Letters to the editor J Cardiovasc Med 2015, 16:72–74
The effects of continuous positive airway pressure in obstructive sleep apnea patients with coronary artery disease: still not completely understood Chiara Lazzeria and Antonio M. Esquinasb a Intensive Cardiac Coronary Unit, Heart and Vessel Department, Azienda, Ospedaliero-Universitaria Careggi, Florence, Italy and bIntensive Care Unit, Hospital Morales Meseguer, Murcia, Spain
Correspondence to Chiara Lazzeri, Intensive Cardiac Coronary Unit, Heart and Vessel Department, Azienda, Ospedaliero-Universitaria Careggi, Viale Morgagni 85, 50184 Florence, Italy Tel: +39 055 7947518; fax: +39 055 7947518; e-mail: [email protected] Received 19 July 2014 Revised 30 July 2014 Accepted 25 July 2014
To the Editor We read with interest the original study by Capodanno et al.,1 documenting that continuous positive airway pressure (CPAP) was associated with a decreased risk of major adverse cardiac or cerebrovascular event (MACCE) in patients with coronary artery disease (CAD) and obstructive sleep apnea (OSAS), whereas no benefit of CPAP was observed in women. The study by Capodanno et al.1 gives us the opportunity to make some reflections. The study population included a small number (only 17 patients are treated with CPAP) and heterogeneous (stable and unstable CAD) patients, and a scarce number of women (no conclusion can be made regarding potential sex differences in outcome). When compared with patients conventionally treated, those submitted to CPAP included a higher percentage of patients with reduced admission of left ventricular ejection fraction (LVEF) (41 vs. 20%) and were more frequently administered medical therapy (30 vs. 17%). In the study, it has not been reported how many patients underwent complete coronary revascularization and this may have influenced the outcome. The relation between CPAP in OSAS patients and CAD is far from being completely understood. There are three key elements: (1) An increased risk of developing CAD has been documented in OSAS patients who are also characterized by worse outcome of CAD.2,3
(2) Most studies focusing on the prevalence of OSAS in patients with acute cardiovascular events included a heterogeneous patient population such as stable angina, unstable angina, myocardial infarction, and heart failure,3,4 and prevalence varied also according to the apnea–hypopnea index (AHI) cut-off value. (3) In patients with acute myocardial infarction (AMI) treated with primary percutaneous coronary intervention (PCI), a high prevalence of previously undiagnosed OSAS was documented and diabetes mellitus was independently associated with OSAS, but there was no significant association between OSAS and impaired microvascular perfusion after primary PCI.5 According to the available evidence, on clinical grounds, screening for OSAS in CAD patients (stable and unstable) is warranted, taking into account the higher prevalence of this condition in CAD. Further studies are needed to evaluate the clinical course and outcome of OSAS patients with CAD, keeping distinct patients with stable CAD and those with acute cardiovascular events, all undergoing optimal treatment. Finally, the effects of CPAP in OSAS patients with CAD should be specifically investigated, ranging from neuro-humoral to cardiac mechanisms, in order to tailor the therapeutic strategy in these patients at a higher risk.
Acknowledgements There are no conflicts of interest.
References 1
2
3
4
5
Capodanno D, Milazzo G, Cumbo M, et al. Positive airway pressure in patients with coronary artery disease and obstructive sleep apnea syndrome. J Cardiovasc Med (Hagerstown) 2014; 15:402–406. Peker Y, Carlson J, Hedner J. Increased incidence of coronary artery disease in sleep apnoea: a long-term follow-up. Eur Respir J 2006; 28:596–602. Yumino D, Tsurumi Y, Takagi A, et al. Impact of obstructive sleep apnea on clinical and angiographic outcomes following percutaneous coronary intervention in patients with acute coronary syndrome. Am J Cardiol 2007; 99:26–30. Turmel J, Se´rie`s F, Boulet LP, et al. Relationship between atherosclerosis and the sleep apnea syndrome: an intravascular ultrasound study. Int J Cardiol 2009; 132:203–209. Lee CH, Khoo SM, Tai BC, et al. Obstructive sleep apnea in patients admitted for acute myocardial infarction: prevalence, predictors, and effect on microvascular perfusion. Chest 2009; 135:1488–1495. DOI:10.2459/JCM.0000000000000205
1558-2027 ß 2015 Italian Federation of Cardiology
Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited.
