Is systematic lymph node dissection mandatory or is sampling adequate in patients with stage I non-small-cell lung cancer?

A best evidence topic in thoracic surgery was written according to a structured protocol. The question addressed was: Is systematic lymph node dissection (SLND) mandatory or is sampling adequate in stage I non-small-cell lung cancer (NSCLC)? Two hundred and eleven papers were identified, of which 12 papers represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and the results of these papers are tabulated. There are 7 retrospective cohort reviews, 3 meta-analyses and 2 randomized controlled clinical trials (RCTs) to answer the clinical question. Four of the 7 retrospective studies demonstrated that the total number of resected lymph nodes and the number of lymph node stations sampled affected the accuracy of staging in patients with early-stage NSCLC and had an impact on overall survival and disease-free survival. Two RCTs, 1 meta-analysis and 1 cohort study revealed no significant benefit in overall survival and disease-free survival in patients undergoing SLND. One meta-analysis, which contained only 1 RCT, revealed significantly better 3- and 5-year survival with SLND. One further meta-analysis revealed improved survival with SLND in cohort studies but no significant difference in the 4 RCTs included. Two further studies identified specific subgroups of patients in whom LN sampling could be justified and SLND avoided. We conclude that there is no significant difference in the recurrence rate when performing either SLND or LN sampling in patients with stage I NSCLC. While retrospective cohort studies implied survival benefit with SLND, this was not borne out in RCTs and meta-analyses. However, there may be a potential survival benefit for patients who are upstaged by SLND identifying mediastinal nodal involvement.

The role of surgical resection in Unicentric Castleman's disease: a systematic review.

INTRODUCTION: Castleman's disease is a rare benign lymphoproliferative disorder of unknown etiology. The disease occurs in two clinical forms with different prognoses, treatments and symptoms: a unicentric form (UCD), which is solitary, localized, and a multicentric form characterized by generalized lymphadenopathy and systemic symptoms. This article aims to review the current literature to consolidate the evidence surrounding the curative potential of surgical treatment to the unicentric type. MATERIAL AND METHODS: A systematic review of English-language literature was performed and databases (Medline, Pubmed, the Cochrane Database and grey literature) were searched to identify articles pertaining to the treatment of unicentric form of Castleman's disease. Each article was critiqued by two authors using a structured appraisal tool, and stratified according to the level of evidence. RESULTS: After application of inclusion criteria, 14 studies were included. There were no prospective randomized control studies identified. One meta-analysis including 278 patients with UCD reported that resective surgery is safe and should be considered the gold standard for treatment. Seven retrospective studies enhance this standpoint. Radiotherapy (RT) has been used in six studies with controversial results. CONCLUSIONS: We conclude that surgical resection appears to be the most effective treatment for Unicentric Castleman's Disease of the thoracic cavity. Radiotherapy can also achieve clinical response and cure in selected patients.

Arterial Thoracic Outlet Syndrome Treated Successfully with Totally Endoscopic First Rib Resection.

Thoracic outlet syndrome (TOS) is a constellation of signs and symptoms caused by compression of the neurovascular structures in the thoracic outlet. TOS may be classified as either neurogenic TOS (NTOS) or vascular TOS: venous TOS (VTOS) or arterial TOS (ATOS), depending on the specific structure being affected. The basis for the surgical treatment of TOS is resection of the first rib, and it may be combined with scalenectomy or cervical rib resection. Herein, we describe a case of arterial thoracic outlet syndrome which was successfully treated with totally endoscopic video-assisted thoracoscopic surgery (VATS) first rib resection.

Totally Endoscopic (VATS) First Rib Resection for Thoracic Outlet Syndrome.

