Direct Mechanical Ventricular Actuation Research Articles

Abstract 15552: Augmentation of Right Ventricular Strain Dynamics During Direct Mechanical Ventricular Actuation

Introduction: Available forms of mechanical circulatory support are associated with significant complications related to blood contact. Direct cardiac compression (DCC) devices avoid blood contact but may impair diastolic function. This derogatory effect of DCC devices may be related to a negative impact on RV function. Direct mechanical ventricular actuation (DMVA) uniquely augments LV diastolic function. The purpose of this study was to evaluate DMVA’s effect on RV function. Methods: Ischemic heart failure (HF) was induced using 5 mins of ventricular fibrillation (VF) circulatory arrest in large mature canines (n=9). Hearts were defibrillated and DMVA applied for 15 mins. VF circulatory arrest was subsequently re-induced for 5 mins to generate progressive HF. The experimental protocol was continued for 3 hrs. Intracardiac echocardiography was used to quantify longitudinal strain and peak strain rates in the RV and LV using speckle-tracking algorithms. Two-way ANOVA with Tukey HSD tests were used to evaluate statistical differences in strain metrics (baseline vs. HF vs. DMVA support and LV vs. RV). Results: DMVA increased RV fractional area change (DMVA: 0.282 ± 0.011, Mean ± SEM) relative to either baseline (0.221 ± 0.15, p=0.004) or HF (0.170 ± 0.006, p<0.001). DMVA statistically significantly augmented all RV strain metrics relative to either baseline or HF (Table). Additionally, all DMVA strain metrics were statistically significantly greater in the RV than the LV (LV strain: 18.8 ± 0.5 %, p<0.001, LV strain rate: systolic, -1.46 ± 0.04 1/s, p<0.001, diastolic, 1.51 ± 0.04 1/s, p<0.001). Conclusions: DMVA substantially improved RV strain dynamics compared to baseline or HF in this model. During DMVA support, strain dynamics in the RV were amplified more than the LV. This RV augmentation is important to achieving balanced biventricular DMVA support. Enhanced diastolic RV and LV augmentation during DMVA remains highly unique when compared to any other devices.

Abstract 14705: Diastolic Function is Uniquely Augmented by Direct Mechanical Ventricular Actuation in the Failing Heart

Introduction: Diastolic dysfunction represents a significant pathophysiology in cardiomyopathies and heart failure (HF), yet limited therapies exist for treatment. Direct Mechanical Ventricular Actuation (DMVA) is a non-blood contacting device highly unique in its ability to provide both diastolic and systolic support. The purpose of this study was to further evaluate DMVA’s effect on diastolic function in the failing heart. Methods: Adult canine (63.7 ± 13.4 lb, n=9) underwent repeated cycles of ventricular fibrillation to generate progressive levels of acute HF. DMVA was applied to support HF after defibrillation. Intracardiac echocardiography was used to quantify LV longitudinal strain/strain rates using speckle-tracking algorithms. Strain/strain rate peak magnitudes and composite waveforms were analyzed during baseline (n = 35), DMVA (n = 127), and non-support HF (n = 127). One-way ANOVA with post-hoc Tukey’s HSD was used to assess statistical differences (p<0.05) for all comparisons. Results: LV strain metrics were augmented during DMVA support (strain: 20.0 ± 0.5 %, strain rate: systolic, -1.64 ± 0.03 1/s, diastolic, 1.68 ± 0.04 1/s) versus non-supported HF (strain: 9.9 ± 0.2 %, p<0.001, strain rate: systolic, -0.83 ± 0.02 1/s, p<0.001, diastolic, 0.86 ± 0.02 1/s, p<0.001). All strain metrics were increased during DMVA compared to baseline (strain: 14.2 ± 0.4 %, p<0.001, strain rate: systolic, -1.11 ± 0.03 1/s, p<0.001, diastolic, 1.14 ± 0.04 1/s, p<0.001). Composite strain waveforms aligned by systolic peak revealed an early diastolic boost during DMVA relative to baseline (see figure). Conclusions: Diastolic strain dynamics were significantly improved during DMVA in this model of progressive HF. Direct cardiac compression devices can impair diastolic function, which limits feasibility for circulatory support. This study further validates that DMVA restores near physiologic LV strain patterns during HF and uniquely augments diastolic function.

