The authors acknowledge the following funding sources: Else Kr&#246;ner-Fresenius-Stiftung (Tienush Rassaf); Hans und Gertie Fischer Stiftung (Tienush Rassaf), grant from the medical faculty, University Duisburg-Essen, Germany (Tienush Rassaf, Lars Michel); Ernst- und Berta Grimmke-Stiftung (Christos Rammos).

All experiments were completed in accordance and compliance with all relevant regulations&#160;(&#8216;European Convention for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes&#8217; (Directive 2010/63/EU) and animal care was in accordance with institutional guidelines. All experiments have been performed with male C57BL/6JRj mice at the age of 6 months.
1. Preparation
<ol>
	<li>Prepare a surgical microscope and a heating pad as well as a rectal probe to monitor the body temperature. Clean and sterilize all surgical instruments.</li>
	<li>Prepare 2 pieces of 10 cm 5-0 silk thread for vessel ligation, 5 cm of 6-0 polypropylene thread, and 2 mm silicon tube for ligation of the LCA.</li>
	<li>Prepare the PV catheter calibration cuvette by pre-heating it to 37 &#176;C and prepare a 100 &#181;L Hamilton syringe filled with 15% sodium chloride (NaCl) in H2O for saline calibration.</li>
	<li>Place the PV catheter (3 cm, 1.4 F) in 37 &#176;C pre-heated 0.9% NaCl in H2O (saline) at least 30 min before measurement. Connect the catheter to the data acquisition device and connect the device to an analog/digital converter. Connect both devices to a computer.</li>
	<li>Set up the software. Perform software-guided pressure calibration and conductance calibration as demanded by the software-guided workflow8.</li>
</ol>
2. Anesthesia and Analgesia
<ol>
	<li>Anesthetize the mouse using ketamine 100 mg/kg body weight and xylazine hydrochloride 10 mg/kg body weight by intraperitoneal injection. At the beginning of I/R surgery, administer 0.05 mg/kg body weight buprenorphine intraperitoneally to maintain analgesia.</li>
	<li>After 10 min, perform an endotracheal intubation using a 20 G intravenous (iv) catheter and ventilate the mouse with 40% oxygen (O2) and 2% (v) isoflurane. Set appropriate ventilation parameters (e.g., 220 &#181;L stroke volume, 150/min for a 25 - 30 g C57BL/6JRj mouse).</li>
	<li>Continuously monitor body temperature via rectal probe. Fasten mouse on the heated plate with the head pointing towards the investigator.&#160;Mouse normal body temperature is 36.5 - 38 &#176;C. Maintain body temperature within 1 degree by adjustment of heated plate temperature.</li>
</ol>
3. Left Ventricular Catheterization
<ol>
	<li>Disinfect chest and neck&#160;with three alternating scrubs of betadine and 70% alcohol.&#160; Wait for skin disinfectant to dry.&#160;Remove the chest hair by using a small animal shaving system.&#160;</li>
	<li>Perform a 10 mm longitudinal median incision 5 mm beneath the bottom lip towards the sternum using small surgical scissors.</li>
	<li>Dissect the left and right part of the submandibular gland via blunt preparation using a forceps. Separate muscle and fat tissue in the right paratracheal region to expose the right commune carotid artery. Mobilize and separate the vessel for a total length of 5 - 10 mm from connective tissue via careful blunt preparation alongside the vessel with a bent forceps. 
	NOTE: Avoid mechanical manipulation of the vagus nerve or the carotid body at all time as this can cause severe hypotension and bradycardia.</li>
	<li>Pass the two prepared silk threads under the vessel. Ligate the distal vessel with a tight knot and place a loose knot on the proximal exposed region that still allows passage of the catheter.</li>
	<li>Fix the threads of the cranial (tight) knot next to the head of the mice to apply a light tension on the vessel as this will facilitate the introduction of the catheter. Place a hemostat vascular clamp on the proximal vessel proximal of the loose knot to reversibly block blood flow.</li>
	<li>Perform a wedge-shaped incision 1 mm proximal to the cranial knot to open the vessel with micro scissors. 
	NOTE: A small drop of blood will indicate proper execution of this step.</li>
	<li>Insert the catheter carefully for 10 mm. Start recording of catheter data. 
	NOTE: Stretching the incision with a forceps can make this process easier.</li>
	<li>Extract the vascular clamp. Add 1 - 2 drops of saline to the incision to facilitate catheter movement. Continue introducing the catheter for approximately another 10 mm. After passing the proximal knot with the sensor tip, fasten the knot carefully just enough to prevent blood reflux alongside the thinner parts of the catheter without impairing catheter movement. 
	NOTE: The size of the sensor at the tip of the catheter prevents reflux of blood when extracting the vascular clamp.</li>
	<li>Gently continue inserting the catheter until pressure analysis shows arterial blood pressure profile indicating that the catheter is placed in the aorta (Figure 3A). 
	NOTE: The catheter reaching the aortic valve will be indicated by light resistance and pulse-synchronized motion of the catheter.</li>