BACKGROUND: Thoracic outlet syndrome (TOS) causes neurologic symptoms in 95% of cases and vascular symptoms in 5% of cases. Surgical resection is curative. Endoscopic-assisted transaxillary first rib resection has been previously reported. In this study we report a totally endoscopic video-assisted thoracoscopic surgery (VATS) approach using tailored endoscopic instruments. METHODS: Ten patients (8 women; average age, 32.3 ± 5.6 years) with TOS underwent VATS first rib resection following failure of symptom improvement with physiotherapy. Symptoms were: unilateral neurogenic (n = = 7), bilateral neurogenic (n = = 2), and bilateral arterial compression (n = = 1). Three standard VATS ports were utilized. The parietal pleura and periosteum overlying the first rib were stripped avoiding injury to the neurovascular bundle. The rib was transected with an endoscopic rib cutter and resected completely in a piecemeal fashion using endoscopic bone nibblers. All periosteal remnants were trimmed releasing the neurovascular bundle completely. RESULTS: Patients were discharged within 72 hours following surgery. One patient had the contralateral side treated 18 months later and another patient is awaiting the second surgery. At follow-up, 9 patients had complete resolution of their main symptoms. One patient with neurogenic TOS developed mild functional and sensational loss of the non-dominant hand that improved within 8 months with physiotherapy. CONCLUSIONS: VATS first rib resection for TOS provides, unlike the classic approaches, a superior, magnified, and well-illuminated view of the thoracic inlet. It allows good posterior trimming of the first rib, release of brachial plexus, and an aesthetically pleasing result, especially in female patients.

A rare case of occult splenic rupture after left pneumonectomy.

Cardiopulmonary resuscitation (CPR) techniques are now well-established and play a crucial role in improving survival in cardiac arrest. Recognized complications associated with CPR include injury to the upper abdominal viscera, including the liver, stomach and spleen. We present a rare case of occult splenic rupture following cardiac arrest in a 63-year-old male immediately after left pneumonectomy. We discuss potential mechanisms predisposing the spleen to injury in this case, and highlight the difficulty of promptly identifying such a traumatic injury within the confines of a cardiac arrest scenario. Clinicians should be aware that anatomical changes following thoracic surgery may render the intra-abdominal viscera at increased risk of injury following CPR.

Advances in chest drain management in thoracic disease.

An adequate chest drainage system aims to drain fluid and air and restore the negative pleural pressure facilitating lung expansion. In thoracic surgery the post-operative use of the conventional underwater seal chest drainage system fulfills these requirements, however they allow great variability amongst practices. In addition they do not offer accurate data and they are often inconvenient to both patients and hospital staff. This article aims to simplify the myths surrounding the management of chest drains following chest surgery, review current experience and explore the advantages of modern digital chest drain systems and address their disease-specific use.

Novel technique in managing bronchobiliary fistula in adults: Endobronchial embolization using silicone spigots in 2 cases.

Bronchobiliary fistula (BBF) can complicate most hepatic pathologies. This is a challenging group of patients, especially when surgery is precluded. The bronchoscopic application of silicon spigots is a recognized technique for the treatment of massive hemoptysis and the management of patients with bronchopleural fistula following lung resection. Their role in the treatment of BBF has never been described. In this paper we report the successful embolization using silicon spigots in two patients with BBF secondary to malignant disease, when all surgical options were exhausted.

Dose-Dependent Hemodynamic, Biochemical, and Tissue Oxygen Effects of OC99 following Severe Oxygen Debt Produced by Hemorrhagic Shock in Dogs.

We determined the dose-dependent effects of OC99, a novel, stabilized hemoglobin-based oxygen-carrier, on hemodynamics, systemic and pulmonary artery pressures, surrogates of tissue oxygen debt (arterial lactate 7.2 ± 0.1 mM/L and arterial base excess -17.9 ± 0.5 mM/L), and tissue oxygen tension (tPO2) in a dog model of controlled severe oxygen-debt from hemorrhagic shock. The dose/rate for OC99 was established from a pilot study conducted in six bled dogs. Subsequently twenty-four dogs were randomly assigned to one of four groups (n = 6 per group) and administered: 0.0, 0.065, 0.325, or 0.65 g/kg of OC99 combined with 10 mL/kg lactated Ringers solution administered in conjunction with 20 mL/kg Hextend IV over 60 minutes. The administration of 0.325 g/kg and 0.65 g/kg OC99 produced plasma hemoglobin concentrations of 0.63 ± 0.01 and 1.11 ± 0.02 g/dL, respectively, improved systemic hemodynamics, enhanced tPO2, and restored lactate and base excess values compared to 0.0 and 0.065 g/kg OC99. The administration of 0.65 g/kg OC99 significantly elevated pulmonary artery pressure. Plasma hemoglobin concentrations of OC99 ranging from 0.3 to 1.1 g/dL, in conjunction with colloid based fluid resuscitation, normalized clinical surrogates of tissue oxygen debt, improved tPO2, and avoided clinically relevant increases in pulmonary artery pressure.

