Patient-specific severity of von Willebrand factor degradation identifies patients with a left ventricular assist device at high risk for bleeding.

BACKGROUND: Continuous-flow left ventricular assist devices (LVADs) cause an acquired von Willebrand factor (VWF) deficiency and bleeding. Models to risk-stratify for bleeding are urgently needed. We developed a model of continuous-flow LVAD bleeding risk from patient-specific severity of VWF degradation. METHODS: In a prospective, longitudinal cohort study, paired blood samples were obtained from patients (n = 67) with a continuous-flow LVAD before and during support. After 640 ± 395 days, patients were categorized as all-cause bleeders, gastrointestinal (GI) bleeders, or nonbleeders. VWF multimers and VWF clotting function were evaluated to determine bleeding risk. RESULTS: Of 67 patients, 34 (51%) experienced bleeding, 26 (39%) experienced GI bleeding, and 33 (49%) did not bleed. In all patients, LVAD support significantly reduced high-molecular-weight VWF multimers (P < .001). Bleeders exhibited greater loss of high-molecular-weight VWF multimers (mean ± standard deviation, -10 ± 5% vs -7 ± 4%, P = .008) and reduced VWF clotting function versus nonbleeders (median [interquartile range], -12% [-31% to 4%] vs 0% [-9 to 26%], P = .01). A combined metric of VWF multimers and VWF function generated the All-Cause Bleeding Risk Score, which stratified bleeders versus nonbleeders (86 ± 56% vs 41 ± 48%, P < .001) with a positive predictive value of 86% (95% confidence interval, 66%-95%) and diagnostic odds ratio of 11 (95% confidence interval, 2.9-44). A separate GI Bleeding Risk Score stratified GI bleeders versus nonbleeders (202 ± 114 vs 120 ± 86, P = .003) with a positive predictive value of 88% (64%-97%) and diagnostic odds ratio of 18 (3.1-140). CONCLUSIONS: The severity of loss of VWF multimers and VWF clotting function generated Bleeding Risk Scores with high predictive value for LVAD-associated bleeding. This model may guide personalized antithrombotic therapy and patient surveillance.

Depression Is Associated With Non-Home Discharge After Coronary Artery Bypass Graft.

INTRODUCTION: Depression is disproportionately high in patients with coronary artery disease and has been associated with adverse outcomes following coronary artery bypass graft (CABG). One quality metric, non-home discharge (NHD), can have substantial implications for patients and health care resource utilization. Depression increases the risk of NHD after many operations, but it has not been studied after CABG. We hypothesized that a history of depression would be associated with an increased risk of NHD following CABG. METHODS: CABG cases were identified from the 2018 National Inpatient Sample using ICD-10 codes. Depression, demographic data, comorbidities, length of stay (LOS), rate of NHD were analyzed using appropriate statistical tests where a P-value < 0.05 was defined as statistically significant. Adjusted multivariable logistic regression models were used to assess independent association between depression and NHD as well as LOS while controlling for confounders. RESULTS: There were 31,309 patients, of which 2743 (8.8%) had depression. Depressed patients were younger, females, in a lower income quartile, and more medically complex. They also demonstrated more frequent NHD and prolonged LOS. After adjusted multivariable analysis, depressed patients had a 70% increased odds of NHD (adjusted odds ratio: 1.70 [1.52-1.89] P < 0.001) and a 24% increased odds of prolonged LOS (AOR: 1.24 [1.12-1.38] P < 0.001). CONCLUSIONS: From a national sample, depressed patients were associated with more frequent NHD following CABG. To our knowledge, this is the first study to demonstrate this, and it highlights the need for improved preoperative identification in order to improve risk stratification and timely allocation of discharge services.

COMPETENCE Trial: The EVAHEART 2 continuous flow left ventricular assist device.

