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 g...

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 border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<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 consi...

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 ...

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3.1K Views.  Loma Linda University Medical Center. 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.

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 ...

Induction of Myocardial Infarction in Adult Zebrafish Using Cryoinjury

The mammalian heart is incapable of significant regeneration following an acute injury such as myocardial infarction1. By contrast, urodele amphibians and teleost fish retain a remarkable capacity for cardiac regeneration with little or no scarring throughout life2,3. It is not known why only some non-mammalian vertebrates can recreate a complete organ from remnant tissues4,5. To understand the molecular and cellular differences between regenerative responses in different species, we need to use similar approaches for inducing acute injuries.
In mammals, the most frequently used model to study cardiac repair has been acute ischemia after a ligation of the coronary artery or tissue destruction after cryoinjury6,7. The cardiac regeneration in newts and zebrafish has been predominantly studied after a partial resection of the ventricular apex2,3. Recently, several groups have established the cryoinjury technique in adult zebrafish8-10. This method has a great potential because it allows a comparative discussion of the results obtained from the mammalian and non-mammalian species.
Here, we present a method to induce a reproducible disc-shaped infarct of the zebrafish ventricle by cryoinjury. This injury model is based on rapid freezing-thawing tissue, which results in massive cell death of about 20% of cardiomyocytes of the ventricular wall. First, a small incision was made through the chest with iridectomy scissors to access the heart. The ventricular wall was directly frozen by applying for 23-25 seconds a stainless steel cryoprobe precooled in liquid nitrogen. To stop the freezing of the heart, fish water at room temperature was dropped on the tip of the cryoprobe. The procedure is well tolerated by animals, with a survival rate of 95%.
To characterize the regenerative process, the hearts were collected and fixed at different days after cryoinjury. Subsequently, the specimen were embedded for cryosectioning. The slides with sections were processed for histological analysis, in situ hybridization and immunofluorescence. This undertaking enhances our understanding of the factors that are required for the regenerative plasticity in the zebrafish, and provide new insights into the machinery of cardiac regeneration. A conceptual and molecular understanding of heart regeneration in zebrafish will impact both developmental biology and regenerative medicine.

Zebrafish represents a valuable model to study the mechanisms of heart regeneration in vertebrates. Here, we present a protocol for induction of a heart infarct in adult zebrafish using cryoinjury. This method results in massive cell death within 20% of the ventricular wall, similar to that observed in mammalian infarcts.

The mammalian heart is incapable of significant regeneration following an acute injury such as myocardial infarction1. By contrast, urodele amphibians and ...

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 ...

Myocardial Infarction and Functional Outcome Assessment in Pigs

Introduction of newly discovered cardiovascular therapeutics into first-in-man trials depends on a strictly regulated ethical and legal roadmap. One important prerequisite is a good understanding of all safety and efficacy aspects obtained in a large animal model that validly reflect the human scenario of myocardial infarction (MI). Pigs are widely used in this regard since their cardiac size, hemodynamics, and coronary anatomy are close to that of humans. Here, we present an effective protocol for using the porcine MI model using a closed-chest coronary balloon occlusion of the left anterior descending artery (LAD), followed by reperfusion. This approach is based on 90 min of myocardial ischemia, inducing large left ventricle infarction of the anterior, septal and inferoseptal walls. Furthermore, we present protocols for various measures of outcome that provide a wide range of information on the heart, such as cardiac systolic and diastolic function, hemodynamics, coronary flow velocity, microvascular resistance, and infarct size. This protocol can be easily tailored to meet study specific requirements for the validation of novel cardioregenerative biologics at different stages (i.e. directly after the acute ischemic insult, in the subacute setting or even in the chronic MI once scar formation has been completed). This model therefore provides a useful translational tool to study MI, subsequent adverse remodeling, and the potential of novel cardioregenerative agents.

This protocol describes the porcine myocardial infarction (MI) model using a 90 min closed-chest coronary balloon occlusion of the left anterior descending artery (LAD), followed by reperfusion. Furthermore, the protocol for several outcome parameters, such as cardiac function, hemodynamics, microvascular resistance, and infarct size, are also presented.

Introduction of newly discovered cardiovascular therapeutics into first-in-man trials depends on a strictly regulated ethical and legal roadmap. One ...

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Myocardial infarction still remains the main cause of death in western countries, despite considerable progress in the stent development area in the last decades. For clarification of the underlying mechanisms and the development of new therapeutic strategies, the availability of valid animal models are mandatory. Since we need new insights into pathomechanisms of cardiovascular diseases under in vivo conditions to combat myocardial infarction, the validity of the animal model is a crucial aspect. However, protection of animals are highly relevant in this context. Therefore, we establish a minimally invasive and simple model of myocardial infarction in mice, which assures a high reproducibility and survival rate of animals. Thus, this models fulfils the requirements of the 3R principle (Replacement, Refinement and Reduction) for animal experiments and assure the scientific information needed for further developing of therapeutical strategies for cardiovascular diseases.

A highly reproducible model for myocardial infarction in mice with minimal invasive manipulations is described. The model can be easily performed, resulting in a high reproducibility and survival rate. Thus, the described model will reduce the number of required animals as requested by the 3R principle (Replacement, Refinement and Reduction).

Myocardial infarction still remains the main cause of death in western countries, despite considerable progress in the stent development area in the last ...

Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction

Mortality after acute myocardial infarction remains substantial and is associated with significant morbidity, like heart failure. Novel therapeutics are therefore required to confine cardiac damage, promote survival and reduce the disease burden of heart failure. Large animal experiments are an essential part in the translational process from experimental to clinical therapies. To optimize clinical translation, robust and representative outcome measures are mandatory. The present manuscript aims to address this need by describing the assessment of three clinically relevant outcome modalities in a pig acute myocardial infarction (AMI) model: infarct size in relation to area at risk (IS/AAR) staining, 3-dimensional transesophageal echocardiography (TEE) and admittance-based pressure-volume (PV) loops. Infarct size is the main determinant driving the transition from AMI to heart failure and can be quantified by IS/AAR staining. Echocardiography is a reliable and robust tool in the assessment of global and regional cardiac function in clinical cardiology. Here, a method for three-dimensional transesophageal echocardiography (3D-TEE) in pigs is provided. Extensive insight into cardiac performance can be obtained by admittance-based pressure-volume (PV) loops, including intrinsic parameters of myocardial function that are pre- and afterload independent. Combined with a clinically feasible experimental study protocol, these outcome measures provide researchers with essential information to determine whether novel therapeutic strategies could yield promising targets for future testing in clinical studies.

Reliable and accurate outcome assessment is the key for translation of preclinical therapies into clinical treatment. The current paper describes how to assess three clinically relevant primary outcome parameters of cardiac performance and damage in a pig acute myocardial infarction model.

Mortality after acute myocardial infarction remains substantial and is associated with significant morbidity, like heart failure. Novel therapeutics are ...

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration

Myocardial infarction induced by coronary artery ligation has been used in many animal models as a tool to study the mechanisms of cardiac repair and regeneration, and to define new targets for therapeutics. For decades, models of complete heart regeneration existed in amphibians and fish, but a mammalian counterpart was not available. The recent discovery of a postnatal window during which mice possess regenerative capabilities has led to the establishment of a mammalian model of cardiac regeneration. A surgical model of mammalian cardiac regeneration in the neonatal mouse is presented herein. Briefly, postnatal day 1 (P1) mice are anesthetized by isoflurane and placed on an ice pad to induce hypothermia. After the chest is opened, and the left anterior descending coronary artery (LAD) is visualized, a suture is placed around the LAD to inflict myocardial ischemia in the left ventricle. The surgical procedure takes 10-15 min. Visualizing the coronary artery is crucial for accurate suture placement and reproducibility. Myocardial infarction and cardiac dysfunction are confirmed by triphenyl-tetrazolium chloride (TTC) staining and echocardiography, respectively. Complete regeneration 21 days post myocardial infarction is verified by histology. This protocol can be used to as a tool to elucidate mechanisms of mammalian cardiac regeneration after myocardial infarction.

This protocol describes a highly reproducible model of cardiac regeneration by surgical induction of myocardial infarction in the left ventricle of postnatal day 1 mice. The method involves induction of hypothermic anesthesia and ligation of the left anterior descending coronary artery.

Myocardial infarction induced by coronary artery ligation has been used in many animal models as a tool to study the mechanisms of cardiac repair and ...

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 ...

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any potential therapeutic approach directed against acute left ventricular (LV) dysfunction. Current imaging modalities (e.g., echocardiography and magnetic resonance imaging) have several limitations since data on LV pressure cannot directly be measured. LV catheterization in mice undergoing coronary artery occlusion could serve as a novel method for a real-time evaluation of LV function.
At the beginning of the procedure, mice were anesthetized followed by endotracheal intubation. For LV catheterization, the right carotid artery was exposed via middle-neck incision. The catheter was introduced and placed into the LV cavity. Left thoracotomy was conducted and the left main coronary artery (LCA) was ligated. To induce reperfusion, the suture was released after 45 min. Pressure-volume data was recorded at all times.
Ligation of the LCA caused a decrease in LV systolic function as evidenced by a 30% reduction in stroke volume, LV ejection fraction (EF), and cardiac output. Maximum dP/dt as a parameter for LV contractility was also significantly reduced and diastolic function was severely impaired (minimum dP/dt -40%). Reperfusion over a period of 20 min did not lead to a complete recovery of LV function.
Real-time pressure-volume analysis served as a valid procedure for monitoring cardiac function during acute myocardial infarction in mice. Maintaining stable anesthesia and a standardized surgical approach was crucial to ensure valid results. As the early phase of acute myocardial infarction is critical for morbidity and mortality, the delineated method could be beneficial for preclinical evaluation of new strategies for cardioprotection.

Acute myocardial infarction in mice induces acute but incompletely characterized changes in left ventricular (LV) function. LV catheterization in mice undergoing coronary artery occlusion serves as a novel method for a real-time evaluation of LV function.

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any ...

Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease

Circulating serum microRNAs (miRNAs) have shown promise as biomarkers for the cardiovascular disease and acute myocardial infarction (AMI), being released from the cardiovascular cells into the circulation. Circulating miRNAs are highly stable and can be quantified. The quantitative expression of specific miRNAs can be linked to the pathology, and some miRNAs show high tissue and disease specificity. Finding novel biomarkers for cardiovascular diseases is of importance for medical research. Quite recently, digital polymerase chain reaction (dPCR) has been invented. dPCR, combined with fluorescent hydrolysis probes, enables specific direct absolute quantification. dPCR exhibits superior technical qualities, including a low variability, high linearity, and high sensitivity compared to the quantitative polymerase chain reaction (qPCR). Thus, dPCR is a more accurate and reproducible method for directly quantifying miRNAs, particularly for the use in large multi-center cardiovascular clinical trials. In this publication, we describe how to effectively perform digital PCR in order to assess the absolute copy number in serum samples.

Circulating microRNAs have shown promise as biomarkers for cardiovascular diseases and acute myocardial infarctions. In this study, we describe a protocol for miRNA extraction, reverse transcription, and digital PCR for the absolute quantification of miRNAs in the serum of patients with cardiovascular disease.

Circulating serum microRNAs (miRNAs) have shown promise as biomarkers for the cardiovascular disease and acute myocardial infarction (AMI), being released ...