This protocol follows the guidelines of institutional human research ethics committee.
1. Pre-insertion preparation
NOTE: The IABP is preferably inserted in the cardiac catheterization lab under fluoroscopic guidance. Bedside placement can be considered in very critical clinical situations.
<ol>
	<li>Begin by preparing the catheterization laboratory for the procedure. Prepare sterile drapes and chlorhexidine or povidone iodine, IABP control unit, IABP catheter, ultrasound for arterial access, 1% lidocaine for local anesthesia, micropuncture needle and wire, micropuncture sheath, 7-8.5 F arterial access sheath for the IABP depending on the balloon size or IABP manufacturer, sutures and sterile dressing.</li>
	<li>Prepare and drape the patient in the usual sterile fashion with a plan to access the femoral artery. 
	&#8203;NOTE: IABP can also be inserted through the axillary artery but this often requires a surgical cut down.</li>
	<li>Have the patient lay down flat on his or her back. Administer moderate conscious sedation if the clinical scenario permits, by infiltrating the groin access site liberally with 1% Lidocaine.</li>
	<li>Prepare the IABP catheter. Use a 50 mL syringe to apply a vacuum and completely deflate the balloon, using the one-way valve at the catheter hub.</li>
	<li>Remove the stylet in the catheter and manually flush the inner lumen with 3-5 mL of saline.</li>
</ol>
2. Insertion of the IABP
<ol>
	<li>Obtain arterial access using the Seldinger technique18. Use ultrasound guided vascular access to improve first pass success and minimize vascular complications.</li>
	<li>Insert a micropuncture needle at a 45&#730; angle and insert the introducer wire once blood return is obtained.</li>
	<li>Insert the micropuncture sheath.</li>
	<li>Exchange the micropuncture sheath for a larger IABP sheath. The sheath size varies by manufacturers and balloon size but is usually 7-8.5 F. 
	NOTE: There are two methods to introduce and advance the IABP catheter. The catheter can either be backloaded with a wire or can be advanced over a wire.</li>
	<li>Advance the IABP catheter through the sheath using short strokes until correct placement is achieved. The optimal balloon position is where the tip is situated distal to the left subclavian artery take off. This is often not easy to identify, and hence, use the carina of the trachea as a landmark, ensuring that the proximal end is above the renal arteries.</li>
	<li>Confirm position by fluoroscopy. Secure the catheter in place either by using sutures or manufacturer provided locking plates and apply sterile dressing. 
	&#8203;CAUTION: Incorrect balloon position results in reduced diastolic augmentation or vascular complications due to direct endovascular injury.</li>
</ol>
3. Switching on and setting up the IABP
<ol>
	<li>Remove the guidewire and aspirate 3 mL of blood from the inner lumen. Flush the inner lumen with 3-5 mL of saline.</li>
	<li>Attach a standard arterial pressure monitoring tubing to the catheter hub. Remove the one-way valve from the catheter and attach the catheter hub to the console using the provided extension catheter.</li>
	<li>Turn IABP On, then open the gas tank. Connect the ECG cable to the console. Connect the fiber optic or pressure cable to the console (depending on the manufacturer).</li>
	<li>Press the Start key on the console. This automatically purges and fills the balloon, calibrates, selects an appropriate ECG lead and trigger, and automatically sets the inflation and deflation timing.
	<ol>
		<li>Select an appropriate operation mode - Automatic, Semi-automatic or Manual depending on the clinical scenario.</li>
		<li>Select a trigger source. The IABP uses a trigger to identify the beginning of the next cardiac cycle. It deflates the balloon when it recognizes a trigger event. Trigger can be either ECG (R wave) or pressure (systolic upstroke).</li>
		<li>Observe the pressure changes on the IABP console by setting a 1:2 frequency. Confirm that the assisted systolic pressure is lower than unassisted one, there is decrease in assisted end-diastolic pressure and that diastolic augmentation is above the systolic pressure - all of which is associated with optimal IABP support (Figure 1).</li>
		<li>Set appropriate IABP frequency which can be 1:1, 1:2 or 1:3. This represents the frequency of balloon inflation with each trigger.</li>
		<li>Confirm that the IABP timing is appropriate. 
		NOTE: An ideal IABP timing consists of the following: a) Inflation occurring at the dicrotic notch which appears as a sharp &#34;V&#34;. Ideally, the diastolic augmentation rises above systole, and b) Deflation occurring just prior to the next systole (Figure 1).</li>
	</ol>
	</li>
	<li>Use a continuous flush through the inner lumen (usually 3 mL/h). 
	NOTE: The patient and the IABP console are now ready to be transported.</li>
	<li>Use systemic anticoagulation to reduce the risk of arterial thromboembolism. 
	&#8203;NOTE: This is institution dependent and some centers do not use systemic anticoagulation for an IABP frequency of 1:119.</li>
</ol>
4. Assessment of the patient after placement of IABP
<ol>
	<li>Check distal pulses. If the left radial pulse is weak, verify the position of the balloon to make sure that it is not occluding the left subclavian artery. If no distal pulses are detected in the lower limb, consider removing the IABP and possibly alternate access.</li>
	<li>Check the insertion site for any bleeding or hematoma.</li>
	<li>Monitor urine output. If there is a drop in urine output or if there is a concern for hematuria, recheck balloon position to confirm that the balloon lies above the level of the renal arteries.</li>
	<li>If there is blood in the IABP tubing, suspect balloon rupture. Immediately stop the IABP (this is usually done automatically) and remove the catheter.</li>
	<li>Obtain a chest X-ray daily to verify optimal device positioning. Also change the sterile dressing daily to reduce the chances of infection.</li>
</ol>
5. Removal of IABP
<ol>
	<li>Stop systemic anticoagulation and set IABP to 1:1.</li>
	<li>Palpate the femoral pulse and check the baseline distal perfusion by obtaining a Doppler of the pedal pulse.</li>
	<li>Check the activated clotting time. It should ideally be less than 150-160 seconds.</li>
	<li>Remove sutures.</li>
	<li>Once ready to pull, press the Stop button on the IABP console screen.</li>
	<li>Pull the IABP until resistance is met against the sheath.</li>
	<li>Pull the sheath and IABP as a unit.</li>
	<li>Hold manual pressure over the femoral artery for 20-30 minutes or until bleeding stops.</li>
	<li>Reassess distal pulses with Doppler. 
	NOTE: Manual pressure has been mentioned here in the protocol because it is universal. However, there are numerous other methods apart from manual pressure to help achieve femoral arterial hemostasis. These are institution dependent and include but are not limited to: external compression devices like FemoStop, vascular closure devices like Angioseal and Perclose ProGlide Suture-Mediated Closure System. The above-mentioned protocol was partly developed by using official device information guides and manuals across various manufactures of IABP.</li>
</ol>