Noninvasive estimation of assist pressure for direct mechanical ventricular actuation.

Direct mechanical ventricular actuation is effective to reestablish the ventricular function with non-blood contact. Due to the energy loss within the driveline of the direct cardiac compression device, it is necessary to acquire the accurate value of assist pressure acting on the heart surface. To avoid myocardial trauma induced by invasive sensors, the noninvasive estimation method is developed and the experimental device is designed to measure the sample data for fitting the estimation models. By examining the goodness of fit numerically and graphically, the polynomial model presents the best behavior among the four alternative models. Meanwhile, to verify the effect of the noninvasive estimation, the simplified lumped parameter model is utilized to calculate the pre-support and the post-support left ventricular pressure. Furthermore, by adjusting the driving pressure beyond the range of the sample data, the assist pressure is estimated with the similar waveform and the post-support left ventricular pressure approaches the value of the adult healthy heart, indicating the good generalization ability of the noninvasive estimation method.

Abstract 11151: Vascular Pulsatility During Mechanical Actuation of the Fibrillating Heart is Equivalent to the Native Beating Heart

Introduction: Direct Mechanical Ventricular Actuation (DMVA) is a non-blood-contacting direct cardiac compression device shown to resuscitate both humans and animals without myocardial injury. The purpose of this study was to determine if DMVA support during ventricular fibrillation (VF) generates pulsatility similar to the native heart. Methods: Large canine (n=10) and swine (n=10) were anesthetized, underwent sternotomy, and instrumented for hemodynamic monitoring and intracardiac echocardiography. VF was induced for 5 mins of circulatory arrest and DMVA applied for 15 mins. Hearts were then defibrillated and allowed to recover. Repeated periods of arrest were used to increase cardiac dysfunction post-resuscitation. Paired t-tests were used to compare the post-sternotomy baseline, supported VF, and unsupported post-resuscitation states. Mean pressures and flows were statistically equalized between supported arrest and unsupported post-resuscitation. Previously described metrics of pulsatility were calculated using 10 sec flow and pressure intervals. Results: Conclusions: DMVA was able to generate physiologic levels of pulsatility even during support of the fibrillating heart across a range of heart sizes. Differences in overall energy (EEP) between the possibly hyperdynamic baseline and support can be explained by discrepancies in mean (continuous) pressures and flows given observed similarities in the pulsatile component (PP, PI, SHE). Mechanical actuation of the fibrillating heart was shown to provide superior pulsatility compared to post-resuscitation hearts with comparable hemodynamic means and power curves.

Abstract 326: Direct Ventricular Compression Improves Mechanical Synchrony of the Acutely Failing Heart

Introduction: Mechanical dyssynchrony during acute cardiac failure contributes to ventricular dysfunction. Direct Mechanical Ventricular Actuation (DMVA) provides non-blood-contacting augmentation of systolic and diastolic ventricular function. The purpose of this study was to determine if DMVA can improve mechanical synchrony in the acutely failing heart. Methods: New Zealand white rabbits (n = 10) were anesthetized, underwent sternotomy, and instrumented for arterial pressures and aortic flow. A 10 MHz transvascular ultrasound probe acquired two-chambered, long-axis transesophageal ventricular images. Heart failure (50% of baseline cardiac output) was modeled using a titrated Esmolol drip. Phenylephrine maintained mean arterial pressure between 60 -70 mm Hg as needed. LV images were analyzed using Siemens speckle tracking software. The LV was divided into six regions which were analyzed for peak strain rate and time to peak strain rate. Average peak systolic and diastolic strain rates were used to assess global myocardial function. Synchrony was determined by analyzing the standard deviation of regional time differences between peak systolic strain rates (dyssynchrony index). Results: Systolic and diastolic global strain rates were significantly reduced during failure and significantly augmented to near normal during DMVA support. Following a similar relationship, DMVA significantly improved mechanical synchrony during acute heart failure. Recovery strain rates and synchrony were significantly improved vs. failure but did not return to baseline values. Conclusion: DMVA effectively augments myocardial function in the acutely failing heart. The improvements in pump function are associated with normalization of mechanical synchrony. DMVA’s ability to restore mechanical synchrony during resuscitative ventricular support has favorable implications on cardiac recovery.