	<li>When experiencing resistance trying to advance through the aortic valve, pull the catheter back 5 mm and advance again until LV catheterization will be indicated in a change in PV analysis as diastolic pressure will reach 0 - 20 mmHg (Figure 3B). Note changes in volume monitoring to further confirm left ventricular placement of the sensor tip (Figure 3C). Fasten the proximal knot more tightly to prevent catheter movement.</li>
</ol>
4. Ischemia/Reperfusion Surgery
<ol>
	<li>Perform skin incision from caudal sternum towards the left axilla for a total length of 15 mm. Proceed with blunt preparation of the two muscle layers until the ribs can be visualized.</li>
	<li>Open the thorax via incision between the third and fourth left rib. Use surgical hooks to gain access to the pericardium. Resect the pericardium above the heart. Before continuing with LCA ligation, wait 30 s without touching the animal to record PV data for valid analysis.</li>
	<li>Localize the LCA emerging under the left auricle and descending at the left side of the heart towards the apex. Use a 6-0 polypropylene suture to encircle the artery with a loop 2 mm underneath the left auricle. Place a small silicon tube under the loop and place a tight knot above. 
	NOTE: Distal myocardium turning grey serves as positive control for LCA occlusion6. I/R surgery should be performed within 5 min independently from the operating investigator.</li>
	<li>Cut the suture at 1 mm length. Release the surgical hooks and manually close the muscle layers above the incision. Wait 45 min while continuously recording PV data.</li>
	<li>After 45 min, re-open the incision and remove the silicon tube to induce reperfusion. Record data for another 20 min. 
	NOTE: A change to a red color as seen before ischemia indicates successful reperfusion.</li>
</ol>
5. Calibration
NOTE: The calibration of the PV catheter system consists of 4 mandatory steps, two of which have to be performed after the measurement. Calibration should be repeated after every experiment to ensure valid results.
<ol>
	<li>Perform pressure calibration and conductance calibration before the experiment as described in Step 1.5.</li>
	<li>Perform saline calibration when the catheter is still placed in the left ventricle after the experiment itself is finished. Localize the right jugular vein lateral of the carotid artery in the prepared area. Inject 10 &#181;L 25% NaCl in H2O via a Hamilton syringe while recording data.</li>
	<li>Calculate the calibration using the acquisition software by highlighting the ascending phase in volume curve (Figure 5C). Repeat this process for a total of 3 times. Avoid loss of blood after syringe extraction by using a vascular clamp to rapidly compress the puncture.</li>
	<li>Perform volume calibration to calibrate volume data acquisition by analysis of standardized volumes. Obtain approximately 500 &#181;L mouse blood from cardiac puncture with a slightly heparinized 1 mL syringe (e.g., 5 &#181;L per 200 IE heparin). Pull back the PV catheter 10 - 15 mm to avoid damaging the catheter.</li>
	<li>Fill the obtained blood into the 37 &#176;C pre-heated calibration cuvette (Figure 5A). Avoid bubbles as it may interfere with the results. Add the catheter tip into each well and record data. Obtain a standard curve by software-guided analysis (Figure 5B). Repeat the process for a total of 3 times.</li>
	<li>Euthanize mice by exsanguination or cervical dislocation while sufficient isoflurane anesthesia is maintained at all time.</li>
</ol>
6. Data Analysis
<ol>
	<li>After completing the calibration steps, perform software-guided data analysis. Therefore, highlight the appropriate section (at least ten cycles) within the Analyze section of the PV Workflow and perform baseline analysis. Exclude cycles with deviations due to ventilation or manipulation if necessary (Figure 3D).</li>
	<li>Perform PV baseline analysis before passage of the aortic valve (arterial pressure only), immediately before and after LCA occlusion. Proceed by conducting PV baseline analysis and in intervals of 5 min. while ischemia and after reperfusion. At the end of the experiment, perform analysis of pressure data after retraction of the catheter from the left ventricle (arterial pressure).</li>
	<li>Analyze at least 10 consecutive cycles to avoid sampling error. When experiencing strong interference of obtained values with the ventilation, transient interruption of the ventilation for a maximum of 5 s can be considered.</li>
	<li>Use the following parameters that are calculated in Baseline Analysis (Figure 3D) to characterize LV function:
	<ol>
		<li>Stroke volume (&#181;L)</li>
		<li>Ejection fraction: Stroke volume / end-diastolic volume (%)</li>
		<li>Cardiac output: Stroke volume * heart rate (&#181;L/min)</li>
		<li>Cardiac index: Cardiac output / body surface area (&#181;L/(min*cm&#178;)</li>
		<li>Stroke work: Inner area of PV curve (mmHg*&#181;L)</li>
		<li>Maximum pressure (Pmax); Mean pressure (Pmean)</li>
		<li>max dP/dt (mmHg/s) as a parameter of LV systolic function</li>
		<li>min dP/dt (mmHg/s) as a parameter for LV compliance</li>
		<li>Time constant of isovolumetric relaxation: Tau (ms)</li>
	</ol>
	</li>
</ol>

