International Journal of Cardiology 176 (2014) e102–e103
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Continuous flow left ventricular assist device placement complicated by aortic valve thrombus and myocardial infarction Juyong Brian Kim a,b, June-Wha Rhee b, Daniel A. Brenner a,b, Richard Ha c, Dipanjan Banerjee a,b, Alan C. Yeung a,b, Jennifer A. Tremmel a,b,⁎ a b c
Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, USA Department of Internal Medicine, Stanford University School of Medicine, USA Department of Cardiothoracic Surgery, Stanford University School of Medicine, USA
a r t i c l e
i n f o
Article history: Received 20 July 2014 Accepted 27 July 2014 Available online 5 August 2014 Keywords: Left ventricular assist device Aortic valve thrombus Acute myocardial infarction Right heart failure
A 75 year-old man with an idiopathic dilated cardiomyopathy underwent Heartmate II (Thoratec Corporation; Pleasanton, Calif) continuous flow left ventricular assist device (cf-LVAD) implantation for destination therapy without complications. An echocardiogram obtained 2-months following implantation showed normal flow through the cannulas with the aortic valve (AV) opening every beat. For his cf-LVAD, he was anti-coagulated with warfarin, but at a lower INR than usual (1.7–2.0) due to a prior gastrointestinal bleed. Approximately 4 months after cf-LVAD implantation, the patient developed acute onset of dyspnea associated with substernal chest pressure and tightness. An initial 12-lead ECG did not show any ischemic changes and a troponin-I was normal at 0.1 ng/mL. His LVAD was interrogated without obvious abnormalities. The lactate dehydrogenase level was b 200 U/L. CT angiography of the thorax revealed no obvious pulmonary emboli. His INR was 1.7 (within goal), but a heparin infusion was started given concern for a thrombotic event. Shortly after these studies, however, the patient developed ventricular arrhythmias requiring 5 defibrillations from his implantable cardioverter defibrillator (ICD) with eventual cardioversion. At that time, his laboratory studies revealed an elevated troponin-I level to 29.8 ng/mL. A coronary angiogram was performed and was remarkable for significant contrast filling defects in the aortic cusps concerning for large thrombi (Fig. 1, Video 1). ⁎ Corresponding author at: Interventional Cardiology, 300 Pasteur Drive, Room H2103, Stanford University Medical Center, Stanford, CA 94305, USA. E-mail address: [email protected] (J.A. Tremmel).
http://dx.doi.org/10.1016/j.ijcard.2014.07.248 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
There was no evidence of AV opening. Following contrast injection into the left coronary artery (LCA), there was left-to-right collateral flow and contrast stasis in the right coronary artery (RCA) (Video 1a). The contrast hanging in the proximal RCA cleared spontaneously before engaging the RCA, as if the vessel suddenly opened. While there was narrowing in the distal vessels, there was TIMI-3 flow to RCA with no overt occlusion, as well as the surprising presence of right-to-left collaterals (Video 1b). No lesion amenable to intervention was identified. An echocardiogram was notable for non-coronary and left coronary cusp thrombi (Fig. 1) and acute dilation of the right ventricle (RV) with reciprocal left ventricular cavity obliteration (Video 2). It was again noted that the AV was not opening. The patient's troponin-I continued to rise and his hemodynamics progressively worsened due to RV failure. He was started on inotropic support and underwent right-sided TandemHeart (Cardiac Assist, Inc., Pittsburgh, PA) placement for RV support. Despite these interventions, the patient's condition continued to decline with incessant ventricular tachycardia. The patient was subsequently transitioned to comfort care and died shortly after VAD supports were withdrawn. Discussion: To the best of our knowledge, this is the first report of a fatal outcome due to myocardial infarction and RV failure from AV thrombus after cf-LVAD implantation. There is currently one published case report of AV thrombus and associated coronary occlusion leading to non-fatal MI [1]. In continuous flow devices, flow from the device supports cardiac output and reduces the pulsatility of the LV by bypassing the native heart and the aortic sinus. One complication that can occur from bypassing the native systemic circulation is fusion of the AV commissures, limiting the AV opening and subsequently causing AV insufficiency. Absent or diminished blood flow across the AV can also turn the AV coronary cusps into niduses for clot formation [2]. These events are rarely described, but can lead to catastrophic outcomes, as demonstrated in our case report. It is possible that the incidence of AV thrombus is more common than currently estimated, as diagnosis is difficult and can only be visualized on echocardiography when it becomes large enough. Most of these thrombi likely remain subclinical, but may contribute to the adverse cardiovascular events associated with LVADs, including stroke and sudden cardiac death. In our patient, one would suspect embolization of microthrombi into the RCA as the likely cause of his infarct. However, the angiogram also suggested a component of vascular collapse from
J.B. Kim et al. / International Journal of Cardiology 176 (2014) e102–e103
e103
Fig. 1. Coronary angiogram and transesophageal echocardiogram demonstrate large thrombi in AV. LCA angiogram shows patent left anterior descending artery. Contrast stasis is seen in the RCA (block arrow) and there are collateral vessels to the distal right (dotted arrows). Large thrombi are seen in the AV cusps (panel A); the RCA angiogram shows diffuse narrowing of distal vessel. (panel B); AV thrombi are seen in the non-coronary and left coronary cusps (panels C, D).
