Name: utilizing percutaneous ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock
Uploaded: 2021-06-12T13:00:00.000+00:00
Duration: 6 min 10 s
Description: Watch this Scientific Journal Video about Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock at JoVE.com

This protocol is the standard of care in our institution.
1. Insertion of the PVAD (e.g., Impella CP)
<ol>
	<li>Obtain common femoral access over the lower half of the femoral head under fluoroscopic and ultrasound guidance using a micro-puncture needle9,10. Position the micro-puncture sheath and obtain an angiogram of the femoral artery to confirm appropriate arteriotomy location11.</li>
	<li>Insert a 6 Fr sheath in the femoral artery.</li>
	<li>If there is concern for ilio-femoral disease, insert a pigtail catheter in the inferior portion of the abdominal aorta and perform an angiogram of the iliofemoral system to ensure there is no significant peripheral artery disease (PAD) that may preclude PVAD insertion. If there is moderate disease or calcification of the iliac arteries consider using a longer 25 cm 14 French sheath so that the tip of the sheath is in a relatively healthy segment of the abdominal aorta.</li>
	<li>Serially dilate the arteriotomy site over a stiff .035&#34; wire using 8, 10 and 12 Fr dilators sequentially. Then, insert the 14 Fr peel away sheath under fluoroscopic guidance, ensuring the tip advances without resistance.</li>
	<li>Administer heparin bolus (~100 U/kg body weight) for an ACT goal of 250 to 300 s. Alternative anticoagulation include bivalirudin and argatroban.</li>
	<li>Use a pigtail catheter to cross into the LV using a .035&#34; J tipped wire. Remove the J wire and check an LVEDP.</li>
	<li>Shape the tip of the exchange length 0.018&#34; wire included in the kit and insert it into the LV so that it forms a stable curve at the LV apex.</li>
	<li>Make sure ACT is at goal (250 to 300 s) before insertion12,13.</li>
	<li>Remove the pigtail catheter and insert the pump by loading the wire on the pre-assembled loading red lumen (e.g., EasyGuide) until it exits near the label.</li>
	<li>Remove the loading red lumen by gently pulling on the label while holding the catheter.</li>
	<li>Advance the device in small increments under fluoroscopic guidance into the LV over the 0.018&#34; wire.</li>
	<li>Position the pump in the LV with its inlet 4 cm below the aortic valve and make sure it is free from the mitral chordae. Being too close to the apex can cause PVCs and trigger &#34;suction alarms&#34;. Remove the .018&#34; wire and once removed, start the pump. Remove excess slack so the pump rests against the lesser curvature of the aorta.</li>
	<li>Monitor the console to make sure the motor current is pulsatile and aortic waveform is displayed. If a ventricular waveform is displayed, the pump may need to be pulled back.</li>
	<li>If the device needs to be left in situ, remove the peal-away sheath and insert the repositioning sheath pre-loaded on the device.</li>
	<li>Check the device position on fluoroscopy and the waveforms on the console again.</li>
	<li>Palpate (or sense with Doppler) the distal lower extremity arterial pulses including dorsalis pedis and posterior tibial prior to and after insertion of the device. Document this appropriately in the patient&#39;s medical record.</li>
	<li>If pulses or dopplers cannot be obtained, consider taking a lower extremity angiogram using the wire re-introducing port located on the side of the device or using another access to ensure non-obstructive flow to the lower limb.</li>
	<li>If flow is obstructed, place a reperfusion sheath prior to transferring the patient to the CCU. In patients with PAD who are at high risk for obstructive flow, strongly consider inserting the reperfusion sheath prior to placement of the 14 Fr sheath (i.e., after step 1.4 listed above).</li>
	<li>Monitor patients treated with a PVAD in the critical care unit (CCU) by personnel trained in its use.</li>
</ol>
2. Post-procedural care
<ol>
	<li>Apply sterile dressing.</li>
	<li>Position the device at a 45&#176; angle when entering the skin (gauze underneath the repositioning sheath can be helpful to maintain this angle). Failure to do so may result in the arteriotomy oozing, leading to formation of a hematoma. It is also helpful to place sutures with forward pressure to avoid device migration and to prevent bleeding. 
	NOTE: Securing the lower extremity with a knee immobilizer can also limit device migration as a reminder to patient not to bend/move the effected limb. This should not be fastened too tightly so as not to compromise circulation.</li>
	<li>Continue to perform routine pulse checks (palpable or Doppler).</li>
</ol>
3. Positioning
<ol>
	<li>Use bedside transthoracic echocardiogram to confirm appropriate device position either prior to transfer or immediately on arrival to the cardiac ICU, depending on availability of a point of care ultrasound.</li>
	<li>Use a parasternal long axis view to assess device position. A subxyphoid view may also be used if parasternal long axis view is not obtainable. A measurement from aortic valve to the device inlet should ideally be 3-4 cm for proper positioning of the device.</li>
	<li>Use echocardiograms to note the position of the device as it relates to the mitral valve.</li>
	<li>When a device needs to be repositioned, turn down the device to P2, unscrew the locking mechanism on the sterile cover to advance or retract the device. One can torque as advancing or retracting if the pigtail or inlet is too close to the mitral valve.</li>
	<li>Lock the device in the new position and document the new position.</li>
	<li>Following this, increase the device to the desired level of support.</li>
	<li>After increasing the level of support, reevaluate the device position as the device can jump forward when speed increases. 
	NOTE: If the device has been pulled back across the aortic valve, repositioning is better done in the cath lab under fluoroscopy guidance.</li>
</ol>
4. Weaning
<ol>
	<li>Consider weaning when vasopressors/inotropes are at low doses or completely weaned off. Hemodynamics should be continuously monitored to maintain a CPO &#62; 0.6 W. Carefully monitor right ventricular (RV) hemodynamics with a goal to maintain right atrial pressure (RAP) &#60;12 mmHg and pulmonary artery pulsatility index (PAPI) &#62;1.014. Also consider obtaining pH, mixed venous saturations and lactate every 2-6 hours to monitor cardiac work and end-organ perfusion.</li>
	<li>Decrease power by 1-2 levels over 2 hours, noting CPO, PAPI, RAP, MAP and urine output. If CPO drops &#60;0.6 W, RAP begins to increase, urine output drops &#62; 20 mL/h or MAP &#60;60 mmHg, increase power to previous level.</li>
</ol>
5. Removal12
<ol>
	<li>Use vascular closure devices to close the arteriotomy access site with complete deployment of the device performed when the large bore sheath is removed14. Temporary endovascular balloon tamponade or &#34;dry field closure technique&#34; is an effective and safe way to ensure hemostasis of the large bore access site15.</li>
	<li>Dial down to P1 and pull back the device into the aorta followed by change to P0 and disconnect the device from the console as the catheter is pulled out of the body.
	<ol>
		<li>Note that the device should not be left across the aortic valve at P0 due to the risk of aortic regurgitation.</li>
	</ol>
	</li>
	<li>If considering manual hemostasis, wait until ACT &#60;150 and hold 3 minutes of pressure per French size.</li>
</ol>