Ventricular Actuation Improves Systolic and Diastolic Myocardial Function in the Small Failing Heart

Direct mechanical ventricular actuation (DMVA) provides non-blood contacting augmentation of ventricular function. The device has promise for supporting the pediatric heart. The purpose of this study was to assess DMVA's effect in a small animal model of heart failure. Anesthetized rabbits (n = 6) underwent sternotomy and were instrumented for hemodynamic monitoring. A 10-MHz ultrasound probe was used for transesophageal echocardiography imaging. Heart failure (cardiac output <50% baseline) was induced with esmolol. Phenylephrine was titrated to maintain baseline mean arterial pressure. Transesophageal echocardiography imaging was acquired at baseline, heart failure, and subsequent DMVA support for 2 hours. Image analysis was used to derive ejection fraction, cardiac output, and stroke work as measures of left ventricular function. Speckle tracking software was used to derive myocardial strain rates as load-independent measures of left ventricular myocardial function. Mean ejection fraction was significantly increased during DMVA support (0.585 +/- 0.035) versus failure (0.215 +/- 0.014; p < 0.001). Peak global left ventricular systolic and diastolic strain rates (1/second) were significantly increased during DMVA (-2.85 +/- 0.33 and 2.92 +/- 0.37) versus failure (-1.69 +/- 0.11 and 1.99 +/- 0.14; p < 0.001 and 0.004, respectively). Peak strain rates during DMVA in the failing heart were similar to baseline. Direct mechanical ventricular actuation augments both systolic and diastolic left ventricular pump function. Diastolic augmentation distinguishes the device from other direct cardiac compression methods. This study demonstrated that DMVA in the small-sized, failing heart improves both systolic and diastolic myocardial function, which has favorable implications for left ventricular recovery. Direct mechanical ventricular actuation's salutary effects can be provided to the failing pediatric heart without complications of blood contact.

DIRECT CARDIAC COMPRESSION DOES NOT RESULT IN PRO-APOPTOTIC CELL SIGNALING

INTRODUCTION: Direct Mechanical Ventricular Actuation (DMVA) is a non-blood contacting method of ventricular support. This study examined DMVA's impact on cellular markers of apoptosis in an isolated working heart model. METHODS: New Zealand white rabbit hearts(n=20) were instrumented in a biventricular working heart platform. Group 1 hearts served as controls and Group 2 hearts were subjected to DMVA. Hemodynamics and cardiac function were analyzed using SPSS statistical software. Two-sample t-tests on change scores were performed to assess group differences. Regional myocardial samples were taken and Caspase-3 fluorometric assay was performed. Results are reported as absolute values ±SEM. RESULTS: LV performance significantly improved with DMVA application (23.3±12.3 ml/min v. 58.83±18.6 ml/min) compared to progressive LV dysfunction in control hearts (62.9±8.7 ml/min v. 45.0±10.0 ml/min), p=0.01. Measurement of Caspase-3 activity in regional myocardial samples revealed no significant differences. Notably, right (32.4±1.5 v.33.9±3.3, p=.87) and left (LV 23.9±1.9 v. 24.3±2.6, p=.96) ventricle epicardial surfaces showed no difference between DMVA and control, respectively. CONCLUSIONS: DMVA effectively augmented ventricular function and cardiac output in the small heart model. Epicardial Caspase-3 activity revealed no significant injury to the epicardial surface caused by DMVA. More study is necessary to further elucidate DMVA's effect on cell wounding and cellular repair.

