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Limited data exist on the circadian blood pressure (BP) and heart rate (HR) variations that occur in heart failure (HF) patients on left ventricular assist device (LVAD) support.We prospectively recorded clinic and 24-hour ambulatory BP and HR data in patients on HeartMate II LVAD support. Results were compared to HF patients with ejection fraction ≤30% and controls with no history of cardiovascular disease. Physiologic nocturnal BP and HR dipping was defined as a ≥10% decline compared to daytime values.Twenty-nine LVAD patients (age 59 ± 15 years, 76% male, 38% ischemic etiology), 25 HF patients (age 64 ± 13 years, 84% male, 32% ischemic etiology) and 26 controls (age 56 ± 9 years, 62% male) were studied. Normal nocturnal BP dipping was less frequent in LVAD patients (10%) than in HF patients (28%) and controls (62%) and reversed BP dipping (BP increase at night) was more common in LVAD patients (24%), compared to HF (16%) and controls (8%), (p0.001, for all comparisons). Physiologic HR reduction was less frequent in LVAD patients (14%), compared to HF (16%) and controls (59%) (p0.001, for all comparisons). Among LVAD patients, 36% exhibited sustained hypertension over the 24-hours and 25% had white-coat hypertension.Treatment of advanced HF with an LVAD does not restore physiologic circadian variability of BP and HR; additionally, BP was not adequately controlled in more than a third of LVAD patients, and a quarter of them exhibited white-coat hypertension. Future studies are warranted to confirm these findings and investigate prognostic and management implications in this population.

While rates of stroke have declined with the HeartMate3 (HM3) continuous- flow (CF) left ventricular assist device (LVAD), the impact of non-pulsatile flow and artificial pulse physiology on cerebrovascular function is not known. We hypothesized that improved hemodynamics and artificial pulse physiology of HM3 patients would augment cerebrovascular metabolic reactivity (CVR) compared with HeartMate II (HMII) CF-LVAD and heart failure (HF) patients.Mean, peak systolic and diastolic flow velocities (MFV, PSV, MinFV, respectively) and cerebral pulsatility index were determined in the middle cerebral artery (MCA) before and after a 30 sec breath-hold challenge in 90 participants: 24 healthy controls; 30 HF, 15 HMII, and 21 HM3 patients.In HM3 patients, breath-holding increased MFV (Δ8 ± 10 cm/sec, p.0001 vs baseline) to levels similar to HF patients (Δ9 ± 8 cm/sec, p.05), higher than HMII patients (Δ2 ± 8 cm/sec, p.01) but lower than healthy controls (Δ13 ± 7 cm/sec, p.05). CF-LVAD altered the proportion of systolic and diastolic flow responses as reflected by a differential cerebral pulsatility index (p = .03). Baseline MFV was not related to CVR (rCompared with HMII, HM3 patients have a significantly improved CVR. However, CVR remains lower in HM3 and HF patients than in healthy controls, therefore suggesting that changes in cerebral hemodynamics are not reversed by CF-LVAD therapy. Further research on the mechanisms and the long-term impact of altered cerebral hemodynamics in this unique patient population are warranted.

In the general population, increased aortic stiffness is associated with an increased risk of cardiovascular events. Previous studies have demonstrated an increase in aortic stiffness in patients with a continuous flow left ventricular assist device (CF-LVAD). However, the association between aortic stiffness and common adverse events is unknown.Forty patients with a HeartMate II (HMII) (51 $ 11 years; 20% female; 25% ischemic) implanted between January 2011 and September 2017 were included. Two-dimensional transthoracic echocardiograms of the ascending aorta, obtained before HMII placement and early after heart transplant, were analyzed to calculate the aortic stiffness index (AO-SI). The study cohort was divided into patients who had an increased vs decreased AO-SI after LVAD support. A composite outcome of gastrointestinal bleeding, stroke, and pump thrombosis was defined as the primary end point and compared between the groups. While median AO-SI increased significantly after HMII support (AO-SI 4.4-6.5, P = .012), 16 patients had a lower AO-SI. Patients with increased (n = 24) AO-SI had a significantly higher rate of the composite end point (58% vs 12%, odds ratio 9.8, P.01). Similarly, those with increased AO-SI tended to be on LVAD support for a longer duration, had higher LVAD speed and reduced use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers.Increased aortic stiffness in patients with a HMII is associated with a significantly higher rates of adverse events. Further studies are warranted to determine the causality between aortic stiffness and adverse events, as well as the effect of neurohormonal modulation on the conduit vasculature in patients with a CF-LVAD.