Dr. Aditya Bharadwaj is a consultant, proctor, and member of the Speakers Bureau for Abiomed.
Dr. Mir Basir is a consultant for Abbott Vascular, Abiomed, Cardiovascular System, Chiesi, Procyrion and Zoll.

Minimizing the Risks and Complications of PVAD (Table 2) 
The hemodynamic benefits of PVAD can be significantly neutralized if complications from large-bore access occur, such as major bleeding and acute limb ischemia28,29. It is thus essential to minimize the risk and complications of the device.
In order to decrease access site complications and reduce the number of access attempts, ultrasound and fluoroscopic guidance should be used when obtaining femoral arterial access10,30. Use of micropuncture allows operators to minimize trauma if the access is deemed to be at an inappropriate site9. Performing an aorto-iliac angiogram prior to placement of PVAD also helps in selecting the more favorable access site15. Vascular closure devices and endovascular balloon tamponade are effective in achieving hemostasis in patients with large-bore access and should be utilized whenever possible at the time of device removal15, 31.
Acute limb ischemia is a catastrophic complication of PVAD use. Assessing distal pulses in the extremity is a crucial step in early detection limb ischemia. If pulses are noted to be diminished from baseline or are absent, it is imperative to restore flow prior to the patient leaving the cardiac catheterization laboratory. The ability to create an external bypass circuit for limb perfusion is thus critical15. Based upon a patient&#39;s vascular anatomy an external ipsilateral, an external contralateral, or an internal contralateral circuit can be created15. Similarly, the ability to obtain and manage an alternative access point such as an axillary artery or transcaval access is essential in patients with PAD in an effort to avoid the risk of limb ischemia7,8.
Hemolysis can occur in patients treated with PVAD. In the EUROSHOCK registry hemolysis was present in 7.5% of patients28. Hemolysis can result in anemia, acute kidney injury and result in activating a systemic inflammatory response. Repositioning the PVAD device to clear the inlet from the mitral apparatus and decreasing the P level (at the cost of decreased flow) may help mitigate hemolysis.
Utilizing Shock Protocols 
The aforementioned best practices led to the conceptualization and implementation of shock protocols for the treat of AMI-CS32. The use of these protocols has demonstrate improved survival when compared to historical controls (Figure 2)14. Quality measures such as PVAD utilization pre-PCI, door to support times, establishment of TIMI III flow in the culprit artery, utilization of right heart catheterization, the ability to wean vasopressors and inotropes and the ability to maintaining CPO &#62; 0.6 Watts, are systemically evaluated and reported to improve outcomes within these institutions. However, while this data shows improved survival compared to prior studies, this data largely stems from single-arm registry rather than randomized controlled trials.
Limitations of the PVAD 
There are several limitations to using PVADs. Severe PAD may limit implantation options, as access may occlude the vessel and lead to limb ischemia14. For example, if bilateral femoral disease or bypasses are present, the device may need to be placed either via the axillary artery or by transcaval access7,8,15. As with other ventricular assist devices, PVADs should not be used in patients with moderate to severe aortic regurgitation, as this device will worsen the aortic regurgitation rather than achieving the desired unloading of the LV12. Finally, for the left-sided PVADs, presence of an LV thrombus is an absolute contraindication due to the risk of stroke or other embolic events12. Furthermore, an Impella CP may not provide enough cardiac output, requiring upgrade to a larger PVAD or ECMO. Finally, a long-term plan should be considered for the patient - if the patient is not a candidate for advanced therapy (bridge to transplant or LVAD), then the likelihood of recovery and the duration of PVAD use should be discussed with the patient and/or family, heart failure specialist and interventionalist.
Limitations in the data 
The aforementioned studies have been significantly limited in the number of patients, and in their retrospective, observational nature. Many are based on of registries, which allow for more confounding factors. There is as yet no large-scale prospective trial which demonstrates mortality benefit of the any MCS device in AMI-CS, though these studies are currently under way33.
Future Studies 
Future studies evaluating the use of PVAD in AMI-CS must come from well powered randomized control trials. These efforts are already underway. The DanGer Shock Trial will be the first adequately powered randomized controlled trial in AMI-CS and will compare standard AMI-CS practice versus standard practice with PVAD33,34.
With increasing utilization of PVAD in AMI-CS it is important for clinicians to identify how to place, manage and wean such devices. In this article we have summarized how to place this device, step-by-step and best practices associated with improved outcomes when utilizing such devices. Formalizing these best practices based on local experience and expertise is encouraged until data from future well-powered trials is available.