BACKGROUND: Continuous flow left ventricular assist devices have improved outcomes in patients with end-stage heart failure that require mechanical circulatory support. Current devices have an adverse event profile that has hindered widespread application. The EVAHEART®2 left ventricular assist device (EVA2) has design features such as large blood gaps, lower pump speeds and an inflow cannula that does not protrude into the left ventricle that may mitigate the adverse events currently seen with other continuous flow devices. METHODS: A prospective, multi-center randomized non-inferiority study, COMPETENCE Trial, is underway to assess non-inferiority of the EVA2 to the HeartMate 3 LVAS when used for the treatment of refractory advanced heart failure. The primary end-point is a composite of the individual primary outcomes: Survival to cardiac transplant or device explant for recovery; Free from disabling stroke; Free from severe Right Heart Failure after implantation of original device. Randomization is in a 2:1 (EVA2:HM3) ratio. RESULTS: The first patient was enrolled into the COMPETENCE Trial in December of 2020, and 25 subjects (16 EVA2 and 9 HM3) are currently enrolled. Enrollment of a safety cohort is projected to be completed by third quarter of 2022 at which time an interim analysis will be performed. Short-term cohort (92 EVA2 subjects) and long-term cohort is expected to be completed by the end of 2023 and 2024, respectively. CONCLUSIONS: The design features of the EVA2 such as a novel inflow cannula and large blood gaps may improve clinical outcomes but require further study. The ongoing COMPETENCE trial is designed to determine if the EVA2 is non-inferior to the HM3.

Abnormalities in the Von Willebrand-Angiopoietin Axis Contribute to Dysregulated Angiogenesis and Angiodysplasia in Children With a Glenn Circulation.

Children with a bidirectional superior cavopulmonary (Glenn) circulation develop angiodysplasia and pulmonary arteriovenous malformations (AVMs). The von Willebrand factor (vWF)-angiopoietin axis plays a major role in AVM formation in multiple diseases. We observed derangements in global angiogenic signaling, vWF metabolism, angiopoietins, and in vitro angiogenesis in children with a Glenn circulation versus controls and within Glenn pulmonary versus systemic circulations. These findings support the novel hypothesis that abnormalities in the vWF-angiopoietin axis may dysregulate angiogenesis and contribute to Glenn pulmonary AVMs. The vWF-angiopoietin axis may be a target to correct angiogenic imbalance in Glenn patients, for whom no targeted therapy exists.

Continuous-Flow Left Ventricular Assist Device Support Improves Myocardial Supply:Demand in Chronic Heart Failure.

Continuous-flow left ventricular assist devices (CF LVADs) are rotary blood pumps that improve mean blood flow, but with potential limitations of non-physiological ventricular volume unloading and diminished vascular pulsatility. In this study, we tested the hypothesis that left ventricular unloading with increasing CF LVAD flow increases myocardial flow normalized to left ventricular work. Healthy (n = 8) and chronic ischemic heart failure (IHF, n = 7) calves were implanted with CF LVADs. Acute hemodynamics and regional myocardial blood flow were measured during baseline (LVAD off, clamped), partial (2-4 L/min) and full (>4 L/min) LVAD support. IHF calves demonstrated greater reduction of cardiac energy demand with increasing LVAD support compared to healthy calves, as calculated by rate-pressure product. Coronary artery flows (p < 0.05) and myocardial blood flow (left ventricle (LV) epicardium and myocardium, p < 0.05) decreased with increasing LVAD support in normal calves. In the IHF model, blood flow to the septum, LV, LV epicardium, and LV myocardium increased significantly with increasing LVAD support when normalized to cardiac energy demand (p < 0.05). In conclusion, myocardial blood flow relative to cardiac demand significantly increased in IHF calves, thereby demonstrating that CF LVAD unloading effectively improves cardiac supply and demand ratio in the setting of ischemic heart failure.

Initial clinical experience with the Symphony heart assist system.