Letters to the editor 73
Reply to the letter: ‘The effects of CPAP in OSAS patients with coronary artery disease: still not completely understood’ Davide Capodanno and Corrado Tamburino Ferrarotto Hospital, University of Catania, Catania, Italy Correspondence to Davide Capodanno, MD, PhD Cardiology Department, Ferrarotto Hospital, University of Catania, Via Citelli 6, 95124 Catania, Italy Tel: +39 0957436202; fax: +39 095362429; e-mail: [email protected] Received 26 July 2014 Revised 31 July 2014 Accepted 8 August 2014
10 times higher (n ¼ 175), and treatment of OSAS was significantly associated with a reduction in the number of cardiac deaths. In their editorial to our article, Agostoni et al.4 mention several reasons for the putative beneficial role of CPAP in cardiovascular medicine, while recognizing that the physiology behind this benefit ‘is not of immediate comprehension’.
References 1
2
To the Editor 1
We thank Lazzeri and Esquinas for their interest in our article exploring the impact of continuous positive airway pressure (CPAP) on clinical outcomes of patients with obstructive sleep apnea–hypopnea syndrome (OSAS) and angiographically documented coronary artery disease (CAD).2 As far as their reflections are concerned, we would like to highlight the following points: patients with unstable CAD were similarly distributed in the CPAP and no CPAP groups (41 vs. 39%; P ¼ 0.88), and presentation with an acute coronary syndrome did not significantly change the adjusted treatment effect of CPAP when forced into the multivariable model [adjusted hazard ratio 0.18, 95% confidence interval (CI) 0.04–0.76, P ¼ 0.02]; similarly, complete revascularization occurred with no significant differences between the two groups (47 vs. 51%; P ¼ 0.77) and, again, forcing this variable in the multivariable model did not change significantly the magnitude of the adjusted treatment effect of CPAP (adjusted hazard ratio 0.18, 95% CI 0.04–0.77, P ¼ 0.021); the multivariable model already included left ventricular ejection fraction below 40%, which was also not found to impact significantly on the treatment estimate of CPAP2; there were no relevant differences in medical therapy at discharge between CPAP-treated patients and those who were not.2 Therefore, the confounders mentioned by Lazzeri and Esquinas1 have been all taken into account and were not found to have an impact on our findings. Obviously, this does not take into consideration the possible presence of other unidentified confounders, which remains a limitation of any nonrandomized study. On the contrary, we agree that the small number of patients in the CPAP group may prevent us from drawing firm conclusions on the causal relationship between reduction of cardiovascular events and initiation of treatment for sleeping disorders. Of note, all patients with moderate or severe OSAS and CAD in our series were offered CPAP therapy (n ¼ 129), but only 13% accepted,2 which underscores the need for further developing and refining this therapy to make it more acceptable and userfriendly. This ‘power’ limitation notwithstanding, it should be noted that our findings remain hypothesisgenerating, but coherent with those of a study by Cassar et al.,3 where the number of CPAP-treated patients was
3
4
Lazzeri C, Esquinas AM. The effects of continuous positive airway pressure in obstructive sleep apnea patients with coronary artery disease: still not completely understood. J Cardiovasc Med (Hagerstown) 2014; 16:72. Capodanno D, Milazzo G, Cumbo M, et al. Positive airway pressure in patients with coronary artery disease and obstructive sleep apnea syndrome. J Cardiovasc Med (Hagerstown) 2014; 15:402–406. Cassar A, Morgenthaler TI, Lennon RJ, et al. Treatment of obstructive sleep apnea is associated with decreased cardiac death after percutaneous coronary intervention. J Am Coll Cardiol 2007; 14:1310–1314. Agostoni P, Contini M, Sciomer S, et al. Continuous positive airway pressure in cardiovascular medicine: the underlying physiology is frequently unknown. J Cardiovasc Med (Hagerstown) 2014; 15:361–363. DOI:10.2459/JCM.0000000000000213
Why not consider PET/CT in the workup of pulmonary tumour thrombotic microangiopathy? Francesco Ciconea and Koichiro Abeb a Unit of Nuclear Medicine, Sant’Andrea Hospital, Faculty of Medicine and Psychology, Sapienza University of Rome, Italy and bDepartment of Diagnostic Imaging and Nuclear Medicine, Tokyo Women’s Medical University, Tokyo, Japan