Cardiogenic shock (CS) is defined as persistent hypotension (systolic blood pressure &#60;90 mmHg for &#62;30 minutes, or the need for vasopressors or inotropes), end-organ hypo-perfusion (urine output &#60;30 mL/h, cool extremities or lactate &#62; 2 mmol/L), pulmonary congestion (pulmonary capillary wedge pressure (PCWP) &#8805; 15 mmHg) and decrease cardiac performance (cardiac index &#60;2.2 <img alt="Equation 1" fo:break-after="column" src="/files/ftp_upload/62110/62110eq01v2.jpg" />)1,2 due to a primary cardiac disorder. Acute myocardial infarction (AMI) is the most common cause of CS3. CS occurs in 5-10% of AMI and historically has been associated with significant mortality3,4. Mechanical circulatory support (MCS) devices such as intra-aortic balloon pump (IABP), percutaneous ventricular assist devices (PVAD), extracorporeal membrane oxygenation (ECMO) and percutaneous left atrial to aortic devices are frequently used in patients with CS5. Routine use of IABP has demonstrated no improvement in clinical outcomes or survival in AMI-CS1. Given the poor outcomes associated with AMI-CS, the difficulties in conducting trials in AMI-CS, and the negative results of IABP use in AMI-CS, clinicians are increasingly looking to other forms of MCS.
PVADs are increasingly utilized in patients with AMI-CS6. In this article, we will focus our discussion primarily on the Impella CP, which is the most common PVAD used currently6. This device utilizes an axial flow Archimedes-screw pump which actively and continuously propels blood from the left ventricle (LV) into the ascending aorta (Figure 1). The device is most frequently placed in the cardiac catheterization laboratory under fluoroscopic guidance via the femoral artery. Alternatively, it can be implanted through an axillary or transcaval access when necessary7,8.

<table><tbody><tr><td>4 Fr-018-10 cm Silhouette Stiffened Micropuncture Set</td><td>Cook</td><td>G48002</td><td>Microvascular access</td></tr><tr><td>5 Fr Infiniti Pigtail Catheter</td><td>Cordis</td><td>524-550S</td><td>pigtail catheter</td></tr><tr><td>Impella CP Intra-cardiac Assist Catheter</td><td>ABIOMED</td><td>0048-0003</td><td>Impella catheter kit</td></tr></tbody></table>

utilizing percutaneous ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock

Cardiogenic shock is defined as persistent hypotension, accompanied by evidence of end organ hypo-perfusion. Percutaneous ventricular assist devices (PVADs) are used for the treatment of cardiogenic shock in an effort to improve hemodynamics. Impella is currently the most common PVAD and actively pumps blood from the left ventricle into the aorta. PVADs unload the left ventricle, increase cardiac output and improve coronary perfusion. PVADs are typically placed in the cardiac catheterization laboratory under fluoroscopic guidance via the femoral artery when feasible. In cases of severe peripheral arterial disease, PVADs can be implanted through an alternative access. In this article, we summarize the mechanism of action of PVAD and the data supporting their use in the treatment of cardiogenic shock.