PURPOSE: Current cardiac assist devices provide full support, require a major operation, and function asynchronously to the native heart. In contrast, we developed a novel circulatory support device that provides synchronous partial support and can be placed with a minor operation. We report the first clinical implantation with the Symphony device (Abiomed, Danvers, MA). DESCRIPTION: Patients with advanced heart failure despite optimal therapy who had exhausted all options were evaluated. A 64-year-old man with ischemic cardiomyopathy underwent implantation of the Symphony device in the right infraclavicular fossa. EVALUATION: After initiating device support, the cardiac index increased from 1.7 to 2.5 L/min/m(2), pulmonary capillary wedge pressure decreased from 26 to 13 mm Hg, right atrial pressure decreased from 12 to 7 mm Hg, creatinine level decreased from 2.3 to 1.5 mg/dL, and New York Heart Association (NYHA) class improved from IIIB to II. CONCLUSIONS: Placement of the Symphony device resulted in improvements in hemodynamics and functional status. Further clinical data will help define the role for this approach of partial synchronous support through a less invasive operation in patients with advanced heart failure.

Nonphysiologic blood flow triggers endothelial and arterial remodeling in vivo: implications for novel left ventricular assist devices with a peripheral anastomosis.

OBJECTIVES: Less invasive circulatory support devices have been developed that require anastomosis to a peripheral artery. The Symphony Heart Assist System (Abiomed, Inc, Danvers, Mass) is a volume-displacement pump sewn to the subclavian artery to provide partial circulatory support. The surgical configuration produces nonphysiologic blood pressure and bidirectional flow in the subclavian artery. Our objective was to identify effects of altered hemodynamics on arterial structure and function. METHODS: In calves (n = 23; 80-100 kg), the Symphony pump was sewn end-to-side to the carotid artery. Acutely, carotid blood pressure and flow were recorded to evaluate hemodynamic changes. After medium-term support (1-4 weeks), carotid artery was studied. Histologic and molecular assays evaluated architectural changes. Quantitative real-time polymerase chain reaction evaluated gene expression of matrix metalloproteinase (MMP)-2, MMP-9, and connective tissue growth factor. In vitro carotid arterial-ring studies evaluated physiologic responses. RESULTS: During Symphony support, carotid arterial pressure was 200/15 mm Hg. Antegrade flow increased significantly (P < .05) from 1.40 ± 0.32 to 4.29 ± 0.33 L/min. Flow during native cardiac diastole reversed completely from 0.25 ± 0.05 to -4.15 ± 0.38 L/min in carotid artery proximal to the anastomosis. After medium-term support, the carotid artery was significantly dilated with significantly thinner tunica media and thicker tunica adventitia than in control carotid arteries. MMP-9 gene expression decreased significantly, connective tissue growth factor gene expression increased significantly, and collagen, elastin, and total extracellular matrix increased significantly. Endothelial cells were significantly hypertrophied and produced significantly more von Willebrand factor. Endothelial apoptosis increased significantly. Platelet-endothelial interactions decreased significantly. Endothelial-independent contraction decreased significantly, whereas endothelial-dependent relaxation increased modestly. CONCLUSIONS: Assisted circulation with a left ventricular assist device triggered arterial remodeling that allowed a peripheral artery to accommodate the altered hemodynamics of a novel partial-support pump. Further delineation of remodeling pathways may be of significance for the emerging field of partial circulatory support.

Insights into the mechanism(s) of von Willebrand factor degradation during mechanical circulatory support.