decreased native flow, similar to what one might see in a poorly collateralized vessel distal to a chronic total occlusion. With the cf-LVAD, there is presumably less flow in the epicardial vessels, because of decreased flow in the ascending aorta (exacerbated in this case by the lack of AV motion) and by decreased myocardial demand. This may lead to some degree of collapse in the epicardial vessels and may promote the role of the microvasculature in supplying the myocardium. Microemboli to this microvasculature may be even less well tolerated, leading to a negative cycle of further epicardial collapse, as flow to that territory decreases even more. Increased anticoagulation in patients with fused AV or decreased pump speed to allow more native flow across the aortic valve may prevent this serious adverse event. Many programs, including ours, currently use a RAMP echocardiogram protocol to maintain AV opening every 2 to 3 cardiac cycles [3]. The optimal frequency of assessing AV opening, however, is not established; more frequent assessment of AV opening could reduce the chance of thrombus formation in the aortic valve/root. Placement of the outflow graft to the ascending aorta, rather than the descending aorta may also provide greater retrograde flow to the AV, thus reducing the stagnation of flow in the AV cusps. Continued
efforts to optimize the management of the AV flow in patients with LVAD are warranted. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ijcard.2014.07.248. Financial support and disclosure The authors report no relationships that could be construed as a conflict of interest. References [1] Freed BH, Jeevanandam V, Jolly N. Aortic root and valve thrombosis after implantation of a left ventricular assist device. J Invasive Cardiol 2011;23:E63–5. [2] Martina JR, Schipper ME, de Jonge N, et al. Analysis of aortic valve commissural fusion after support with continuous-flow left ventricular assist device. Interact Cardiovasc Thorac Surg 2013;17:616–24. [3] Uriel N, Morrison KA, Garan AR, et al. Development of a novel echocardiography ramp test for speed optimization and diagnosis of device thrombosis in continuous-flow left ventricular assist devices: the Columbia ramp study. J Am Coll Cardiol 2012;60: 1764–75.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Continuous flow left ventricular assist device placement complicated by aortic valve thrombus and myocardial infarction Juyong Brian Kim a,b, June-Wha Rhee b, Daniel A. Brenner a,b, Richard Ha c, Dipanjan Banerjee a,b, Alan C. Yeung a,b, Jennifer A. Tremmel a,b,⁎ a b c
Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, USA Department of Internal Medicine, Stanford University School of Medicine, USA Department of Cardiothoracic Surgery, Stanford University School of Medicine, USA
a r t i c l e
i n f o
Article history: Received 20 July 2014 Accepted 27 July 2014 Available online 5 August 2014 Keywords: Left ventricular assist device Aortic valve thrombus Acute myocardial infarction Right heart failure
A 75 year-old man with an idiopathic dilated cardiomyopathy underwent Heartmate II (Thoratec Corporation; Pleasanton, Calif) continuous flow left ventricular assist device (cf-LVAD) implantation for destination therapy without complications. An echocardiogram obtained 2-months following implantation showed normal flow through the cannulas with the aortic valve (AV) opening every beat. For his cf-LVAD, he was anti-coagulated with warfarin, but at a lower INR than usual (1.7–2.0) due to a prior gastrointestinal bleed. Approximately 4 months after cf-LVAD implantation, the patient developed acute onset of dyspnea associated with substernal chest pressure and tightness. An initial 12-lead ECG did not show any ischemic changes and a troponin-I was normal at 0.1 ng/mL. His LVAD was interrogated without obvious abnormalities. The lactate dehydrogenase level was b 200 U/L. CT angiography of the thorax revealed no obvious pulmonary emboli. His INR was 1.7 (within goal), but a heparin infusion was started given concern for a thrombotic event. Shortly after these studies, however, the patient developed ventricular arrhythmias requiring 5 defibrillations from his implantable cardioverter defibrillator (ICD) with eventual cardioversion. At that time, his laboratory studies revealed an elevated troponin-I level to 29.8 ng/mL. A coronary angiogram was performed and was remarkable for significant contrast filling defects in the aortic cusps concerning for large thrombi (Fig. 1, Video 1). ⁎ Corresponding author at: Interventional Cardiology, 300 Pasteur Drive, Room H2103, Stanford University Medical Center, Stanford, CA 94305, USA. E-mail address: [email protected] (J.A. Tremmel).