Table 1 shows the safety and efficacy of PVAD implantation35,36,37,38,39,40.
Optimizing PVAD Outcomes 
PVADs are a resource-heavy intervention that requires significant experience and expertise to optimize outcomes. The following best practices should be considered:
1. Utilizing PVAD early after shock onset
2. Utilizing PVAD prior to escalating doses of vasopressors and inotropes
3. Utilizing PVAD prior to PCI
4. Utilizing invasive hemodynamics for PVAD escalation and de-escalation
5. Minimizing PVAD complications
6. Utilizing Shock Protocols
Utilizing PVAD early after shock onset 
AMI-CS is caused by coronary ischemia leading to diastolic failure, increasing LV wall tension, systolic failure and systemic hypo-perfusion. If not promptly treated, CS results in lactic acidosis, end-organ failure and death3. It is imperative to support patients prior to the onset of refractory shock. Patients in refractory shock go on to develop systemic inflammatory response syndrome, triggering a cascade of neurohormonal changes which are difficult to reverse3. This was demonstrated in the cVAD registry where patients who received MCS early, with a duration of shock before PVAD initiation of &#60;1.25 hours, had higher survival to discharge compared with those who received PVAD after 1.25 hours16. This was also demonstrated by Tehrani et al. who demonstrated that for patients requiring PVAD, every 1-hour delay in escalation of therapy was associated with a 9.9% increased risk of death17.Notably, small randomized controlled trials which compared IABP to PVADs demonstrated a superior hemodynamic effect, but not a mortality benefit18,19.
Utilize PVAD prior to escalating doses of vasopressors and inotropes 
Use of vasopressors and inotropes is typically needed in patients presenting with AMI-CS. These medications rapidly improve blood pressure and cardiac output. Unfortunately, they also increase heart rate and afterload, resulting in increasing myocardial oxygen consumption and work20. They are also associated with increasing arrythmogenicity and infarct size. Given these hemodynamic effects, PVADs should be considered at the time of initiation of an inotrope or vasopressor and/or when escalating their use in patients with AMI-CS. This was demonstrated in the cVAD registry where the rate of survival to discharge was inversely proportional to the amount of inotropic support used before initiation of MCS. Patients who received 0, 1, 2, 3, or 4 or more inotropes had a 68%, 45%, 35%, 35%, and 26% rate of survival to discharge, respectively (odds ratio 2.3, 95% confidence interval 0.99 to 5.32, p=0.05)21.
Utilize PVAD pre-PCI in AMI-CS 
PCI causes a transient cessation of blood flow resulting in increasing LV volume and decreasing systolic pressure. In patients with normal LV function, these physiologic changes are typically transient and quickly recover. In patients with poor LV reserve and those presenting in AMI-CS, the physiologic effects of PCI can be catastrophic. PCI can also result in micro-embolization and reperfusion injury resulting in infarct zone expansion. Early initiation of hemodynamic support prior to PCI has been shown to improve outcomes in patients with AMI-CS. The USPella registry (n=154) demonstrated survival to discharge was significantly higher in the group which received PVAD pre-PCI as compared to post-PCI (65% vs 40%, p=0.01, OR =0.37 CI 0.19-0.72)22. In the cVAD registry, an analysis of 287 patients demonstrated that MCS implantation before PCI was independently associated with improved survival16. Lastly in the IQ database, analysis of 5,571 patients demonstrated that PVAD use pre-PCI was associated with improved survival21.
Utilizing invasive hemodynamics to PVAD management 
Use of invasive hemodynamic monitoring with pulmonary artery catheters has been associated with improved outcomes in AMI-CS patients requiring PVAD. PA catheters help to guide the effectiveness of PVAD, the need for MCS escalation, the identification of RV failure as well in aiding weaning of such devices21. In a retrospective cohort study of the national inpatient sample, patients with PA catheters who were admitted with AMI-CS had decreased mortality and lower in-hospital cardiac arrest23. Tehrani et al also demonstrated that use of a PA catheter, along with a standardized cardiogenic shock protocol, was associated with a 39% absolute increase in survival (71% vs. 32.0%; p &#60; 0.01)17. Recent data published from the cardiogenic shock working group also demonstrated a benefit in mortality when PA catheters were used24. PA catheters allowed for serial monitoring of cardiac function by parameters such as cardiac power output (<img alt="Equation 2" src="/files/ftp_upload/62110/62110eq02v2.jpg" />), right atrial pressure and PAPI (<img alt="Equation 3" src="/files/ftp_upload/62110/62110eq03.jpg" />), which are important predictors of outcomes in AMI-CS16,25. PAPI, like many measures of RV function, is sensitive to loading conditions, and varies by population of patient (e.g., chronic heart failure vs pulmonary hypertension vs ACS)26. In the future, a more specific PAPI cut off may be provided in AMI-CS versus other conditions such as chronic advanced heart failure or post LVAD or cardiac transplant implantation26. It is our clinical practice to use &#60;1.0 as the cut off for consideration of right ventricular support in AMI-CS patients27.
<img alt="Figure 1" class="xfigimg" src="/files/ftp_upload/62110/62110fig01.jpg" /> 
Figure 1: PVAD, Detailed Anatomy and Hemodynamic Effects. (A)&#160;Detailed anatomy of a PVAD (This figure has been modified from Abiomed). (B) Hemodynamic effects of PVAD. CPO: cardiac power output, O2: oxygen, MAP: mean arterial pressure, PCWP: pulmonary capillary wedge pressure, LVEDP: left ventricular end diastolic pressure, LVEDP: left ventricular end diastolic pressure. <a href="https://www-jove-com.remotexs.ntu.edu.sg/files/ftp_upload/62110/62110fig01large.jpg" target="_blank">Please click here to view a larger version of this figure.</a>
<img alt="Figure 2" class="xfigimg" src="/files/ftp_upload/62110/62110fig02.jpg" /> 
