Copulsation balloon for right ventricular assistance: preliminary trials. (1/805)

BACKGROUND: Options for management of acute right ventricular (RV) failure are limited. This report describes preliminary testing of a temporary RV assist device that acts by direct compression of the RV. The system comprises a pancake-shaped silicone balloon (5 cm diameter) connected to a drive console that delivers a 65-mL pneumatic pulse during cardiac systole. METHODS AND RESULTS: Initial in vivo tests were performed on 6 pigs (weight, 41+/-4 kg). RV wall motion and stroke volume were monitored via transesophageal echocardiography. Acute RV failure was created by graded right coronary ligation, which yielded a 63% reduction in RV stroke volume (39.9+/-8.2 to 14.7+/-1.9 mL; P<0.002). We secured the balloon over the RV free wall by attaching it to the edges of the opened pericardium. The sternum was then reapproximated, and data were collected with the device off and on (every beat). Device placement had no deleterious effect on RV function. Balloon activation returned RV stroke volumes to normal (37.8+/-9.2 mL) and increased mean pulmonary artery pressures from 13+/-2 to 16+/-3 mm Hg (P<0.01). RV compression did not induce or exacerbate tricuspid regurgitation. Mean aortic pressure improved from postinfarction levels but did not return to normal. CONCLUSIONS: We conclude that the pulmonary circulation can be supported in the short term via cardiac compression and that balloon copulsation techniques for short-term RV failure should be tested in long-term models.  (+info)

Improved survival rates support left ventricular assist device implantation early after myocardial infarction. (2/805)

OBJECTIVES: Implantation of left ventricular assist devices (LVADs) early after acute myocardial infarction (MI) has traditionally been thought to be associated with high mortality rates due to technical limitations and severe end-organ dysfunction. At some experienced centers, doctors have refrained from earlier operation after MI to allow for a period of hemodynamic and end-organ stabilization. METHODS: We retrospectively investigated the effect of preoperative MI on the survival rates of 25 patients who received a Thermocardiosystems Incorporated LVAD either <2 weeks (Early) (n = 15) or >2 weeks (Late) (n = 10) after MI. Outcome variables included perioperative right ventricular assistance (and right-sided circulatory failure), hemodynamic indexes, percent transplanted or explanted, and mortality. RESULTS: No statistically significant differences were demonstrated between demographic, perioperative or hemodynamic variables between the Early and Late groups. Patients in the Early group demonstrated a lower rate of perioperative mechanical right ventricular assistance, but had a higher rate of perioperative inhaled nitric oxide use. In addition, 67% of patients in the Early group survived to transplantation and 7% to explantation, findings comparable to those in the Late group (60% and 0% respectively). CONCLUSIONS: This clinical experience suggests that patients may have comparable outcomes whether implanted early or late after acute MI. These data therefore support the early identification and timely application of this modality in post-MI LVAD candidates, as this strategy may also reveal a subgroup of patients for whom post-MI temporary LVAD insertion may allow for full ventricular recovery.  (+info)

Children may survive severe myocarditis with prolonged use of biventricular assist devices. (3/805)

The outcome of acute myocarditis with cardiogenic shock is poor. In some children in whom aggressive medical treatment fails, artificial replacement of heart function may offer lifesaving support until the myocardium has recovered. Four previously healthy children (three boys aged 4, 6, and 1 years; one girl aged 5) developed acute myocarditis with ventricular failure and multiorgan dysfunction caused by low cardiac output. Biventricular assist devices (BVAD) were implanted for prolonged support. In three children cardiac function improved and after up to 21 days mechanical support could be withdrawn. They had full recovery of heart function. In the fourth patient there was no myocardial recovery after a period of 20 days. He underwent orthotopic heart transplantation with an uneventful postoperative course. Prolonged circulatory support with BVAD is an effective method for bridging until cardiac recovery or transplantation in children.  (+info)

Decreased expression of tumor necrosis factor-alpha in failing human myocardium after mechanical circulatory support : A potential mechanism for cardiac recovery. (4/805)