<ol>
	<li>Sanchis-Gomar, F., Perez-Quilis, C., Leischik, R., Lucia, A. <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+coronary+heart+disease+and+acute+coronary+syndrome.">Epidemiology of coronary heart disease and acute coronary syndrome.</a> Annals of Translational Medicine. 4 (13), 256 (2016).</li><li>Anderson, J. L., Morrow, D. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Acute+Myocardial+Infarction.">Acute Myocardial Infarction.</a> New England Journal of Medicine. 376 (21), 2053-2064 (2017).</li><li>McNamara, R. L., 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=Predicting+in-hospital+mortality+in+patients+with+acute+myocardial+infarction.">Predicting in-hospital mortality in patients with acute myocardial infarction.</a> Journal of the American College of Cardiology. 68 (6), 626-635 (2016).</li><li>Kurian, G. A., Rajagopal, R., Vedantham, S., Rajesh, M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+Role+of+Oxidative+Stress+in+Myocardial+Ischemia+and+Reperfusion+Injury+and+Remodeling:+Revisited.">The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited.</a> Oxidative Medicine and Cellular Longevity. , (2016).</li><li>Turer, A. T., Hill, J. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Pathogenesis+of+myocardial+ischemia-reperfusion+injury+and+rationale+for+therapy.">Pathogenesis of myocardial ischemia-reperfusion injury and rationale for therapy.</a> American Journal of Cardiology. 106 (3), 360-368 (2010).</li><li>Totzeck, M., Hendgen-Cotta, U. B., French, B. A., Rassaf, T. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=A+practical+approach+to+remote+ischemic+preconditioning+and+ischemic+preconditioning+against+myocardial+ischemia/reperfusion+injury.">A practical approach to remote ischemic preconditioning and ischemic preconditioning against myocardial ischemia/reperfusion injury.</a> Journal of Biological Methods. 3 (4), (2016).</li><li>Respress, J. L., Wehrens, X. H. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Transthoracic+echocardiography+in+mice.">Transthoracic echocardiography in mice.</a> Journal of Visualized Experiments. (39), (2010).</li><li>Pacher, P., Nagayama, T., Mukhopadhyay, P., Batkai, S., Kass, D. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Measurement+of+cardiac+function+using+pressure-volume+conductance+catheter+technique+in+mice+and+rats.">Measurement of cardiac function using pressure-volume conductance catheter technique in mice and rats.</a> Nature Protocols. 3 (9), 1422-1434 (2008).</li><li>Zhang, B., Davis, J. P., Ziolo, M. T. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Cardiac+catheterization+in+mice+to+measure+the+pressure+volume+relationship:+Investigating+the+Bowditch+effect.">Cardiac catheterization in mice to measure the pressure volume relationship: Investigating the Bowditch effect.</a> Journal of Visualized Experiments. (100), e52618 (2015).</li><li>Rossello, X., Hall, A. R., Bell, R. M., Yellon, D. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Characterization+of+the+Langendorff+perfused+isolated+mouse+heart+model+of+global+ischemia-reperfusion+injury:+Impact+of+ischemia+and+reperfusion+length+on+infarct+size+and+LDH+release.">Characterization of the Langendorff perfused isolated mouse heart model of global ischemia-reperfusion injury: Impact of ischemia and reperfusion length on infarct size and LDH release.</a> Journal of Cardiovascular Pharmacology and Therapeutics. 21 (3), 286-295 (2016).</li><li>Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC). <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=ESC+Guidelines+for+the+management+of+acute+myocardial+infarction+in+patients+presenting+with+ST-segment+elevation.">ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation.</a> European Heart Journal. 33 (20), 2569-2619 (2012).</li><li>Shigemitsu, O., 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=Acute+myocardial+infarction+due+to+left+main+coronary+artery+occlusion.+Therapeutic+strategy.">Acute myocardial infarction due to left main coronary artery occlusion. 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The authors have nothing to disclose.

