Christos Charitos

Right heart failure post left ventricular assist device implantation

Right heart failure (RHF) is a frequent complication following left ventricular assist device (LVAD) implantation. The incidence of RHF complicates 20-50% (range, 9-44%) of cases and is a major factor of postoperative morbidity and mortality. Unfortunately, despite the fact that many risk factors contributing to the development of RHF after LVAD implantation have been identified, it seems to be extremely difficult to avoid them. Prevention of RHF consists of the management of the preload and the afterload of the right ventricle with optimum inotropic support. The administration of vasodilators designed to reduce pulmonary vascular resistance is standard practice in most centers. The surgical attempt of implantation of a right ventricular assist device does not always resolve the problem and is not available in all cardiac surgery centers.

Comparison of pulsatile with nonpulsatile mechanical support in a porcine model of profound cardiogenic shock.

The aim of this study was to examine whether pulsatility by intraaortic balloon counterpulsation (IABP) is an important adjunct to the treatment of profound cardiogenic shock (CS) with a widely used, nonpulsatile centrifugal pump (CP). In each of 18 anesthetized, open chest pigs, the outflow cannula of the CP was inserted in the aortic arch through the right external carotid artery, and the inflow cannula of the CP was placed in the left atrium. A 40 cc IABP was subsequently placed in the descending aorta through the left external carotid artery. CS was induced by occlusion of coronary arteries and the infusion of propranolol and crystalloid fluid. Mean aortic pressure, pulse pressure, aortic end diastolic pressure, left ventricular end diastolic pressure, right atrial pressure, and heart rate were monitored. Cardiac output and left anterior descending artery flow were measured with a transit time ultrasound flowmeter. During profound CS, life sustaining hemodynamics were maintained only with the support of the assist devices. Hemodynamic support with the CP was associated with a nearly nonpulsatile flow and a pulse pressure of 7 ± 4 mm Hg, which increased to 33 ± 10 mm Hg (p = 0.000) after combining the CP with the IABP. Compared with the hemodynamic support offered by the CP alone, addition of the IABP increased mean aortic pressure from 40 ± 15 to 50 ± 16 mm Hg (p = 0.000), cardiac output from 810 ± 194 to 1,200 ± 234 ml/min (p = 0.003), and left anterior descending artery flow from 26 ± 10 to 39 ± 14 ml/min (p = 0.001). In profound CS, mechanical support provided by a continuous flow CP is enhanced by the added pulsatility of the IABP.

Mechanical Assistance by Intra-Aortic Balloon Pump Counterpulsation During Reperfusion Increases Coronary Blood Flow and Mitigates the No-Reflow Phenomenon: An Experimental Study

The effects of the intra-aortic balloon pump (IABP) counterpulsation on the extent of myocardial infarction (MI), the no-reflow phenomenon (NRP), and coronary blood flow (CBF) during reperfusion in an ischemia-reperfusion experimental model have not been clarified. Eleven pigs underwent occlusion of the mid left anterior descending coronary artery for 1 h, followed by reperfusion for 2 h. CBF, distal to the occlusion site, was measured. In six experiments, IABP support began 10 min before, and continued throughout reperfusion (IABP Group). Five pigs without IABP support served as controls. At the end of each experiment, the myocardial area at risk (MAR) of infarction and the extent of MI and NRP were measured. Hemodynamic measurements at baseline and during coronary occlusion were similar in both groups. During reperfusion, systolic aortic blood pressure was significantly lower in the IABP Group than in controls. In the IABP Group, CBF reached a peak at 5 min of reperfusion, gradually decreased, but remained higher than at baseline, and significantly higher than in controls throughout the 2 h of reperfusion. In controls, CBF increased significantly above baseline immediately after the onset of reperfusion, then returned to baseline within 90 min. The extent of NRP (37 ± 25% vs. 68 ± 17%, P = 0.047) and MI (39 ± 23% vs. 67 ± 13%, P = 0.036), both expressed as percentage of MAR, was significantly less in the IABP group than in controls. After prolonged myocardial ischemia, IABP assistance started just 10 min before and throughout reperfusion increased CBF and limited infarct size and extent of NRP.