Background Preclinical studies have reported that a single treadmill session performed 24 h prior to doxorubicin provides cardio-protection. We aimed to characterize the acute change in cardiac function following an initial doxorubicin treatment in humans and determine whether an exercise session performed 24 h prior to treatment changes this response. Methods Breast cancer patients were randomized to either 30 min of vigorous-intensity exercise 24 h prior to the first doxorubicin treatment (n = 13), or no vigorous exercise for 72 h prior to treatment (control, n = 11). Echocardiographically-derived left ventricular volumes, longitudinal strain, twist, E/A ratio, and circulating NT-proBNP, a marker of later cardiotoxicity, were measured before and 24–48 h after the treatment. Results Following treatment in the control group, NT-proBNP, end-diastolic and stroke volumes, cardiac output, E/A ratio, strain, diastolic strain rate, twist, and untwist velocity significantly increased (all p ≤ 0.01). Whereas systemic vascular resistance (p < 0.01) decreased, and ejection fraction (p = 0.02) and systolic strain rate (p < 0.01) increased in the exercise group only. Relative to control, the exercise group had a significantly lower NT-proBNP (p < 0.01) and a 46% risk reduction of exceeding the cut-point used to exclude acute heart failure. Conclusion The first doxorubicin treatment is associated with acutely increased NT-proBNP, echocardiographic parameters of myocardial relaxation, left ventricular volume overload, and changes in longitudinal strain and twist opposite in direction to documented longer-term changes. An exercise session performed 24 h prior to treatment attenuated NT-proBNP release and increased systolic function. Future investigations should verify these findings in a larger cohort and across multiple courses of doxorubicin. Background Preclinical studies have reported that a single treadmill session performed 24 h prior to doxorubicin provides cardio-protection. We aimed to characterize the acute change in cardiac function following an initial doxorubicin treatment in humans and determine whether an exercise session performed 24 h prior to treatment changes this response. Methods Breast cancer patients were randomized to either 30 min of vigorous-intensity exercise 24 h prior to the first doxorubicin treatment (n = 13), or no vigorous exercise for 72 h prior to treatment (control, n = 11). Echocardiographically-derived left ventricular volumes, longitudinal strain, twist, E/A ratio, and circulating NT-proBNP, a marker of later cardiotoxicity, were measured before and 24–48 h after the treatment. Results Following treatment in the control group, NT-proBNP, end-diastolic and stroke volumes, cardiac output, E/A ratio, strain, diastolic strain rate, twist, and untwist velocity significantly increased (all p ≤ 0.01). Whereas systemic vascular resistance (p < 0.01) decreased, and ejection fraction (p = 0.02) and systolic strain rate (p < 0.01) increased in the exercise group only. Relative to control, the exercise group had a significantly lower NT-proBNP (p < 0.01) and a 46% risk reduction of exceeding the cut-point used to exclude acute heart failure. Conclusion The first doxorubicin treatment is associated with acutely increased NT-proBNP, echocardiographic parameters of myocardial relaxation, left ventricular volume overload, and changes in longitudinal strain and twist opposite in direction to documented longer-term changes. An exercise session performed 24 h prior to treatment attenuated NT-proBNP release and increased systolic function. Future investigations should verify these findings in a larger cohort and across multiple courses of doxorubicin.