http://dx.doi.org/10.1016/j.ijcard.2014.07.248 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
There was no evidence of AV opening. Following contrast injection into the left coronary artery (LCA), there was left-to-right collateral flow and contrast stasis in the right coronary artery (RCA) (Video 1a). The contrast hanging in the proximal RCA cleared spontaneously before engaging the RCA, as if the vessel suddenly opened. While there was narrowing in the distal vessels, there was TIMI-3 flow to RCA with no overt occlusion, as well as the surprising presence of right-to-left collaterals (Video 1b). No lesion amenable to intervention was identified. An echocardiogram was notable for non-coronary and left coronary cusp thrombi (Fig. 1) and acute dilation of the right ventricle (RV) with reciprocal left ventricular cavity obliteration (Video 2). It was again noted that the AV was not opening. The patient's troponin-I continued to rise and his hemodynamics progressively worsened due to RV failure. He was started on inotropic support and underwent right-sided TandemHeart (Cardiac Assist, Inc., Pittsburgh, PA) placement for RV support. Despite these interventions, the patient's condition continued to decline with incessant ventricular tachycardia. The patient was subsequently transitioned to comfort care and died shortly after VAD supports were withdrawn. Discussion: To the best of our knowledge, this is the first report of a fatal outcome due to myocardial infarction and RV failure from AV thrombus after cf-LVAD implantation. There is currently one published case report of AV thrombus and associated coronary occlusion leading to non-fatal MI [1]. In continuous flow devices, flow from the device supports cardiac output and reduces the pulsatility of the LV by bypassing the native heart and the aortic sinus. One complication that can occur from bypassing the native systemic circulation is fusion of the AV commissures, limiting the AV opening and subsequently causing AV insufficiency. Absent or diminished blood flow across the AV can also turn the AV coronary cusps into niduses for clot formation [2]. These events are rarely described, but can lead to catastrophic outcomes, as demonstrated in our case report. It is possible that the incidence of AV thrombus is more common than currently estimated, as diagnosis is difficult and can only be visualized on echocardiography when it becomes large enough. Most of these thrombi likely remain subclinical, but may contribute to the adverse cardiovascular events associated with LVADs, including stroke and sudden cardiac death. In our patient, one would suspect embolization of microthrombi into the RCA as the likely cause of his infarct. However, the angiogram also suggested a component of vascular collapse from
J.B. Kim et al. / International Journal of Cardiology 176 (2014) e102–e103
e103
Fig. 1. Coronary angiogram and transesophageal echocardiogram demonstrate large thrombi in AV. LCA angiogram shows patent left anterior descending artery. Contrast stasis is seen in the RCA (block arrow) and there are collateral vessels to the distal right (dotted arrows). Large thrombi are seen in the AV cusps (panel A); the RCA angiogram shows diffuse narrowing of distal vessel. (panel B); AV thrombi are seen in the non-coronary and left coronary cusps (panels C, D).
decreased native flow, similar to what one might see in a poorly collateralized vessel distal to a chronic total occlusion. With the cf-LVAD, there is presumably less flow in the epicardial vessels, because of decreased flow in the ascending aorta (exacerbated in this case by the lack of AV motion) and by decreased myocardial demand. This may lead to some degree of collapse in the epicardial vessels and may promote the role of the microvasculature in supplying the myocardium. Microemboli to this microvasculature may be even less well tolerated, leading to a negative cycle of further epicardial collapse, as flow to that territory decreases even more. Increased anticoagulation in patients with fused AV or decreased pump speed to allow more native flow across the aortic valve may prevent this serious adverse event. Many programs, including ours, currently use a RAMP echocardiogram protocol to maintain AV opening every 2 to 3 cardiac cycles [3]. The optimal frequency of assessing AV opening, however, is not established; more frequent assessment of AV opening could reduce the chance of thrombus formation in the aortic valve/root. Placement of the outflow graft to the ascending aorta, rather than the descending aorta may also provide greater retrograde flow to the AV, thus reducing the stagnation of flow in the AV cusps. Continued
efforts to optimize the management of the AV flow in patients with LVAD are warranted. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ijcard.2014.07.248. Financial support and disclosure The authors report no relationships that could be construed as a conflict of interest. References [1] Freed BH, Jeevanandam V, Jolly N. Aortic root and valve thrombosis after implantation of a left ventricular assist device. J Invasive Cardiol 2011;23:E63–5. [2] Martina JR, Schipper ME, de Jonge N, et al. Analysis of aortic valve commissural fusion after support with continuous-flow left ventricular assist device. Interact Cardiovasc Thorac Surg 2013;17:616–24. [3] Uriel N, Morrison KA, Garan AR, et al. Development of a novel echocardiography ramp test for speed optimization and diagnosis of device thrombosis in continuous-flow left ventricular assist devices: the Columbia ramp study. J Am Coll Cardiol 2012;60: 1764–75.