Arterial blood pressure as a predictor of the response to fluid administration in euvolemic nonhypotensive or hypotensive isoflurane-anesthetized dogs.

OBJECTIVE: To determine the effects of rapid small-volume fluid administration on arterial blood pressure measurements and associated hemodynamic variables in isoflurane-anesthetized euvolemic dogs with or without experimentally induced hypotension. DESIGN: Prospective, randomized, controlled study. ANIMALS: 13 healthy dogs. PROCEDURES: Isoflurane-anesthetized dogs were randomly assigned to conditions of nonhypotension or hypotension (mean arterial blood pressure, 45 to 50 mm Hg) and treatment with lactated Ringer's solution (LRS) or hetastarch (3 or 10 mL/kg [1.4 or 4.5 mL/lb] dose in a 5-minute period or 3 mL/kg dose in a 1-minute period [4 or 5 dogs/treatment; ≥ 10-day interval between treatments]). Hemodynamic variables were recorded before and for up to 45 minutes after fluid administration. RESULTS: IV administration of 10 mL/kg doses of LRS or hetastarch in a 5-minute period increased right atrial and pulmonary arterial pressures and cardiac output (CO) when dogs were nonhypotensive or hypotensive, compared with findings before fluid administration; durations of these effects were greater after hetastarch administration. Intravenous administration of 3 mL of hetastarch/kg in a 5-minute period resulted in an increase in CO when dogs were nonhypotensive. Intravenous administration of 3 mL/kg doses of LRS or hetastarch in a 1-minute period increased right atrial pressure and CO when dogs were nonhypotensive or hypotensive. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of LRS or hetastarch (3 or 10 mL/kg dose in a 5-minute period or 3 mL/kg dose in a 1-minute period) improved CO in isoflurane-anesthetized euvolemic dogs with or without hypotension. Overall, arterial blood pressure measurements were a poor predictor of the hemodynamic response to fluid administration.

The expanded role of extracellular matrix patch in malignant and non-malignant chest wall reconstruction in thoracic surgery.

OBJECTIVES: The extracellular matrix (XCM Biologic Tissue Matrix) is a non-cross-linked 3D patch derived from porcine dermis. Once implanted, it is infiltrated by recipient's cells and becomes incorporated in the repair. Here, we report the first series of using this device for chest wall reconstruction. METHODS: The XCM Biologic Tissue Matrix was utilized to provide the restoration of chest wall defects. It was used either alone or in conjunction with the Synthes titanium system to provide additional support. The decision was made intraoperatively. RESULTS: Since April 2010, 21 (12 females) patients received the device. Average age at operation was 47 ± 17 years. Eleven (52%) patients had the patch inserted alone, while the remaining 10 received it in combination with another implantable medical device. The biological tissue matrix was used to reconstruct chest wall defects in cancer involving chest wall (n = 9), chest wall deformity (n = 6), chest wall hernia (n = 5) and chest wall repair following empyema drainage (n = 1). Complications were witnessed in 3 patients receiving the combined XCM and Synthes bar mechanisms; infection (n = 2) and bar displacement and infection (n = 1). CONCLUSIONS: The XCM patch can be safely used to provide the strength required for chest wall reconstruction and to replace previously infected reconstructions.

Cardiovascular autonomic control in patients undergoing left ventricular assist device (LVAD) support and pharmacologic therapy.