Purpose We previously showed that cerebrovascular reactivity (CVR) is reduced in heart failure (HF) patients and does not improve after left ventricular assist device (LVAD) HeartMate II (HMII) implantation, possibly because of low pulsatile physiology. Therefore, it is possible that the artificial pulse of the latest generation LVAD, the HeartMate3 (HM3), restores normal CVR. HM3 patients will have an increased CVR to a CO2-retention challenge compared with HF and HMII. Methods A total of 79 subjects (17 healthy, 30 HF, 15 HMII and 17 HM3) underwent angle-corrected transcranial Doppler sonography. Middle cerebral artery (MCA) velocity profiles were recorded before and at the end of a 30s breath hold. Mean flow velocity (MFV), peak flow velocity (Vmax), minimal flow velocity (Vmin), Pulsatility Index (PI) and Resistance Index (RI) were quantified. Statistical differences were determined using 2-way ANOVA (Breathhold x group). Results At baseline, HF patients with and without LVAD implantation had a decreased Vmax, MFV, PI and RI compared to healthy (all P Conclusion HM3 patients have a significantly improved CVR to a CO2-retention challenge compared with HMII patients. However, the acute CVR is not altered by the artificial pulse. Since CVR of HM3 patients remains reduced compared with healthy controls, further research is needed to understand the pathophysiology of cerebrovascular complications in LVAD.

Purpose Lack of nocturnal blood pressure (BP) reduction (BP dipping) has been associated with cerebrovascular and cardiovascular events in the general population. However, the effect of a deranged circadian BP variability between day and night has never been studied in patients on left ventricular assist device (LVAD) support, where stroke still represents a major complication. We hypothesized that decreased BP dipping significantly increases the risk of stroke in patients on LVAD support. Methods HeartMate II (HMII) outpatients were prospectively studied with an ambulatory BP monitor (Mobil-O-Graph) previously validated in this patient population. Systolic BP (SBP), diastolic BP (DBP) and mean arterial pressure (MAP) were recorded every 30 minutes during the day and every hour during the night for 24 hours. Circadian patterns, expressed as the percentage of nocturnal SBP, DBP, and MAP reduction from daytime values, were assessed in Cox regression models with stroke as primary endpoint. Results 29 patients were studied (age 59 ±15 yrs, 76% male, 38% ischemic, 69% DT). 6 patients (20%) experienced a stroke 879±591 days post LVAD implant. Nocturnal reductions of SBP, DBP, and MAP were 5.0 ± 6.1%, 5.0 ± 5.6% and 5.0 ± 5.5%, respectively. Preserved nocturnal reductions of SBP (HR 0.790 [95% CI 0.658 - 0.949]), DBP (HR 0.707 [95% CI 0.559 - 0.894]) and MAP (HR 0.703 [95% CI 0.554 - 0.894]) were associated with a decreased risk of stroke. When patients were grouped by the median nocturnal reduction in MAP (5.4%), patients with reduced dipping had a significantly greater risk of stroke (Figure 1). Conclusion This study is the first to indicate that reduced BP dipping at night increases the risk of stroke in patients on HMII support. Further studies are warranted to investigate, mechanistically, the relationship between reduced BP dipping and sympathetic nervous system activation, and, clinically, its association with the risk of stroke in patients on HM3 support.