<ol>
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Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock.</a> New England Journal of Medicine. 341 (9), 625-634 (1999).</li><li>Thiele, H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Intraaortic+Balloon+Support+for+Myocardial+Infarction+with+Cardiogenic+Shock.">Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock.</a> New England Journal of Medicine. 367 (14), 1287-1296 (2012).</li><li>Berg, D. D., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Epidemiology+of+Shock+in+Contemporary+Cardiac+Intensive+Care+Units.">Epidemiology of Shock in Contemporary Cardiac Intensive Care Units.</a> Circulation Cardiovascular Quality and Outcomes. 12 (3), 005618 (2019).</li><li>Jeger, R. 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Ganesh Gajanan MD has no conflicts of interests to declare
Emmanouil S. Brilakis, MD, PhD has the following disclosures : Consulting/speaker honoraria from Abbott Vascular, American Heart Association (associate editor Circulation), Amgen, Biotronik, Boston Scientific, Cardiovascular Innovations Foundation (Board of Directors), ControlRad, CSI, Ebix, Elsevier, GE Healthcare, InfraRedx, Medtronic, Siemens, and Teleflex; research support from Regeneron and Siemens. Shareholder: MHI Ventures.
Jolanta M. Siller-Matula, MD, PhD has the following disclosures: Lecture or consultant fees from AstraZeneca, Daiichi-Sankyo, Eli Lilly, Bayer and research grant from Roche Diagnostics;
Ronald L. Zolty, MD, PhD has the following disclosures: Consultant for Actelion, Bayer, United Therapeutics and Alnhylam
Poonam Velagapudi MD has no conflicts of interests to declare.