OBJECTIVES: The objective of the study is to determine cardiac autonomic control in patients undergoing assessment for and/or LVAD therapy. METHODS: Heart rate variability (HRV) was measured in 17 explanted LVAD, 17 implanted LVAD and 23 NYHA III-IV classified chronic heart failure (CHF) patients and ten healthy matched controls under three conditions: supine free breathing, standing and supine controlled breathing. Five measures of HRV were assessed: mean R-R interval (mR-R), high frequency (HF) and low frequency (LF) spectral power, LF in normalised units (LFnu), and LF to HF (LF:HF) ratio. RESULTS: Repeat measures ANOVA showed significant (p < 0.05) differences in HRV between all three conditions within groups. Lower values were observed in CHF for LF(in log natural units) compared with explanted patients (-1.4 [95% CI -2.6 to -0.7], p = 0.04) and controls (-2.1 [-3.5 to -0.7], p = 0.001) and for LF:HF compared with implanted patients under paced breathing conditions (z = -2.7, p = 0.007) and controls in standing (z = -2.9, p = 0.004) and paced breathing conditions (z = -2.3, p = 0.02). However, no significant differences were seen between explanted, implanted and control groups under any condition. CONCLUSIONS: Patients implanted with an LVAD and explanted from a LVAD following myocardial recovery demonstrate a more normal dynamic response to autonomic stimuli and have a lower HRV risk profile compared to CHF patients.

The effect of long-term left ventricular assist device support on myocardial sympathetic activity in patients with non-ischaemic dilated cardiomyopathy.

AIMS: Dilated cardiomyopathy (DCM) patients have abundant levels of norepinephrine secondary to failure of the norepinephrine transporter uptake mechanism. Little is known about the effects of an LV assist device (LVAD) on cardiac sympathetic innervations and norepinephrine transporter dysfunction. This study examines the effects of continuous-flow HeartMate II LVAD on cardiac sympathetic innervations using [(123)I]metaiodobenzylguanidine ([(123)I]MIBG) nuclear imaging. METHODS AND RESULTS: After injecting 431 ± 21 MBq of [(123)I]MIBG, planar scintigraphy was performed at 15 min and 4 h in 14 consecutive non-diabetic non-ischaemic DCM patients. Scans were executed early post-LVAD implantation (T1) and prior to either device explantation for myocardial recovery or transplant listing (T2). [(123)I]MIBG measured parameters included early and delayed heart-mediastinum (H/M) ratios and washout rate (W/O). Catecholamine levels were measured using liquid chromatography-mass spectrometry. Following 208.4 ± 85.5 days of LVAD support, both early and delayed H/M ratios increased by 42.1% (P < 0.001) and 54.7% (P < 0.001), respectively. The W/O rate decreased by 46% (P = 0.003). Plasma norepinephrine, epinephrine, and dopamine decreased significantly in correlation with [(123)I]MIBG parameters. Ten patients had recovered and had their device explanted as they had demonstrated a higher percentage change in delayed H/M ratio, W/O rate, and norepinephrine levels. Linear regression analysis revealed a strong correlation between percentage changes in both norepinephrine and epinephrine and myocardial recovery. CONCLUSION: Combination therapy with LVAD and drug resulted in enhancement of [(123)I]MIBG uptake in DCM patients.

Cardiac iodine-123 metaiodobenzylguanidine imaging predicts ventricular arrhythmia in heart failure patients receiving an implantable cardioverter-defibrillator for primary prevention.