Figure 2: A Shock Protocol. The algorithm for the National Cardiogenic Shock Initiative. AMI: acute MI, NSTEMI: non-ST elevation myocardial infarction, STEMI: ST-elevation myocardial infarction, LVEDP: left ventricular end diastolic pressure, MAP: mean arterial pressure, CO: cardiac output, sPAP: systolic pulmonary artery pressure, dPAP: diastolic pulmonary artery pressure, RA: right atrial pressure <a href="https://www-jove-com.remotexs.ntu.edu.sg/files/ftp_upload/62110/62110fig02large.jpg" target="_blank">Please click here to view a larger version of this figure.</a>
<table border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<tbody>
		<tr>
			<td>Study</td>
			<td>Patient Population</td>
			<td>N</td>
			<td>Devices Compared</td>
			<td>Findings</td>
		</tr>
		<tr>
			<td rowspan="5">Seyfarth et al</td>
			<td rowspan="5">Acute myocardial infarction and Cardiogenic Shock</td>
			<td rowspan="5">25</td>
			<td rowspan="5">IABP vs Impella 2.5</td>
			<td>No device-related technical failure</td>
		</tr>
		<tr>
			<td>Non-statistically significant &#8593;pRBC transfusion in Impella group</td>
		</tr>
		<tr>
			<td>Non-statistically significant &#8593;FFP in Impella Group</td>
		</tr>
		<tr>
			<td>&#8593;Hemolysis in Impella group</td>
		</tr>
		<tr>
			<td>No difference in mortality or LVEF</td>
		</tr>
		<tr>
			<td rowspan="2">Schrage et al.</td>
			<td rowspan="2">Acute myocardial infarction and Cardiogenic Shock</td>
			<td rowspan="2">237</td>
			<td rowspan="2">IABP vs Impella CP and 2.5</td>
			<td>No difference in Mortality, Stroke</td>
		</tr>
		<tr>
			<td>&#8593;Bleeding and ischemic complications inImpella group compared to IABP group</td>
		</tr>
		<tr>
			<td rowspan="3">Casassus et al.</td>
			<td rowspan="3">Refractory cardiogenic shock from acute myocardial infartion</td>
			<td rowspan="3">22</td>
			<td rowspan="3">Impella 2.5</td>
			<td>Transfusion due to bleeding: 18.2%</td>
		</tr>
		<tr>
			<td>limb ischemia: 10%</td>
		</tr>
		<tr>
			<td>aortic insufficiency: 5.6%</td>
		</tr>
		<tr>
			<td rowspan="4">Joseph et al.</td>
			<td rowspan="4">Acute myocardial infarction and cardiogenic shock</td>
			<td rowspan="4">180</td>
			<td rowspan="4">Impella 2.5</td>
			<td>Hemolysis: 8.9%</td>
		</tr>
		<tr>
			<td>No aortic regurgitation</td>
		</tr>
		<tr>
			<td>Bleeding requiring transfusion: 15.6%</td>
		</tr>
		<tr>
			<td>Vascular complication: 11.7%</td>
		</tr>
		<tr>
			<td rowspan="2">Lauten et al.</td>
			<td rowspan="2">Acute Myocardial Infarction and Cardiogenic Shock</td>
			<td rowspan="2">120</td>
			<td rowspan="2">Impella 2.5</td>
			<td>Major Bleeding 28.6%</td>
		</tr>
		<tr>
			<td>Hemolysis: 7.5%</td>
		</tr>
		<tr>
			<td rowspan="5">Ouweneel et al</td>
			<td rowspan="5">Acute myocardial infarction and cardiogenic shock</td>
			<td rowspan="5">48</td>
			<td rowspan="5">IABP vs Impella CP</td>
			<td>Hemolysis: 8%</td>
		</tr>
		<tr>
			<td>No incidence of device failure</td>
		</tr>
		<tr>
			<td>Device-related bleeding: 13%</td>
		</tr>
		<tr>
			<td>Major Vascular complication: 4%</td>
		</tr>
		<tr>
			<td>No significant difference in mortality</td>
		</tr>
	</tbody>
</table>
Table 1. Safety and Efficacy of PVAD implantation35,36,37,38,39,40.&#160;IABP: Intra-aortic balloon pump, pRBC: packed red blood cells, FFP: fresh-frozen plasma, LVEF: left ventricular ejection fraction.
<table border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<tbody>
		<tr>
			<td>Complication</td>
			<td>Diagnosis</td>
			<td>Management</td>
			<td>Prevention</td>
		</tr>
		<tr>
			<td rowspan="3">Acute Limb Ischemia</td>
			<td>&#183; Clinical: Decreased or absent pulses on limb, limb pain, change in color to pale, blue.</td>
			<td>&#183; Internal or External percutaneous bypass, restoring antegrade flow</td>
			<td>&#183; Routine assessment of distal pulses</td>
		</tr>
		<tr>
			<td>&#183; Imaging: Minimal or no pulse via Doppler ultrasound.</td>
			<td>&#183; Removal of Impella device, re-insertion at another arterial site with less vascular disease if needed for hemodynamic support</td>
			<td>&#183; If distal pulse is compromised, recommend creation of external or internal bypass to restore flow</td>
		</tr>
		<tr>
			<td>&#183; Laboratory: elevation in lactate</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td rowspan="3">Vascular Pseudoaneurysm</td>
			<td>&#183; Clinical: large, pulsatile mass, painful at access site, +thrill/bruit</td>
			<td>&#183;&#60;2-3cm, may resolve spontaneously</td>
			<td rowspan="3">&#183; Meticulous access techniques including use of Ultrasound, Fluoroscopy and micro-puncture access</td>
		</tr>
		<tr>
			<td>&#183; Imaging: Doppler Ultrasound</td>
			<td>&#183; Ultrasound-guided thrombin injection</td>
		</tr>
		<tr>
			<td></td>
			<td>&#183; Surgical intervention (rapid increase in size, peripheral neuropathy, distal/cutaneous ischemia)</td>
		</tr>
		<tr>
			<td rowspan="3">Bleeding (external hematoma or internal retroperitoneal bleed)&#160;</td>
			<td>&#183; Clinical: hypotension despite improved cardiac output, visible hematoma, suction alarms</td>
			<td>&#183; If hematoma or oozing around access site, reposition angle of Impella</td>
			<td rowspan="3">&#183; Meticulous access technique with Ultrasound, Fluoroscopy and micro-puncture sheath to prevent &#8216;high stick&#8217; (prevents retroperitoneal bleed) and minimize access attempts (prevents hematoma)&#160;</td>
		</tr>
		<tr>
			<td>&#183; Laboratory: &#8595;hemoglobin</td>
			<td>&#183; Low-pressure balloon inflation at site of bleeding or covered stent deployment in extreme cases</td>
		</tr>
		<tr>
			<td>&#183; Imaging: CT scan without contrast to diagnose retroperitoneal bleed</td>
			<td>&#183; Coil embolization for retroperitoneal bleed</td>
		</tr>
		<tr>
			<td rowspan="3">Hemolysis</td>
			<td>&#183; Clinical: change in color of urine to dark yellow, brown.</td>
			<td>&#183; Reposition device, generally away from mitral leaflet</td>
			<td rowspan="3">&#183; Good Impella position with inlet away from mitral apparatus</td>
		</tr>
		<tr>
			<td>&#183; Laboratory: &#8593; plasma-free hemoglobin, lactate dehydrogenase, bilirubin. &#8595; hemoglobin, haptoglobin.</td>
			<td>&#183; Decrease power level</td>
		</tr>
		<tr>
			<td></td>
			<td>&#183; Removal of device if requiring significant blood transfusions (&#62; 2 units) or causing renal function compromise.</td>
		</tr>
	</tbody>
</table>
Table 2. Complications of PVAD15,41.&#160;Diagnosis and management of complications that arise from use of left-sided PVADs.