OBJECTIVE: Left ventricular assist device support produces a bleeding diathesis. Evidence suggests a major role for von Willebrand factor (vWF). We examined vWF metabolism in a preclinical model of short-term mechanical circulatory support. METHODS: In 25 calves (weight, 80-110 kg), the inflow/outflow graft of the Symphony Heart Assist System was sewn end-to-side to the carotid artery. Support was initiated (acute, n = 4; 1 week, n = 16; 2 weeks, n = 5). Acutely, carotid artery pressure and flow were measured to evaluate the hemodynamic changes near the anastomosis. At baseline and after ≤2 weeks of support, platelet aggregometry with adenosine 5'-diphosphate, collagen, and ristocetin was performed. Gel electrophoresis and wet immunoblotting qualitatively evaluated vWF multimers and quantified plasma ADAMTS-13, the vWF-cleaving protease. Carotid arterial rings near the anastomosis were studied with immunohistochemical staining for ADAMTS-13 and were cultured to quantify endothelial ADAMTS-13 production. Fluorescent resonance energy transfer was used to evaluate the enzymatic activity of ADAMTS-13 in the plasma and in supernatant from cultured carotid arterial rings. Plasma interleukin-6, which inhibits ADAMTS-13 activity, was measured using an enzyme-linked immunosorbent assay. RESULTS: During support, statistically significant (P < .05) changes in the carotid endothelium arterial hemodynamics were observed. The highest molecular weight vWF multimers were absent, and the vWF-ristocetin platelet aggregation pathway was significantly impaired. A modest but significant increase in plasma ADAMTS-13 protein and activity was observed. ADAMTS-13 decreased significantly in the carotid near the anastomosis but increased significantly in supernatant from cultured carotid arterial rings. The plasma interleukin-6 levels did not change significantly. CONCLUSIONS: Hemodynamic activation of vWF and increased plasma ADAMTS-13 activity may have reduced high-molecular-weight vWF multimers and thereby impaired the vWF-platelet aggregation pathway. Additional delineation of these pathways may improve management of left ventricular assist device-associated bleeding.

Counterpulsation with symphony prevents retrograde carotid, aortic, and coronary flows observed with intra-aortic balloon pump support.

A counterpulsation device (Symphony) is being developed to provide long-term circulatory support for advanced heart failure (HF) patients. In acute animal experiments, flow waveform patterns in the aortic, carotid, and coronary arteries were compared during Symphony and intra-aortic balloon pump (IABP) support. Human data were examined for similarities. The 30-mL Symphony was compared to a 40-mL IABP in calves with cardiac dysfunction (80-100 kg, n = 8). Aortic pressures and aortic, carotid, and coronary artery flows were simultaneously recorded at baseline (devices off) and during 1:1 and 1:2 support. Forward, retrograde, and mean flows were calculated and compared for each test condition. Findings were also compared to aortic flow measurements recorded in HF patients (n = 21) supported by 40-mL IABP. IABP caused significant retrograde flows in the aorta, coronary (IABP: -24 ± 8 mL/min, Symphony: -6 ± 2 mL/min, baseline: -2 ± 1 mL/min, P < 0.05), and carotid arteries (IABP: -30 ± 5 mL/min, Symphony: -0 ± 0 mL/min, baseline: -0 ± 0 L/min, P < 0.05) during ventricular systole compared to the Symphony. IABP support produced higher diastolic pressure and flow augmentation compared to Symphony. Due to retrograde flows during IABP support, Symphony provided higher overall coronary, carotid, and aortic flows. Similar reduction in total aortic flows due to retrograde flow was observed in HF patients during IABP support. Counterpulsation with an IABP via aortic volume displacement produces retrograde flows during rapid balloon deflation that reduces total flow. Counterpulsation with Symphony via volume removal eliminates retrograde flow and improves total flow more than that achieved with IABP. The Symphony may provide long-term hemodynamic benefits in HF patients.

Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva.

OBJECTIVE: An ectopic coronary artery that courses between the aortic root and the pulmonary trunk may lead to sudden cardiac death, especially in athletes. It has been speculated that during exercise, compression of the coronary artery between the great vessels may impair coronary blood flow and produce myocardial ischemia and fatal arrhythmia. However, this hypothesis cannot be tested in humans, and little experimental data exist to explain this phenomenon. To this end, in a calf with an anomalous left coronary artery that coursed from the right sinus of Valsalva between the great vessels, we assessed for myocardial ischemia during pharmacologically induced tachycardia and hypertension. METHODS: We identified a juvenile male calf (103 kg) with an anomalous left coronary artery from the right sinus of Valsalva that coursed between the great vessels. Via thoracotomy, the animal was instrumented for hemodynamic measurements. Intravenous dobutamine increased heart rate and myocardial metabolic demands. Intravenous phenylephrine produced arterial hypertension and increased myocardial metabolic demands. Fluorescent-labeled microspheres were used to map regional myocardial blood flow, and hemodynamics were recorded during each condition. Masson's trichrome staining for fibrosis, wheat-germ agglutinin staining for myocyte size, terminal deoxynucleotidyl transferase dUTP nick end-label staining for apoptosis, and isolectin-B4 staining for capillary density were performed. RESULTS: For the first time, empiric data documented that an ectopic coronary artery produced myocardial ischemia during elevated myocardial metabolic demands. Left coronary artery resistance increased in a cardiac cycle-dependent pattern that was consistent with systolic compression between the great vessels. Increased cardiac fibrosis, myocyte hypertrophy, cardiac apoptosis, and capillary density indicated that regional ischemic, inflammatory-mediated myocardial remodeling was present. CONCLUSIONS: These findings confirm the proposed mechanism of sudden death and support early surgical repair of coronary arteries that course between the aortic root and the pulmonary trunk.