OBJECTIVE: To assess the prognostic value of cardiac iodine-123 metaiodobenzylguanidine ((123)I-MIBG) scintigraphy to predict ventricular arrhythmias in patients with heart failure (HF) listed for implantable cardioverter-defibrillator (ICD) devices as primary prevention. DESIGN, SETTING AND PATIENTS: A prospective cohort study in 27 patients with HF referred for ICD implantation (alone or in combination with cardiac resynchronisation therapy) at a tertiary cardiac centre. METHODS: Cardiac (123)I-MIBG scintigraphy was performed with calculation of early and late heart-to-mediastinum (H:M) ratios, washout rate, and summed defect score from single photon emission computed tomography (SPECT) acquisition. Resting myocardial perfusion SPECT using (99m)Tc-tetrofosmin was also performed and a summed score calculated. Innervation-perfusion mismatch was evaluated by comparing SPECT scores. MAIN OUTCOME MEASURE: Ventricular arrhythmia requiring ICD therapy. RESULTS: At 16 months median follow-up, 10 (37%) patients experienced a significant arrhythmic event. Compared with patients who suffered no event, these individuals had lower early and late H:M ratio and higher (123)I-MIBG SPECT defect scores: 1.83 ± 0.43 versus 2.34 ± 0.33 (p<0.001); 1.54 ± 0.38 versus 1.96 ± 0.38 (p=0.005); 37.0 ± 9.4 versus 25.5 ± 7.7 (p=0.001). Mismatch scores were also higher: 18.5 ± 8.5 versus 8.4 ± 5.0 (p<0.01). Optimal thresholds for predicting arrhythmia were <1.94 for early H:M ratio (sensitivity 70%, specificity 88%); <1.54 for late H:M ratio (sensitivity 60%, specificity 88%); (123)I-MIBG SPECT defect score ≥31 (sensitivity 78%, specificity 77%). CONCLUSIONS: In HF patients without prior ventricular arrhythmia, (123)I-MIBG imaging strongly predicts future arrhythmic risk. This may inform the process of case selection for ICD therapy on an individual basis, although no single measurement provides sufficient reassurance to obviate device implantation if otherwise clinically indicated.

Long-term outcomes of patients bridged to recovery versus patients bridged to transplantation.

OBJECTIVE: The proportion of patients who can be bridged with left ventricular assist devices to myocardial recovery and the long-term outcome of these patients is unknown. METHODS: We investigated the outcomes of patients bridged to recovery compared with those bridged to transplantation. All left ventricular assist devices were implanted as a bridge to transplantation with a very proactive program of promoting myocardial recovery. A total of 40 patients were bridged to recovery and 52 to transplantation. Of the bridged to recovery (explanted) group, 33 were men (age, 32.8 ± 11.8 years), 37 had dilated cardiomyopathy (familial in 3, peripartum cardiomyopathy in 3) and 3 had myocarditis. Of the bridged to transplantation (transplanted) group, 42 were men (age, 42.3 ± 12.5 years; P < .0005 vs bridged to recovery). The diagnosis was ischemic heart disease in 24, dilated cardiomyopathy in 21 (only 13 received drug therapy), hypertrophic obstructive cardiomyopathy in 2, arrythmogenic right ventricular dysplasia in 2, myocarditis in 1, and congestive heart disease in 2. RESULTS: The survival rate was 89.9%, 73.9%, and 73.9% and 80.4%, 78.3, and 78.3% in the explanted and transplanted groups at 1, 5, and 7 years, respectively. In total, 12 (23%) patients bridged transplantation either died from, or required ventricular assist device support, for primary graft failure. Of the explanted patients, 4 (10%) subsequently required transplantation at 34, 512, 1019, and 1213 days (2 died 25 and 1867 days after transplantation and 2 were well after 1523 and 3199 days). The rate of transplant or ventricular assist device-free survival less noncardiac death for the bridged to recovery and bridged to transplantation groups, respectively, was 89.9%, 73.9%, and 73.9% and 80.4%, 78.3%, and 78.3% at 1, 3, and 7 years. At latest follow-up (1394 ± 1195 days for the bridged to recovery and 1913 ± 941 days for the bridged to transplantation group), 5 of the bridged to transplantation patients (9.6%) had malignancy, 34 (65.4%) had hypercholesterolemia, 25 (48.1%) had hypertension, and 7 (13.5%) had coronary disease. The creatinine was 125.5 ± 43.5 vs 95.2 ± 16.5 µmol/L for the bridged to transplantation and bridged to recovery groups (P < .001). CONCLUSIONS: The outcome after explantation for myocardial recovery is comparable, if not better than, after bridge to transplantation.

Relationship between peak cardiac pumping capability and selected exercise-derived prognostic indicators in patients treated with left ventricular assist devices.