Mechanical circulatory support is a rapidly evolving field. Even with the arrival of newer support devices, IABP remains the most widely used and simplest to deploy mechanical circulatory support device available currently25. In this article we describe in detail, the procedure for percutaneous insertion of IABP, the indications, evidence, troubleshooting and complications. Despite conflicting evidence regarding the use of IABP in AMI-related cardiogenic shock, it remains the most widely used form...

Cardiogenic shock is a clinical condition characterized by decreased end organ perfusion due to severe cardiac dysfunction. The most widely accepted definition of cardiogenic shock is based on the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock trial (SHOCK)1 and Intra-aortic Balloon Support for Myocardial Infarction with Cardiogenic Shock (IABP-SHOCK-II) trial2 and includes the following parameters:
1. Systolic blood pressure &#60;90 mm Hg for &#8805;30 min or vasopressor and/or mechanical support to maintain SBP &#8805;90 mm Hg
2. Evidence of end-organ hypoperfusion (urine output &#60;30 mL/h or cool extremities)
3. Hemodynamic criteria: cardiac index &#8804;2.2 L/min/m2 and pulmonary capillary wedge pressure &#8805;15 mm Hg
Acute myocardial infarction (AMI) is the most common cause of cardiogenic shock accounting for approximately 30% of cases3. Despite advances in the treatment of patients with AMI with early invasive revascularization, the mortality of cardiogenic shock remains high4. The mechanism of diastolic augmentation showing improvement in coronary perfusion and decreased left ventricular work was first demonstrated in 19585. Subsequently, in 1962 the first experimental prototype of IABP was developed6. Six years later, Kantrowitz et al.7 presented the first clinical experience of IABP use in four patients with AMI and cardiogenic shock unresponsive to medical therapy.
The IABP&#39;s mechanism of action involves inflation of the balloon during diastole and deflation during systole. This results in two important hemodynamic consequences: When the balloon inflates in diastole, the blood in the aorta is displaced proximally towards the aortic root thereby increasing coronary blood flow. When the balloon deflates in systole, it causes a vacuum or suction effect decreasing afterload and augmenting cardiac output8. The hemodynamic changes caused by IABP are listed below9 (Table 1):
1.Increase in aortic diastolic pressure
2.Decrease in systolic blood pressure
3.Increase in mean arterial pressure
4.Decrease in pulmonary capillary wedge pressure
5.Increase in cardiac output by ~20%
6.Increase in coronary blood flow10
The major indications of IABP are cardiogenic shock (due to AMI and other causes like ischemic and non-ischemic cardiomyopathy, myocarditis), mechanical complications of AMI like ventricular septal defect or severe mitral regurgitation, mechanical support during high risk percutaneous coronary interventions11, as a bridge to coronary artery bypass surgery in patients with critical CAD, inability to wean off cardiopulmonary bypass and as a bridge to decision or advanced therapies like left ventricular assist devices (LVAD) or cardiac transplantation in end stage heart failure12,13,14,15. Contraindications to use of IABP include moderate or severe aortic regurgitation which can worsen with counterpulsation, severe peripheral vascular disease which would preclude optimal arterial access and placement of the device and aortic pathologies like dissection12,15.
The IABP device consists of a console to control the unit and a vascular catheter with the balloon.
The console includes the following four components:
a) Monitor unit which helps to process and determine a trigger signal for the balloon. The signal can be either electrocardiographic (ECG) triggering or pressure signal triggering;
b) Control unit: Processes the trigger signal and activates the gas valve to help with inflation or deflation;
c) A gas cylinder that contains helium. Carbon dioxide is an alternative but is less preferred than helium. Helium has a lower density and provides better balloon inflation characteristics with more rapid inflation and deflation16;
d) A valve unit which helps with gas delivery.
The IABP (balloon) catheter is a 7-8.5 F vascular catheter with distance markings. The catheter has a polyethylene balloon mounted at the tip. The balloon size can vary from 20-50 mL. The ideal balloon has a length to cover from the left subclavian artery to the celiac artery take off, the inflated diameter measuring 90 to 95% of that of the descending aorta. The most commonly used balloon size in adult patients (height 5&#39;4&#8243;/162 cm to 6&#39;/182 cm) is 40 mL. A 50 mL balloon is used for patients &#62;6&#39;/182 cm and 34 cm balloon for 5&#39;/152 cm to 5&#39;4&#8243;/162 cm tall patients12,17 (Table 2).

