Abstract
In many cases, hemodynamic instability limits the ability to perform activation mapping during scar-related ventricular tachycardia (VT). Catecholamines may support blood pressure, but overall perfusion may be suboptimal, and these agents can produce cardiotoxicity. Mechanical hemodynamic support can facilitate mapping by maintaining perfusion to vital organs for extended periods of time during ongoing VT. Types of hemodynamic support include intraaortic balloon counterpulsation and percutaneous left ventricular assist devices of several types. In this chapter, different methods of hemodynamic support for facilitating activation mapping during VT will be discussed, including advantages and disadvantages to their use.
Keywords
hemodynamic monitoring, hemodynamic support, mapping, ventricular assist, ventricular tachycardia
Key Points
- •
Hemodynamic instability precludes detailed activation and entrainment mapping in a significant percentage of patients presenting for scar-related ventricular tachycardia (Sc-VT) ablation. As a result, ablation of Sc-VT is often limited to substrate mapping and ablation performed in sinus rhythm.
- •
Substrate-based ablation is thought to be less effective in certain patient populations, such as those with nonischemic cardiomyopathy—because of the paucity of targets (late potentials, fractionated electrograms, etc.) in sinus rhythm.
- •
Percutaneous hemodynamic support devices are being increasingly used during Sc-VT ablation to maintain cardiac output and systemic perfusion to allow for extensive mapping during VT and unload the left ventricle during periods of sinus rhythm.
- •
To date, the cumulative data suggest that percutaneous left ventricular assist extends the duration of mapping during unstable VT and allow for mapping and ablation of a greater number of unstable VTs (per patient). However, whether percutaneous left ventricular assist devices (pLVADs) will improve acute or long-term procedural success remains to be seen.
In patients with structural heart disease, scar-related ventricular tachycardia (Sc-VT) is often associated with hemodynamic instability. During catheter ablation of VT, this instability frequently precludes detailed entrainment and activation mapping during ongoing VT, and often limits procedural success. Indeed, in up to one-third of patients presenting for VT ablation, all inducible VTs are hemodynamically unstable and frequently termed unmappable. Even when brief episodes of entrainment and activation mapping can be achieved with repetitive VT inductions and terminations, this strategy can have a detrimental cumulative effect and exposes patients to progressive hemodynamic compromise, congestive heart failure, and end-organ hypoperfusion, without necessarily improving the ability to identify successful ablation targets. In addition, even well-tolerated prolonged episodes of induced VT may induce venous congestion and acute heart failure exacerbations, increasing the short-term morbidity and mortality of the procedure. In fact, in patients with Sc-VT, heart failure is a major cause of morbidity and mortality during late follow-up. As a result, ablation strategies in patients with unstable VT are often limited to substrate mapping and ablation performed in sinus rhythm, an approach that limits the ability to differentiate and target clinically relevant VT substrate. Furthermore, recent evidence suggests that only a minority of scar-related potentials (fractionated electrograms and late potentials) participate in the channels that support VT. The impact of a substrate-based mapping and ablation strategy is further limited in patients with nonischemic cardiomyopathy (NICM) because of the fewer number of putative channels in this increasingly prevalent population (≈35% of all Sc-VT ablation patients). In fact, the inability to achieve complete procedural success (i.e., persistent inducibility of any VT at the end of the procedure) in NICM is a strong predictor of VT recurrence. In addition, there are situations in which a pure substrate-based ablation is not technically feasible. Fig. 37.1 is an example of a patient with NICM whose putative channel sites were directly adjacent to critical structures (coronary artery, phrenic nerve) and in which minimization of ablation was necessary to achieve the proper balance between safety and efficacy. To avoid the adverse hemodynamic effects associated with prolonged VT episodes, and permit safe detailed entrainment/activation mapping during ablation, increasing focus has been placed on using temporary mechanical cardiac support in the electrophysiology laboratory.
Intravenous vasopressor and inotropic agents are often used to support cardiac output and maintain systemic blood pressure during ablation; however, they are typically unable to assist cardiac output to the extent necessary to provide sufficient hemodynamic support during prolonged episodes of VT. Furthermore, prolonged use of these agents can result in cardiotoxicity, multiorgan dysfunction, and acute and long-term morbidity and increased mortality.
Key Points
- •
Hemodynamic instability precludes detailed activation and entrainment mapping in a significant percentage of patients presenting for scar-related ventricular tachycardia (Sc-VT) ablation. As a result, ablation of Sc-VT is often limited to substrate mapping and ablation performed in sinus rhythm.