Antigens of persistent Chlamydia pneumoniae within coronary atheroma from patients undergoing heart transplantation.

AIMS: In order for Chlamydia pneumoniae to play a causative role in chronic human disease, it would need to persist within infected tissue for extended periods of time. Current theory suggests that C pneumoniae may persist at the site of infection via an alternative replicative form, known as an aberrant body. METHODS: A panel of C pneumoniae-specific antibodies upregulated by the aberrant body was used to probe tissue specimens from the coronary atheroma from 13 explanted hearts to identify patterns of reactivity in these tissues, as well as to determine the presence and prevalence of C pneumoniae aberrant bodies. RESULTS: Six of 13 patients had an ischaemic cardiomyopathy secondary to coronary atherosclerosis, while another six patients had an idiopathic, dilated cardiomyopathy. One additional patient, a young (24 years) woman with cardiomyopathy, had no history of atherosclerotic disease. Eleven patients were positive by immunohistochemistry with at least one antibody. Coronary arteries of the two other patients were negative by immunohistochemistry with all antibodies. One of these patients was the 24-year-old woman with grade I disease and no risk factors for coronary artery disease. CONCLUSIONS: The protein antigens of persistent C pneumoniae infection found in the atheromatous lesions from patients in this study could potentially be used as markers to detect such infections and some may be virulence factors or immunogens specific to C pneumoniae, thus serving as target molecules for diagnostic use or therapeutic intervention.

The future of adult cardiac assist devices: novel systems and mechanical circulatory support strategies.

The recent, widespread success of mechanical circulatory support has prompted the development of numerous implantable devices to treat advanced heart failure. It is important to raise awareness of novel device systems, the mechanisms by which they function, and implications for patient management. This article discusses devices that are being developed or are in clinical trials. Devices are categorized as standard full support, less-invasive full support, partial support: rotary pumps, partial support: counterpulsation devices, right ventricular assist device, and total artificial heart. Implantation strategy, mechanism of action, durability, efficacy, hemocompatibility, and human factors are considered. The feasibility of novel strategies for unloading the failing heart is examined.

Intraaortic balloon pump timing discrepancies in adult patients.

The objective of this clinical study was to quantify the incidence and magnitude of intraaortic balloon pump (IABP) inflation and deflation landmark discrepancies associated with the IABP catheter arterial pressure waveform. Cardiac surgery patients with an IABP inserted prior to surgery were recruited. Following cardiac exposure, a high-fidelity pressure catheter was inserted into the aortic root for digital recording. The radial artery pressure signal was simultaneously recorded from the patient monitor along with the arterial pressure and electrocardiogram waveforms from the IABP console while operating at 1:1 and 1:2 synchronization. In selected patients, recordings were obtained with the IABP timed to the high-fidelity aortic root waveform. In all 11 patients, inflation and deflation landmark delays were observed when comparing the aortic root waveforms to the IABP arterial pressure waveforms (inflation delay = 74 ± 29 [23-117] ms; deflation delay = 71 ± 37 [24-141] ms, mean ± standard deviation [min-max]). Delays were greater when compared to the radial artery waveform (inflation delay = 175 ± 50 [100-233] ms; deflation delay = 168 ± 52 [100-274] ms). In all cases, the landmark delays were statistically different from zero (P < 0.001). Diastolic augmentation and afterload reduction varied with waveform source. Conflicting indications of afterload reduction occurred in four patients. Timing to the aortic root waveform resulted in greater diastolic pressure augmentation and afterload reduction but mixed changes in stroke volume. Delay and distortion of the arterial waveform was consistently found when measured through the IABP catheter lumen. These delays can alter IABP efficacy and may be eliminated by using high-fidelity sensing of aortic pressure.