Watch this Scientific Journal Video about Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock at JoVE.com

Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock

Percutaneous ventricular assist devices are increasingly being utilized in patients with acute myocardial infarction and cardiogenic shock. Herein, we discuss the mechanism of action and hemodynamic effects of such devices. We also review algorithms and best practices for the implantation, management and weaning of these complex devices.

Cardiogenic shock is defined as persistent hypotension, accompanied by evidence of end organ hypo-perfusion. Percutaneous ventricular assist devices ...

utilizing-percutaneous-ventricular-assist-devices-acute-myocardial

Nanyang Technological University

Research

JoVE Journal

Medicine

3.2K Views.  Loma Linda University Medical Center. Percutane ventriculaire hulpmiddelen worden steeds vaker gebruikt bij patiënten met een acuut myocardinfarct en cardiogene shock. Deze video demonstreert best practices voor het inbrengen van de impellakatheter. Het gebruik van best practices voor femorale arteriële toegang en het inbrengen van percutane ventriculaire hulpmiddelen is uiterst belangrijk om het risico op vasculaire complicaties bij patiënten met cardiogene shock te verminderen.Begin met het gebruik van een micropunctu...

Video: Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock

Acute Myocardial Infarction in Rats

With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular diseases. Animal models that mimic human cardiac disease, such as myocardial infarction (MI) and ischemia-reperfusion (IR) that induces heart failure as well as pressure-overload (transverse aortic constriction) that induces cardiac hypertrophy and heart failure (Goldman and Tarnavski), are useful models to study cardiovascular disease. In particular, myocardial ischemia (MI) is a leading cause for cardiovascular morbidity and mortality despite controlling certain risk factors such as arteriosclerosis and treatments via surgical intervention (Thygesen). Furthermore, an acute loss of the myocardium following myocardial ischemia (MI) results in increased loading conditions that induces ventricular remodeling of the infarcted border zone and the remote non-infarcted myocardium. Myocyte apoptosis, necrosis and the resultant increased hemodynamic load activate multiple biochemical intracellular signaling that initiates LV dilatation, hypertrophy, ventricular shape distortion, and collagen scar formation. This pathological remodeling and failure to normalize the increased wall stresses results in progressive dilatation, recruitment of the border zone myocardium into the scar, and eventually deterioration in myocardial contractile function (i.e. heart failure). The progression of LV dysfunction and heart failure in rats is similar to that observed in patients who sustain a large myocardial infarction, survive and subsequently develops heart failure (Goldman). The acute myocardial infarction (AMI) model in rats has been used to mimic human cardiovascular disease; specifically used to study cardiac signaling mechanisms associated with heart failure as well as to assess the contribution of therapeutic strategies for the treatment of heart failure. The method described in this report is the rat model of acute myocardial infarction (AMI). This model is also referred to as an acute ischemic cardiomyopathy or ischemia followed by reperfusion (IR); which is induced by an acute 30-minute period of ischemia by ligation of the left anterior descending artery (LAD) followed by reperfusion of the tissue by releasing the LAD ligation (Vasilyev and McConnell). This protocol will focus on assessment of the infarct size and the area-at-risk (AAR) by Evan's blue dye and triphenyl tetrazolium chloride (TTC) following 4-hours of reperfusion; additional comments toward the evaluation of cardiac function and remodeling by modifying the duration of reperfusion, is also presented. Overall, this AMI rat animal model is useful for studying the consequence of a myocardial infarction on cardiac pathophysiological and physiological function.

The rat model of acute myocardial infarction (AMI) is useful to study the consequence of a MI on cardiac pathophysiological and physiological function.

With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular ...

Implantation of the Syncardia Total Artificial Heart

With advances in technology, the use of mechanical circulatory support devices for end stage heart failure has rapidly increased. The vast majority of such patients are generally well served by left ventricular assist devices (LVADs). However, a subset of patients with late stage biventricular failure or other significant anatomic lesions are not adequately treated by isolated left ventricular mechanical support. Examples of concomitant cardiac pathology that may be better treated by resection and TAH replacement includes: post infarction ventricular septal defect,&#160;aortic root aneurysm / dissection, cardiac allograft failure, massive ventricular thrombus, refractory malignant arrhythmias (independent of filling pressures), hypertrophic / restrictive cardiomyopathy, and complex congenital heart disease. Patients often present with cardiogenic shock and multi system organ dysfunction. Excision of both ventricles and orthotopic replacement with a total artificial heart (TAH) is an effective, albeit extreme, therapy for rapid restoration of blood flow and resuscitation. Perioperative management is focused on end organ resuscitation and physical rehabilitation. In addition to the usual concerns of infection, bleeding, and thromboembolism common to all mechanically supported patients, TAH patients face unique risks with regard to renal failure and anemia. Supplementation of the abrupt decrease in brain natriuretic peptide following ventriculectomy appears to have protective renal effects. Anemia following TAH implantation can be profound and persistent. Nonetheless, the anemia is generally well tolerated and transfusion are limited to avoid HLA sensitization. Until recently, TAH patients were confined as inpatients tethered to a 500 lb pneumatic console driver. Recent introduction of a backpack sized portable driver (currently under clinical trial) has enabled patients to be discharged home and even return to work. Despite the profound presentation of these sick patients, there is a 79-87% success in bridge to transplantation.

The purpose of this manuscript is to briefly review indications, management, and outcomes for the total artificial heart. Video operative techniques for device implantation are presented.

With advances in technology, the use of mechanical circulatory support devices for end stage heart failure has rapidly increased. The vast majority of ...