PV monitoring of LV hemodynamics in acute myocardial infarction serves as a novel method for real-time in vivo assessment of cardiogenic shock and impaired LV function in I/R injury. PV catheterization can provide a broad spectrum of parameters with regard to LV systolic and diastolic function. In addition to the LV volumetric parameters typically obtained by echocardiography or MRI (chamber volumes, EF, stroke volume, and cardiac output), PV analysis yields a more complete profile of LV function by simultaneously providing measures of LV systolic performance (contractility dP/dt, stroke work) and LV compliance (-dP/dt, Tau) as a parameter for diastolic function.
As acute heart failure in patients with acute myocardial infarction is a critical predictor for early in-hospital morbidity and mortality2, monitoring of acute hemodynamic impairment and cardiogenic shock in acute myocardial infarction could serve as a valuable tool for identifying possible protective mechanisms in an experimental setting.
Several factors turned out to be critical for successful data acquisition. Stable anesthesia was crucial for valid PV data since isoflurane showed a strong cardiodepressive effect with drops in pressure, LV EF, and stroke volume. Atraumatic preparation of the carotid artery was important to avoid hypovolemia due to blood loss. Furthermore, compression or injury of the vagus nerve and the carotid body could result in severe impairment of hemodynamics.
Saline calibration and cuvette calibration appeared to be another critical step to maintain valid data. For saline calibration, injection of 15% NaCl solution led to increased conductance indicated by a temporary increase in volume level (Figure 5C). Maintaining the same speed when injecting was crucial for stable data. When conducting cuvette calibration, it was important to avoid bubbles within the cuvettes to ensure valid results.
The obtained PV data furthermore indicate the importance of a simultaneous acquisition of pressure and volume data for a valid hemodynamic characterization since pressure data alone did not show significant changes throughout the experiment (Figure 4A). The combined PV analysis offered both baseline parameters for LV systolic function (e.g., ejection fraction) as well as parameters for LV contractility (dP/dt) and LV relaxation (-dP/dt, Tau).
Interestingly, acute occlusion of the LCA in patients usually causes a severe deficit of LV function with immediate necessity for mechanical hemodynamic support and is associated with a high mortality rate11,12. LCA occlusion in mice showed less hemodynamic impairment and LCA occlusion-associated death during the procedure was not observed. As a sign of persisting hemodynamic stability during ischemia, systolic LV blood pressure was stable at all time (Figure 4A). However, this effect could be caused by more distal ligations in mice compared to LCA occlusions in humans.
Taken together, real-time hemodynamic monitoring of acute myocardial infarction in mice could serve as a new method for studying cardioprotective mechanisms in severe LV dysfunction aiming to improve early-phase treatment of patients undergoing acute myocardial infarction.