Repair of mitral valve and left atrioventricular disruption caused by blunt chest trauma.

We describe a case of acute cardiac failure in a patient involved in a motor vehicle accident. A diagnosis of acute mitral regurgitation and left atrioventricular disruption was made with transesophageal echocardiography. Successful repair was performed using the mitral valve leaflets to patch the disruption followed by valve replacement.

Intraoperative evaluation of the HeartMate II flow estimator.

BACKGROUND: Direct measurement of blood flow output has been incorporated into ventricular assist devices (VADs), but long-term reliability of the additional device components has raised concerns regarding sensor drift and failure. As an alternative approach, the HeartMate II axial VAD (Thoratec Corp, Pleasanton, CA) estimates device flow output from power consumption and rotational speed of the device motor. This study evaluated the accuracy of HeartMate II flow estimation at the time of implantation. METHODS: In 20 patients, intraoperative blood flow measurement of the HeartMate II flow estimator was compared with flow values obtained with an ultrasonic flow probe placed around the device outflow graft. Estimated and measured VAD flow data were simultaneously recorded and digitally stored while the device motor speed varied from 7,800 to 11,000 rpm and while achieving device flow outputs of 2 to 7 liters/min. Estimated and measured flows were compared using linear regression analyses and root mean square error. RESULTS: HeartMate II flow estimation (FE) demonstrated a linear correlation with ultrasonic flow probe (FP) measurements: FE = 0.74 FP + 0.99 (R(2) = 0.56, p = 0.0001). A root mean square error of 0.8 liters/min was observed between flow estimation and direct flow measurement and suggests a 15% to 20% difference at flows of 4 of 6 liters/min. CONCLUSIONS: These results suggest that HeartMate II flow estimation may be used to provide directional information for trend purposes rather than absolute values of device blood flow output. Patient management should include but not be limited to this information.

Human, bovine and porcine systematic vascular input impedances are not equivalent: implications for device testing and xenotransplantation in heart failure.

BACKGROUND: Advanced therapies for heart failure (HF), such as mechanical circulatory support (MCS) devices and xenotransplantation, are usually tested in bovine and porcine models. This approach assumes a priori that animal (patho)physiology will closely match that of humans. Systemic aortic input impedance (Z(ART)) is an important physiologic determinant of left ventricular (LV) performance. We tested the hypothesis that Z(ART) is lower in bovine and porcine than in humans with normal or failing hearts. METHODS: High-fidelity aortic pressure and flow waveforms were recorded intra-operatively at native and paced heart rates of 100 beats per minute (bpm) in adult human patients with normal LV function (n = 13) or end-stage HF (n = 15), and normal calves (n = 10) and pigs (n = 18). Fast Fourier transformation was used to calculate Z(ART), and arterial resistance and compliance were estimated using a 4-element Windkessel model. RESULTS: Humans with HF had greater Z(ART) than those with normal LV function, characterized by higher resistance (1.16 +/- 0.12 vs 1.00 +/- 0.10 mm Hg x s/ml, p < 0.05) and lower compliance (1.53 +/- 0.21 vs 1.88 +/- 0.33 ml x mm Hg, p < 0.05). Healthy calves and pigs had significantly lower resistance (calf: 0.63 +/- 0.07 mm Hg x s/ml; pig: 0.90 +/- 0.07 mm Hg x s/ml) and higher compliance (calf: 2.79 +/- 0.37 ml x mm Hg; pig: 2.80 +/- 0.64 ml x mm Hg) when compared to humans (p < 0.05) with normal or failing hearts. CONCLUSIONS: Z(ART) is significantly lower in calves and pigs than in humans with or without HF. This finding has important implications for the pre-clinical testing of MCS devices and xenotransplants, which are usually examined in bovine and porcine models, respectively. Specifically, these therapies may respond differently in humans than animals due to non-equivalence of systemic after-load.