Purpose The optimal method for blood pressure (BP) measurement among pts implanted with HeartMate 3 (HM3), a centrifugal pump that features an artificial pulse, is presently unknown. We aimed to: 1) assess success rate and validity of Doppler opening BP (DOBP) and automated BP (ABP) monitor; 2) test a novel approach to estimate mean arterial pressure (MAP) by combining DOBP and HM3 parameters. Methods BP and HM3 parameters (Speed, Power, Pulsatility Index [PI], Flow) were prospectively collected in a derivation cohort (DC, n=50) and a validation cohort (VC, n=11). BP was measured by arterial line (A-line) in all pts. DOBP and ABP were concurrently measured in a subgroup of DC (DCs, n=31) and in VC. In DC, a multiple linear regression model was fit with A-line systolic BP (SBP) and HM3 parameters as predictor variables and A-line MAP as the dependent variable to derive the HM3 MAP Formula. In DCs and VC, the accuracy of the Formula in estimating A-line MAP was tested using DOBP as non-invasive equivalent of A-line SBP. Mean observed differences (MOD) and mean absolute differences (MAD) against A-line were calculated for each method. Results The success rate for Doppler and ABP monitor was 100% and 49%, respectively. In DCs, DOBP reflected A-line SBP (MAD 4.6, MOD +1.7 mmHg) but markedly overestimated A-line MAP (Fig A). MAD and MOD of ABP monitor were 7.7 and +3.5 and 7.0 and +1.1 mmHg for SBP and MAP, respectively (Fig B). In DC, the best model to predict A-line MAP included PI and Flow in addition to A-line SBP (HM3 MAP Formula, r2=0.77). In DCs, the Formula accurately predicted A-line MAP when using A-line SBP (Fig C) and DOBP (Fig D). In a preliminary analysis of VC, the accuracy of the Formula was similar (MAD: A-line SBP 4.1, DOBP 6.8 mmHg). Conclusion In HM3 pts, DOBP accurately estimates SBP, but overestimates MAP. ABP monitor has limited success rate and accuracy, possibly due to the artificial pulse. The HM3 MAP Formula represents a uniformly successful and valid tool to estimate MAP by combining DOBP and pump parameters.

Purpose It is well established that continuous-flow left ventricular assist devices (LVAD) reduce pulsatility in the circulation. Consequently, the addition of an ‘artificial pulse’ to the HeartMate3 (HM3) LVAD has been expected to increase pulsatility. Yet, there has been no prospective study that has examined arterial hemodynamics of HM3 patients across the whole circulation, from large to muscular and microcirculatory arteries.Compared with HMII patients, HM3 patients will have a significantly increased arterial pulsatility across the whole circulation, and similar pulsatility to healthy individuals. Methods Pulsatility index (PI), peak systolic velocity (PSV), minimum velocity (Vmin) and mean flow velocity (MFV) of the common carotid, middle cerebral and central retinal arteries were quantified with angle-corrected 2D ultrasound in 141 volunteers (32 healthy controls, 42 heart failure (HF), 28 HM II, and 39 HM3 patients). To test the study hypothesis, data were statistically evaluated using 1-way ANOVA with Tukey's honestly significant difference test. Results Across all three artery locations, both PI and PSV of HM3 patients were significantly lower compared with healthy controls and HF (all P 0.05, Fig.1). Similarly, Vmin and MFV were not significantly different between HM3 and HMII (all P>0.05). Conclusion Despite the presence of an ‘artificial pulse’, pulsatility in patients implanted with the HM3 remains significantly lower than healthy controls and similar to HM II patients. Importantly, the lack of increased pulsatility in HM3 was explained by the flow pattern caused by the artificial pulse, which did not increase peak systolic velocity. These findings add insight into the remaining cardiovascular complications in HM3 patients and warrant further investigation.

