Long-term incidence of upper extremity venous obstruction in implantable cardioverter defibrillator patients.

BACKGROUND: Very little is known about the long-term prevalence of severe venous obstruction and occlusion in patients with transvenous implantable cardioverter-defibrillator leads. The objective of the current investigation was to elucidate the incidence and prevalence and to identify predisposing conditions in an ICD cohort over a long follow-up period. METHODS: Based on a prospective database, we analyzed consecutive patients who received an ICD implantation in our hospital between 06/1988 and 2009 as well as all corresponding follow-up data until 02/2018. Cavographies were used for analysis, and all patients with at least one device replacement and one follow-up cavography were included. RESULTS: Over a mean follow-up period of 94 ± 50 months, severe venous obstruction was found in 147 (33%) of 448 patients. Kaplan-Meier analysis shows a severe obstruction or occlusion in 50% of patients after a period of 14.3 years. The total number of leads (p < .001, HR 2.01, CI 2.000-2.022), an advanced age (p = .004, HR 1.023 per year, CI 1.022-1.024) and the presence of dilated cardiomyopathy (p = .035, HR 1.49, CI 1.47-1.51) were predictive of venous obstruction whereas the presence of anticoagulation was not. CONCLUSION: Severe obstruction of the access veins after ICD implantation occurs frequently and its prevalence shows a nearly linear increase over long-time follow-up. Multiple leads, an advanced age and DCM as underlying disease are associated with an increased risk of venous obstruction while the role of anticoagulation to prevent venous obstruction in ICD patients is unclear.

TAVR outcome after reclassification of aortic valve stenosis by using a hybrid continuity equation that combines computed tomography and echocardiography data.

BACKGROUND: In the continuity equation, assumption of a round-shaped left ventricular outflow tract (LVOT) leads to underestimation of the true aortic valve area in two-dimensional echocardiography. The current study evaluated whether inclusion of the LVOT area, as measured by computed tomography (CT), reclassifies the degree of aortic stenosis (AS) and assessed the impact on patient outcome after transcatheter aortic valve replacement (TAVR). METHODS AND RESULTS: Four hundred and twenty-two patients with indexed aortic valve area index (AVAi) of <0.6 cm2 /m2 , assessed by using the classical continuity equation (mean age: 81.5 ± 6.1 years, 51% female, mean left ventricular ejection fraction: 53.2 ± 13.6%), underwent TAVR and were included. After inclusion of the CT measured LVOT area into the continuity equation, the hybrid AVAi led to a reclassification of 30% (n = 128) of patients from severe to moderate AS. Multivariate predictors for reclassification were male sex, lower mean aortic gradient, and lower annulus/LVOT ratio (all p < .01). Reclassified patients had significantly higher sST2 at baseline and higher NT-proBNP values at baseline and 6 months follow-up compared to non-reclassified patients. Acute kidney injury was experienced more frequently after TAVR by reclassified patients, but no significant mortality difference occurred during 2 years of follow-up. CONCLUSION: The hybrid AVAi reclassifies a significant portion of low-gradient severe AS patients into moderate AS. Reclassified patients showed increased fibrosis and heart failure markers at baseline compared to non-reclassified patients. But reclassification had no significant impact on mortality up to 2 years after TAVR. Routine assessment of hybrid AVAi seems not to improve further risk stratification of TAVR patients.

Modulation of carotid strain by statin therapy in atherosclerosis patients.

BACKGROUND: The beneficial effect of statin therapy on the progress of atherosclerotic disease has been demonstrated by numerous studies. Vascular strain imaging is an arising method to evaluate arterial stiffness. Our study examined whether an influence of statin therapy on the vessel wall could be detected by vascular strain imaging. PATIENTS AND METHODS: 88 patients with recently detected atherosclerosis underwent an angiological examination including ankle-brachial index (ABI), pulse wave index (PWI), central puls ewave velocity and duplex ultrasound. Captures for vascular strain analysis were taken in B-mode during ultrasound examination of the common carotid artery and evaluated using a workstation equipped with a speckle tracking based software. A statin therapy was recommended and after six months a follow-up examination took place. Meanwhile, the non-adherence of a group of patients (N = 18) lead to a possibility to observe statin effects on the vascular strain. RESULTS: In the statin non-adherent group the ABI decreased significantly to a still non-pathological level (1.2 ± 0.2 vs. 1.0 ± 0.2; p = 0.016) whereas it stagnated in the adherent group (1.0 ± 0.2 vs. 1.0 ± 0.2; p = 0.383). The PWI did not differ in the non-adherent group (180.5 ± 71.9 vs. 164.4 ± 75.8; p = 0.436) but under statin therapy it decreased significantly (261.8 ± 238.6 vs. 196.4 ± 137.4; p = 0.016). In comparison to the adherent group (4.2 ± 2.0 vs. 4.0 ± 1.8; p = 0.548) under statin therapy the radial strain decreased significantly in the non-adherent group (4.7 ± 2.0 vs. 3.3 ± 1.1; p = 0.014). CONCLUSIONS: Our findings reveal a beneficial influence of statin therapy on the arterial wall detected by vascular strain analysis.

