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Virtual histology findings in rapid cardiac allograft vasculopathy progression and bioresorbable vascular scaffolds
Letters to the Editor
References [1] Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol 2004;43:1731–7. [2] Niu W, Liu Y, Qi Y, Wu Z, Zhu D, Jin W. Association of interleukin-6 circulating levels with coronary artery disease: a meta-analysis implementing Mendelian randomization approach. Int J Cardiol 2012;157:243–52. [3] Elliott P, Chambers JC, Zhang W, et al. Genetic Loci associated with C-reactive protein levels and risk of coronary heart disease. JAMA 2009;302:37–48. [4] Humphries SE, Luong LA, Ogg MS, Hawe E, Miller GJ. The interleukin-6 −174 G/C promoter polymorphism is associated with risk of coronary heart disease and systolic blood pressure in healthy men. Eur Heart J 2001;22:2243–52. [5] Jenny NS, Tracy RP, Ogg MS, et al. In the elderly, interleukin-6 plasma levels and the −174G N C polymorphism are associated with the development of cardiovascular disease. Arterioscler Thromb Vasc Biol 2002;22:2066–71. [6] Brull DJ, Leeson CP, Montgomery HE, et al. The effect of the interleukin-6 −174G N C promoter gene polymorphism on endothelial function in healthy volunteers. Eur J Clin Invest 2002;32:153–7.
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[7] Sarecka B, Zak I, Krauze J. Synergistic effects of the polymorphisms in the PAI-1 and IL-6 genes with smoking in determining their associated risk with coronary artery disease. Clin Biochem 2008;41:467–73. [8] Sunyer J, Forastiere F, Pekkanen J, et al. Interaction between smoking and the interleukin-6 gene affects systemic levels of inflammatory biomarkers. Nicotine Tob Res 2009;11:1347–53. [9] Papaoikonomou S, Tentolouris N, Tousoulis D, et al. The association of the 174G N C polymorphism of interleukin 6 gene with diabetic nephropathy in patients with type 2 diabetes mellitus. J Diabetes Complications 2013;27:576–9. [10] Papaoikonomou S, Tousoulis D, Tentolouris N, et al. The role of C-reactive protein genetic variability in the onset of carotid artery disease and renal function impairment in patients with diabetes mellitus type 2. Int J Cardiol 2013;168:4331–2. [11] Papageorgiou N, Tousoulis D, Miliou A, et al. Combined effects of fibrinogen genetic variability on atherosclerosis in patients with or without stable angina pectoris: focus on the coagulation cascade and endothelial function. Int J Cardiol 2013;168:4602–7. [12] Rodriguez S, Gaunt TR, Day IN. Hardy–Weinberg equilibrium testing of biological ascertainment for Mendelian randomization studies. Am J Epidemiol 2009;169:505–14.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.06.058
Virtual histology findings in rapid cardiac allograft vasculopathy progression and bioresorbable vascular scaffolds Flavio Ribichini a,⁎, Michele Pighi a, Carlo Zivelonghi a, Giuseppe Faggian b, Corrado Vassanelli a a b
Department of Medicine, University of Verona, Verona, Italy Cardiac Surgery, University of Verona, Verona, Italy
a r t i c l e
i n f o
Article history: Received 28 April 2014 Accepted 28 June 2014 Available online 15 July 2014 Keywords: Bioresorbable vascular scaffold Heart transplant Percutaneous coronary intervention
