- Email: [email protected]
Electrophysiological interactions between implantable cardioverter defibrillators and left ventricular assist device
620
Letters to the Editor
this case, a spheric balloon with a diameter of about 0.5 mm larger than the stent used was employed to obtain a funnel-like shape at the ostium of the stent. In ideal conditions the stent should be deployed with a minimal protrusion inside the main branch. The protruding struts will then be expanded by the spheric balloon, thus obtaining the final funnel-like shape. In addition, doing that, we obtain a reduction of the main branch wall trauma. In the next cases we are going to perform a detailed IVUS monitoring during the procedure, to demonstrate the modifications of the shape of the stent which can be obtained by the spheric balloon. The authors certified that they comply with the principles of ethical publishing in the International Journal of Cardiology [7].
[2] Melikian N, Di Mario C. Treatment of bifurcation coronary lesions: a review of current techniques and outcome. J Interv Cardiol Dec 2003;16(6):507–13. [3] Lefèvre T, Louvard Y, Morice MC, Loubeyre C, Piéchaud JF, Dumas P. Stenting of bifurcation lesions: a rational approach. J Interv Cardiol Dec 2001;14(6):573–85. [4] Rizik DG, Klag JM, Tenaglia A, Hatten TR, Barnhart M, Warnack B. Evaluation of a bifurcation drug-eluting stent system versus provisional T-stenting in a perfused synthetic coronary artery model. J Interv Cardiol Dec 2009;22(6):537–46 Epub 2009 Nov 13. [5] Jilaihawi H, Farah B, Laborde JC. The use of self-expanding stents in coronary bifurcations and beyond: a paradigm revisited. EuroIntervention Mar 2009;4(5): 669–75. [6] Brunel P, Martin G, Bressollette E, Leurent B, Banus Y. “Inverted” provisional T stenting, a new technique for Medina 0, 0, 1 coronary bifurcation lesions: feasibility and follow-up. EuroIntervention Feb 2010;5(7):814–20. [7] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
References [1] Sharma SK, Mares AM, Kini AS. Coronary bifurcation lesions. Minerva Cardioangiol Oct 2009;57(5):667–82.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.09.035
Electrophysiological interactions between implantable cardioverter defibrillators and left ventricular assist device Stefano Maffè a,⁎, Antonello Perucca a, Fabiana Signorotti a, Massimo Pistono b, Paola Paffoni a, Umberto Parravicini a, Pierfranco Dellavesa a, Lorenzo Cucchi a, Anna Maria Paino a, Franco Zenone a, Nicolò Franchetti Pardo a, Massimo Bielli a, Marco Zanetta a a b
Division of Cardiology, SS Trinità Hospital, ASL No, Borgomanero (NO), Italy Division of Cardiology, Salvatore Maugeri Foundation, IRCCS, Veruno (NO), Italy
a r t i c l e
i n f o
Article history: Received 14 June 2010 Accepted 16 September 2010 Available online 20 October 2010 Keywords: Implantable cardioverter-defibrillator Left ventricular assist device
Left ventricular assist devices (LVAD) have become not only an excellent bridge to cardiac transplantation, but also a valid alternative, in selected populations, as destination therapy in patients with advanced congestive heart failure [1]. Since recent clinical trials have demonstrated the survival benefit associated with implantable cardioverter defibrillators (ICD) in patients with heart failure [2], many LVAD candidates have an ICD in place prior to LVAD surgery. Clinical evidence suggests that a combined management strategy of electrical and mechanical support is both feasible and adds benefits in the treatment of end-stage heart failure [3]. While many studies have analyzed the hemodynamic interaction between LVAD and ICD [4,5], little has been published about the electrophysiological changes after a LVAD implant. This report ⁎ Corresponding author. Via Sesalli 15, 28100 NOVARA. Tel.: + 39 3355912520; fax: + 39 0322848430. E-mail address: [email protected] (S. Maffè).
describes the electrophysiological and not only the hemodynamic impact of a Jarvik 2000 pump implant in patients with a prior ICD and an end-stage heart failure. The Jarvik 2000 is a titanium axial-flow impeller pump (5.5 cm– 2.5 cm, weight 90 g) that is implanted into the apex of the failing left ventricle. Pump output is delivered to the descending thoracic aorta, thereby perfusing the brachiocephalic and coronary arteries in retrograde fashion. The device provides a continuous non-pulsatile flow from 2.5 to 6 L/min, working from 8000 up to 12,000 rpm, depending on the afterload [6]. The Jarvik 2000 pumps, which incorporate axial-flow and rotary pump technology, represent the last generation of devices. The use of the latter devices is associated with significant co-morbidity, primarily as a result of their large size and limited durability. The clinical use of these newer axial-flow pumps has resulted in better outcomes, including significantly reduced complication rates with improved durability. These characteristics have allowed to use successfully the Jarvik 2000 pump as destination therapy [7]. In our institution we have analyzed three patients with dilated hypokinetic cardiomyopathy and refractory heart failure, submitted to a LVAD Jarvik 2000 implant as destination therapy. The first patient is a 67-year-old man, with prior anterior myocardial infarction in 1991 treated with two coronary artery by-pass graft. In the space of ten years he has been repeatedly hospitalized for recurrent heart failure. His clinical condition deteriorated over time and the implantation of bicameral–biventricular ICD (Promote® RF CRT-D, St Jude Medical) proved only a transient clinical improvement. On the basis of clinical condition, age and important co-morbidity (previous prostatic cancer), he was submitted to a LVAD Jarvik 2000
Letters to the Editor
621
Fig. 1. a–b, ICD periodically measures intrinsic P and R-wave amplitudes; in the figures are graphically represented a marked and significant reduction of R-wave amplitude in the month after the LVAD implant in our patients.