Cardiovascular disease is the most common cause of death in western civilization1. Acute myocardial infarction is a critical event, which is associated with high acute and chronic mortality2. Even if revascularization is achieved via emergency percutaneous coronary intervention (PCI), mortality remains high, particularly within the first 48 h after onset of symptoms in patients with acute myocardial infarction3. Cardiogenic shock caused by acute reduction in left ventricular (LV) function is a major cause for in-hospital mortality in these patients3. This early reduction in LV function is caused by myocardial damage following ischemia and reperfusion. This so-called ischemia/reperfusion (I/R) injury is mediated by changes in cellular metabolome such as exaggerated generation of reactive oxygen species4,5.
To explore possible protective mechanisms leading to a decrease in myocardial damage in a preclinical setting, reliable mouse models are essential including methods for evaluation of post-I/R LV function6. In this setting, transthoracic echocardiography7 and magnetic resonance imaging (MRI)6 are widely used for functional phenotyping8,9. However, these methods are not suitable for the assessment of severe LV dysfunction and cardiogenic shock in an ongoing acute myocardial infarction and cannot directly show data on LV pressure. The Langendorff apparatus using isolated heart in an ex vivo assay provides information about the underlying pathomechanisms of early-phase I/R injury10. This method is limited due to its inability to reproduce in vivo adaptive mechanisms such as regulation of the autonomous nervous system or hormonal regulation and acid-base homeostasis. There is currently no method available for a complete functional phenotyping of cardiogenic shock and left ventricular dysfunction during an ongoing myocardial I/R injury.
A synchronized approach with combination of pressure-volume (PV) catheterization and transient surgical left main coronary artery (LCA) occlusion could be beneficial but technically challenging. Stable extracardiac hemodynamics during I/R injury are essential for valid results since unstable anesthesia or blood loss could heavily influence the results. A novel approach for hemodynamic phenotyping of I/R injury via LV PV catheterization and transient LCA occlusion could bring new insights on cardiogenic shock and LV dysfunction in acute myocardial infarction and serve as a method for future analysis on cardioprotection.