Cardiac allograft vasculopathy (CAV) is a unique form of accelerated atherosclerosis and represents the leading cause of late morbidity and mortality after heart transplantation (HTx). Unlike native coronary artery disease, CAV is more typically a diffuse disease that produces concentric narrowing and affects the entire length of the coronary tree from epicardial to intra-myocardial segments. The most crucial problem regarding CAV is its indefinite progression with time. This peculiar characteristic leads to the belief that revascularisation procedures for CAV have only a marginal palliative meaning, with no long-term benefit on mortality [1]. We have recently published a first case of bioresorbable vascular scaffold (BVS) implantation in a 40-year old male, subjected to HTx ten years before and being symptomatic for typical ischemic chest pain during exercise due to a severe stenosis of the left anterior descending artery (LAD) [2]. Interestingly, the proximal segment of the dominant right coronary artery (RCA) sowed a non-critical stenosis (angiographic diameter stenosis 50%) with no functional relevance (FFR 0.91); therefore,
this non-culprit lesion was left on optimal medical treatment. Details of intravascular ultrasound (IVUS) evaluation, by grey-scale and virtualhistology (VH) modalities of this baseline examination are shown in Fig. 1. Six months later the patient was readmitted for rapid worsening of typical ischemic chest pain after 5 months of complete wellbeing. The repeated angiogram disclosed the good result of the previous BVS implantation in the LAD and a sub-total occlusion of the proximal RCA. The IVUS and VH details of this follow-up examination are shown in Fig. 2 and put in evidence the rapid and aggressive progression of the thin-cap fibroatheroma observed 6 months before. A 28 mm long BVS was implanted from the ostium of the RCA up to the zone where a new thin-cap fibro-atheroma was observed at VH run. The angiography showed also the good result of the previous BVS implantation on the LAD. Our observations show the potential prognostic importance of VH in the rapidly progressing context of aggressive CAV. We speculate that BVS in patients with CAV may be an option to the rapid progression of some native plaques that present VH risk features [3] despite the lack of evidence of flow limitation. BVS can by hypothesized as a new therapeutic option for CAV in HTx recipients not only to treat flow-limiting stenosis, but also to prevent rapid progression of plaques according to VH features. Dedicated studies should be pursued to investigate this hypothesis with the aim of testing an alternative to this largely unmet need. F. Ribichini, M. Pighi performed the case, conceived and drafted the manuscript. All other authors have read and approved the manuscript to which they contributed significant intellectual content after critical revision. References
⁎ Corresponding author at: Division of Cardiology, Cardiovascular Interventional Unit, University of Verona, Piazzale Aristide Stefani n°1, 37126 Verona, Italy. Tel.: + 39 045 812 2039. E-mail address: fl[email protected] (F. Ribichini).
[1] Schmauss D, Weis M. Cardiac allograft vasculopathy: recent developments. Circulation 2008;117:2131–41. [2] Ribichini F, Pighi M, Faggian G, Vassanelli C. Bioresorbable vascular scaffolds in cardiac allograft vasculopathy: a new therapeutic option. Am J Med 2013;126:e11–4. [3] Stone GW, Maehara A, Lansky AJ, et al. A prospective natural-history study of coronary atherosclerosis. N Engl J Med 2011;364:226–35.
258
Letters to the Editor
Fig. 1. Left anterior oblique angiographic incidence of the right coronary artery at baseline in March 2013 showing a moderate, stenosis of the proximal segment (arrow) that causes no significant obstruction to the coronary flow according to the fractional flow reserve calculation = 0.91.Grey-scale IVUS images and co-respective virtual histology: a) section of the proximal vessel showing pathological intimal thickening, b) fibro-calcific plaque with a small area of thin-cap fibro-atheroma, c) thick-cap fibro-atheroma with a lipid empty core, and d) fibro-calcific plaque distal to the stenotic segment.