<table border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<tbody>
		<tr>
			<td>IABP catheter and console</td>
			<td>Getinge</td>
			<td>Sensation Plus</td>
			<td></td>
		</tr>
		<tr>
			<td>Micropuncture Introducer Set</td>
			<td>Cook Medical</td>
			<td>G48006</td>
			<td></td>
		</tr>
		<tr>
			<td>Sterile drapes</td>
			<td>Haylard</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td>Ultrasound</td>
			<td>GE</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td>Lidocaine</td>
			<td>Pfizer</td>
			<td></td>
			<td></td>
		</tr>
	</tbody>
</table>

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.

Despite being used for many decades now, the evidence on IABP use has been controversial. Routine use of IABP in patients with AMI and cardiogenic shock is not recommended. The previous guidelines of the American Heart Association/American College of Cardiology (AHA/ACC) and the European Society of Cardiology (ESC) strongly recommended the use of the IABP in patients with AMI-associated cardiogenic shock (Class I B and Class I C) on the basis of pathophysiological considerations, non-randomized trials and registry data. ...

Watch this Scientific Journal Video about The Intra-Aortic Balloon Pump at JoVE.com

The Intra-Aortic Balloon Pump

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 ...

Research

JoVE Journal

Medicine

20.2K Views.  University of Nebraska Medical Center. 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.

Video: The Intra-Aortic Balloon Pump

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

The carotid artery balloon injury model in rats has been well established for over two decades. It remains an important method to study the molecular and cellular mechanisms involved in vascular smooth muscle dedifferentiation, neointima formation and vascular remodeling. Male Sprague-Dawley rats are the most frequently employed animals for this model. Female rats are not preferred as female hormones are protective against vascular diseases and thus introduce a variation into this procedure. The left carotid is typically injured with the right carotid serving as a negative control. Left carotid injury is caused by the inflated balloon that denudes the endothelium and distends the vessel wall. Following injury, potential therapeutic strategies such as the use of pharmacological compounds and either gene or shRNA transfer can be evaluated. Typically for gene or shRNA transfer, the injured section of the vessel lumen is locally transduced for 30 min with viral particles encoding either a protein or shRNA for delivery and expression in the injured vessel wall. Neointimal thickening representing proliferative vascular smooth muscle cells usually peaks at 2 weeks after injury. Vessels are mostly harvested at this time point for cellular and molecular analysis of cell signaling pathways as well as gene and protein expression. Vessels can also be harvested at earlier time points to determine the onset of expression and/or activation of a specific protein or pathway, depending on the experimental aims intended. Vessels can be characterized and evaluated using histological staining, immunohistochemistry, protein/mRNA assays, and activity assays. The intact right carotid artery from the same animal is an ideal internal control. Injury-induced changes in molecular and cellular parameters can be evaluated by comparing the injured artery to the internal right control artery. Likewise, therapeutic modalities can be evaluated by comparing the injured and treated artery to the control injured only artery.

This protocol uses a balloon catheter to cause an intraluminal injury on the rat carotid artery and henceforth elicit neointimal hyperplasia. This is a well-established model for studying the mechanisms of vascular remodeling in response to injury. It is also widely used to determine the validity of potential therapeutic approaches.

The carotid artery balloon injury model in rats has been well established for over two decades. It remains an important method to study the molecular and ...

Evaluation of a Novel Laser-assisted Coronary Anastomotic Connector - the Trinity Clip - in a Porcine Off-pump Bypass Model

To simplify and facilitate beating heart (i.e., off-pump), minimally invasive coronary artery bypass surgery, a new coronary anastomotic connector, the Trinity Clip, is developed based on the excimer laser-assisted nonocclusive anastomosis technique. The Trinity Clip connector enables simplified, sutureless, and nonocclusive connection of the graft to the coronary artery, and an excimer laser catheter laser-punches the opening of the anastomosis. Consequently, owing to the complete nonocclusive anastomosis construction, coronary conditioning (i.e., occluding or shunting) is not necessary, in contrast to the conventional anastomotic technique, hence simplifying the off-pump bypass procedure. Prior to clinical application in coronary artery bypass grafting, the safety and quality of this novel connector will be evaluated in a long-term experimental porcine off-pump coronary artery bypass (OPCAB) study. In this paper, we describe how to evaluate the coronary anastomosis in the porcine OPCAB model using various techniques to assess its quality. Representative results are summarized and visually demonstrated.