Purpose While the impact of mean arterial pressure (MAP) on adverse events during left ventricular assist device (LVAD) support has been well established, there remains significant controversy regarding the impact of pulse pressure (PP) on clinical outcomes. We evaluated the impact of PP on post-implant hemocompatibility related adverse events (HRAE). Methods Using the INTERMACS registry, we identified patients who received a primary, durable continuous-flow LVAD with distinct systolic and diastolic blood pressure readings at 3-months post-implant. Patients requiring mechanical right ventricular assist devices or inotropic support were excluded. Patients were then stratified into low, medium, and high pulsatility tertiles. Kaplan-Meier survival estimates and Cox Proportional Hazard Models were used to assess the impact of pulsatility on HRAEs. Results A total of 4745 patients were classified into low (n=1508), medium (n=1675), and high (n=1562) pulsatility groups. There was no correlation between PP and MAP in this population (Figure 1A) and no clinically significant difference in MAP between the groups. Significant pre-implant determinants of pulsatility included female sex, BMI, race, device type, and peripheral vascular disease. Patients with lower pulsatility had more RV dysfunction and higher pro-BNP levels as compared to those with higher pulsatility. PP was a significant risk factor for stroke (HR: 1.09, CI: 1.04 - 1.15, p=0.001 per 10mmHg increase) independent of MAP. Patients with high MAP and high PP had the highest stroke risk (Figure 1B). PP was not associated with GI bleeding, device thrombosis. thromboembolic events, or post-implant survival. Conclusion High PP is associated with increased risk of stroke during LVAD support. Pulsatility may represent an additional therapeutic target in this patient population.

Purpose Blood flow through the left ventricular assist device (LVAD) is dependent on the rotation speed of the impeller, and inversely dependent on the differential pressure across the LVAD (HQ relationship). We developed a novel approach to estimate intraventricular pressure difference (IVPD) in patients with LVAD and assess the change of IVPD according to pump speed during ramp study. Methods We developed in-house code of 1-dimensional incompressible Euler equation written in MATLAB (MathWorks, Natick, MA, USA) which allows us to measure IVPD by analyzing transesophageal echocardiographic images. Color M-mode images in mid-esophageal long axis view were obtained at 3 different pump speeds (low, optimized, high) in 10 patients who had LVAD implant (Figure). The optimal rotation speed was defined by stable hemodynamic conditions and the septal shape on transesophageal imaging. Pairwise comparison between each group was performed using Steel-Dwass analysis. Results Images were successfully obtained in all patients. Median IVPD values were 0.88 mmHg [IQR 0.73 - 1.02] at pre-LVAD implant, 1.86 mmHg [IQR 1.50 - 2.15] at low speed, 2.12 mmHg [IQR 1.72 - 2.71] at optimal speed, 2.09 mmHg [IQR1.72 - 2.31] at high speed, respectively (figure). There was significant difference between pre-implantation and the remaining 3 groups ( p Conclusion These data illustrate a novel approach to estimate IVPD during early diastole in patients with LVAD. Importantly, data suggests that setting of pump speed can be informed by analyzing IVPD during early diastole.

Purpose De novo aortic insufficiency is one of unresolved complications after left ventricular assist device (LVAD) implant. It has been hypothesized that decreased and oscillatory wall shear stress (WSS) on the aortic valve following LVAD implantation cause leaflet degeneration resulting in AI. We developed novel approach to measure WSS on the aortic valve using vector flow mapping (VFM) images. Methods Aortic root color Doppler image was obtained using intraoperative epiaortic echocardiogram in 6 patients who received LVAD implant and 8 patients undergoing LVAD explant and heart transplant. As a control group, we enrolled 5 patients undergoing CABG surgery. Using obtained images, WSS and oscillatory shear index (OSI) on the right coronary cusp (RCC) was calculated with off-line software, Echo VFM® (Cardio Flow Design, Tokyo, Japan) (Figure). Results Image analysis was successful in all patients. The WSS on the ventricularis of the RCC was significantly lower in the LVAD group compared to control (0.09±0.06 vs. 0.35±0.27 Pa, p Conclusion Significantly lower WSS on the ventricularis may be accountable for AV degeneration and subsequent De Novo AI in patients with LVAD.