Use of continuous subcutaneous anesthetic infusion in cardiac surgical patients after median sternotomy

The use of opioid analgesics to control pain after median sternotomy in cardiac surgical patients is worldwide accepted and established. However, opioids have a wide range of possible side effects, concerning prolonged extubation time, gastrointestinal tract dyskinesia and urinary tract disorders mostly retention. All these may lead to a prolonged ICU stay or overall hospitalization time increase.ObjectiveTo determine whether a continuous subcutaneous regional anesthetic infusion delivered directly to the sternotomy site would result in decreased levels of postoperative pain and opioid requirements in cardiac surgical patients undergoing median sternotomy.MethodThe continuous subcutaneous infusion (OnQ Painbuster system) was applied in 37 patients. 3 patients were exempted due to prolonged ICU stay. 29 patients underwent CABG, 5 had AVR, 1 MVR and modified Maze, 1 patient had a 3-valve repair due to endocarditis and another one had reconstruction of the left ventricle. Requirements of opioid analgesics were recorded for 96 hours after operation. Pain was assessed using the visual analog scale and the total postoperative hospital length of stay was also measured.ResultsThe postoperative pain was significantly diminished (0 – 3 at VAS). The mean postoperative length of stay was 5,8 days, rather improved compared to the average stay of 6,7 days.ConclusionContinuous subcutaneous infusion of ropivacaine directly at the median sternotomy significantly diminishes postoperative pain and the need for opioid analgesic use. Moreover, it seems to reduce overall postoperative length of stay for all cardiac surgical patients.

No effect of stem cell mobilization with GM-CSF on infarct size and left ventricular function in experimental acute myocardial infarction.

Abstract.Objectives:To evaluate the effect of bone marrowpluripotent stem cell mobilization with granulocyte-monocyte colony stimulating factor (GMCSF) on infarct size and left ventricular function, in the setting of acute myocardial infarction, with a protocol easily applicable in clinical practice.Methods:Ten pigs underwent left thoracotomy and left anterior descending coronary artery occlusion for 1 h, followed by reperfusion. After 50 min of arterial occlusion, the animals were randomly divided between treatment with placebo (Group 1) and subcutaneous GM-CSF (Group 2). The thoracotomy was closed and the animals recovered. In Group 2, GM-CSF, 20 µg/kg, was administered daily, 5 days/week, for 3 weeks. Echocardiograms were obtained at 5 and 28 days after acute myocardial infarction. At 30 days, infarct size, expressed as a percentage of the whole left ventricular mass, was measured.Results:The white blood cell count increased from 13000 ± 3338/µl to 28700 ± 4916/µl (p = 0.001) in the GM-CSF-treated group. Infarct size was 7.8 ± 6.1% in Group 1 vs 7.5 ± 7.7% in Group 2 (ns). Similarly, no significant difference was observed between the 2 study groups in any of the echocardiographic measurements made at 28 days.Conclusions:Subcutaneous GMCSF administered during the early post acute myocardial infarction period neither decreased infarct size nor improved left ventricular function. Other protocols for mobilization of stem cells and their concentration in the injured area should be developed to combine efficacy and clinical applicability.

A vavleless high stroke volume counterpulsation device restores hemodynamics in patients with congestive heart failure and intractable cardiogenic shock awaiting heart transplantation

The paraaortic counterpulsation device is a round pumping chamber with one valveless opening 20 mm in diameter and a 100 ml stroke volume. The paraaortic counterpulsation device was implanted on the ascending aorta of three male patients with intractable cardiogenic shock. Patients were assisted for 4 hours and 8 and 54 days, respectively; the first patient died as a result of nonresponding peripheral vasodilation and the other two died of septic shock. The two patients who were assisted for 8 and 54 days were conscious and able to function in a limited manner during the mechanical assistance. Discontinuation of the mechanical support for a few seconds was followed by low systolic arterial pressure (30 to 60 mm Hg) and syncopal episodes. Biochemical tests and autopsy results in these patients showed no evidence of blood cell destruction, thrombus formation, brain infarction, or other distal emboli. In conclusion, satisfactory hemodynamic effects, excellent biocompatibility, and simplicity of the implantation procedure in these patients encourage the use of the paraaortic counterpulsation device as a bridge to heart transplantation.

Effects of transient myocardial ischemia on the ventricular defibrillation threshold

Background: Acute myocardial ischemia and the mode of ventricular fibrillation (VF) induction influence the ventricular defibrillation threshold (DFT).