Correspondence to Francesco Cicone, MD, Sant’Andrea Hospital, Faculty of Medicine and Psychology, ‘Sapienza’ University of Rome, Rome, Italy E-mail: [email protected] Received 29 July 2013 Accepted 10 November 2013
To the Editor We read with interest the paper by Patrignani et al.,1 describing a case of post-mortem diagnosis of pulmonary tumour thrombotic microangiopathy (PTTM) from unknown primary, a clinical condition which is gaining interest among the scientific community.2 Its extremely severe prognosis makes imperative an early diagnosis, which may possibly allow to start appropriate treatments.3 We particularly appreciated the authors’ proposal of a flow chart for differential diagnosis as we completely agree that PTTM should be considered among the possible causes of acute cor pulmonale and pulmonary hypertension. Unfortunately, we notice that, in the proposed flow chart, a potentially very helpful technique such as positron emission tomography/computed tomography (PET/CT) with fluorodeoxyglucose (FDG) has been overlooked. At least twice previously,4,5 FDG PET/CT has been employed in the workup of ‘breathless’ patients who were eventually diagnosed as having PTTM at autopsy. In these two cases, the patients were referred for PET/ CT to search for the suspected, occult primary tumour.
Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited.
74 Journal of Cardiovascular Medicine 2015, Vol 16 No 1
Interestingly, different pulmonary pictures and various systemic disease involvements were shown. Although, as extensively discussed,5 the identification of the primary tumour failed, extra-pulmonary tumour metastatic sites were found, including bone and lymph nodes. This highlights the additional potential value of PET/CT in the identification of metastatic tumour sites liable to an easy biopsy. Both search of unknown primary and guidance of bioptic procedures represent common indications for PET/CT imaging.6 Additionally, PET/CT can provide relevant metabolic information on the severity of cardiac overload induced by pulmonary hypertension. Indeed, an increased FDG uptake in the right ventricle has been suggested as an indirect sign of right-ventricular dysfunction.5,7 As a consequence, the degree of right-ventricular FDG uptake may have prognostic significance. Of course, we are aware that PET/CT is still perceived as an expensive and not promptly available technique; however, the number of PET scanners has sensibly increased over the years, and many centres with a decent workload can offer this service within a few days. Moreover, it should be noted that PET/CT is generally performed without the injection of potentially toxic contrast
media and gives far less radiation dose than a fully diagnostic contrast-enhanced CT. In conclusion, we think that once a pulmonary thromboembolism has been excluded, either by CT-angiogram or lung scintigraphy, an FDG PET/CT can represent a one-step diagnostic procedure for staging and outcome prognostication of a suspected PTTM.
References 1
2 3 4 5
6
7
Patrignani A, Purcaro A, Calcagnoli F, et al. Pulmonary tumor thrombotic microangiopathy: the challenge of the antemortem diagnosis. J Cardiovasc Med 2013; [Epub ahead of print]. Gavin MC, Morse D, Partridge AH, et al. Clinical problem-solving. Breathless. N Engl J Med 2012; 366:75–81. Miyano S, Izumi S, Takeda Y, et al. Pulmonary tumor thrombotic microangiopathy. J Clin Oncol 2007; 25:597–599. Tashima Y, Abe K, Matsuo Y, et al. Pulmonary tumor thrombotic microangiopathy: FDG-PET/CT findings. Clin Nucl Med 2009; 34:175–177. Cicone F, Del Forno M, Papa A, et al. Fatal pulmonary tumour thrombotic microangiopathy: do typical FDG-PET findings exist? Nuklearmedizin 2012; 51:N6–9. Boellaard R, O’Doherty MJ, Weber WA, et al. FDG PET and PET/CT: EANM procedure guidelines for tumour PET imaging: version 1.0. Eur J Nucl Med Mol Imaging 2010; 37:181–200. Mielniczuk LM, Birnie D, Ziadi MC, et al. Relation between right ventricular function and increased right ventricular [18F]fluorodeoxyglucose accumulation in patients with heart failure. Circ Cardiovasc Imaging 2011; 4:59–66. DOI:10.2459/JCM.0000000000000071
Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited.