<table border="0" cellpadding="0" cellspacing="0" width="762">
	<tbody>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Calibration cuvette</td>
			<td style="width:164px;">Millar instruments</td>
			<td style="width:119px;">910-1049</td>
			<td style="width:243px;">Calibration cuvette</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Contura professional hair trimmer</td>
			<td style="width:164px;">Wella</td>
			<td style="width:119px;">HS-60</td>
			<td>Small animal shaving system</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Eclipse Needle 27G</td>
			<td style="width:164px;">BD</td>
			<td style="width:119px;">REF 305770</td>
			<td>27G needle</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Forceps</td>
			<td style="width:164px;">FST</td>
			<td>11203-25, 11069-08, 11616-15, 11506-12, 11051-10</td>
			<td style="width:243px;">Surgical forceps</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Forceps</td>
			<td style="width:164px;">Aesculap Braun</td>
			<td>BN731R, BD 311R</td>
			<td style="width:243px;">Surgical forceps</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Foris FS2434</td>
			<td style="width:164px;">Eizo</td>
			<td style="width:119px;">0FTD2033</td>
			<td>Monitor</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Hamilton Syringe 100 &#181;l needle</td>
			<td style="width:164px;">Hamilton</td>
			<td style="width:119px;">80621</td>
			<td>100&#181;l syringe with needle</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Heated Small animal OP table</td>
			<td style="width:164px;">Harvard Apparatus</td>
			<td style="width:119px;">15001</td>
			<td>Heated OP table</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Heparin-Natrium 25000</td>
			<td style="width:164px;">Ratiopharm</td>
			<td style="width:119px;">N68542.04</td>
			<td>Heparin</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Ketamin 10% 100 mg/ml</td>
			<td style="width:164px;">bela-pharm</td>
			<td style="width:119px;">FS1670041</td>
			<td>Ketamin</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Labchart Pro 8 + Pro modules</td>
			<td style="width:164px;">AD Instruments</td>
			<td style="width:119px;">MLS260/8</td>
			<td>PV data analysis software</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">LAS EZ</td>
			<td style="width:164px;">Leica</td>
			<td style="width:119px;">LAS EZ</td>
			<td>Microscope camera software</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Leica IC80 HD</td>
			<td style="width:164px;">Leica</td>
			<td style="width:119px;">IC80 HD</td>
			<td>Microscope camera</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Leica M80</td>
			<td style="width:164px;">Leica</td>
			<td style="width:119px;">M80</td>
			<td>Microscope</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Micro-tip catheter transducer</td>
			<td style="width:164px;">Millar instruments</td>
			<td style="width:119px;">SPR-839</td>
			<td>PV catheter</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">MiniVent</td>
			<td style="width:164px;">Harvard Apparatus</td>
			<td style="width:119px;">845</td>
			<td>ventilation</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">MPVS Ultra</td>
			<td style="width:164px;">Millar instruments</td>
			<td style="width:119px;">PL3508B48/M</td>
			<td>PV catheter data acquisition device</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Octenisept</td>
			<td style="width:164px;">Sch&#252;lke</td>
			<td style="width:119px;">20000832-A</td>
			<td>disinfectant</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Plastipak 1ml</td>
			<td style="width:164px;">PD</td>
			<td style="width:119px;">REF 303172</td>
			<td>1ml syringe</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">PowerLab 8/35</td>
			<td style="width:164px;">AD Instruments</td>
			<td style="width:119px;">PL3508</td>
			<td>analog/digital converter</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Prolene 6-0</td>
			<td style="width:164px;">Ethicon</td>
			<td style="width:119px;">XNEH7814.P31</td>
			<td>Polypropylene suture</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Retraction Kit</td>
			<td style="width:164px;">FST</td>
			<td>18200-20</td>
			<td>retraction of surgical situs</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Seraflex 5-0</td>
			<td style="width:164px;">Naila</td>
			<td style="width:119px;">IC108000</td>
			<td>silk suture</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Small and micro-scissors</td>
			<td style="width:164px;">FST Essen</td>
			<td style="width:119px;">14059-11, 15007-08, 14064-11</td>
			<td>Surgical scissors</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Small silicon tube</td>
			<td style="width:164px;">Reichelt Chemietechnik</td>
			<td style="width:119px;"></td>
			<td>tube for LCA occlusion</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">Sodium Chloride</td>
			<td style="width:164px;">Sigma-Aldrich</td>
			<td style="width:119px;">S7653</td>
			<td>Sodium Chloride</td>
		</tr>
		<tr height="26">
			<td height="26" style="height:27px;width:237px;">testo 108</td>
			<td style="width:164px;">testo</td>
			<td>5631080</td>
			<td>rectal thermometer</td>
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			<td height="26" style="height:27px;width:237px;">Thinkcentre desktop computer</td>
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			<td height="26" style="height:27px;width:237px;">Windows 10</td>
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			<td style="width:119px;">6324464.00.00</td>
			<td>Xylazine hydrochloride</td>
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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.