surgery, as destination therapy. Left ventricular ejection fraction (LVEF) was 13% at pre-implant echocardiogram, while the right ventricular function was normal (tricuspid annular systolic plane excursion — TAPSE 19 mm). With the LVAD support the clinical conditions improved, and actually the patient is in NYHA III. The ICD periodically measures lead impedance (both pace and shock) and intrinsic P and R-wave amplitudes; in the patient it revealed a marked and significant reduction of the R-wave amplitude in the month after the LVAD implant (Fig.1a), with a decrease of approximately 50% (from N12 mV to 7 mV). Similarly the echocardiogram showed a reduction of the left and right ventricular functions (LVEF 10% and TAPSE 15 mm). Besides the important decrease in the R-wave amplitude, we recorded a small increase in lead impedances; the right ventricular stimulation threshold remained stable, while the left ventricular stimulation threshold was slightly increased. After a few months from the LVAD implant all the electrophysiological parameters returned to the basal pre-implant values. The second patient is a 72-year-old male, with a history of anterior myocardial infarction in 2008, complicated by cardiogenic shock and treated with intra-aortic balloon pump. He was submitted to a percutaneous coronary angioplasty (PCI) with a bare metal stent implant on the proximal left anterior descending artery. In the following months he developed a dilated hypokinetic cardiomyopathy with a left ventricular anterior–apical aneurysm and important reduction of systolic function. Five months later the patient underwent implantation of ventricular ICD (Vitality 2 ICD®, Boston Scientific) for the primary prevention of sudden death. In March 2009 the patient was submitted to LVAD Jarvik 2000 implant as destination therapy; before the implant, the echocardiographic LVEF was 13% and the right ventricular function was normal (TAPSE 19 mm). In the first month
after the implant we noticed a decrease in the R-wave amplitude of approximately 70% (from 18 mV to 50.3 mV), and in the following months a gradual normalization (Fig. 1b). Right ventricular impedances and right ventricular stimulation threshold remained substantially stable, without important variations. After a month with LVAD support, the LVEF was 9% and TAPSE 18 mm. The third patient is a 65-year-old male, diabetic, obese, and affected from dilated idiopathic cardiomyopathy, with normal coronary tree; in three years he was hospitalized several times for chronic heart failure. In 2008 the patient underwent implantation of bicameral–biventricular ICD (Contak Renewal 3RF®, Boston Scientific), with only transient clinical improvement. In September 2009 he was submitted to LVAD Jarvik 2000 implant; the pre-implant LVEF was 25%, with TAPSE 23 mm. At one month follow up LVEF was 30% and TAPSE 19 mm. In this patient we didn't find R-wave amplitude modifications after LVAD implant, and no significant variations in lead impedance and right ventricular stimulation threshold (see echocardiographic and electrophysiological parameters in Table 1). There is little information regarding potential interactions between non-pulsatile LVAD and cardiac pacemakers or defibrillators. The present case-reports document the cardiac alterations, not only hemodynamic but also electrophysiological, after a LVAD implant. Right ventricular hemodynamic alterations after LVAD implant have been broadly documented in literature. Acute right heart failure is one of the most important problems following a LVAD implant, which represents a prognostically negative event. The hemodynamic effects of LVAD are different in the two chambers: while the LV may be greatly unloaded, the right ventricle (RV) generally does not receive such benefits [8]. In the first 30 days after LVAD implant, the left ventricular volume is significantly reduced, obtaining a reverse
Table 1 Echocardiographic and electrophysiological parameters. LVEF (%)
Patient 1 Patient 2 Patient 3
TAPSE (mm)
R-wave amplitude (mV)
RV lead impedance (Ω)
RV stimulation threshold (V)
Pre
Post
Pre
Post
Pre
Post
Pre
Post
Pre
Post
13 13 25
10 9 30
19 19 23
15 18 19
N 12 18 17
7 5.3 16
500 485 830
450 510 900
0.5 0.7 0.5
0.5 0.8 0.5
622
Letters to the Editor
structural remodeling. On the contrary the right ventricular volume, gradually increases and only after the first month, if a right heart failure doesn't appear, it begins a gradual normalization [9]. Previous studies report the preoperative risk factors for RV failure after LVAD insertion by analysis of data from 100 patients implanted with LVAD. In this population, one of the most important risk factors identified by univariate analysis was the cardiac output [10]. When LVAD is used as a bridge to heart transplant, the procedure may be still complicated by early peri-operative right ventricular failure, leading to poor filling of the left ventricle, and thus, to low pump output. Severe right ventricular failure sometimes needs placement of right ventricular assist devices as well; this is the last resort of treatment to sustain LVAD output [11]. After LVAD support, the end-diastolic pressure–volume relationship shifts leftward, toward normal volumes [9], as a consequence of reduced left ventricular mass, size, and myocyte diameter [12]. Unlike the left ventricle, the right ventricle does not exhibit significant reverse structural remodeling during LVAD support, despite reduced right ventricular afterload, as evidenced by marked decreases in left atrial and pulmonary pressure during LVAD support [13]. The principal explanation of the limited recovery of the right ventricular cardiomyocyte function during LVAD support is the persistence of high central venous pressure with relative volume overload of the impaired right ventricle [14]. Univentricular hemodynamic support of the left ventricle reduces right ventricular afterload (i.e. pulmonary arterial and wedge pressure) but does not reduce right ventricular preload conditions. In this case, there is no evidence of reverse structural remodeling and evidence of only limited reverse functional remodeling. On the contrary, the biventricular VAD support normalizes right ventricular passive pressure–volume relationship, right ventricular mass, myocyte diameter, and chamber stiffness [13]. In the last years, thanks to improved peri-operative management and advanced clinical experience, the incidence for