MRI and PET in Mouse Models of Myocardial Infarction

Myocardial infarction is one of the leading causes of death in the Western world. The similarity of the mouse heart to the human heart has made it an ideal model for testing novel therapeutic strategies.
In vivo magnetic resonance imaging (MRI) gives excellent views of the heart noninvasively with clear anatomical detail, which can be used for accurate functional assessment. Contrast agents can provide basic measures of tissue viability but these are nonspecific. Positron emission tomography (PET) is a complementary technique that is highly specific for molecular imaging, but lacks the anatomical detail of MRI. Used together, these techniques offer a sensitive, specific and quantitative tool for the assessment of the heart in disease and recovery following treatment.
In this paper we explain how these methods are carried out in mouse models of acute myocardial infarction. The procedures described here were designed for the assessment of putative protective drug treatments. We used MRI to measure systolic function and infarct size with late gadolinium enhancement, and PET with fluorodeoxyglucose (FDG) to assess metabolic function in the infarcted region. The paper focuses on practical aspects such as slice planning, accurate gating, drug delivery, segmentation of images, and multimodal coregistration. The methods presented here achieve good repeatability and accuracy maintaining a high throughput.

We describe how to perform MRI and PET imaging of the mouse heart. The protocol is tailored to assess treatment efficacy in models of myocardial infarction and heart failure.

Myocardial infarction is one of the leading causes of death in the Western world. The similarity of the mouse heart to the human heart has made it an ...

Implantation of Total Artificial Heart in Congenital Heart Disease

In patients with end-stage heart failure (HF), a total artificial heart (TAH) may be implanted as a bridge to cardiac transplant. However, in congenital heart disease (CHD), the malformed heart presents a challenge to TAH implantation. 
In the case presented here, a 17 year-old patient with congenital transposition of the great arteries (CCTGA) experienced progressively worsening HF due to his congenital condition. He was hospitalized multiple times and received an implantable cardioverter defibrillator (ICD). However, his condition soon deteriorated to end-stage HF with multisystem organ failure. 
Due to the patient's grave clinical condition and the presence of complex cardiac lesions, the decision was made to proceed with a TAH. The abnormal arrangement of the patient's ventricles and great arteries required modifications to the TAH during implantation.
With the TAH in place, the patient was able to return home and regain strength and physical well-being while awaiting a donor heart. He was successfully bridged to heart transplantation 5 months after receiving the device. This report highlights the TAH is feasible even in patients with structurally abnormal hearts, with technical modification.

This is a case report of a patient with congenitally corrected transposition of the great arteries (CCTGA) who received a total artificial heart (TAH) as a bridge to heart transplant. The TAH was successfully implanted with modifications to accommodate the patient's congenitally malformed heart.

In patients with end-stage heart failure (HF), a total artificial heart (TAH) may be implanted as a bridge to cardiac transplant. However, in congenital ...

Use of Two Intracorporeal Ventricular Assist Devices As a Total Artificial Heart

Mechanical circulatory support (MCS) has been introduced as a viable alternative to heart transplantation primarily through the use of intracorporeal ventricular assist devices (VADs) for support of the left ventricle. However, certain clinical scenarios warrant biventricular mechanical support. One strategy for some patients is the excision of both ventricles and the implantation of two VAD pumps as a total artificial heart (TAH). This has recently been made possible by the improvements in device design and the small profile of centrifugal devices. This TAH approach remains experimental with many important challenges such as the device settings to balance the right and left circulation, the orientation of the devices and the outflow graft with their influence on hemolysis and stability, and the outcome of chronic support using such an orientation. This protocol aims to provide a reproducible approach for total artificial heart replacement with two intracorporeal centrifugal VADs in a cow model.

Here, we present a protocol using two centrifugal pumps as a total artificial heart replacement.

Mechanical circulatory support (MCS) has been introduced as a viable alternative to heart transplantation primarily through the use of intracorporeal ...

In Vitro Thrombosis Test for Ventricular Assist Devices

The risk of thrombosis remains a significant concern in the development and clinical use of ventricular assist devices (VADs). Traditional assessments of VAD thrombogenicity, primarily through animal studies, are costly and time-consuming, raise ethical concerns, and ultimately may not accurately reflect human outcomes. To address these limitations, we developed an aggressive in vitro testing protocol designed to provoke thrombosis and identify potential high-risk areas within the blood flow path. This protocol, motivated by the work of Maruyama et al., employs a modified anticoagulation strategy and utilizes readily available components, making it accessible to most laboratories conducting in vitro blood testing of VADs. We demonstrated the utility of this method through iterative testing and refinement of a miniature magnetically levitated pediatric VAD (PediaFlow PF5). The method has been effective in identifying thrombogenic hotspots caused by design and manufacturing flaws in early VAD prototypes, enabling targeted improvements before advancing to animal studies. Despite its limitations, including the absence of pulsatile flow and the influence of donor blood characteristics, this protocol serves as a practical tool for early-stage VAD development and risk mitigation.

We present a benchtop protocol to induce thrombosis in ventricular assist devices (VAD) within a recirculating test platform. This method serves to identify thrombogenic hotspots in the blood flow path and can help improve thromboresistance ahead of preclinical testing in animal models.

The risk of thrombosis remains a significant concern in the development and clinical use of ventricular assist devices (VADs). Traditional assessments of ...

Bioengineering

The Intra-Aortic Balloon Pump

Cardiogenic shock remains one of the most challenging clinical syndromes in modern medicine. Mechanical support is being increasingly used in the management of cardiogenic shock. Intra-aortic balloon pump (IABP) is one of the earliest and most widely used types of mechanical circulatory support. The device acts by external counterpulsation and uses systolic unloading and diastolic augmentation of aortic pressure to improve hemodynamics. Although IABP provides less hemodynamic support when compared with newer mechanical circulatory support devices, it can still be the mechanical support device of choice in appropriate situations because of its relative simplicity of insertion and removal, need for smaller size vascular access and better safety profile. In this review, we discuss the equipment, procedural and technical aspects, hemodynamic effects, indications, evidence, current status and recent advances in the use of IABP in cardiogenic shock.