Purpose Left ventricular assist device (LVAD) surgery is a life-prolonging therapy for advanced heart failure (HF). Despite many improvements over the years, LVADs continue to be associated with a high incidence of stroke and other vascular complications such as gastrointestinal bleeding (GIB). At present, the pathogenesis of these complications during LVAD support remains unclear. Abnormal structure and hemodynamics in large arteries are a potential contributor. We hypothesized that structural abnormalities and flow alterations will be significantly associated with stroke and a composite outcome of stroke, GIB, and death in HF patients before and during LVAD support. Methods We conducted a retrospective analysis of 141 carotid duplex studies in adult patients who received the HeartMate II LVAD. Clinical Doppler exams were evaluated before and after LVAD implantation. Parameters evaluated included peak-systolic velocity (PSV), end-diastolic velocity (EDV), mean velocity (MV), pulsatility index (PI), ICA/CCA PSV ratio, plaque burden, and ICA stenosis. In addition, we noted demographics, outcomes, and LVAD speed parameters. Results Compared with HF patients, LVAD patients had decreased PSV (CCA: 80 vs. 50 cm/s, ICA: 72 vs. 56 cm/s; both P Conclusion We conclude that structural arterial disease in HF patients, namely carotid artery stenosis and plaque as evidenced by Doppler evaluation, was associated with stroke, GIB, and death during LVAD support while arterial flow parameters were not. Flow parameters during LVAD support were likewise unrelated to adverse events. Our findings support routine carotid duplex evaluation for clinical outcome prediction and encourage further study of the unique vascular physiology resulting from LVAD support.

Purpose In the normal, pulsatile circulation, the hemodynamic pattern of the middle cerebral artery (MCA) differs from the central retinal artery (CRA). Whether continuous flow from a left ventricular assist device (LVAD) alters this relationship is not known. Since serious adverse events in different end-organs, such as stroke and GI bleeding, are frequent in LVAD patients, comparing hemodynamics in different arterial beds may enhance our understanding of the specific pathophysiology of these complications. Hypothesis Because of continuous flow, hemodynamic patterns between the MCA and CRA are more similar in HeartMate II (HM II) patients compared with healthy individuals. Methods MCA and CRA time-averaged maximal flow velocity (TAMAX), pulsatility index (PI) and resistance index (RI) were determined using Doppler ultrasound with angle correction, in 20 HM II pts and 21 healthy individuals. To test the study hypothesis, data were statistically analysed for both group differences and group variances. Results Although PI and RI were markedly lower in HM II patients in both the MCA and CRA (P Conclusion The typical differences that are observed in small- and microcirculatory hemodynamics of healthy individuals are altered in HM II patients. Notably, the wide ranges of haemodynamics observed in the HM II group may carry important implications with respect to the pathophysiology of specific end-organ complications, and, eventually, the identification of high-risk patients.

Purpose It has been proposed that the high prevalence of bleeding events in continuous-flow left ventricular assist device (CF-LVAD) patients may be lowered by increasing von Willebrand factor-release via augmented peripheral pulsatility (PI). However, the hemostatic effects of increased PI may be offset by concomitant increases in local wall shear stress (WSS) - which is known to stimulate the endothelial release of anti-thrombotic factors (NO, prostacyclin, thrombomodulin). Hypothesis Higher pulsatility in the middle cerebral artery of CF-LVAD patients will be significantly associated with increased local WSS. Methods Video loops of color Doppler recordings from the middle cerebral artery were obtained in 8 HeartMate II (HM II) patients and 8 healthy controls. Data were analyzed offline with validated vector flow mapping software. WSS was calculated as: viscosity*(du/dy), according to Newton's law. Viscosity was corrected by using individuals’ hematocrit. Importantly, we determined not only peak WSS but also WSS per beat (area under the curve) and WSS/min (WSS/beat * heart rate). PI was measured from angle-corrected pulsed-wave Doppler velocities. Results Peak WSS and WSS/beat were lower in HM II (P = 0.05) but WSS/min was not different (P > 0.05). Supporting our hypothesis, WSS and pulsatility index (PI) were strongly correlated non-linearly in HM II patients (r2 = 0.94) and shared a common linear slope with healthy controls between a PI of ∼0.45 and ∼0.90 (Fig. 1). Conclusion In CF-LVAD patients, a strong curvilinear relationship was noted between cerebral PI and WSS, with linear increases in WSS shown above a PI of ∼0.45. These data suggest a threshold for PI and its interaction with endothelium-dependent hemostatic and anti-thrombotic activity. Future work is warranted to investigate whether alteration of the PI-WSS relationship will influence the release of hemostatic or anti-thrombotic factors and reduce cerebral bleeding in CF-LVAD patients.