AIM: Exercise-derived variables have been used in the assessment of functional capacity and prognosis in patients with chronic heart failure. The aim of this study was to assess the relationship between cardiac pumping capability represented by peak cardiac power output and peak oxygen consumption, anaerobic threshold, ventilatory efficiency slope, and peak circulatory power in patients undergoing the 'Harefield Protocol'. METHODS AND RESULTS: Haemodynamic and gas exchange measurements were undertaken during a graded treadmill exercise test. They were performed on 54 patients-18 implanted with left ventricular assist devices (LVADs), 16 explanted (recovered), and 20 moderate-to-severe heart failure patients. Peak oxygen consumption was only highly correlated with peak cardiac power output in explanted LVAD (r = 0.85, P< 0.01), but not in implanted LVAD and heart failure patients (r = 0.55 and 0.53, P< 0.05). The anaerobic threshold was only modestly correlated with peak cardiac power output in heart failure and explanted (r = 0.46 and 0.54, P< 0.05) and weakly in implanted LVAD patients (r = 0.37, P< 0.05). Peak cardiac power output was well correlated with peak circulatory power in LVAD explanted and implanted (r = 0.82, P< 0.01; r = 0.63, P< 0.01) but not in heart failure patients (r = 0.31, P> 0.05). Ventilatory efficiency slope was only moderately correlated with peak cardiac power output in LVAD-explanted patients (r = -0.52, P< 0.05). CONCLUSION: Exercise-derived prognostic indicators demonstrate limited capacity in reflecting cardiac pumping capability in patients treated with LVADs and should therefore be used with caution in interpretation of cardiac organ function.

Reversal of severe heart failure with a continuous-flow left ventricular assist device and pharmacological therapy: a prospective study.

BACKGROUND: We have previously shown that a specific combination of drug therapy and left ventricular assist device unloading results in significant myocardial recovery, sufficient to allow pump removal, in two thirds of patients with dilated cardiomyopathy receiving a Heartmate I pulsatile device. However, this protocol has not been used with nonpulsatile devices. METHODS AND RESULTS: We report the results of a prospective study of 20 patients who received a combination of angiotensin-converting enzymes, ß-blockers, angiotensin II inhibitors, and aldosterone antagonists followed by the ß2-agonist clenbuterol and were regularly tested (echocardiograms, exercise tests, catheterizations) with the pump at low speed. Before left ventricular assist device insertion, patient age was 35.2 ± 12.6 years (16 male patients), patients were on 2.0 ± 0.9 inotropes, 7 (35) had an intra-aortic balloon pump, 2 were hemofiltered, 2 were ventilated, 3 had a prior Levitronix device, and 1 had extracorporeal membrane oxygenation. Cardiac index was 1.39 ± 0.43 L · min⁻¹ · m⁻², pulmonary capillary wedge pressure was 31.5 ± 5.7 mm Hg, and heart failure history was 3.4 ± 3.5 years. One patient was lost to follow-up and died after 240 days of support. Of the remaining 19 patients, 12 (63.2) were explanted after 286 ± 97 days. Eight had symptomatic heart failure for ≤6 months and 4 for >6 months (48 to 132 months). Before explantation, at low flow for 15 minutes, ejection fraction was 70 ± 7, left ventricular end-diastolic diameter was 48.6 ± 5.7 mm, left ventricular end-systolic diameter was 32.3 ± 5.7 mm, mV(O2) was 21.6 ± 4 mL · kg⁻¹ · min⁻¹, pulmonary capillary wedge pressure was 5.9 ± 4.6 mm Hg, and cardiac index was 3.6 ± 0.6 L · min⁻¹ · m⁻². Estimated survival without heart failure recurrence was 83.3 at 1 and 3 years. After a 430.7 ± 337.1-day follow-up, surviving explants had an ejection fraction of 58.1 ± 13.8, left ventricular end-diastolic diameter of 59.0 ± 9.3 mm, left ventricular end-systolic diameter of 42.0 ± 10.7 mm, and mV(O2) of 22.6 ± 5.3 mL · kg⁻¹ · min⁻¹. CONCLUSIONS: Reversal of end-stage heart failure secondary to nonischemic cardiomyopathy can be achieved in a substantial proportion of patients with nonpulsatile flow through the use of a combination of mechanical and pharmacological therapy.