Letters to the Editor
259
Fig. 2. Left anterior oblique angiographic incidence of the right coronary artery six months later (September 2013) showing a rapid plaque progression causing a sub-occlusive stenosis of the proximal segment (arrow).The grey-scale IVUS shows the minimum lumen area (bottom right).Virtual histology of the proximal segment of the right coronary artery. First line: guiding catheter, and images of thin-cap fibro-atheroma in the para-ostial segment. Second line: sections of the minimum lumen area and largest plaque burden showing similar VH components. Third line: from right to left, a section of large vessel area and more distally, the same fibro-calcific plaque observed at baseline (Fig. 1c–d) showing thinning of the fibrous cap.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.06.056
References [1] Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol 2004;43:1731–7. [2] Niu W, Liu Y, Qi Y, Wu Z, Zhu D, Jin W. Association of interleukin-6 circulating levels with coronary artery disease: a meta-analysis implementing Mendelian randomization approach. Int J Cardiol 2012;157:243–52. [3] Elliott P, Chambers JC, Zhang W, et al. Genetic Loci associated with C-reactive protein levels and risk of coronary heart disease. JAMA 2009;302:37–48. [4] Humphries SE, Luong LA, Ogg MS, Hawe E, Miller GJ. The interleukin-6 −174 G/C promoter polymorphism is associated with risk of coronary heart disease and systolic blood pressure in healthy men. Eur Heart J 2001;22:2243–52. [5] Jenny NS, Tracy RP, Ogg MS, et al. In the elderly, interleukin-6 plasma levels and the −174G N C polymorphism are associated with the development of cardiovascular disease. Arterioscler Thromb Vasc Biol 2002;22:2066–71. [6] Brull DJ, Leeson CP, Montgomery HE, et al. The effect of the interleukin-6 −174G N C promoter gene polymorphism on endothelial function in healthy volunteers. Eur J Clin Invest 2002;32:153–7.
257
[7] Sarecka B, Zak I, Krauze J. Synergistic effects of the polymorphisms in the PAI-1 and IL-6 genes with smoking in determining their associated risk with coronary artery disease. Clin Biochem 2008;41:467–73. [8] Sunyer J, Forastiere F, Pekkanen J, et al. Interaction between smoking and the interleukin-6 gene affects systemic levels of inflammatory biomarkers. Nicotine Tob Res 2009;11:1347–53. [9] Papaoikonomou S, Tentolouris N, Tousoulis D, et al. The association of the 174G N C polymorphism of interleukin 6 gene with diabetic nephropathy in patients with type 2 diabetes mellitus. J Diabetes Complications 2013;27:576–9. [10] Papaoikonomou S, Tousoulis D, Tentolouris N, et al. The role of C-reactive protein genetic variability in the onset of carotid artery disease and renal function impairment in patients with diabetes mellitus type 2. Int J Cardiol 2013;168:4331–2. [11] Papageorgiou N, Tousoulis D, Miliou A, et al. Combined effects of fibrinogen genetic variability on atherosclerosis in patients with or without stable angina pectoris: focus on the coagulation cascade and endothelial function. Int J Cardiol 2013;168:4602–7. [12] Rodriguez S, Gaunt TR, Day IN. Hardy–Weinberg equilibrium testing of biological ascertainment for Mendelian randomization studies. Am J Epidemiol 2009;169:505–14.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.06.058
Virtual histology findings in rapid cardiac allograft vasculopathy progression and bioresorbable vascular scaffolds Flavio Ribichini a,⁎, Michele Pighi a, Carlo Zivelonghi a, Giuseppe Faggian b, Corrado Vassanelli a a b
Department of Medicine, University of Verona, Verona, Italy Cardiac Surgery, University of Verona, Verona, Italy
a r t i c l e
i n f o
Article history: Received 28 April 2014 Accepted 28 June 2014 Available online 15 July 2014 Keywords: Bioresorbable vascular scaffold Heart transplant Percutaneous coronary intervention
Cardiac allograft vasculopathy (CAV) is a unique form of accelerated atherosclerosis and represents the leading cause of late morbidity and mortality after heart transplantation (HTx). Unlike native coronary artery disease, CAV is more typically a diffuse disease that produces concentric narrowing and affects the entire length of the coronary tree from epicardial to intra-myocardial segments. The most crucial problem regarding CAV is its indefinite progression with time. This peculiar characteristic leads to the belief that revascularisation procedures for CAV have only a marginal palliative meaning, with no long-term benefit on mortality [1]. We have recently published a first case of bioresorbable vascular scaffold (BVS) implantation in a 40-year old male, subjected to HTx ten years before and being symptomatic for typical ischemic chest pain during exercise due to a severe stenosis of the left anterior descending artery (LAD) [2]. Interestingly, the proximal segment of the dominant right coronary artery (RCA) sowed a non-critical stenosis (angiographic diameter stenosis 50%) with no functional relevance (FFR 0.91); therefore,