Purpose In advanced heart failure (HF) patients, a normal cardiac output is restored after continuous-flow left ventricular assist device (CF-LVAD) implantation. Previous studies have suggested that cerebral autoregulation is preserved. However, it is not known whether CF-LVAD therapy affects the cerebrovascular reactivity to a metabolic challenge. Hypothesis CF-LVAD patients will have a similar cerebrovascular response to a CO2-retention challenge compared with HF patients and healthy controls. Methods Angle-corrected Doppler ultrasound images of the middle cerebral artery (MCA) were recorded immediately before and at the end of a 30s breathhold in 10 healthy controls, 4 HF and 7 CF-LVAD (HM II) patients. Time-averaged maximum blood velocity (TAMAX), peak flow velocity (Vmax), Pulsatility Index (PI) and Resistance Index (RI) were determined by tracing of the blood velocity envelope. Statistical differences were determined with 2-way ANOVA (% change is illustrated graphically). Results In the MCA, significant baseline differences in TAMAX, Vmax, PI and RI existed between groups (all P Conclusion A metabolic challenge has a differential impact on cerebrovascular hemodynamics of HF and CF-LVAD patients compared with healthy controls. The pilot data suggest that cerebrovascular reserve may be altered already in HF and not further modulated after CF-LVAD implantation.

Investigations were performed on the selective non-catalytic reduction (SNCR) of nitric oxide (NO) at TAMARA, the pilot-scale waste incineration plant of the Karlsruhe Research Center. Aqueous ammonia (NH{sub 3}) was injected into the combustion chamber as reductant. The influence of NH{sub 3} on various inorganic and organic compounds in the flue gas was investigated. The concentrations of NO were reduced by up to about 90% by NH{sub 3} injection. The concentrations of most of the other inorganic and organic compounds, including in particular PCDD and PCDF, did not change significantly.

Forced by legislation, a series of catalytic converters have been installed in German municipal waste incineration (MWI) plants to reduce nitrogen oxides and/or polychlorinated dibenzodioxins/furans (PCDD/F). The catalytic material is usually based on TiO{sub 2} doped with V{sub 2}O{sub 5} and WO{sub 3}. During the past 2 years, problems arose especially in new installations in connection with disturbances in the combustion chamber. The mission of great amounts of carbon monoxide and other products of incomplete combustion caused fast temperature excursions in the catalytic converters. As a result, some of these installations were heavily damaged. For this reason the oxidation of pyrolytic gases was investigated with several types of catalysts in the laboratory. The gases detected during periods of low oxygen concentrations in an incinerator behave quite differently when they pass a catalytic converter. While hydrogen and some unsaturated hydrocarbons like benzene or ethyne are easily oxidized at the operating temperature of about 300 C, others like carbon monoxide or methane are rather inert at this temperature. Oxidation of the compounds first mentioned will produce enough energy to rise the temperature of the catalytic converter up to values where even CO and CH{sub 4} will react. In this case, temperatures willmore » exceed 700 C, which can be concluded from the changes in the physical properties of the catalytic material. Under certain conditions, these changes may result in a complete destruction of the catalytic converter. The first measure to prevent such damage could be a bypass and additionally catalytic materials that withstand high temperatures better than catalysts based on TiO{sub 2} could be used.« less

The temporal and spatial propagation of heat in a dielectric medium has been studied by observing the thermal expansion using a differential laser interferometer which was initially built for profilometry. It is demonstrated that topographical and thermal information can be obtained simultaneously. Measurements were compared with calculations using a simple model and found to be in good agreement.