requirement of RVAD placement after LVAD insertion is decreasing [15]. However, once such severe RV failure occurs, mortality is still quite high. [16]. Even when the RVAD is not required, patients with severe RV failure may require prolonged inotropes, which interferes with their physical rehabilitation. In addition a persistent elevation of the central venous pressure may lead to liver dysfunction and make it difficult to avoid multiple organ failure. Therefore, to predict potential RV failure after LVAD replacement is essential for optimal device selection and improved clinical outcome. In case of implantable LVAD as destination therapy it is important to avoid implanting the device in a population (significant although small) with risk for considerable RV failure. The underlying reasons for lead parameter changes remain speculative. Postulated mechanisms include removal of a plug of LV apical myocardium near the RV apical lead; alteration of the underlying myocardial substrate post-LVAD; myocardial scarring and fibrosis; or pharmacologic, metabolic, and electrolyte changes that are prevalent in this patient group [17]. In addition, changes in cardiac geometry after LVAD placement may be an important factor as well. Alternatively, the natural progression of end-stage cardiomyopathy may influence lead parameters. Microdislodgement would be less likely for all leads that were implanted at least 6 months before the LVAD. Our hypothesis is that LVAD implant effects a rapid increase in cardiac output, causing a right ventricular volume overload and a right ventricular myocardial “stunning”, which reduces the endocavitary potential amplitude. The same phenomenon occurs in patients with previous pace-maker implant, who have a myocardial infarction involving the right ventricle, and who present a lowering of the right ventricular endocavitary potential [18]. The endocavitary potential reduction is strictly related to the LVAD implant, and not to cardiac surgery: in fact we didn't see any change in the potential amplitude recorded by the right ventricular lead in those patients with previous ICD implant undergoing traditional cardiac surgery (valvular or coronary artery by-pass graft). Why did the reduction of the potential
occur in the first two patients and not in the third one? Our explanation is that the third patient showed a less compromised systolic function than the others before and after LVAD implantation. This might be interpreted as a preserved contractile reserve that supports the device made. In all the patients we have noted a reduction of the left ventricular systolic function; however such data are not sufficient to show a correlation between reduction of the potential and reduction of right contractility. Our data are not the first one concerning the interferences between ICD and LVAD; Foo et al. demonstrated that right ventricular sensing decreases in the first 6 months post-LVAD; the impedance also decreases and there is a significant increase in right ventricular stimulation threshold following implantation of the LVAD [17]. In our experience the stimulation threshold didn't change, only the impedances increased slightly in the first month after LVAD implant. The device measures daily lead impedance (both pace and shock) and intrinsic P and R-wave amplitudes. These measurements do not affect normal bradycardia pacing therapy. The measurements are taken during a 255-cardiac cycle period at approximately the same time each day. Daily amplitude measurements are stored for 7 days. After 7 days, the device calculates and stores a weekly average measurement. These measurements are stored for 52 weeks. At any time, you can access the daily measurements for the last 7 days, and the weekly measurements for the last 52 weeks. The data are displayed in graphical or tabular format (Fig. 1a–b). A decrease in R-wave amplitude occurs frequently in cardiac sarcoidosis, arrhythmogenic hypertrophy cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy [19], but low Rwave amplitude was also found in patients with dilated cardiomyopathy and severe left ventricular dysfunction. All these pathological conditions are characterized by reduction in the number and function of myocardial fibers with interstitial fibrosis [20]. Left ventricular dysfunction can increase right ventricular overload and may cause extensive fibrosis, possibly resulting in a decrease of R-wave. In our case, after LVAD implant, the right ventricular overload is transient and in the long term is compensated by the improvement of the cardiac output and by the reduction of the peripheral resistance. For this reason the reduction of the R-wave is transitory in the first months after the implant and then the R-wave normalizes again. A lowering of the R-wave amplitude could potentially involve alterations in the ICD and provoke missed recognition of ventricular arrhythmias, and delayed or missed intervention of the device. ICD discriminates ventricular tachyarrhythmia by measuring the cycle length and amplitude on intracardiac electrograms by its algorithm for sensing; as a consequence a decrease in the R-wave may cause an undersensing of ventricular tachyarrhythmias. Furthermore, as the thresholds of sensing are defined automatically by the amplitude of an R-wave in the algorithm, in case of a low R-wave, the device makes sense signals that are not R-wave ones (e.g. T-wave) and can provide inappropriate therapy [19]. Recent observational studies report that patients with LVAD may be subject to more frequent ventricular tachyarrhythmias [21] and therefore appropriate sensing of ventricular tachyarrhythmias is of paramount importance. Inappropriate detection and treatment of ventricular arrhythmias can reduce pump flows, resulting in poor cardiac output through the LVAD. In conclusion, a LVAD implant improves the cardiac function and the clinical status, but may have adverse hemodynamic and electrophysiological consequences on the right ventricle in the first period of follow up. The interaction between LVAD and ICD may influence the appropriateness and optimal function of the devices. Bradycardia and tachycardia parameters and settings in ICD should be judiciously evaluated and optimized regularly in order to derive the maximal benefits from these devices. Our data must be evaluated on a more numerous population, to confirm the discussed explanations and to analyze its statistical significance.