After LV catheterization, reversible LCA ligation was performed for 45 min followed by 10 min of reperfusion. PV data was recorded at all times (Figure 1).
Correct placement of the PV catheter was confirmed by obtaining the characteristic LV PV graph (Figure 2A). LV catheter placement showed the typical ventricular pressure range with a minimum of 0 - 20 mmHg whereas false placement of the PV-catheter in the aorta would have shown a typical arterial pressure curve with a minimum pressure of 30 - 60 mmHg (diastolic blood pressure) and a small excursion at the end of systole indicating the aortic valve closing (Figure 3B and 3C). Successful occlusion of the LCA was visually confirmed by blanching of the distal LV myocardium (Figure 2B).
After LCA occlusion, PV data was acquired in 5 min intervals. Pressure data analysis demonstrated no changes in maximum LV systolic pressure indicating preserved peripheral perfusion and stable anesthesia (Figure 4A). Analysis of LV volume revealed a significant decrease in both EF (52% vs. 40%, p&#160;= 0.008) and absolute stroke volume (Figure 4B and 4C). These changes happened within the early phase of ischemia and LV functional data remained unchanged in the later phase of ischemia. Maximum dP/dt as a parameter of LV contractility showed a 30% reduction in mice undergoing myocardial ischemia. Stroke work was 30% reduced (Figure 4D and 4E). As a parameter for diastolic function, minimum dP/dt was significantly decreased indicating impaired LV compliance (Figure 4F). Reperfusion by extraction of the silicon tube was visually validated. Reperfusion did not show significant changes in PV data analysis within a period of 20 min (Figure 4A-4D). Sham-operated animals did not show a significant reduction in LV systolic or diastolic parameters (Figure 4I-4J).
At the end of data acquisition, cuvette calibration and saline calibration were performed (Figure 5).
<img alt="Figure 1" class="xfigimg" src="/files/ftp_upload/57621/57621fig1v3.jpg" /> 
Figure 1: Scheme of the method. Sequence of left ventricular (LV) catheterization, left main coronary artery (LCA) occlusion and reperfusion.&#160;
<img alt="Figure 2" class="xfigimg" src="/files/ftp_upload/57621/57621fig2.jpg" /> 
Figure 2: Surgical procedures. (A) Left ventricular catheterization placed via the right common carotid artery. (B) Left main coronary artery occlusion with polypropylene suture and silicon tube. <a href="/files/ftp_upload/57621/57621fig2large.jpg" target="_blank">Please click here to view a larger version of this figure.</a>
<img alt="Figure 3" class="xfigimg" src="/files/ftp_upload/57621/57621fig3.jpg" /> 
Figure 3: Representative pressure-volume data. (A) Representative arterial pressure indicated by a minimal pressure of &#62;30 mmHg and a typical excursion at the end of systole indicating closing of the aortic valve. (B) Representative left ventricular pressure data showing diastolic values &#60;20 mmHg. (C) Representative left ventricular pressure-volume diagram. (D) Screenshot of software-based PV baseline analysis. <a href="/files/ftp_upload/57621/57621fig3large.jpg" target="_blank">Please click here to view a larger version of this figure.</a>
<img alt="Figure 4" class="xfigimg" src="/files/ftp_upload/57621/57621fig4.jpg" /> 
Figure 4: Pressure/volume data in mice undergoing ischemia/reperfusion. (A) Systolic left ventricular blood pressure (Pmax). (B) Left ventricular (LV) ejection fraction (EF) (%). (C) LV stroke volume (&#181;L). (D) Maximum dP/dT (max dP/dt) (mmHg/s). (E) LV Stroke work (SW). (F) Minimum dP/dt (min dP/dt) (mmHg/s). (G) Time constant of isovolumetric relaxation Tau (ms). (H) Pressure/volume diagram before and 45 min after induction of myocardial ischemia. (I-J) Stroke volume (SV) (&#181;L) and maximum dP/dt (max dP/dt) (mmHg/s) in sham-operated animals compared to animals after 15/30 min ischemia. Data (A-G) are presented as mean &#177; SEM. * p &#60;0.05 via Student&#39;s t-test or ratio-paired t-test, n&#160;= 4 mice/group (A+D-G)) or n&#160;= 3 mice/group (B, C). +45: 45 min ischemia; rep.: reperfusion. <a href="/files/ftp_upload/57621/57621fig4large.jpg" target="_blank">Please click here to view a larger version of this figure.</a>
<img alt="Figure 5" class="xfigimg" src="/files/ftp_upload/57621/57621fig5.jpg" /> 
Figure 5: Post-hoc calibration. (A) Schematic of calibration cuvette. Volumes in &#181;L. (B) Representative linear regression analysis of obtained volume data to perform cuvette calibration. (C) Representative volume data after injection of 10 &#181;L of 25% sodium chloride in H2O into the right jugular vein to perform saline calibration. <a href="/files/ftp_upload/57621/57621fig5large.jpg" target="_blank">Please click here to view a larger version of this figure.</a>