- •
Substrate-based ablation is thought to be less effective in certain patient populations, such as those with nonischemic cardiomyopathy—because of the paucity of targets (late potentials, fractionated electrograms, etc.) in sinus rhythm.
- •
Percutaneous hemodynamic support devices are being increasingly used during Sc-VT ablation to maintain cardiac output and systemic perfusion to allow for extensive mapping during VT and unload the left ventricle during periods of sinus rhythm.
- •
To date, the cumulative data suggest that percutaneous left ventricular assist extends the duration of mapping during unstable VT and allow for mapping and ablation of a greater number of unstable VTs (per patient). However, whether percutaneous left ventricular assist devices (pLVADs) will improve acute or long-term procedural success remains to be seen.
In patients with structural heart disease, scar-related ventricular tachycardia (Sc-VT) is often associated with hemodynamic instability. During catheter ablation of VT, this instability frequently precludes detailed entrainment and activation mapping during ongoing VT, and often limits procedural success. Indeed, in up to one-third of patients presenting for VT ablation, all inducible VTs are hemodynamically unstable and frequently termed unmappable. Even when brief episodes of entrainment and activation mapping can be achieved with repetitive VT inductions and terminations, this strategy can have a detrimental cumulative effect and exposes patients to progressive hemodynamic compromise, congestive heart failure, and end-organ hypoperfusion, without necessarily improving the ability to identify successful ablation targets. In addition, even well-tolerated prolonged episodes of induced VT may induce venous congestion and acute heart failure exacerbations, increasing the short-term morbidity and mortality of the procedure. In fact, in patients with Sc-VT, heart failure is a major cause of morbidity and mortality during late follow-up. As a result, ablation strategies in patients with unstable VT are often limited to substrate mapping and ablation performed in sinus rhythm, an approach that limits the ability to differentiate and target clinically relevant VT substrate. Furthermore, recent evidence suggests that only a minority of scar-related potentials (fractionated electrograms and late potentials) participate in the channels that support VT. The impact of a substrate-based mapping and ablation strategy is further limited in patients with nonischemic cardiomyopathy (NICM) because of the fewer number of putative channels in this increasingly prevalent population (≈35% of all Sc-VT ablation patients). In fact, the inability to achieve complete procedural success (i.e., persistent inducibility of any VT at the end of the procedure) in NICM is a strong predictor of VT recurrence. In addition, there are situations in which a pure substrate-based ablation is not technically feasible. Fig. 37.1 is an example of a patient with NICM whose putative channel sites were directly adjacent to critical structures (coronary artery, phrenic nerve) and in which minimization of ablation was necessary to achieve the proper balance between safety and efficacy. To avoid the adverse hemodynamic effects associated with prolonged VT episodes, and permit safe detailed entrainment/activation mapping during ablation, increasing focus has been placed on using temporary mechanical cardiac support in the electrophysiology laboratory.
Intravenous vasopressor and inotropic agents are often used to support cardiac output and maintain systemic blood pressure during ablation; however, they are typically unable to assist cardiac output to the extent necessary to provide sufficient hemodynamic support during prolonged episodes of VT. Furthermore, prolonged use of these agents can result in cardiotoxicity, multiorgan dysfunction, and acute and long-term morbidity and increased mortality.
Options for Intraprocedural Cardiac Mechanical Support
Mechanical hemodynamic support during VT ablation is designed to maintain cardiac output and mean arterial pressure in the setting of suboptimal contractile properties present during VT, while promoting diuresis, preventing significant increases in pulmonary artery pressures, reducing the incidence of acute heart failure and multisystem organ failure, and perhaps improving safety and permitting more rapid recovery following the procedure. During periods of induced VT, the goals of strategies for hemodynamic support are to maintain acceptable systemic perfusion allowing for prolonged arrhythmia mapping and preventing rapid hemodynamic deterioration. The percutaneous support devices that have been used during VT ablation are intraaortic balloon pump (IABP) counterpulsation, the TandemHeart left atrial-to-iliac artery bypass (CardiacAssist Inc, Pittsburgh, PA), and percutaneous left ventricular assist devices (pLVADs), which are impeller-driven axial flow pumps placed temporarily through the aortic valve to pump blood directly from the left ventricle to the ascending aorta (Impella; Abiomed, Danvers, MA).