Preclinical evaluation of the abdominal aortic counterpulsation device

A valveless, single-orifice abdominal aortic counterpulsation device (AACD) was implanted retroperitoneally on the abdominal aorta and was pumped continuously, providing aortic diastolic augmentation for 45 +/- 4.9 days in four calves (group A). The hematocrit, lactate dehydrogenase (LDH), bilirubin, blood urea nitrogen, and creatinine were obtained before implantation and weekly thereafter. Biocompatibility data were compared to those obtained from 11 calves (group B) that received a total artificial heart (TAH) and were electively terminated 50.0 +/- 19.5 days after implantation. The hematocrit values in the first week were 20.9 +/- 11.5% and 39.8 +/- 11.5% below control values for group A and group B, respectively (p less than 0.02); in the sixth week they were 5.1 +/- 14.6% above control values (group A) and 22.6 +/- 9.0% below control values (group B) (p less than 0.05). LDH did not change in group A, while in group B it was constantly about 100% above control values. Autopsy revealed one to three infarcts 1 to 3 mm in diameter in 63% of the kidneys in group A, while in all of group B kidneys there were multiple infarcts of more than 10 mm. After the induction of left ventricular (LV) failure, the AACD decreased the LV end-diastolic pressure (EDP) by 21.2% (p less than 0.005) and the aortic (AO) EDP by 18% (p less than 0.005). It increased the endocardial viability ratio by 300% (p less than 0.0005), and the cardiac index by 66.9% (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Increase in coronary blood flow by intra-aortic balloon counterpulsation in a porcine model of myocardial reperfusion

BACKGROUND Studies of the IABP have reported variable effects on coronary blood flow (CBF). The purpose of the present study was to measure the changes in coronary blood flow induced by intra-aortic balloon pump (IABP) counterpulsation in normal and reperfused porcine myocardium. METHODS A 30-ml IABP was placed in the descending aorta of 6 open-chest pigs. Each pig underwent occlusion of the mid-left anterior descending (LAD) coronary artery for 1 h, followed by reperfusion for 2 h. The effects of IABP support on systolic aortic pressure (SAP) and aortic end-diastolic pressure were recorded. The mean CBF, distal to the LAD occlusion site was measured at baseline and during reperfusion, with and without IABP counterpulsation. RESULTS The IABP decreased SAP and aortic end-diastolic pressure in normal and reperfused myocardium, and maintained a peak aortic diastolic augmentation at the level of SAP. In normal myocardium, the IABP decreased mean CBF by 8.4+/-2.2% (p<0.001). At 2, 15, 30, 60, 90 and 120 min of reperfusion, the IABP increased mean CBF by 11.5+/-6.8%, 8.0+/-7.0%, 11.2+/-6.9%, 12.4+/-12.9%, 23.5+/-9.9% and 8.9+/-6.9%, of the corresponding value without the assistance of the IABP (all p<0.05). CONCLUSIONS In the normal heart, IABP counterpulsation decreased CBF, probably because of a decrease in myocardial oxygen demand from a decreased afterload. During reperfusion the IABP increased CBF, suggesting that it might effectively mitigate the no-reflow phenomenon.

Late-onset right ventricular dysfunction after mechanical support by a continuous-flow left ventricular assist device.

BACKGROUND Right heart failure (RHF) is a serious post-operative complication of left ventricular assist device (LVAD) implantation, with significant morbidity and mortality. Many clinical, hemodynamic and laboratory variables have been shown to have prognostic value for appearance of RHF. We sought to investigate the incidence of new-onset right ventricular dysfunction (RVD) complicating the long-term use of LVADs. METHODS We retrospectively examined all patients supported with a continuous-flow LVAD for >1 year at our center. RESULTS Twenty patients (mean age 54 ± 10 years, 95% men, 60% with ischemic cardiomyopathy, left ventricular ejection fraction 22 ± 6%, pulmonary capillary wedge pressure 23.5 ± 7.5 mm Hg, brain natriuretic peptide [BNP] 1,566 ± 1,536 pg/ml, serum creatinine 1.6 ± 0.64 mg/dl, furosemide dose 643 ± 410 mg/day) underwent long-term mechanical support as destination therapy support with a continuous-flow LVAD (HeartMate II) at our center. During follow-up (1,219 ± 692 days), 9 patients (45%) manifested symptoms and signs of RVD (increase in right atrial pressure [RAP], BNP and daily furosemide dose compared with the early post-operative period). In these patients, RAP was increased by 6.6 ± 2.6 mm Hg and BNP by 526 ± 477 pg/ml, whereas furosemide dose increased by 145 ± 119 mg. The mean and median times of RVD onset were 2.3 ± 1.5 and 2.1 years, respectively, after LVAD implantation (range 0.4 to 4.8 years). Four of these patients (44.4%) demonstrated further deterioration of RV function and died 73 ± 106 days (median 25 days, range 9 to 231 days) after first manifestation of RVD. Comparisons of baseline variables regarding medical history and clinical status did not demonstrate significant differences between the patients with or without RVD, including parameters related to RV function at the time of implantation. CONCLUSIONS Late-onset RVD is a complication of LVAD support, which can manifest several months to years from device implantation. This complication has significant adverse implications with regard to patient outcome. Prognostic factors need to be identified to follow and treat high-risk patients more efficiently.