Non-blood contacting biventricular support for severe heart failure

Background. Direct mechanical ventricular actuation (DMVA) is a non-blood contacting method of biventricular support. DMVA employs a vacuum attached, pneumatically regulated, flexible membrane to transfer both systolic and diastolic forces to the ventricular myocardium. The purpose of this study was to determine if DMVA effectively restores pump performance when applied to the severely failing heart. Methods. Bovines (n = 10) underwent thoracotomy and were instrumented for continuous hemodynamic monitoring. Cardiac failure was induced by β 1-blockade to achieve a cardiac index of < 1.5 l/min/m 2 for 1 hour. Heart rate was maintained at 100 bpm by atrioventricular sequential pacing. Synchronous DMVA support was then applied for 3 hours. Results. Eight animals achieved significant reductions in cardiac index and mean arterial pressures (35%* and 43%* control, respectively; * p < 0.05). DMVA restored cardiac index to baseline and significantly increased arterial pressures ( p < 0.05; DMVA versus cardiac failure). Pulmonary flow and mean pulmonary artery pressures were similar to baseline during DMVA ( p = NS). Pathologic exam did not demonstrate evidence of significant device trauma. Conclusions. DMVA support can effectively restore pump performance of the acutely failing heart. Synchronization may be inherent to the stimulus of cardiac compression. These data further substantiate DMVA’s potential as an adjunct to the field of circulatory support.

RV AND LY DYNAMICS DURING DIRECT MECHANICAL VENTRICULAR ACTUATION OF THE FAILING HEART

Purpose of study: Direct Mechanical Ventricular Actuation (DMVA) is a non-blood contacting, vaccum attached, pneumatically regulated biventricular, systolic and diastolic assist device. Its effectiveness has already been demonstrated clinically when applied to the fibrillating heart. This study assesses DMVA's effect on left and right ventricular dynamics when applied to biventricular failure state. Methods: After general anesthesia 10 bovine (113±8kg) underwent left thoracotomy and were instrumented for continuous hemodynamic monitoring. Cardiac Index <1,5 l/min/m2 was achieved by a β 1 blockade for one hour, while heart rate was maintained at 100 bpm by AV-sequential pacing, before synchronous DMVA support was applied for 3 hours. Results: β1 blockade lead to reduction of Cardiac Index (C1) by 68% and 71% (*p<0,05) of the left and right ventricle respectively. Supported by DMVA CI increased immediately by 203% and 225%* with a maximum of 318% and 348%* respectively. RV versus LV output was elevated by 35% to 45% with RV unloading occuring earlier than LV unloading during DMVA support. Arterial pressures increased significantly*, while pulmonary artery pressures remained unchanged throughout DMVA support period. Elevated central venous pressures during failure returned to baseline during DMVA while left atrial pressures remained relatively unchanged. Conclusion: DMVA supports left and right ventricular function equally. RV unloading occurs prior to the LV during DMVA support as similar compressive forces are applied to both ventricular chambers. Lower pressures in pulmonary circulation, therefore, lead to a distinct separtion in peak pulmonary and systemic pressures. Pulmonary congestion is effectively avoided by ensuring complete LV assist.

Non–Blood-Contacting Biventricular Support: Direct Mechanical Ventricular Actuation

The concept of nierlianicall~ conipr ing the ventrirles of a failing heart into a sy stolic cwnfiguration followed I)! pa5sive or mechanicall\. assisted diastole is not new. 4 variety of bellows. wrap-around devices, antl cups have lteen prOl~’5t3etl t o angment forward cardiac flow after cardiac arrest. For example, 27 patents have Iieen issued in the United States alone for a Fariety of such tlevices 1)eginning as early as 1936. Although seemingly simple antl elegant , no one has yet to qufficiently stud) and refine this concept to pi-oduce an accepted. commercially available means to support the failing circulation. In fact, the overwhelming majority of patents issued were for totally unassemhled antl untested devices. Direct mechanical ventricular actuation (DMVA), as deeloped to date in our laboratory, is the only non-hloodcontacting means to achieve rapid, biventricular circulatory support.’ l’ D y n amic cardiomyoplasty using blood-contacting latissimus dorsi muscle requires weeks of muscle preconditioning before transfer around the heart and provides only limited assistance in its present state of development antl has largely been abandoned. Non-blood-contacting biventricular support using DMVA has the following advantages:

Future directions for resuscitation research. V. Ultra-advanced life support

Standard external cardiopulmonary resuscitation (SECPR) frequently produces very low perfusion pressures, which are inadequate to achieve restoration of spontaneous circulation (ROSC) and intact survival, particularly when the heart is diseased. Ultra-advanced life support (UALS) techniques may allow support of vital organ systems until either the heart recovers or cardiac repair or replacement is performed. Closed-chest emergency cardiopulmonary bypass (CPB) provides control of blood flow, pressure, composition and temperature, but has so far been applied relatively late. This additional low-flow time may preclude conscious survival. An easy, quick method for vessel access and a small preprimed system that could be taken into the field are needed. Open-chest CPR (OCCPR) is physiologically superior to SECPR, but has also been initiated too late in prior studies. Its application in the field has recently proven feasible. Variations of OCCPR, which deserve clinical trials inside and outside hospitals, include `minimally invasive direct cardiac massage' (MIDCM), using a pocket-size plunger-like device inserted via a small incision and `direct mechanical ventricular actuation' (DMVA), using a machine that pneumatically drives a cup placed around the heart. Other novel UALS approaches for further research include the use of an aortic balloon catheter to improve coronary and cerebral blood flow during SECPR, aortic flush techniques and a double-balloon aortic catheter that could allow separate perfusion (and cooling) of the heart, brain and viscera for optimal resuscitation of each. Decision-making, initiation of UALS methods and diagnostic evaluations must be rapid to maximize the potential for ROSC and facilitate decision-making regarding long-term circulatory support versus withdrawal of life support for hopeless cases. Research and development of UALS techniques needs to be coordinated with cerebral resuscitation research.

Experimental Aortocoronary Saphenous Vein Graft Function After Mechanical Cardiac Massage With the Anstadt Cup

Direct mechanical ventricular actuation (DMVA) using the Anstadt Cup can achieve total circulatory support by massaging the fibrillating, asystolic, or failing heart. The device does not contact the blood or cause significant myocardial trauma. The purpose of this study was to assess the functional integrity of saphenous vein grafts (SVGs) subjected to DMVA vs cardiopulmonary bypass (CPB). Human SVGs were used to bypass the ligated left anterior descending coronary artery in 11 dogs. Animals then received 2 hrs of either DMVA (n = 5) or CPB (n = 6) during sustained ventricular fibrillation. Grafted and non grafted (control) SVG segments were then studied in vitro. SVG patency was confirmed by radiolabeled microspheres and pathologic evaluation. Matched SVG specimens (control) were not exposed to circulatory support. All SVGs were subjected to isometric tension studies. SVG contractile responses to norepinephrine, bradykinin, serotonin, and histamine were assessed. Maximal response to all agonists were similar between control SVG segments compared to either CPB or DMVA support (p = NS, ANOVA). All cumulative dose response curves were similar after DMVA vs CPB support. In conclusion, the smooth muscle function of SVGs in this study was not significantly altered by DMVA support. Therefore, short-term DMVA support does not impair patency or adversely effect the functional integrity of smooth muscle within SVGs.