Letters to the Editor
The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [22]. References [1] Wilson SR, Mudge GH, Garrick C, Givertz S, Givertz MM. Evaluation for a ventricular assist device: selecting the appropriate candidate. Circulation 2009;119:2225–32. [2] Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, et al. Sudden cardiac death in heart failure trial (SCDHeFT) investigators: amiodorone or an implantable-cardioverter defibrillator for congestive heart failure. N Engl J Med 2005;352:225–37. [3] Duru F, Candinas R, Lachat M, Rahn M, Noll G, Luscher TF, et al. Electrical and mechanical support in advanced heart failure. Rationale and feasibility of a combined management strategy. Eur Heart J 2002;23:1005–10. [4] Matthews JC, Betley D, Morady F, Pelosi F. Adverse interaction between a left ventricular assist device and an implantable cardioverter defibrillator. J Cardiovasc Electrophysiol 2007;18:1107–8. [5] Kuhne M, Sakamura M, Reich SS, Sarrazin JF, Wells D, Chalfoun N, et al. Simultaneous use of implantable cardioverter-defibrillators and left ventricular assist devices in patients with severe heart failure. Am J Cardiol 2010;105:378–82. [6] Westaby S, Banning AP, Saito S, Pigott DW, Jin XY, Catarino PA. Circulatory support for long-term treatment of heart failure. Circulation 2002:2588–91. [7] John R. Current axial-flow devices—the HeartMate II and Jarvik 2000 left ventricular assist devices. Semin Thorac Cardiovasc Surg 2008;20:264–72. [8] Nakatani S, Thomas JD, Savage RM. Prediction of right ventricular dysfunction after left ventricular assist device implantation. Circulation 1996;94:II-216–21 (suppl II). [9] Barbone A, Holmes JW, Heerdt PM, Thè AHS, Naka Y, Joshi N, et al. Comparison of right and left ventricular responses to left ventricular assist device support in patients with severe heart failure: a primary role of mechanical unloading underlying reverse remodeling. Circulation 2001;104:670–5. [10] Fukamachi K, McCarthy PM, Smedira NG, et al. Preoperative risk factors for right ventricular failure after implantable left ventricular assist device insertion. Ann Thorac Surg 1999;68:2181–4.
623
[11] Ochiai Y, McCarthy PM, Smedira NG, Banbury MK, Navia JL, Feng J, et al. Predictors of severe right ventricular failure after implantable left ventricular assist device insertion: analysis of 245 patients. Circulation 2002;106(12 Suppl 1):I198–202. [12] Zafeiridis A, Jeevanandam V, Houser SR, Margulies KB. Regression of cellular hypertrophy after left ventricular assist device support. Circulation 1998;98: 656–62. [13] Kucuker SA, Stetson SJ, Becker KA, et al. Evidence of improved right ventricular structure after LVAD support in patients with end-stage cardiomyopathy. J Heart Lung Transplant 2004;23:28–35. [14] Farrar DJ. Physiology of ventricular interactions during ventricular assistance. In: Goldstein DJ, Oz MC, editors. Cardiac assist devices. New York: Futura Publishing Company; 2000. p. 15–26. [15] Deng MC, Loebe M, El-Banayosy A, et al. Mechanical circulatory support for advanced heart failure: effect of patient selection on outcome. Circulation 2001;103:231–7. [16] El-Banayosy A, Körfer R, Arusoglu L, et al. Device and patient management in a bridge-to-transplant setting. Ann Thorac Surg. 2001;71: S98–S102; discussion S114–S115 [17] Foo D, Walker BD, Kuchar DL, Thorburn CW, Tay A, Hayward CS, et al. Left ventricular mechanical assist devices and cardiac device interactions: an observational case series. Pacing Clin Electrophysiol 2009;32:879–87. [18] Gapstein L, Goldin A, Lessick J, Hayam G, Shpun S, Schwartz Y, et al. Electromechanical characterization of chronic myocardial infarction in the canine coronary occlusion model. Circulation 1998;98:2055–64. [19] Watanabe H, Chinushi M, Izumi D, Sato A, Okada S, Okamura K, et al. Decrease in amplitude of intracardiac ventricular electrogram and inappropriate therapy in patients with an implantable cardioverter defibrillator. Int Heart J 2006;47: 363–70. [20] Hughes SE, McKenna WJ. New insights into the pathology of inheredited cardiomyopathy. Heart 2005;91:257–64. [21] Bedi M, Kormos R, Winowich S, McNamara DM, Mathier MA, Murali S. Ventricular arrhythmias during left ventricular assist device support. Am J Cardiol 2007;99: 1151–3. [22] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.09.036
Association of right coronary artery (RCA) motion at 75% phase with heart rate during multi-row detector cardiac tomography angiography Souraya Sourayanezhad, Yasmin Hamirani, Sandeep Pagali, Vahid Nabavi, Subu Nair, Matthew J. Budoff ⁎ Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, 1124 West Carson Street, RB2, Torrance, CA 90502, USA
a r t i c l e
i n f o
Article history: Received 11 June 2010 Accepted 15 September 2010 Available online 13 October 2010 Keywords: Multidetector computed tomography Image quality RCA motion Heart rate Motion artifact
Abbreviations: RCA, right coronary artery; MDCT, multi-row detector computed tomography; CT, computed tomography; CTA, computed tomography angiography; CCT, coronary computed tomography; HR, heart rate; bpm, beat per minute; SPSS, snap shot pulse acquisition; EBCT, electron beam computed tomography; MRI, magnetic resonance imaging. ⁎ Corresponding author. Tel.: + 1 310 222 4107; fax: + 1 310 787 0448. E-mail address: [email protected] (M.J. Budoff).
Coronary artery disease is one of the major causes of hospital admissions. Ever since the development of cardiac computed tomography (CCT) more than twenty five years ago, CCT angiography has been increasingly used for the diagnostic evaluation of patients with clinically suspected obstructive disease or with abnormal cardiac or coronary anatomy [1]. With the advent of multi-slice scanners with higher spatial and temporal resolution there has been a tremendous improvement in the diagnostic accuracy of CCT. However there are limitations of cardiac imaging by this modality, the most important of which is coronary motion which can make a scan non-evaluable [2]. Motion artifact on multi-row detector computed tomography (MDCT) can be minimized by using electrocardiographic gating of CCT scans; this allows reconstruction of images at different phases of the cardiac cycle. Increasing use of prospective imaging, which only allows a short phase range of acquisition, limits the ability to change phase and correct for motion artifacts. Studies have been done in the past to evaluate the relationship of heart rate and image quality [3]; however no study has looked at optimal heart rates using prospective triggering during CCTangiography. The right coronary artery (RCA) is most likely to
Letters to the Editor
this case, a spheric balloon with a diameter of about 0.5 mm larger than the stent used was employed to obtain a funnel-like shape at the ostium of the stent. In ideal conditions the stent should be deployed with a minimal protrusion inside the main branch. The protruding struts will then be expanded by the spheric balloon, thus obtaining the final funnel-like shape. In addition, doing that, we obtain a reduction of the main branch wall trauma. In the next cases we are going to perform a detailed IVUS monitoring during the procedure, to demonstrate the modifications of the shape of the stent which can be obtained by the spheric balloon. The authors certified that they comply with the principles of ethical publishing in the International Journal of Cardiology [7].