We describe the steps for the percutaneous implantation of the intra-aortic balloon pump (IABP), a mechanical circulatory support device. It acts by counterpulsation, inflating at the onset of diastole, augmenting diastolic aortic pressure and improving coronary blood flow and systemic perfusion, and deflating before systole, reducing left ventricular afterload.

Cardiogenic shock remains one of the most challenging clinical syndromes in modern medicine. Mechanical support is being increasingly used in the ...

Use of a Percutaneous Ventricular Assist Device/Left Atrium to Femoral Artery Bypass System for Cardiogenic Shock

The left atrial to femoral artery bypass (LAFAB) system is a mechanical circulatory support (MCS) device used in cardiogenic shock (CS) that bypasses the left ventricle by draining blood from the left atrium (LA) and returning it to the systemic arterial circulation via the femoral artery. It can provide flows ranging from 2.5-5 L/min depending on the size of the cannula. Here, we discuss the mechanism of action of LAFAB, available clinical data, indications for its use in cardiogenic shock, steps of implantation, post-procedural care, and complications associated with the use of this device and their management.
We also provide a brief video of the procedural component of device therapy, including the pre-placement preparation, percutaneous placement of the device via transseptal puncture under echocardiographic guidance and the post-operative management of device parameters.

The following article describes the stepwise procedure for placement of a device (e.g., Tandemheart) in cardiogenic shock (CS) that is a percutaneous left ventricular assist device (pLVAD) and a left atrial to femoral artery bypass (LAFAB) system that bypasses and supports the left ventricle (LV) in CS.

The left atrial to femoral artery bypass (LAFAB) system is a mechanical circulatory support (MCS) device used in cardiogenic shock (CS) that bypasses the ...

Insertion, Maintenance, and Removal of the Percutaneous Dual Lumen Cannula Right Ventricular Assist Device

Right ventricular (RV) shock, classically characterized by elevated central venous pressure (CVP) with&#160;normal to low pulmonary artery (PA) and pulmonary capillary wedge pressures (PCWP),&#160;remains a significant cause of morbidity and mortality worldwide if left untreated.&#160;Therapies for the treatment of RV shock range&#160;from medical management to durable or percutaneous mechanical circulatory support (MCS). A unique MCS device, a percutaneous right ventricular assist device (pRVAD), approved for use by the Food and Drug Administration (FDA) in 2014, works by temporarily off-loading the RV through a single, dual lumen catheter with extracorporeal mechanical support and is capable of shunting blood from the right atrium (RA) to the main PA. Although initially approved as venous-venous extracorporeal membrane oxygenation (VV-ECMO) device, this work will focus on the use of RV support, as ambulatory VV-ECMO strategies have been described previously. The catheter is most commonly inserted through the right internal jugular (IJ) vein into the PA and connected to an external pump, allowing flow up to 5 L/min. This device may be an attractive choice for the treatment of RV shock due to its percutaneous, minimally invasive insertion and removal and its ability to allow patient ambulation while the device is in place. This protocol discusses in detail the equipment, hemodynamic effects, indications, contraindications, complications, currently available research in the literature, and step-by-step instructions on how to implant, manage, and extract the device, along with the guidance on use and troubleshooting complications from one of the largest, single-center experiences with the device.

The present protocol provides a detailed description of a percutaneous dual lumen right ventricular assist device and illustrates step-by-step instructions on the safe implanting, managing, and removing the device. Guidance on its use and troubleshooting complications from one of the most significant single-center experiences is also included.

Right ventricular (RV) shock, classically characterized by elevated central venous pressure (CVP) with&#160;normal to low pulmonary artery (PA) and ...

Veno-Arterial Extracorporeal Membrane Oxygenation for Cardiogenic Shock

Cardiogenic shock (CS) is a clinical condition characterized by inadequate tissue perfusion in the setting of low cardiac output. CS is the leading cause of death following acute myocardial infarction (AMI). Several temporary mechanical support devices are available for hemodynamic support in CS until clinical recovery ensues or until more definitive surgical procedures have been performed. Veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) has evolved as a powerful treatment option for short-term circulatory support in refractory CS. In the absence of randomized clinical trials, the utilization of ECMO has been guided by clinical experience and based on data from registries and observational studies. Survival to hospital discharge with the use of VA-ECMO ranges from 28-67%. The initiation of ECMO requires venous and arterial cannulation, which can be performed either percutaneously or by surgical cutdown. Components of an ECMO circuit include an inflow cannula that draws blood from the venous system, a pump, an oxygenator, and an outflow cannula that returns blood to the arterial system. Management considerations post ECMO initiation include systemic anticoagulation to prevent thrombosis, left ventricle unloading strategies to augment myocardial recovery, prevention of limb ischemia with a distal perfusion catheter in cases of femoral arterial cannulation, and prevention of other complications such as hemolysis, air embolism, and Harlequin syndrome. ECMO is contraindicated in patients with uncontrolled bleeding, unrepaired aortic dissection, severe aortic insufficiency, and in futile cases such as severe neurological injury or metastatic malignancies. A multi-disciplinary shock team approach is recommended while considering patients for ECMO. Ongoing studies will evaluate whether the addition of routine ECMO improves survival in AMI patients with CS who undergo revascularization.

The following article highlights various steps involved in initiating and maintaining veno-arterial extracorporeal membrane oxygenation in patients with cardiogenic shock.

Cardiogenic shock (CS) is a clinical condition characterized by inadequate tissue perfusion in the setting of low cardiac output. CS is the leading cause ...

Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock

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