This paper describes a novel nonocclusive coronary anastomotic connector in a porcine off-pump coronary artery bypass (OPCAB) model. This easy-to-use coronary connector has intrinsic potential to facilitate minimally invasive OPCAB surgery.

To simplify and facilitate beating heart (i.e., off-pump), minimally invasive coronary artery bypass surgery, a new coronary anastomotic connector, the ...

A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics

The rat carotid balloon injury is a well-established surgical model that has been used to study arterial remodeling and vascular cell proliferation. It is also a valuable model system to test, and to evaluate therapeutics and drugs that negate maladaptive remodeling in the vessel. The injury, or barotrauma, in the vessel lumen caused by an inflated balloon via an inserted catheter induces subsequent neointimal growth, often leading to hyperplasia or thickening of the vessel wall that narrows, or obstructs the lumen. The method described here is sufficiently sensitive, and the results can be obtained in relatively short time (2 weeks after the surgery). The efficacy of the drug or therapeutic against the induced-remodeling can be evaluated either by the post-mortem pathological and histomorphological analysis, or by ultrasound sonography in live animals. In addition, this model system has also been used to determine the therapeutic window or the time course of the administered drug. These studies can leadto the development of a better administrative strategy and a better therapeutic outcome. The procedure described here provides a tool for translational studies that bring drug and therapeutic candidates from bench research to clinical applications.

The rat carotid balloon injury model described below allows researchers to evaluate drugs or therapeutics that negate injury-induced arterial hyperplasia. Detailed pre-surgical preparation, surgical procedure, and post-surgical cares of the animal are described.

The rat carotid balloon injury is a well-established surgical model that has been used to study arterial remodeling and vascular cell proliferation. It is ...

Fabrication of Small Caliber Stent-grafts Using Electrospinning and Balloon Expandable Bare Metal Stents

Stent-grafts are widely used for the treatment of various conditions such as aortic lesions, aneurysms, emboli due to coronary intervention procedures and perforations in vasculature. Such stent-grafts are manufactured by covering a stent with a polymer membrane. An ideal stent-graft should have a biocompatible stent covered by a porous, thromboresistant, and biocompatible polymer membrane which mimics the extracellular matrix thereby promoting injury site healing. The goal of this protocol is to manufacture a small caliber stent-graft by encapsulating a balloon expandable stent within two layers of electrospun polyurethane nanofibers. Electrospinning of polyurethane has been shown to assist in healing by mimicking native extracellular matrix, thereby promoting endothelialization. Electrospinning polyurethane nanofibers on a slowly rotating mandrel enabled us to precisely control the thickness of the nanofibrous membrane, which is essential to achieve a small caliber balloon expandable stent-graft. Mechanical validation by crimping and expansion of the stent-graft has shown that the nanofibrous polyurethane membrane is sufficiently flexible to crimp and expand while staying patent without showing any signs of tearing or delamination. Furthermore, stent-grafts fabricated using the methods described here are capable of being implanted using a coronary intervention procedure using standard size guide catheters.

In the protocol, we present a method to manufacture a small caliber stent-graft by sandwiching a balloon expandable stent between two electrospun nanofibrous polyurethane layers.

Stent-grafts are widely used for the treatment of various conditions such as aortic lesions, aneurysms, emboli due to coronary intervention procedures and ...