this non-culprit lesion was left on optimal medical treatment. Details of intravascular ultrasound (IVUS) evaluation, by grey-scale and virtualhistology (VH) modalities of this baseline examination are shown in Fig. 1. Six months later the patient was readmitted for rapid worsening of typical ischemic chest pain after 5 months of complete wellbeing. The repeated angiogram disclosed the good result of the previous BVS implantation in the LAD and a sub-total occlusion of the proximal RCA. The IVUS and VH details of this follow-up examination are shown in Fig. 2 and put in evidence the rapid and aggressive progression of the thin-cap fibroatheroma observed 6 months before. A 28 mm long BVS was implanted from the ostium of the RCA up to the zone where a new thin-cap fibro-atheroma was observed at VH run. The angiography showed also the good result of the previous BVS implantation on the LAD. Our observations show the potential prognostic importance of VH in the rapidly progressing context of aggressive CAV. We speculate that BVS in patients with CAV may be an option to the rapid progression of some native plaques that present VH risk features [3] despite the lack of evidence of flow limitation. BVS can by hypothesized as a new therapeutic option for CAV in HTx recipients not only to treat flow-limiting stenosis, but also to prevent rapid progression of plaques according to VH features. Dedicated studies should be pursued to investigate this hypothesis with the aim of testing an alternative to this largely unmet need. F. Ribichini, M. Pighi performed the case, conceived and drafted the manuscript. All other authors have read and approved the manuscript to which they contributed significant intellectual content after critical revision. References
⁎ Corresponding author at: Division of Cardiology, Cardiovascular Interventional Unit, University of Verona, Piazzale Aristide Stefani n°1, 37126 Verona, Italy. Tel.: + 39 045 812 2039. E-mail address: fl[email protected] (F. Ribichini).
[1] Schmauss D, Weis M. Cardiac allograft vasculopathy: recent developments. Circulation 2008;117:2131–41. [2] Ribichini F, Pighi M, Faggian G, Vassanelli C. Bioresorbable vascular scaffolds in cardiac allograft vasculopathy: a new therapeutic option. Am J Med 2013;126:e11–4. [3] Stone GW, Maehara A, Lansky AJ, et al. A prospective natural-history study of coronary atherosclerosis. N Engl J Med 2011;364:226–35.
258
Letters to the Editor
Fig. 1. Left anterior oblique angiographic incidence of the right coronary artery at baseline in March 2013 showing a moderate, stenosis of the proximal segment (arrow) that causes no significant obstruction to the coronary flow according to the fractional flow reserve calculation = 0.91.Grey-scale IVUS images and co-respective virtual histology: a) section of the proximal vessel showing pathological intimal thickening, b) fibro-calcific plaque with a small area of thin-cap fibro-atheroma, c) thick-cap fibro-atheroma with a lipid empty core, and d) fibro-calcific plaque distal to the stenotic segment.
Letters to the Editor
259
Fig. 2. Left anterior oblique angiographic incidence of the right coronary artery six months later (September 2013) showing a rapid plaque progression causing a sub-occlusive stenosis of the proximal segment (arrow).The grey-scale IVUS shows the minimum lumen area (bottom right).Virtual histology of the proximal segment of the right coronary artery. First line: guiding catheter, and images of thin-cap fibro-atheroma in the para-ostial segment. Second line: sections of the minimum lumen area and largest plaque burden showing similar VH components. Third line: from right to left, a section of large vessel area and more distally, the same fibro-calcific plaque observed at baseline (Fig. 1c–d) showing thinning of the fibrous cap.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.06.056