Experimental Aortocoronary Saphenous Vein Graft Function After Mechanical Cardiac Massage With the Anstadt Cup

Direct mechanical ventricular actuation (DMVA) using the Anstadt Cup can achieve total circulatory support by massaging the fibrillating, asystolic, or failing heart. The device does not contact the blood or cause significant myocardial trauma. The purpose of this study was to assess the functional integrity of saphenous vein grafts (SVGs) subjected to DMVA vs cardiopulmonary bypass (CPB). Human SVGs were used to bypass the ligated left anterior descending coronary artery in 11 dogs. Animals then received 2 hrs of either DMVA (n = 5) or CPB (n = 6) during sustained ventricular fibrillation. Grafted and non grafted (control) SVG segments were then studied in vitro. SVG patency was confirmed by radiolabeled microspheres and pathologic evaluation. Matched SVG specimens (control) were not exposed to circulatory support. All SVGs were subjected to isometric tension studies. SVG contractile responses to norepinephrine, bradykinin, serotonin, and histamine were assessed. Maximal response to all agonists were similar between control SVG segments compared to either CPB or DMVA support (p = NS, ANOVA). All cumulative dose response curves were similar after DMVA vs CPB support. In conclusion, the smooth muscle function of SVGs in this study was not significantly altered by DMVA support. Therefore, short-term DMVA support does not impair patency or adversely effect the functional integrity of smooth muscle within SVGs.

Prolonged total circulatory support using direct mechanical ventricular actuation.

Direct mechanical ventricular actuation (DMVA) is a unique, non blood contacting method for biventricular cardiac assist. Although DMVA has successfully provided cardiac assist for more than 7 days in humans, with long-term survival, its potential for long-term circulatory support has not been adequately investigated. DMVA has not been studied in the large ruminants commonly used to evaluate support devices. To develop a large animal experimental model of prolonged total circulatory support using DMVA, Suffolk sheep (n = 10) underwent sterile instrumentation for hemodynamic and chemistry monitoring. After baseline values were obtained, a left lateral thoracotomy and pericardotomy were performed. Upon electrical ventricular fibrillation (VF), DMVA was begun and the thoracotomy closed. Total circulatory support was continued until mean arterial pressure (MAP) persisted below 50% of the baseline value for more than 1 hr, with a goal of 7 days' support. Mean duration (plus or minus the standard deviation [SD]) of circulatory support was 65.9 +/- 56.8 hr (range, 10-168 hr). Pressors were not used during DMVA support. The subject supported for the maximal time (7 days) was defibrillated into sinus rhythm. No CK-MB fraction was greater than 1%, suggesting that DMVA, even with prolonged application during VF, does not result in myocardial injury. Blood urea nitrogen and creatinine levels indicate renal function was preserved. The model described represents the longest period any animal has been supported in VF using DMVA. This new model will be useful in determining what limitations, if any, exist to the prolonged use of DMVA for circulatory support.

The effect of cardiac compression on defibrillation efficacy and the upper limit of vulnerability.

We determined the effects of decreasing the ventricular blood volume and altering cardiac geometry on defibrillation, the upper limit of vulnerability (ULV), and the relationship between them. In six pigs, fibrillation/defibrillation trials were performed with a left ventricular apex patch to a superior vena cava catheter electrode configuration and a biphasic waveform. Thirty trials each were performed on a compressed versus noncompressed (normal) heart. Compression was achieved using direct mechanical ventricular actuation. Dose-response curves were constructed, and the 50% probability points (ED50) were compared for leading edge voltage (LEV), leading edge current (LEI), and total energy (TE). In another 12 pigs, triplicate defibrillation thresholds (DFTs) and ULVs were determined for each heart state. The T wave was scanned with shocks in 10-msec steps for determining the ULV. Compression resulted in decreased ED50s for LEV (delta = 138 +/- 77 V, P < 0.05, mean +/- SD), LEI (delta = 1.57 +/- 0.7 A, P < 0.05), and TE (delta = 4.9 +/- 3.6 J, P < 0.05) compared to normal. In the second study, compression significantly reduced DFT (P < 0.02) and ULV (P < 0.02) for LEV, LEI, and TE compared to normal. The ULV tended to be lower than the DFT for the normal heart state (delta = 23 +/- 46 V LEV: P = NS). However, the ULV was significantly greater than the DFT for the compressed heart state (delta = 19 +/- 25 V LEV; P < 0.03). Shock delivery during cardiac compression improves defibrillation efficacy. Additionally, cardiac compression decreases both DFT and ULV, which supports the ULV hypothesis of defibrillation. Finally, maintaining the heart's geometric and volumetric state during ULV testing in paced rhythm and DFT testing in ventricular fibrillation moves the ULV higher than the DFT-the position predicted by the ULV hypothesis for defibrillation.