[2] Melikian N, Di Mario C. Treatment of bifurcation coronary lesions: a review of current techniques and outcome. J Interv Cardiol Dec 2003;16(6):507–13. [3] Lefèvre T, Louvard Y, Morice MC, Loubeyre C, Piéchaud JF, Dumas P. Stenting of bifurcation lesions: a rational approach. J Interv Cardiol Dec 2001;14(6):573–85. [4] Rizik DG, Klag JM, Tenaglia A, Hatten TR, Barnhart M, Warnack B. Evaluation of a bifurcation drug-eluting stent system versus provisional T-stenting in a perfused synthetic coronary artery model. J Interv Cardiol Dec 2009;22(6):537–46 Epub 2009 Nov 13. [5] Jilaihawi H, Farah B, Laborde JC. The use of self-expanding stents in coronary bifurcations and beyond: a paradigm revisited. EuroIntervention Mar 2009;4(5): 669–75. [6] Brunel P, Martin G, Bressollette E, Leurent B, Banus Y. “Inverted” provisional T stenting, a new technique for Medina 0, 0, 1 coronary bifurcation lesions: feasibility and follow-up. EuroIntervention Feb 2010;5(7):814–20. [7] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
References [1] Sharma SK, Mares AM, Kini AS. Coronary bifurcation lesions. Minerva Cardioangiol Oct 2009;57(5):667–82.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.09.035
Electrophysiological interactions between implantable cardioverter defibrillators and left ventricular assist device Stefano Maffè a,⁎, Antonello Perucca a, Fabiana Signorotti a, Massimo Pistono b, Paola Paffoni a, Umberto Parravicini a, Pierfranco Dellavesa a, Lorenzo Cucchi a, Anna Maria Paino a, Franco Zenone a, Nicolò Franchetti Pardo a, Massimo Bielli a, Marco Zanetta a a b
Division of Cardiology, SS Trinità Hospital, ASL No, Borgomanero (NO), Italy Division of Cardiology, Salvatore Maugeri Foundation, IRCCS, Veruno (NO), Italy
a r t i c l e
i n f o
Article history: Received 14 June 2010 Accepted 16 September 2010 Available online 20 October 2010 Keywords: Implantable cardioverter-defibrillator Left ventricular assist device
Left ventricular assist devices (LVAD) have become not only an excellent bridge to cardiac transplantation, but also a valid alternative, in selected populations, as destination therapy in patients with advanced congestive heart failure [1]. Since recent clinical trials have demonstrated the survival benefit associated with implantable cardioverter defibrillators (ICD) in patients with heart failure [2], many LVAD candidates have an ICD in place prior to LVAD surgery. Clinical evidence suggests that a combined management strategy of electrical and mechanical support is both feasible and adds benefits in the treatment of end-stage heart failure [3]. While many studies have analyzed the hemodynamic interaction between LVAD and ICD [4,5], little has been published about the electrophysiological changes after a LVAD implant. This report ⁎ Corresponding author. Via Sesalli 15, 28100 NOVARA. Tel.: + 39 3355912520; fax: + 39 0322848430. E-mail address: [email protected] (S. Maffè).
describes the electrophysiological and not only the hemodynamic impact of a Jarvik 2000 pump implant in patients with a prior ICD and an end-stage heart failure. The Jarvik 2000 is a titanium axial-flow impeller pump (5.5 cm– 2.5 cm, weight 90 g) that is implanted into the apex of the failing left ventricle. Pump output is delivered to the descending thoracic aorta, thereby perfusing the brachiocephalic and coronary arteries in retrograde fashion. The device provides a continuous non-pulsatile flow from 2.5 to 6 L/min, working from 8000 up to 12,000 rpm, depending on the afterload [6]. The Jarvik 2000 pumps, which incorporate axial-flow and rotary pump technology, represent the last generation of devices. The use of the latter devices is associated with significant co-morbidity, primarily as a result of their large size and limited durability. The clinical use of these newer axial-flow pumps has resulted in better outcomes, including significantly reduced complication rates with improved durability. These characteristics have allowed to use successfully the Jarvik 2000 pump as destination therapy [7]. In our institution we have analyzed three patients with dilated hypokinetic cardiomyopathy and refractory heart failure, submitted to a LVAD Jarvik 2000 implant as destination therapy. The first patient is a 67-year-old man, with prior anterior myocardial infarction in 1991 treated with two coronary artery by-pass graft. In the space of ten years he has been repeatedly hospitalized for recurrent heart failure. His clinical condition deteriorated over time and the implantation of bicameral–biventricular ICD (Promote® RF CRT-D, St Jude Medical) proved only a transient clinical improvement. On the basis of clinical condition, age and important co-morbidity (previous prostatic cancer), he was submitted to a LVAD Jarvik 2000
Letters to the Editor
621
Fig. 1. a–b, ICD periodically measures intrinsic P and R-wave amplitudes; in the figures are graphically represented a marked and significant reduction of R-wave amplitude in the month after the LVAD implant in our patients.