The effects of continuous positive airway pressure in obstructive sleep apnea patients with coronary artery disease: still not completely understood Chiara Lazzeria and Antonio M. Esquinasb a Intensive Cardiac Coronary Unit, Heart and Vessel Department, Azienda, Ospedaliero-Universitaria Careggi, Florence, Italy and bIntensive Care Unit, Hospital Morales Meseguer, Murcia, Spain
Correspondence to Chiara Lazzeri, Intensive Cardiac Coronary Unit, Heart and Vessel Department, Azienda, Ospedaliero-Universitaria Careggi, Viale Morgagni 85, 50184 Florence, Italy Tel: +39 055 7947518; fax: +39 055 7947518; e-mail: [email protected] Received 19 July 2014 Revised 30 July 2014 Accepted 25 July 2014
To the Editor We read with interest the original study by Capodanno et al.,1 documenting that continuous positive airway pressure (CPAP) was associated with a decreased risk of major adverse cardiac or cerebrovascular event (MACCE) in patients with coronary artery disease (CAD) and obstructive sleep apnea (OSAS), whereas no benefit of CPAP was observed in women. The study by Capodanno et al.1 gives us the opportunity to make some reflections. The study population included a small number (only 17 patients are treated with CPAP) and heterogeneous (stable and unstable CAD) patients, and a scarce number of women (no conclusion can be made regarding potential sex differences in outcome). When compared with patients conventionally treated, those submitted to CPAP included a higher percentage of patients with reduced admission of left ventricular ejection fraction (LVEF) (41 vs. 20%) and were more frequently administered medical therapy (30 vs. 17%). In the study, it has not been reported how many patients underwent complete coronary revascularization and this may have influenced the outcome. The relation between CPAP in OSAS patients and CAD is far from being completely understood. There are three key elements: (1) An increased risk of developing CAD has been documented in OSAS patients who are also characterized by worse outcome of CAD.2,3
(2) Most studies focusing on the prevalence of OSAS in patients with acute cardiovascular events included a heterogeneous patient population such as stable angina, unstable angina, myocardial infarction, and heart failure,3,4 and prevalence varied also according to the apnea–hypopnea index (AHI) cut-off value. (3) In patients with acute myocardial infarction (AMI) treated with primary percutaneous coronary intervention (PCI), a high prevalence of previously undiagnosed OSAS was documented and diabetes mellitus was independently associated with OSAS, but there was no significant association between OSAS and impaired microvascular perfusion after primary PCI.5 According to the available evidence, on clinical grounds, screening for OSAS in CAD patients (stable and unstable) is warranted, taking into account the higher prevalence of this condition in CAD. Further studies are needed to evaluate the clinical course and outcome of OSAS patients with CAD, keeping distinct patients with stable CAD and those with acute cardiovascular events, all undergoing optimal treatment. Finally, the effects of CPAP in OSAS patients with CAD should be specifically investigated, ranging from neuro-humoral to cardiac mechanisms, in order to tailor the therapeutic strategy in these patients at a higher risk.
Acknowledgements There are no conflicts of interest.
References 1
2
3
4
5
Capodanno D, Milazzo G, Cumbo M, et al. Positive airway pressure in patients with coronary artery disease and obstructive sleep apnea syndrome. J Cardiovasc Med (Hagerstown) 2014; 15:402–406. Peker Y, Carlson J, Hedner J. Increased incidence of coronary artery disease in sleep apnoea: a long-term follow-up. Eur Respir J 2006; 28:596–602. Yumino D, Tsurumi Y, Takagi A, et al. Impact of obstructive sleep apnea on clinical and angiographic outcomes following percutaneous coronary intervention in patients with acute coronary syndrome. Am J Cardiol 2007; 99:26–30. Turmel J, Se´rie`s F, Boulet LP, et al. Relationship between atherosclerosis and the sleep apnea syndrome: an intravascular ultrasound study. Int J Cardiol 2009; 132:203–209. Lee CH, Khoo SM, Tai BC, et al. Obstructive sleep apnea in patients admitted for acute myocardial infarction: prevalence, predictors, and effect on microvascular perfusion. Chest 2009; 135:1488–1495. DOI:10.2459/JCM.0000000000000205
1558-2027 ß 2015 Italian Federation of Cardiology
Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited.