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury

Acute coronary syndrome resulting from coronary occlusion following atherosclerotic plaque development and rupture is the leading cause of death in the industrialized world. New Zealand White (NZW) rabbits are widely used as an animal model for the study of atherosclerosis. They develop spontaneous lesions when fed with atherogenic diet; however, this requires long time of 4 - 8 months. To further enhance and accelerate atherogenesis, a combination of atherogenic diet and mechanical endothelial injury is often employed. The presented procedure for inducing atherosclerotic plaques in rabbits uses a balloon catheter to disrupt the endothelium in the left iliac artery of NZW rabbits fed with atherogenic diet. Such mechanical damage caused by the balloon catheter induces a chain of inflammatory reactions initiating neointimal lipid accumulation in a time dependent fashion. Atherosclerotic plaque following balloon injury show neointimal thickening with extensive lipid infiltration, high smooth muscle cell content and presence of macrophage derived foam cells. This technique is simple, reproducible and produces plaque of controlled length within the iliac artery. The whole procedure is completed within 20 - 30 min. The procedure is safe with low mortality and also offers high success in obtaining substantial intimal lesions. The procedure of balloon catheter induced arterial injury results in atherosclerosis within two weeks. This model can be used for investigating the disease pathology, diagnostic imaging and to evaluate new therapeutic strategies.

Animal models of atherosclerosis are essential to understand the mechanism and to investigate newer approaches to prevent plaque development or rupture, a leading cause of death in the industrialized world. This protocol uses a combination of balloon injury and cholesterol rich diet to induce atherosclerotic plaques in rabbit iliac artery.

Acute coronary syndrome resulting from coronary occlusion following atherosclerotic plaque development and rupture is the leading cause of death in the ...

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

The use of animal models is essential for a better understanding of MH, one major cause for arterial stenosis.In this article, we demonstrate a murine balloon denudation model, which is comparable with established vessel injury models in large animals. The aorta denudation model with balloon catheters mimics the clinical setting and leads to comparable pathobiological and physiological changes. Briefly, after performing a horizontal incision in the aorta abdominalis, a balloon catheter will be inserted into the vessel, inflated, and introduced retrogradely. Inflation of the balloon will lead to intima injury and overdistension of the vessel. After removing the catheter, the aortic incision will be closed with single stiches. The model shown in this article is reproducible, easy to perform, and can be established quickly and reliably. It is especially suitable for evaluating expensive experimental therapeutic agents, which can be applied in an economical fashion. By using different knockout-mouse strains, the impact of different genes on MH development can be assessed.

This article demonstrates a murine model to study the development of myointimal hyperplasia (MH) after aortic balloon injury.

The use of animal models is essential for a better understanding of MH, one major cause for arterial stenosis.In this article, we demonstrate a murine ...

Harvest of Endothelial Cells from the Balloon Tips of Swan-Ganz Catheters after Right Heart Catheterization

A variety of pathologies lead to pulmonary hypertension (PH), which is defined as a mean pulmonary artery pressure exceeding 25 mmHg at rest. To further diagnose and manage PH, patients undergo repeated right heart catheterizations (RHC) wherein a Swan-Ganz catheter is advanced into a branch of the pulmonary artery and a balloon is inflated to wedge the catheter tip. This article illustrates a protocol whereby pulmonary artery endothelial cells (PAECs) may be harvested from the balloon tips of Swan-Ganz catheters after RHC, and purified with an anti- CD146 affinity column technique to purify putative PAECs. These cells might be used to provide an in situ snapshot of the biological state of the pulmonary vasculature endothelium to complement hemodynamic measurements obtained during RHC. Harvested and purified PAECs may be used for either cell culture or for subsequent analytical assays such as flow cytometery.

This protocol describes the removal and purification of pulmonary artery endothelial cells (PAECs) that adhere to the balloon tips of Swan-Ganz catheters while they are wedged in the pulmonary artery during right heart catheterization and remain adherent to the deflated balloon following removal from the patient's body.

A variety of pathologies lead to pulmonary hypertension (PH), which is defined as a mean pulmonary artery pressure exceeding 25 mmHg at rest. To further ...

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Isoproterenol (ISO), is a non-selective beta-adrenergic agonist, that is used widely to induce cardiac injury in mice. While the acute model mimics stress-induced cardiomyopathy, the chronic model, administered through an osmotic pump, mimics advanced heart failure in humans. The purpose of the described protocol is to create the chronic ISO-induced heart failure model in mice using an implanted mini-pump. This protocol has been used to induce heart failure in 100+ strains of inbred mice. Techniques on surgical pump implantation are described in detail and may be relevant to anyone interested in creating a heart failure model in mice. In addition, the weekly cardiac remodeling changes based on echocardiographic parameters for each strain and expected time to model development are presented. In summary, the method is simple and reproducible. Continuous ISO administered via the implanted mini-pump over 3 to 4 weeks is sufficient to induce cardiac remodeling. Finally, the success for ISO model creation may be assessed in vivo by serial echocardiography demonstrating hypertrophy, ventricular dilation, and dysfunction.