Most clinical experience with temporary mechanical support has been with IABPs, which are routinely implanted percutaneously by cardiac interventionalists. As the IABP augments diastolic pressure and diminishes afterload, its greatest benefit is in support of coronary blood flow in patients with active myocardial ischemia. However, IABPs are only able to augment cardiac output by 0.5 L per minute, and the increases in mean arterial pressure and stroke volume afforded by the IABP may not be sufficient to meet the hemodynamic demands of patients in ongoing VT. Furthermore, the IABP is dependent on timing of balloon inflation and deflation to pressure- or electrocardiogram-based triggers, and thus its optimal function requires a stable, regular, and nontachycardic rhythm, and thus is not ideally suited for patients undergoing VT ablation. Although the IABP is likely the most common percutaneous support device used during VT ablation, there is limited published experience demonstrating its safety or effectiveness. The benefits of the IABP are its (1) relatively small arterial sheath size (7 F); (2) ease of insertion; and (3) familiarity to most operators and laboratory personnel.
The TandemHeart device is a percutaneous left atrial to iliac artery bypass system, which uses an external centrifugal pump that provides up to 3.5 to 4 L per minute of forward flow. It received approval from the Food and Drug Administration in the United States for extracorporeal circulatory support of procedures not requiring full cardiopulmonary bypass for up to 6 hours, and longer durations of use have been tolerated in clinical trials. As hemodynamic benefit tracks directly with the degree of continuous flow provided, the TandemHeart appears to achieve greater hemodynamic support than that provided by the smaller Impella 2.5 pLVAD. However, the TandemHeart requires a relatively complicated insertion technique including both arterial and venous access at the level of the femoral vessels. To access the left atrium, venous access is obtained followed by transseptal puncture and dilation to accommodate the 21 F inflow cannula in the left atrium, and a separate arterial access is necessary to place the outflow cannula in the iliac artery. Potential complications of this system are cardiac tamponade, major bleeding, critical limb ischemia, sepsis, arrhythmias, and residual atrial septal defects. Bleeding complications in particular range from 40% to 90%.
The Impella pLVADs use a miniaturized axial flow pump to deliver blood directly from the left ventricle to the atrium. An advantage of this device is its relatively simple implantation technique, which requires a single femoral arterial access and retrograde placement across the aortic valve. Three Impella devices with different pump flow capabilities currently exist: the Impella 2.5, placed through a 13 F introducer sheath in the femoral artery and allowing a maximal flow rate of 2.5 L per minute; the more recently introduced Impella CP, capable of delivering approximately 3.5 L per minute of flow placed through a 14 F access sheath; and the Impella 5.0, which is capable of providing a maximal support of approximately 5.0 L per minute, although this latter device has a larger maximal catheter diameter (21 F) that requires a surgical cutdown for arterial access. Most clinical experience thus far with pLVAD-assisted VT ablation has been with the Impella 2.5 device. Table 37.1 includes selected case series and studies of percutaneous hemodynamic support during Sc-VT ablation.
| Study | Design | Device | Substrate | No. Patients a | Follow-Up | Outcome Assessed |
|---|---|---|---|---|---|---|
| Abuissa et al. | Retrospective | Impella 2.5 | Nonischemic and ischemic | 3 | 6–9 months | Acute procedural success and VT recurrence |
| Miller et al. | Retrospective | Impella 2.5 and IABP | Nonischemic and ischemic | 22 | 3 months | Acute procedural success and VT recurrence |
| Bunch et al. | Retrospective | TandemHeart | Nonischemic and ischemic | 31 | 9 months | Acute procedural success and VT recurrence |
| Lu et al. | Retrospective | Impella 2.5, CPB and surgical LVADs | Nonischemic and ischemic | 16 | 3 months | Acute procedural success and VT recurrence |
| Miller et al. | Prospective | Impella 2.5 | Nonischemic and ischemic | 20 | 1 month | Acute procedural success, VT recurrence, hemodynamics during simulated VT, effects on end-organ perfusion |
| Aryana et al. | Retrospective | Impella 2.5 Impella CP | Nonischemic and ischemic | 68 | 19 months | Acute procedural success, VT recurrence, hospital LOS, 30-day rehospitalization, redo VT ablation, recurrent ICD therapies, 3-month mortality |
| Reddy et al. | Retrospective | Impella 2.5 Impella CP TandemHeart | Nonischemic and ischemic | 66 | 12 months | Acute procedural success, VT recurrence, mortality |
| Kusa et al. | Retrospective | Impella 2.5 Impella CP | Nonischemic and ischemic | 194 | 7 months | Acute procedural success, heart transplantation, and recurrent VT |
| Aryana et al. | Retrospective | pLVAD IABP (based on ICD 9 codes) | Nonischemic and ischemic | 345 | 12 months | In-hospital cardiogenic shock, acute renal failure, hospital LOS, 30-day readmission, mortality, redo VT ablation |
| Mathuria et al. | Retrospective | Impella TandemHeart | Nonischemic and ischemic | 93 | 3 months | 30-day mortality, 3-month freedom from VT |
| Turagam et al. | Retrospective | Impella 2.5 Impella CP TandemHeart ECMO | Nonischemic and ischemic | 1655 | 17 months | Acute procedural success, in-hospital mortality, 12-month mortality, VT recurrence |
a No patients refers to the total number of patients included within the study, but not necessarily the total number in which a percutaneous hemodynamic support device was used.