Acute hemodynamic efficacy of a 32-ml subcutaneous counterpulsation device in a calf model of diminished cardiac function.

The acute hemodynamic efficacy of an implantable counterpulsation device (CPD) was evaluated. The CPD is a valveless single port, 32-ml stroke volume blood chamber designed to be connected to the human axillary artery using a simple surface surgical procedure. Blood is drawn into the pump during systole and ejected during diastole. The acute hemodynamic effects of the 32-ml CPD were compared to a standard clinical 40-ml intra-aortic balloon pump (IABP) in calves (80 kg, n = 10). The calves were treated by a single oral dose of Monensin to produce a model of diminished cardiac function (DCF). The CPD and IABP produced similar increases in cardiac output (6% CPD vs. 5% IABP, p > 0.5) and reduction in left ventricular external work (14% CPD vs. 13% IABP, p > 0.5) compared to DCF (p < 0.05). However, the ratio of diastolic coronary artery flow to left ventricular external work increase from DCF baseline (p < 0.05) was greater with the CPD compared to the IABP (15% vs. 4%, p < 0.05). The CPD also produced a greater reduction in left ventricular myocardial oxygen consumption from DCF baseline (p < 0.05) compared to the IABP (13% vs. 9%, p < 0.05) despite each device providing similar improvements in cardiac output. There was no early indication of hemolysis, thrombus formation, or vascular injury. The CPD provides hemodynamic efficacy equivalent to an IABP and may become a therapeutic option for patients who may benefit from prolonged counterpulsation.

Vascular pulsatility in patients with a pulsatile- or continuous-flow ventricular assist device.

OBJECTIVE: We sought to investigate differences in indices of pulsatility between patients with normal ventricular function and patients with heart failure studied at the time of implantation with continuous-flow or pulsatile-flow left ventricular assist devices. METHODS: Eight patients with normal ventricular function and 22 patients with heart failure were studied. A high-fidelity aortic and left ventricular pressure catheter was inserted retrograde through the aortic valve into the left ventricle, and transit-time flow probes were placed on the aorta and device outflow graft. Hemodynamic waveforms were recorded at native heart rate before cardiopulmonary bypass and over a range of device flow rates controlled by adjusting beat rate or rpm. These data were used to calculate vascular input impedance and 2 indices of vascular pulsatility: energy-equivalent pressure and surplus hemodynamic energy. RESULTS: At low support levels, pulsatile support restored surplus hemodynamic energy to within 2.5% of normal values, whereas continuous support diminished surplus energy by more than 93%. At high support levels, pulsatile support augmented surplus energy by 49% over normal values, whereas continuous support further diminished surplus energy by 97%. Pulsatile support diminished vascular impedance from baseline failure values, whereas continuous support increased impedance. Vascular impedances at baseline for patients undergoing pulsatile and continuous support and during pulsatile support revealed normal vascular compliance, whereas impedance during continuous support indicated a loss of compliance (or "stiffening") of the vasculature. CONCLUSION: These results suggest that selection of device type and flow rate can influence vascular pulsatility and input impedance, which might affect clinical outcomes.

Traumatic intramyocardial left ventricular dissection: a case report.

In this report, we present an unusual case of a patient who sustained and survived an intramyocardial dissecting hematoma with subacute ventricular rupture complicating a motor vehicle accident. In conclusion, we report on the diagnosis, management, and prior literature of this highly unusual and often lethal condition.

Improved technique to diagnose a patent foramen ovale during left ventricular assist device insertion.

Diagnosis of a patent foramen ovale prior to left ventricular assist device placement can be quite difficult, and if missed may result in a significant hypoxemia due to a right to left shunt. We describe a simple and precise way to increase the diagnostic accuracy of patent foramen ovale detection prior to initiating cardiopulmonary bypass for left ventricular assist device placement.