Molecular changes occurring during reverse remodelling following left ventricular assist device support.

Remodelling is the central feature that occurs in the progression of heart failure. However, unloading of the heart with a left ventricular assist device (LVAD) can lead to reversal of many of the remodelling changes even in patients with advanced heart failure. LVAD unloading can also lead to improved myocardial function and this improvement can be sufficient to allow removal of the device leaving the patient to lead a normal life. We review the molecular changes that have been demonstrated with LVAD unloading in patients bridged to transplantation and also those that have occurred in the myocardium of patients that have recovered their myocardial function enough to have the device removed. Changes in both the myocyte and the matrix are reviewed.

Echocardiographic assessment of flow across continuous-flow ventricular assist devices at low speeds.

BACKGROUND: Testing of native myocardial function in patients with continuous-flow pumps is challenging as reduction/cessation of the pump could result in regurgitation, although the amount and significance of this regurgitation remains unknown. The aim of this study was to determine the optimal speed at which to assess the native left ventricular (LV) function and the physiologic response to speed reduction. METHODS: Fifteen male patients with a HeartMate II (HMII) device were studied prospectively on 46 occasions. Measurements were performed serially at three device speed settings: baseline speed; 6,000 rpm; and either 5,000 rpm (Group A) or 4,000 rpm (Group B). The device's forward and reverse velocity (Vmax(f), Vmax(r)), forward and reverse velocity time integral (VTI(f), VTI(r)) and blood volume (BV) were also measured using Doppler with LV echocardiographic parameters and peripheral hemodynamics. RESULTS: No adverse incidents were reported. Speed reduction to 6,000 rpm resulted in a significant decrease in Vmax(f), VTI(f) and BV. There was no significant difference in either forward or reverse flow with further speed reduction in either group. Speed reduction to <6,000 rpm did not have a significant effect on LV loading. CONCLUSIONS: Speed reduction in patients with the HMII device is safe. There was no difference between 6,000 rpm and lower speeds, suggesting that 6,000 rpm is sufficient to assess native myocardial function. The absence of significant retrograde filling suggests that LV loading is a physiologic response to speed reduction at 6,000 rpm.

The impact of acute reduction of continuous-flow left ventricular assist device support on cardiac and exercise performance.

BACKGROUND: The use of the HeartMate II continuous-flow left ventricular assist device (LVAD) improves survival, quality of life and functional capacity of patients with advanced heart failure. However, no study so far has shown the benefits of these devices for cardiac function during peak exercise. OBJECTIVE: To assess cardiac and exercise performance in patients implanted with the HeartMate II LVAD under two settings: (i) optimal device support and (ii) reduced device support. METHODS: Twelve patients implanted with a HeartMate II LVAD performed a graded cardiopulmonary exercise test with respiratory gas exchange and non-invasive (rebreathing) haemodynamic measurements. After a 4 h resting period, patients performed an additional cardiopulmonary exercise test with reduced LVAD support (pump speed was reduced from optimal 9000-9600 to 6000 revs/min). RESULTS: In response to reduced HeartMate II LVAD support, resting cardiac power output and cardiac output decreased by 21% and 13%, respectively. Also at reduced device support, peak exercise cardiac power output was 39% lower (1.40+/-0.50 vs 2.31+/-0.58 W; p<0.05), peak cardiac output 30% lower (8.6+/-2.5 vs 12.2+/-2.1 l/min; p<0.05) and mean blood pressure 13% lower (74.3+/-14.9 vs 85.4+/-15.4 vs mm Hg; p<0.05). Exercise capacity was also diminished with 23% lower peak oxygen consumption (14.1+/-5.3 vs 18.2+/-4.5 ml/kg/min; p<0.05) and an 18% shorter exercise duration (516+/-119 vs 628+/-192 s; p<0.05). CONCLUSION: It has been shown for the first time that the HeartMate II LVAD can confer both resting and peak cardiac functional benefits to patients with end-stage heart failure, thus improving exercise capacity.