BACKGROUND: An increasing number of observations in patients with end-stage heart failure suggest that chronic ventricular unloading by mechanical circulatory support may lead to recovery of cardiac function. Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine capable of producing pulmonary edema, dilated cardiomyopathy, and death. TNF-alpha is produced in the myocardium in response to volume overload; however, the effects of normalizing ventricular loading conditions on myocardial TNF-alpha expression are not known. We hypothesize that chronic ventricular unloading by the placement of a left ventricular assist device (LVAD) may eliminate the stress responsible for persistent TNF-alpha expression in human failing myocardium. METHODS AND RESULTS: Myocardial tissue was obtained from normal hearts and from paired samples of 8 patients with nonischemic end-stage cardiomyopathy at the time of LVAD implantation and removal. Tissue sections were stained for TNF-alpha, and quantitative analysis of the stained area was performed. We found that TNF-alpha content decreased significantly after LVAD support. Furthermore, the magnitude of the changes did not correlate with the length of LVAD support, although greater reductions in myocardial TNF-alpha content were found in patients who were successfully weaned off the LVAD who did not require transplantation. CONCLUSIONS: These data show for the first time that chronic mechanical circulatory assistance decreases TNF-alpha content in failing myocardium; furthermore, we suggest that the magnitude of the change may predict which patients will recover cardiac function.  (+info)

Surgical management of the patient with an implanted cardiac device: implications of electromagnetic interference. (5/805)

OBJECTIVE: To identify the sources of electromagnetic interference (EMI) that may alter the performance of implanted cardiac devices and develop strategies to minimize their effects on patient hemodynamic status. SUMMARY BACKGROUND DATA: Since the development of the sensing demand pacemaker, EMI in the clinical setting has concerned physicians treating patients with such devices. Implanted cardiovertor defibrillators (ICDs) and ventricular assist devices (VADs) can also be affected by EMI. METHODS: All known sources of interference to pacemakers, ICDs, and VADs were evaluated and preventative strategies were devised. RESULTS: All devices should be thoroughly evaluated before and after surgery to make sure that its function has not been permanently damaged or changed. If electrocautery is to be used, pacemakers should be placed in a triggered or asynchronous mode; ICDs should have arrhythmia detection suspended before surgery. If defibrillation is to be used, the current flow between the paddles should be kept as far away from and perpendicular to the lead system as possible. Both pacemakers and ICDs should be properly shielded if magnetic resonance imaging, positron emission tomography, or radiation therapy is to be used. The effect of EMI on VADs depends on the model. Magnetic resonance imaging adversely affects all VADs except the Abiomed VAD, and therefore its use should be avoided in this population of patients. CONCLUSIONS: The patient with an implanted cardiac device can safely undergo surgery as long as certain precautions are taken.  (+info)

Extracorporeal life support to left ventricular assist device bridge to heart transplant: A strategy to optimize survival and resource utilization. (6/805)

BACKGROUND: The use of extracorporeal life support (extracorporeal membrane oxygenation [ECMO]) as a direct bridge to heart transplant in adult patients is associated with poor survival. Similarly, the use of an implantable left ventricular assist device (LVAD) to salvage patients with cardiac arrest, severe hemodynamic instability, and multiorgan failure results in poor outcome. The use of LVAD implant in patients who present with cardiogenic shock who have not been evaluated for transplantation or who have sustained a recent myocardial infarction also raises concerns. ECMO may provide reasonable short-term support to patients with severe hemodynamic instability, permit recovery of multiorgan injury, and allow time to complete a transplant evaluation before long-term circulatory support with an implantable LVAD is instituted. After acquisition of the HeartMate LVAD (Thermo Cardiosystems, Inc), we began using ECMO as a bridge to an implantable LVAD and, subsequently, to transplantation in selected high-risk patients. METHODS AND RESULTS: From October 1, 1996, through September 30, 1998, 32 adult patients who presented with refractory cardiogenic shock (cardiac index <2.0 L. min(-1). m(-2), with systolic blood pressure <100 mm Hg and pulmonary capillary wedge pressure >/=24 mm Hg and dependent on >/=2 inotropes with or without intra-aortic balloon pump) were evaluated and accepted as candidates for mechanical assistance as a bridge to transplant. Of the 32 patients, 14 (group I) had a cardiac arrest or severe hemodynamic instability (systolic blood pressure 3 mg/dL or oliguria; international normalized ratio >1.5 or transaminases >5 times normal or total bilirubin >3 mg/dL; and needing mechanical ventilation). Group I patients were placed on ECMO support; 7 underwent subsequent LVAD implant and 1 was bridged directly to transplant. Six patients in group I survived to transplant hospitalization discharge. The remaining 18 patients (group II) underwent LVAD implant without ECMO support; 12 survived to transplant hospitalization discharge and 2 remained alive with ongoing LVAD support and awaited transplant. One-year actuarial survival from the initiation of circulatory support was 43% in group I and 75% in group II. One-year actuarial survival from the time of LVAD implant in group I, conditional on surviving ECMO, was 71% (P=NS compared with group II). CONCLUSIONS: In appropriately selected high-risk patients, the rate of LVAD survival after initial ECMO support was not significantly different from the survival rate after LVAD support alone. An initial period of resuscitation with ECMO is an effective strategy to salvage patients with extreme hemodynamic instability and multiorgan injury. Use of LVAD resources is improved by avoiding LVAD implant in a very-high-risk cohort of patients who do not survive ECMO.  (+info)