Letters to the editor 73
Reply to the letter: ‘The effects of CPAP in OSAS patients with coronary artery disease: still not completely understood’ Davide Capodanno and Corrado Tamburino Ferrarotto Hospital, University of Catania, Catania, Italy Correspondence to Davide Capodanno, MD, PhD Cardiology Department, Ferrarotto Hospital, University of Catania, Via Citelli 6, 95124 Catania, Italy Tel: +39 0957436202; fax: +39 095362429; e-mail: [email protected] Received 26 July 2014 Revised 31 July 2014 Accepted 8 August 2014
10 times higher (n ¼ 175), and treatment of OSAS was significantly associated with a reduction in the number of cardiac deaths. In their editorial to our article, Agostoni et al.4 mention several reasons for the putative beneficial role of CPAP in cardiovascular medicine, while recognizing that the physiology behind this benefit ‘is not of immediate comprehension’.
References 1
2
To the Editor 1
We thank Lazzeri and Esquinas for their interest in our article exploring the impact of continuous positive airway pressure (CPAP) on clinical outcomes of patients with obstructive sleep apnea–hypopnea syndrome (OSAS) and angiographically documented coronary artery disease (CAD).2 As far as their reflections are concerned, we would like to highlight the following points: patients with unstable CAD were similarly distributed in the CPAP and no CPAP groups (41 vs. 39%; P ¼ 0.88), and presentation with an acute coronary syndrome did not significantly change the adjusted treatment effect of CPAP when forced into the multivariable model [adjusted hazard ratio 0.18, 95% confidence interval (CI) 0.04–0.76, P ¼ 0.02]; similarly, complete revascularization occurred with no significant differences between the two groups (47 vs. 51%; P ¼ 0.77) and, again, forcing this variable in the multivariable model did not change significantly the magnitude of the adjusted treatment effect of CPAP (adjusted hazard ratio 0.18, 95% CI 0.04–0.77, P ¼ 0.021); the multivariable model already included left ventricular ejection fraction below 40%, which was also not found to impact significantly on the treatment estimate of CPAP2; there were no relevant differences in medical therapy at discharge between CPAP-treated patients and those who were not.2 Therefore, the confounders mentioned by Lazzeri and Esquinas1 have been all taken into account and were not found to have an impact on our findings. Obviously, this does not take into consideration the possible presence of other unidentified confounders, which remains a limitation of any nonrandomized study. On the contrary, we agree that the small number of patients in the CPAP group may prevent us from drawing firm conclusions on the causal relationship between reduction of cardiovascular events and initiation of treatment for sleeping disorders. Of note, all patients with moderate or severe OSAS and CAD in our series were offered CPAP therapy (n ¼ 129), but only 13% accepted,2 which underscores the need for further developing and refining this therapy to make it more acceptable and userfriendly. This ‘power’ limitation notwithstanding, it should be noted that our findings remain hypothesisgenerating, but coherent with those of a study by Cassar et al.,3 where the number of CPAP-treated patients was
3
4
Lazzeri C, Esquinas AM. The effects of continuous positive airway pressure in obstructive sleep apnea patients with coronary artery disease: still not completely understood. J Cardiovasc Med (Hagerstown) 2014; 16:72. Capodanno D, Milazzo G, Cumbo M, et al. Positive airway pressure in patients with coronary artery disease and obstructive sleep apnea syndrome. J Cardiovasc Med (Hagerstown) 2014; 15:402–406. Cassar A, Morgenthaler TI, Lennon RJ, et al. Treatment of obstructive sleep apnea is associated with decreased cardiac death after percutaneous coronary intervention. J Am Coll Cardiol 2007; 14:1310–1314. Agostoni P, Contini M, Sciomer S, et al. Continuous positive airway pressure in cardiovascular medicine: the underlying physiology is frequently unknown. J Cardiovasc Med (Hagerstown) 2014; 15:361–363. DOI:10.2459/JCM.0000000000000213
Why not consider PET/CT in the workup of pulmonary tumour thrombotic microangiopathy? Francesco Ciconea and Koichiro Abeb a Unit of Nuclear Medicine, Sant’Andrea Hospital, Faculty of Medicine and Psychology, Sapienza University of Rome, Italy and bDepartment of Diagnostic Imaging and Nuclear Medicine, Tokyo Women’s Medical University, Tokyo, Japan