The chronic administration of isoproterenol via an implanted osmotic pump has been used widely to mimic advanced heart failure in mice. Here, we describe detailed methods in surgical mini-pump implantation for the continuous isoproterenol administration over 3 weeks, as well as, echocardiographic assessment for the successful model creation.

Isoproterenol (ISO), is a non-selective beta-adrenergic agonist, that is used widely to induce cardiac injury in mice. While the acute model mimics ...

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application

Cardiovascular disease remains the leading cause of death and disability worldwide, in part due to atherosclerosis. Atherosclerotic plaque narrows the luminal surface area in arteries thereby reducing adequate blood flow to organs and distal tissues. Clinically, revascularization procedures such as balloon angioplasty with or without stent placement aim to restore blood flow. Although these procedures reestablish blood flow by reducing plaque burden, they damage the vessel wall, which initiates the arterial healing response. The prolonged healing response causes arterial restenosis, or re-narrowing, ultimately limiting the long-term success of these revascularization procedures. Therefore, preclinical animal models are integral for analyzing the pathophysiological mechanisms driving restenosis, and provide the opportunity to test novel therapeutic strategies. Murine models are cheaper and easier to operate on than large animal models. Balloon or wire injury are the two commonly accepted injury modalities used in murine models. Balloon injury models in particular mimic the clinical angioplasty procedure and cause adequate damage to the artery for the development of restenosis. Herein we describe the surgical details for performing and histologically analyzing the modified, pressure-controlled rat carotid artery balloon injury model. Additionally, this protocol highlights how local periadventitial application of therapeutics can be used to inhibit neointimal hyperplasia. Lastly, we present light sheet fluorescence microscopy as a novel approach for imaging and visualizing the arterial injury in three-dimensions.

The rat carotid artery balloon injury mimics the clinical angioplasty procedure performed to restore blood flow in atherosclerotic vessels. This model induces the arterial injury response by distending the arterial wall, and denuding the intimal layer of endothelial cells, ultimately causing remodeling and an intimal hyperplastic response.

Cardiovascular disease remains the leading cause of death and disability worldwide, in part due to atherosclerosis. Atherosclerotic plaque narrows the ...

Complete and Partial Resuscitative Endovascular Balloon Occlusion of the Aorta for Hemorrhagic Shock

Resuscitative endovascular balloon occlusion of the aorta (REBOA) devices grew out of a military-civilian partnership to develop new capabilities for hemorrhage control. With the advent of purpose-built devices, REBOA has become increasingly common in civilian trauma and acute care settings. Currently available REBOA catheters were designed as complete aortic occlusion devices. However, the therapeutic window for complete aortic occlusion is time-limited due to ischemia-reperfusion injury. The partial procedure allows blood flow past the level of occlusion while maintaining targeted proximal pressure, which has been shown to reduce distal ischemia and adjunctive resuscitation requirements in preclinical studies with prolonged occlusion times as compared to traditional complete occlusion.
pREBOA-PRO is the first catheter designed to enable partial and complete aortic occlusion and is currently in limited market release at seven Level I trauma centers in North America. This paper will focus on procedural considerations for REBOA, including patient selection criteria and a comparison of complete and partial aortic occlusion in a simulator, along with highlighting critical steps to improve clinical outcomes. Additionally, this paper reviews a contrast-enhanced CT scan from a trauma patient that shows distal perfusion after 2 h of partial aortic occlusion using this newly designed catheter and discusses representative results from the limited market release to highlight the profound effect of technological innovation on outcomes in vascular emergencies.

A commercial catheter was designed to facilitate true partial resuscitative endovascular balloon occlusion of the aorta (REBOA) and address the complications associated with complete aortic occlusion. Initial clinical reports indicate that partial REBOA improves transition to reperfusion, reduction of distal ischemia, and extension of safe occlusion time compared to complete occlusion.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) devices grew out of a military-civilian partnership to develop new capabilities for ...