injury in aneurysmal subarachnoid hemorrhage (SAH) using the more sensitive cardiac troponin I (cTnI) assay, correlated changes in cTnI with creatine kinase, MB fraction (CK-MB), myoglobin, and catecholamine metabolite assays, and examined the predictive value of changes in cTnI for myocardial dysfunction.Myocardial injury in aneurysmal SAH as evidenced by elevated CK-MB fraction has been reported. Little published data exist on the value of cTnI measurements in aneurysmal SAH.Thirty-nine patients were studied for seven days. Clinical cardiovascular assessment, electrocardiographic (ECG), echocardiography, cTnI, CK, CK-MB and CK-MB index, myoglobin and 24-h urinary catecholamine assays were performed in all patients. The ECG abnormalities were defined by the presence of ST-T changes, prolonged QT intervals, and arRhythmias. An abnormal echocardiogram was defined by the presence of wall-motion abnormalities and a reduced ejection fraction. The severity of SAH was graded clinically and radiologically.Eight patients demonstrated elevations in cTnI (upper limit of normal is 0.1 microg/liter with the immunoenzymatic assay and 0.4 microg/liter with the sandwich immunoassay), while five had abnormal CK-MB levels (upper limit of normal is 8 microg/liter). Patients with more severe grades of SAH were more likely to develop a cTnI leak (p < 0.05). Patients with cTnI elevations were more likely to demonstrate ECG abnormalities (p < 0.01) and manifest clinical myocardial dysfunction (p < 0.01) as evidenced by the presence of a Gallop Rhythm on auscultation and clinical or radiological evidence of pulmonary edema as compared to those with CK-MB elevations. The sensitivity and specificity of cTnI to predict myocardial dysfunction were 100% and 91%, respectively, whereas the corresponding figures for CK-MB were 60% and 94%, respectively. Elevations in myoglobin levels (upper limit of norma
Martino Marianna - One of the best experts on this subject based on the ideXlab platform.
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
Springer, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
country:ITA, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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) Mart\ued V, Ballester M, Obrador D, Udina C, Moya C, Pons-Llad\uf3 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
Viticchi Giovanna - One of the best experts on this subject based on the ideXlab platform.
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
Springer, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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
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Uncommon causes of heart failure with reduced ejection fraction in internal medicine: a case report
country:ITA, 2016Co-Authors: Capeci William, Tarquinio Nicola, Falsetti Lorenzo, Fioranelli Agnese, Viticchi Giovanna, Martino Marianna, Pellegrini FrancescoAbstract: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) Mart\ued V, Ballester M, Obrador D, Udina C, Moya C, Pons-Llad\uf3 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