Correspondence to Francesco Cicone, MD, Sant’Andrea Hospital, Faculty of Medicine and Psychology, ‘Sapienza’ University of Rome, Rome, Italy E-mail: [email protected] Received 29 July 2013 Accepted 10 November 2013
To the Editor We read with interest the paper by Patrignani et al.,1 describing a case of post-mortem diagnosis of pulmonary tumour thrombotic microangiopathy (PTTM) from unknown primary, a clinical condition which is gaining interest among the scientific community.2 Its extremely severe prognosis makes imperative an early diagnosis, which may possibly allow to start appropriate treatments.3 We particularly appreciated the authors’ proposal of a flow chart for differential diagnosis as we completely agree that PTTM should be considered among the possible causes of acute cor pulmonale and pulmonary hypertension. Unfortunately, we notice that, in the proposed flow chart, a potentially very helpful technique such as positron emission tomography/computed tomography (PET/CT) with fluorodeoxyglucose (FDG) has been overlooked. At least twice previously,4,5 FDG PET/CT has been employed in the workup of ‘breathless’ patients who were eventually diagnosed as having PTTM at autopsy. In these two cases, the patients were referred for PET/ CT to search for the suspected, occult primary tumour.
Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited.
74 Journal of Cardiovascular Medicine 2015, Vol 16 No 1
Interestingly, different pulmonary pictures and various systemic disease involvements were shown. Although, as extensively discussed,5 the identification of the primary tumour failed, extra-pulmonary tumour metastatic sites were found, including bone and lymph nodes. This highlights the additional potential value of PET/CT in the identification of metastatic tumour sites liable to an easy biopsy. Both search of unknown primary and guidance of bioptic procedures represent common indications for PET/CT imaging.6 Additionally, PET/CT can provide relevant metabolic information on the severity of cardiac overload induced by pulmonary hypertension. Indeed, an increased FDG uptake in the right ventricle has been suggested as an indirect sign of right-ventricular dysfunction.5,7 As a consequence, the degree of right-ventricular FDG uptake may have prognostic significance. Of course, we are aware that PET/CT is still perceived as an expensive and not promptly available technique; however, the number of PET scanners has sensibly increased over the years, and many centres with a decent workload can offer this service within a few days. Moreover, it should be noted that PET/CT is generally performed without the injection of potentially toxic contrast
media and gives far less radiation dose than a fully diagnostic contrast-enhanced CT. In conclusion, we think that once a pulmonary thromboembolism has been excluded, either by CT-angiogram or lung scintigraphy, an FDG PET/CT can represent a one-step diagnostic procedure for staging and outcome prognostication of a suspected PTTM.
References 1
2 3 4 5
6
7
Patrignani A, Purcaro A, Calcagnoli F, et al. Pulmonary tumor thrombotic microangiopathy: the challenge of the antemortem diagnosis. J Cardiovasc Med 2013; [Epub ahead of print]. Gavin MC, Morse D, Partridge AH, et al. Clinical problem-solving. Breathless. N Engl J Med 2012; 366:75–81. Miyano S, Izumi S, Takeda Y, et al. Pulmonary tumor thrombotic microangiopathy. J Clin Oncol 2007; 25:597–599. Tashima Y, Abe K, Matsuo Y, et al. Pulmonary tumor thrombotic microangiopathy: FDG-PET/CT findings. Clin Nucl Med 2009; 34:175–177. Cicone F, Del Forno M, Papa A, et al. Fatal pulmonary tumour thrombotic microangiopathy: do typical FDG-PET findings exist? Nuklearmedizin 2012; 51:N6–9. Boellaard R, O’Doherty MJ, Weber WA, et al. FDG PET and PET/CT: EANM procedure guidelines for tumour PET imaging: version 1.0. Eur J Nucl Med Mol Imaging 2010; 37:181–200. Mielniczuk LM, Birnie D, Ziadi MC, et al. Relation between right ventricular function and increased right ventricular [18F]fluorodeoxyglucose accumulation in patients with heart failure. Circ Cardiovasc Imaging 2011; 4:59–66. DOI:10.2459/JCM.0000000000000071
Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited.