First successful bridge to cardiac transplantation using direct mechanical ventricular actuation

Currently available ventricular assist devices are technically difficult to implant, require continuous anticoagulation, and are associated with hemorrhagic and thromboembolic complications. Direct mechanical ventricular actuation is a biventricular assist device that can be applied in 3 to 5 minutes through a left anterior thoracotomy and has no direct blood contact or need for anticoagulation. The present study was designed to determine the effects of direct mechanical ventricular actuation in total biventricular circulatory support. Cardiogenic shock refractory to standard therapy developed in 2 patients awaiting cardiac transplantation. Direct mechanical ventricular actuation was applied and provided immediate hemodynamic stabilization in both. All inotropic agents and intraaortic balloon support were then discontinued. Fifty-six hours of circulatory support bridged the first patient to successful cardiac transplantation without complication. The patient is alive and well more than 1 year later without incident of infection or rejection. The second patient suffered cardiac arrest and required closed chest cardiopulmonary resuscitation before device application. After 45 hours of support, it was determined that irreversible neurologic injury had occurred and direct mechanical ventricular actuation was discontinued. Neither patient's native heart exhibited any histologic evidence of device-related trauma. Direct mechanical ventricular actuation has undergone limited clinical investigation since its original description 25 years ago, but in these initial trials, the device has proved effective. The concept of mechanically actuating the ventricles appears to be a valuable, yet under-utilized method of total circulatory support.

Direct Mechanical Ventricular Actuation for Cardiac Arrest in Humans: A Clinical Feasibility Trial

Direct mechanical ventricular actuation (DMVA) is a non-blood-contacting method of biventricular cardiac massage which may be applied expediently for total circulatory support. The purpose of this study was to assess the feasibility of DMVA application for patients suffering refractory cardiac arrest. Following informed consent, DMVA was applied in 22 patients. Vascular access for hemodynamic monitoring was possible in only 12 patients, whose outcomes serve as the basis for this report. The mean age of the patients was 48.2 +/- 4.2 years (seven men; five women). The average time from witnessed cardiac arrest to DMVA application was 81 +/- 9 minutes. Application took less than two minutes from the time of skin incision and resulted in immediate hemodynamic improvement. Systolic and diastolic blood pressures averaged 78 +/- 4 and 41 +/- 4 mm Hg, respectively, with a mean cardiac output of 3.14 +/- 0.18 L/min during a mean of 228 +/- 84 minutes of circulatory support (range, 25 minutes to 18 hours). In selected cases the device was temporarily removed for 2 to 3 minutes and open-chest cardiac massage (OCCM) performed at similar compression rates. DMVA increased arterial pressures 65 percent and cardiac output 190 percent compared to OCCM. Initial arterial pH (7.12 +/- 0.04) improved by the time the device was removed (7.24 +/- 0.05). Serum lactate levels decreased from 18.0 +/- 2.3 mumol/L to 14.9 +/- 2.9 mumol/L. Four patients were successfully defibrillated: two had inadequate cardiac function and died within 1 h, and two were successfully resuscitated, but later died from cardiac failure and respiratory insufficiency. Another patient regained normal neurologic function during DMVA and was successfully bridged to cardiopulmonary bypass for emergent coronary artery bypass grafting, but died later from myocardial infarction. There were only two complications: (1) a cardiac laceration during pericardiotomy (1/22 patients); and (2) a ventricular rupture during OCCM (1/22). No complication resulted from the device. We found DMVA to be a feasible method for acute cardiovascular stabilization in victims suffering refractory cardiac arrest. Human clinical trials employing earlier DMVA application are required to determine its resuscitative potential.