Quantitative changes in T-cell populations after left ventricular assist device implantation: relationship to T-cell apoptosis and soluble CD95. (7/805)

BACKGROUND: Left ventricular assist devices (LVADs) are currently being evaluated as permanent therapy for end-stage heart failure. Because life-threatening infections limit successful long-term device implantation, we investigated the relationship between quantitative T-cell defects in LVAD recipients and CD95-mediated T-cell apoptosis. METHODS AND RESULTS: Immunological studies were performed in NYHA class IV patients awaiting cardiac transplantation who received either a TCI Heartmate left ventricular assist device (LVAD) or medical management. Fluorochrome-labeled Mabs were used in T-cell phenotypic analyses. T-cell apoptosis was measured by annexin V binding of T cells cultured in medium for 24 hours. Circulating serum levels of soluble CD95 were measured by ELISA. LVAD recipients had a relative lymphopenia and reduction in CD4 T-cell levels compared with NYHA class IV heart failure controls. These observations were confirmed in a longitudinal study in LVAD recipients, which showed that device implantation was accompanied by progressive and sustained reductions in circulating CD4 T-cell levels. These abnormalities in LVAD recipients were accompanied by increased levels of circulating soluble CD95 and by excessive CD4 and CD8 T-cell apoptosis. Susceptibility to induction of apoptosis was >2-fold greater for CD4 T cells than for CD8 T cells. CONCLUSIONS: These results suggest that the reduction in CD4 T-cell levels accompanying LVAD implantation is a consequence of an augmented pathway of CD95-mediated apoptosis. The clinical consequences of these abnormalities may include increased prevalence of systemic infections.  (+info)

Myocardial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. (8/805)

BACKGROUND: In patients with end-stage heart failure, characterized by an increased susceptibility to cardiomyocyte apoptosis and a labile cardiomyocyte calcium homeostasis, a ventricular assist device (VAD) is implanted for bridging to cardiac transplantation and results in myocardial unloading. Although phenotype changes in the failing heart are assumed to result from hemodynamic overload, the reversibility of these changes under unloading is unknown. METHODS AND RESULTS: By use of quantitative reverse-transcription polymerase chain reaction, mRNA expression analyses were performed on left ventricular specimens obtained from 10 nonfailing donor hearts (from 8 patients with dilated cardiomyopathy and 2 patients with coronary heart disease) at the time of VAD implantation and 36 to 169 days later during VAD removal with subsequent cardiac transplantation. In terminally failing hearts before VAD support, left ventricular mRNA analyses revealed increased Pro-ANP, reduced antiapoptotic Bcl-x(L) and antiapoptotic Fas isoform FasExo6Del, and a decreased ratio of sarcoplasmic reticulum Ca(2+)-ATPase per sarcolemmal Na(+)-Ca(2+) exchanger in comparison with nonfailing ventricles. After VAD unloading, ventricular transcription of Pro-ANP was immediately normalized, and apoptotic DNA fragmentation was attenuated. In patients with dilated cardiomyopathy, mRNAs of Bcl-x(L) and FasExo6Del/Fas were enhanced depending on time on VAD. The Bcl-x(L) mRNA level correlated positively with that of the Bcl-x(L) protein. Transcription of sarcoplasmic reticulum Ca(2+)-ATPase/Na(+)-Ca(2+) exchanger demonstrated recovery in only 4 of 10 patients. CONCLUSIONS: Mechanical support of the failing heart induces a time-dependent change in myocardial gene expression compatible with a decreased susceptibility to apoptosis.  (+info)