Watch this Scientific Journal Video about Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice at JoVE.com

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

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 ...

real-time-pressure-volume-analysis-acute-myocardial-infarction

Nanyang Technological University

Research

JoVE Journal

Medicine

9.0K Views.  University Hospital Essen. 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.

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

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 ...

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 ...

Biventricular Assessment of Cardiac Function and Pressure-Volume Loops by Closed-Chest Catheterization in Mice

Assessment of cardiac function is essential to conduct cardiovascular and pulmonary-vascular preclinical research. Pressure-volume loops (PV loops) generated by recording both pressure and volume during cardiac catheterization are vital when assessing both systolic and diastolic cardiac function. Left and right heart function are closely related, reflected in ventricular interdependence. Thus, recording biventricular function in the same animal is important to get a complete assessment of cardiac function. In this protocol, a closed chest approach to cardiac catheterization consistent with the way catheterization is performed in patients is adopted in mice. While challenging, the closed chest strategy is a more physiological approach, because opening the chest results in major changes in preload and afterload that create artifacts, most notably a fall in systemic blood pressure. While high-resolution echocardiography is used to assess rodents, cardiac catheterization is invaluable, particularly when assessing diastolic pressures in both ventricles.
Described here is a procedure to perform invasive, closed chest, sequential left and right ventricular pressure-volume (PV) loops in the same animal. PV loops are acquired using&#160;admittance technology with a mouse pressure-volume catheter and pressure-volume system acquisition. The procedure is described, beginning with the neck dissection, which is required to access the right jugular vein and the right carotid artery, to the insertion and positioning of the catheter, and finally the data acquisition. Then, the criteria required to ensure the acquisition of high-quality PV loops are discussed. Finally, the analysis of the left and right ventricular PV loops and the different hemodynamic parameters available to quantify systolic and diastolic ventricular function are briefly described.

Presented here is a protocol to assess biventricular heart function in mice by generating pressure-volume (PV) loops from the right and left ventricle in the same animal using closed chest catheterization. The focus is on the technical aspect of surgery and data acquisition.

Assessment of cardiac function is essential to conduct cardiovascular and pulmonary-vascular preclinical research. Pressure-volume loops (PV loops) ...

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.

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 ...