Direct mechanical ventricular actuation: A review

Direct mechanical ventricular actuation (DMVA) is a non-blood contacting method of circulatory support that can be rapidly instituted for resuscitation. DMVA is superior to conventional methods (open and closed-chest cardiac massage) in providing reliable cardiovascular stabilization for resuscitation following cardiac arrest. Furthermore, DMVA has important advantages including rapid application, technical simplicity, and avoidance of blood contact compared to other resuscitation devices (cardiopulmonary bypass and blood pumps). This review summarizes laboratory and clinical applications of DMVA.

Comparison of direct mechanical ventricular actuation and cardiopulmonary bypass.

Direct mechanical ventricular actuation (DMVA) is a non-blood-contacting method for biventricular support. To compare effects of DMVA and cardiopulmonary bypass (CPB), 13 swine were supported by DMVA or CPB during 4 hours of ventricular fibrillation. Hearts were then rapidly excised and sectioned into right ventricular (RV) and left ventricular (LV) free wall slabs and subjected to total normothermic ischemia. Time to peak ischemic contracture (TIC) of LV endocardium (endo), LV epicardium (epi) and RV were determined using Millar needle transducers. Mean TIC was compared between DMVA (n = 6), CPB (n = 7), and control (n = 18). Significant decreases in LV endo TIC were found after DMVA (53.3 +/- 3.3 min) and CPB (56.2 +/- 2.4 min) compared with control (62.5 +/- 1.0), p less than 0.05. Myocardial blood flow was measured using microspheres during normal sinus rhythm and after 2 and 4 hr of circulatory support. Nonsignificant decreases in endo flow occurred during CPB and DMVA compared with control. LV endo adenosine triphosphate (ATP) levels (mumol/g dry weight) were significantly decreased after DMVA (9.0 +/- 2.5) and CPB (4.0 +/- 2.7) compared with control (17.8 +/- 0.6), p less than 0.05. Although CPB maintained mean arterial pressure by increased pump flows (mean, 129 ml/kg/min) and LV intracavitary pressures were kept below 5 mmHg with LV venting, resulting endo flows and ATP levels were decreased. DMVA generated decreased cardiac outputs (mean, 67 ml/kg/min) under these vasodilated states, yet maintained endo flow and ATP levels as well as CPB. These experimental data show that different mechanisms of myocardial perfusion and metabolism result from CPB and DMVA.

Comparison of Direct Mechanical Ventricular Actuation and Cardiopulmonary Bypass

Direct mechanical ventricular actuation (DMVA) is a nonblood-contacting method for biventricular support. To compare effects of DMVA and cardiopulmonary bypass (CPB), 13 swine were supported by DMVA or CPB during 4 hours of ventricular fibrillation. Hearts were then rapidly excised and sectioned into right ventricular (RV) and left ventricular (LV) free wall slabs and subjected to total nor-mothermic ischemia. Time to peak ischemic contracture (TIC) of LV endocardium (endo), LV epicardium (epi) and RV were determined using Millar needle transducers. Mean TIC was compared between DMVA (n = 6), CPB (n = 7), and control (n = 18). Significant decreases in LV endo TIC were found after DMVA (53.3 ± 3.3 min) and CPB (56.2 ± 2.4 min) compared with control (62.5 ± 1.0), p < 0.05. Myocardial blood flow was measured using microspheres during normal sinus rhythm and after 2 and 4 hr of circulatory support. Nonsignificant decreases in endo flow occurred during CPB and DMVA compared with control. LV endo adenosine triphosphate (ATP) levels (μmol/g dry weight) were significantly decreased after DMVA (9.0 ± 2.5) and CPB (4.0 ± 2.7) compared with control (17.8 ± 0.6), p < 0.05. Although CPB maintained mean arterial pressure by increased pump flows (mean, 129 ml/kg/min) and LV in-tracavitary pressures were kept below 5 mmHg with LV venting, resulting endo flows and ATP levels were decreased. DMVA generated decreased cardiac outputs (mean, 67 ml/kg/min) under these vasodilated states, yet maintained endo flow and ATP levels as well as CPB. These experimental data show that different mechanisms of myocardial perfusion and metabolism result from CPB and DMVA.