surgery, as destination therapy. Left ventricular ejection fraction (LVEF) was 13% at pre-implant echocardiogram, while the right ventricular function was normal (tricuspid annular systolic plane excursion — TAPSE 19 mm). With the LVAD support the clinical conditions improved, and actually the patient is in NYHA III. The ICD periodically measures lead impedance (both pace and shock) and intrinsic P and R-wave amplitudes; in the patient it revealed a marked and significant reduction of the R-wave amplitude in the month after the LVAD implant (Fig.1a), with a decrease of approximately 50% (from N12 mV to 7 mV). Similarly the echocardiogram showed a reduction of the left and right ventricular functions (LVEF 10% and TAPSE 15 mm). Besides the important decrease in the R-wave amplitude, we recorded a small increase in lead impedances; the right ventricular stimulation threshold remained stable, while the left ventricular stimulation threshold was slightly increased. After a few months from the LVAD implant all the electrophysiological parameters returned to the basal pre-implant values. The second patient is a 72-year-old male, with a history of anterior myocardial infarction in 2008, complicated by cardiogenic shock and treated with intra-aortic balloon pump. He was submitted to a percutaneous coronary angioplasty (PCI) with a bare metal stent implant on the proximal left anterior descending artery. In the following months he developed a dilated hypokinetic cardiomyopathy with a left ventricular anterior–apical aneurysm and important reduction of systolic function. Five months later the patient underwent implantation of ventricular ICD (Vitality 2 ICD®, Boston Scientific) for the primary prevention of sudden death. In March 2009 the patient was submitted to LVAD Jarvik 2000 implant as destination therapy; before the implant, the echocardiographic LVEF was 13% and the right ventricular function was normal (TAPSE 19 mm). In the first month
after the implant we noticed a decrease in the R-wave amplitude of approximately 70% (from 18 mV to 50.3 mV), and in the following months a gradual normalization (Fig. 1b). Right ventricular impedances and right ventricular stimulation threshold remained substantially stable, without important variations. After a month with LVAD support, the LVEF was 9% and TAPSE 18 mm. The third patient is a 65-year-old male, diabetic, obese, and affected from dilated idiopathic cardiomyopathy, with normal coronary tree; in three years he was hospitalized several times for chronic heart failure. In 2008 the patient underwent implantation of bicameral–biventricular ICD (Contak Renewal 3RF®, Boston Scientific), with only transient clinical improvement. In September 2009 he was submitted to LVAD Jarvik 2000 implant; the pre-implant LVEF was 25%, with TAPSE 23 mm. At one month follow up LVEF was 30% and TAPSE 19 mm. In this patient we didn't find R-wave amplitude modifications after LVAD implant, and no significant variations in lead impedance and right ventricular stimulation threshold (see echocardiographic and electrophysiological parameters in Table 1). There is little information regarding potential interactions between non-pulsatile LVAD and cardiac pacemakers or defibrillators. The present case-reports document the cardiac alterations, not only hemodynamic but also electrophysiological, after a LVAD implant. Right ventricular hemodynamic alterations after LVAD implant have been broadly documented in literature. Acute right heart failure is one of the most important problems following a LVAD implant, which represents a prognostically negative event. The hemodynamic effects of LVAD are different in the two chambers: while the LV may be greatly unloaded, the right ventricle (RV) generally does not receive such benefits [8]. In the first 30 days after LVAD implant, the left ventricular volume is significantly reduced, obtaining a reverse
Table 1 Echocardiographic and electrophysiological parameters. LVEF (%)
Patient 1 Patient 2 Patient 3
TAPSE (mm)
R-wave amplitude (mV)
RV lead impedance (Ω)
RV stimulation threshold (V)
Pre
Post
Pre
Post
Pre
Post
Pre
Post
Pre
Post
13 13 25
10 9 30
19 19 23
15 18 19
N 12 18 17
7 5.3 16
500 485 830
450 510 900
0.5 0.7 0.5
0.5 0.8 0.5
622
Letters to the Editor
structural remodeling. On the contrary the right ventricular volume, gradually increases and only after the first month, if a right heart failure doesn't appear, it begins a gradual normalization [9]. Previous studies report the preoperative risk factors for RV failure after LVAD insertion by analysis of data from 100 patients implanted with LVAD. In this population, one of the most important risk factors identified by univariate analysis was the cardiac output [10]. When LVAD is used as a bridge to heart transplant, the procedure may be still complicated by early peri-operative right ventricular failure, leading to poor filling of the left ventricle, and thus, to low pump output. Severe right ventricular failure sometimes needs placement of right ventricular assist devices as well; this is the last resort of treatment to sustain LVAD output [11]. After LVAD support, the end-diastolic pressure–volume relationship shifts leftward, toward normal volumes [9], as a consequence of reduced left ventricular mass, size, and myocyte diameter [12]. Unlike the left ventricle, the right ventricle does not exhibit significant reverse structural remodeling during LVAD support, despite reduced right ventricular afterload, as evidenced by marked decreases in left atrial and pulmonary pressure during LVAD support [13]. The principal explanation of the limited recovery of the right ventricular cardiomyocyte function during LVAD support is the persistence of high central venous pressure with relative volume overload of the impaired right ventricle [14]. Univentricular hemodynamic support of the left ventricle reduces right ventricular afterload (i.e. pulmonary arterial and wedge pressure) but does not reduce right ventricular preload conditions. In this case, there is no evidence of reverse structural remodeling and evidence of only limited reverse functional remodeling. On the contrary, the biventricular VAD support normalizes right ventricular passive pressure–volume relationship, right ventricular mass, myocyte diameter, and chamber stiffness [13]. In the last years, thanks to improved peri-operative management and advanced clinical experience, the incidence for