Compared with the TandemHeart, the percutaneously implanted pLVADs have smaller catheter diameters and avoid additional venous access and transseptal puncture, circumventing related complications and permitting shorter implantation times. As the Impella device directly unloads the left ventricle, it efficiently reduces myocardial oxygen demand and consumption, augments mean arterial pressure, and decreases left ventricular end-diastolic pressure, likely to a greater degree than the TandemHeart at comparable flow rates, particularly in conditions of low cardiac output. Most clinical experience with the Impella thus far has been in patients undergoing high-risk percutaneous coronary intervention with or without cardiogenic shock, in which cases the Impella 2.5 has provided greater augmentation of cardiac index and mean arterial pressure, and greater improvements in left ventricular ejection fraction (LVEF), than in procedures supported by IABP. Contraindications to Impella placement are any mechanical aortic valve, aortic valve stenosis/calcification (with aortic valve area ≤1.5 cm 2 ), moderate or greater degrees of aortic insufficiency, and significant vascular disease precluding percutaneous implantation, such as aneurysms and extreme tortuosity or calcifications. Vascular access complications are less common with the smaller Impella 2.5 device than with the larger Impella 5.0. For interventional procedures in which patients are typically hemodynamically stable at the start of the procedure, the Impella 2.5 may be particularly attractive given its ease of use, small profile, and minimal access site trauma, coupled with its superior ability to improve systemic perfusion and relieve elevated venous pressure. By contrast, in patients with severe heart failure and for those in cardiogenic shock, the greater degree of hemodynamic support provided by the Impella 5.0 or the TandemHeart may be required despite associated higher complication rates and longer times to implantation. Table 37.2 is a comparison of commonly used percutaneous hemodynamic support devices.
| Insertion Technique | Major Complications | Effect On Circulation | Advantages | Limitations | Contra-Indications |
|---|---|---|---|---|---|
| IABP | |||||
| Percutaneous or surgical | Limb ischemia (minimal risk) | Augment CO by up to 0.5 L/min | Allows longer duration of support | Requires stable rhythm | Moderate to severe AI Aortic disease |
| Single arterial | Stroke | — | Indirectly unloads LV | Lowest level of support | Uncontrolled sepsis Coagulopathy |
| 8 to 9 F | — | — | Familiarity Ease of insertion | — | — |
| TandemHeart | |||||
| Percutaneous or surgical | Cardiac tamponade | Augment CO by up to 3.5 L/min | Prolonged support duration | Large arterial cannulas | VSD PAD |
| Transseptal puncture required | Aortic puncture Limb ischemia (most risk) | — | Partial LV support Indirectly unloads LV | Requires transseptal puncture | RV failure |
| 21 F inflow (venous) | Bleeding and transfusion (most risk) | — | — | Requires two access sites | — |
| 15 F outflow (arterial) | Residual ASD | — | — | — | — |
| Impella 2.5 | |||||
| Percutaneous or surgical | Limb ischemia (moderate risk) | Augment CO by up to 2.5 L/min | Prolonged support duration | Relatively large arterial cannulas | LV thrombus VSD |
| Single arterial access | Bleeding (minimal risk) | — | Partial LV support | Interference with mapping catheter | Severe aortic stenosis |
| 13 F | — | — | Directly unloads LV Ease of use | — | RV failure |
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