requirement of RVAD placement after LVAD insertion is decreasing [15]. However, once such severe RV failure occurs, mortality is still quite high. [16]. Even when the RVAD is not required, patients with severe RV failure may require prolonged inotropes, which interferes with their physical rehabilitation. In addition a persistent elevation of the central venous pressure may lead to liver dysfunction and make it difficult to avoid multiple organ failure. Therefore, to predict potential RV failure after LVAD replacement is essential for optimal device selection and improved clinical outcome. In case of implantable LVAD as destination therapy it is important to avoid implanting the device in a population (significant although small) with risk for considerable RV failure. The underlying reasons for lead parameter changes remain speculative. Postulated mechanisms include removal of a plug of LV apical myocardium near the RV apical lead; alteration of the underlying myocardial substrate post-LVAD; myocardial scarring and fibrosis; or pharmacologic, metabolic, and electrolyte changes that are prevalent in this patient group [17]. In addition, changes in cardiac geometry after LVAD placement may be an important factor as well. Alternatively, the natural progression of end-stage cardiomyopathy may influence lead parameters. Microdislodgement would be less likely for all leads that were implanted at least 6 months before the LVAD. Our hypothesis is that LVAD implant effects a rapid increase in cardiac output, causing a right ventricular volume overload and a right ventricular myocardial “stunning”, which reduces the endocavitary potential amplitude. The same phenomenon occurs in patients with previous pace-maker implant, who have a myocardial infarction involving the right ventricle, and who present a lowering of the right ventricular endocavitary potential [18]. The endocavitary potential reduction is strictly related to the LVAD implant, and not to cardiac surgery: in fact we didn't see any change in the potential amplitude recorded by the right ventricular lead in those patients with previous ICD implant undergoing traditional cardiac surgery (valvular or coronary artery by-pass graft). Why did the reduction of the potential
occur in the first two patients and not in the third one? Our explanation is that the third patient showed a less compromised systolic function than the others before and after LVAD implantation. This might be interpreted as a preserved contractile reserve that supports the device made. In all the patients we have noted a reduction of the left ventricular systolic function; however such data are not sufficient to show a correlation between reduction of the potential and reduction of right contractility. Our data are not the first one concerning the interferences between ICD and LVAD; Foo et al. demonstrated that right ventricular sensing decreases in the first 6 months post-LVAD; the impedance also decreases and there is a significant increase in right ventricular stimulation threshold following implantation of the LVAD [17]. In our experience the stimulation threshold didn't change, only the impedances increased slightly in the first month after LVAD implant. The device measures daily lead impedance (both pace and shock) and intrinsic P and R-wave amplitudes. These measurements do not affect normal bradycardia pacing therapy. The measurements are taken during a 255-cardiac cycle period at approximately the same time each day. Daily amplitude measurements are stored for 7 days. After 7 days, the device calculates and stores a weekly average measurement. These measurements are stored for 52 weeks. At any time, you can access the daily measurements for the last 7 days, and the weekly measurements for the last 52 weeks. The data are displayed in graphical or tabular format (Fig. 1a–b). A decrease in R-wave amplitude occurs frequently in cardiac sarcoidosis, arrhythmogenic hypertrophy cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy [19], but low Rwave amplitude was also found in patients with dilated cardiomyopathy and severe left ventricular dysfunction. All these pathological conditions are characterized by reduction in the number and function of myocardial fibers with interstitial fibrosis [20]. Left ventricular dysfunction can increase right ventricular overload and may cause extensive fibrosis, possibly resulting in a decrease of R-wave. In our case, after LVAD implant, the right ventricular overload is transient and in the long term is compensated by the improvement of the cardiac output and by the reduction of the peripheral resistance. For this reason the reduction of the R-wave is transitory in the first months after the implant and then the R-wave normalizes again. A lowering of the R-wave amplitude could potentially involve alterations in the ICD and provoke missed recognition of ventricular arrhythmias, and delayed or missed intervention of the device. ICD discriminates ventricular tachyarrhythmia by measuring the cycle length and amplitude on intracardiac electrograms by its algorithm for sensing; as a consequence a decrease in the R-wave may cause an undersensing of ventricular tachyarrhythmias. Furthermore, as the thresholds of sensing are defined automatically by the amplitude of an R-wave in the algorithm, in case of a low R-wave, the device makes sense signals that are not R-wave ones (e.g. T-wave) and can provide inappropriate therapy [19]. Recent observational studies report that patients with LVAD may be subject to more frequent ventricular tachyarrhythmias [21] and therefore appropriate sensing of ventricular tachyarrhythmias is of paramount importance. Inappropriate detection and treatment of ventricular arrhythmias can reduce pump flows, resulting in poor cardiac output through the LVAD. In conclusion, a LVAD implant improves the cardiac function and the clinical status, but may have adverse hemodynamic and electrophysiological consequences on the right ventricle in the first period of follow up. The interaction between LVAD and ICD may influence the appropriateness and optimal function of the devices. Bradycardia and tachycardia parameters and settings in ICD should be judiciously evaluated and optimized regularly in order to derive the maximal benefits from these devices. Our data must be evaluated on a more numerous population, to confirm the discussed explanations and to analyze its statistical significance.
Letters to the Editor
The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [22]. References [1] Wilson SR, Mudge GH, Garrick C, Givertz S, Givertz MM. Evaluation for a ventricular assist device: selecting the appropriate candidate. Circulation 2009;119:2225–32. [2] Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, et al. Sudden cardiac death in heart failure trial (SCDHeFT) investigators: amiodorone or an implantable-cardioverter defibrillator for congestive heart failure. N Engl J Med 2005;352:225–37. [3] Duru F, Candinas R, Lachat M, Rahn M, Noll G, Luscher TF, et al. Electrical and mechanical support in advanced heart failure. Rationale and feasibility of a combined management strategy. Eur Heart J 2002;23:1005–10. [4] Matthews JC, Betley D, Morady F, Pelosi F. Adverse interaction between a left ventricular assist device and an implantable cardioverter defibrillator. J Cardiovasc Electrophysiol 2007;18:1107–8. [5] Kuhne M, Sakamura M, Reich SS, Sarrazin JF, Wells D, Chalfoun N, et al. Simultaneous use of implantable cardioverter-defibrillators and left ventricular assist devices in patients with severe heart failure. Am J Cardiol 2010;105:378–82. [6] Westaby S, Banning AP, Saito S, Pigott DW, Jin XY, Catarino PA. Circulatory support for long-term treatment of heart failure. Circulation 2002:2588–91. [7] John R. Current axial-flow devices—the HeartMate II and Jarvik 2000 left ventricular assist devices. Semin Thorac Cardiovasc Surg 2008;20:264–72. [8] Nakatani S, Thomas JD, Savage RM. Prediction of right ventricular dysfunction after left ventricular assist device implantation. Circulation 1996;94:II-216–21 (suppl II). [9] Barbone A, Holmes JW, Heerdt PM, Thè AHS, Naka Y, Joshi N, et al. Comparison of right and left ventricular responses to left ventricular assist device support in patients with severe heart failure: a primary role of mechanical unloading underlying reverse remodeling. Circulation 2001;104:670–5. [10] Fukamachi K, McCarthy PM, Smedira NG, et al. Preoperative risk factors for right ventricular failure after implantable left ventricular assist device insertion. Ann Thorac Surg 1999;68:2181–4.
623
[11] Ochiai Y, McCarthy PM, Smedira NG, Banbury MK, Navia JL, Feng J, et al. Predictors of severe right ventricular failure after implantable left ventricular assist device insertion: analysis of 245 patients. Circulation 2002;106(12 Suppl 1):I198–202. [12] Zafeiridis A, Jeevanandam V, Houser SR, Margulies KB. Regression of cellular hypertrophy after left ventricular assist device support. Circulation 1998;98: 656–62. [13] Kucuker SA, Stetson SJ, Becker KA, et al. Evidence of improved right ventricular structure after LVAD support in patients with end-stage cardiomyopathy. J Heart Lung Transplant 2004;23:28–35. [14] Farrar DJ. Physiology of ventricular interactions during ventricular assistance. In: Goldstein DJ, Oz MC, editors. Cardiac assist devices. New York: Futura Publishing Company; 2000. p. 15–26. [15] Deng MC, Loebe M, El-Banayosy A, et al. Mechanical circulatory support for advanced heart failure: effect of patient selection on outcome. Circulation 2001;103:231–7. [16] El-Banayosy A, Körfer R, Arusoglu L, et al. Device and patient management in a bridge-to-transplant setting. Ann Thorac Surg. 2001;71: S98–S102; discussion S114–S115 [17] Foo D, Walker BD, Kuchar DL, Thorburn CW, Tay A, Hayward CS, et al. Left ventricular mechanical assist devices and cardiac device interactions: an observational case series. Pacing Clin Electrophysiol 2009;32:879–87. [18] Gapstein L, Goldin A, Lessick J, Hayam G, Shpun S, Schwartz Y, et al. Electromechanical characterization of chronic myocardial infarction in the canine coronary occlusion model. Circulation 1998;98:2055–64. [19] Watanabe H, Chinushi M, Izumi D, Sato A, Okada S, Okamura K, et al. Decrease in amplitude of intracardiac ventricular electrogram and inappropriate therapy in patients with an implantable cardioverter defibrillator. Int Heart J 2006;47: 363–70. [20] Hughes SE, McKenna WJ. New insights into the pathology of inheredited cardiomyopathy. Heart 2005;91:257–64. [21] Bedi M, Kormos R, Winowich S, McNamara DM, Mathier MA, Murali S. Ventricular arrhythmias during left ventricular assist device support. Am J Cardiol 2007;99: 1151–3. [22] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.09.036
Association of right coronary artery (RCA) motion at 75% phase with heart rate during multi-row detector cardiac tomography angiography Souraya Sourayanezhad, Yasmin Hamirani, Sandeep Pagali, Vahid Nabavi, Subu Nair, Matthew J. Budoff ⁎ Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, 1124 West Carson Street, RB2, Torrance, CA 90502, USA
a r t i c l e
i n f o
Article history: Received 11 June 2010 Accepted 15 September 2010 Available online 13 October 2010 Keywords: Multidetector computed tomography Image quality RCA motion Heart rate Motion artifact
Abbreviations: RCA, right coronary artery; MDCT, multi-row detector computed tomography; CT, computed tomography; CTA, computed tomography angiography; CCT, coronary computed tomography; HR, heart rate; bpm, beat per minute; SPSS, snap shot pulse acquisition; EBCT, electron beam computed tomography; MRI, magnetic resonance imaging. ⁎ Corresponding author. Tel.: + 1 310 222 4107; fax: + 1 310 787 0448. E-mail address: [email protected] (M.J. Budoff).
Coronary artery disease is one of the major causes of hospital admissions. Ever since the development of cardiac computed tomography (CCT) more than twenty five years ago, CCT angiography has been increasingly used for the diagnostic evaluation of patients with clinically suspected obstructive disease or with abnormal cardiac or coronary anatomy [1]. With the advent of multi-slice scanners with higher spatial and temporal resolution there has been a tremendous improvement in the diagnostic accuracy of CCT. However there are limitations of cardiac imaging by this modality, the most important of which is coronary motion which can make a scan non-evaluable [2]. Motion artifact on multi-row detector computed tomography (MDCT) can be minimized by using electrocardiographic gating of CCT scans; this allows reconstruction of images at different phases of the cardiac cycle. Increasing use of prospective imaging, which only allows a short phase range of acquisition, limits the ability to change phase and correct for motion artifacts. Studies have been done in the past to evaluate the relationship of heart rate and image quality [3]; however no study has looked at optimal heart rates using prospective triggering during CCTangiography. The right coronary artery (RCA) is most likely to