Increased vascular occlusion in patients with pseudoxanthoma elasticum.

BACKGROUND: Pseudoxanthoma elasticum (PXE) is an autosomal recessive inherited multisystem disorder of the connective tissue caused by a loss-of-function mutation of the ABCC6 gene. It can affect the cardiovascular system, presumably leading to a high prevalence of atherosclerosis. PATIENTS AND METHODS: 46 PXE patients and 18 controls underwent an angiological examination consisting of measurement of ankle-brachial index (ABI), strain-gauge arterial reserve (SGAR), arterial resting perfusion, pulse wave index (PWI), central pulse wave velocity, and ultrasound examination. RESULTS: With an average age of 51.4 ± 12.4 years, 35/46 (76.1 %) of the PXE patients had atherosclerotic lesions, and 10 of them (28.6 %) had a chronic vascular occlusion of one or more peripheral vessels. 34/46 (73.9 %) had a pathologic ABI < 0.9, 15/42 (35.7 %) had a pathological SGAR < 10 mL/100 mL tissue/min, and 23/38 (60.5 %) had a pathological PWI > 180. The differences between the groups were statistically significant for ABI, arterial reserve, and PWI. CONCLUSIONS: In PXE patients atherosclerosis was found with a much higher prevalence than expected. Moreover, they were at very high risk for total vessel occlusions.
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Underdiagnosis of Obstructive Sleep Apnoea in Peripheral Arterial Disease.

Background: Obstructive sleep apnoea (OSA) has interdependently been related to the onset and progression of a large portion of atherosclerotic cardiovascular disorders. In due consideration of OSA-mediated endothelial dysfunction, its impact on peripheral artery disease is conceivable, but undefined. Objectives: The aim of this study was to identify the prevalence of OSA in a lower extremity artery disease (LEAD) study population. Methods: A total of 91 patients receiving in- and outpatient treatment for LEAD were included in this prospectively conducted trial. In addition to an angiological examination, all patients underwent nocturnal screening for sleep-disordered breathing by use of SOMNOcheck micro® (SC micro) and - depending on the results obtained - polysomnography. Results: Patients were principally late middle-aged (69.3 ± 10.8 years), male (71.4%) and slightly overweight (BMI 26.8 ± 3.9). Overnight screening determined a sleep apnoea prevalence of 78.0%, of which 90.1% exhibited a predominantly obstructive genesis. The mean apnoea-hypopnoea index (AHI; events/h) and oxygen desaturation index (events/h) averaged 11.8 ± 13.4 and 8.9 ± 14.2, respectively. The individual AHI categories of non-pathological (<5), mild (5 to <15), moderate (15 to <30) and severe sleep apnoea (≥30) accounted for 22.0, 59.3, 13.2 and 5.5%, respectively. A distributive examination of AHI within LEAD severity groups evinced a significant association (p = 0.047). In cases of at least moderate sleep apnoea (AHI ≥15) polysomnography was performed (n = 17, 18.7% of the whole collective). Correlative analysis revealed a significant correlation between values obtained by SC micro recording and polysomnography, establishing the diagnostic accuracy of the screening results. Conclusions: OSA exhibits an important prevalence of 70.3% in LEAD patients with prior undiagnosed sleep-disordered breathing, indicating major OSA unawareness in this cardiovascular cohort. However, the impact of OSA treatment on LEAD propagation remains to be determined. © 2015 S. Karger AG, Basel.

Safety, feasibility, and diagnostic value of cardiac magnetic resonance imaging in patients with cardiac pacemakers and implantable cardioverters/defibrillators at 1.5 T.

BACKGROUND: Recent studies suggest that magnetic resonance (MR) imaging of the brain and spine may safely be performed in patients with pacemakers (PMs) and implantable cardioverter/defibrillators (ICDs), when taking adequate precautions. The aim of this study was to investigate safety, feasibility, and diagnostic value (DV) of MR imaging in cardiac applications (cardiac MR [CMR]) in patients with PMs and ICDs for the first time. METHODS: Thirty-two PM/ICD patients with a clinical need for CMR were examined. The specific absorption rate was limited to 1.5 W/kg. Devices were reprogrammed pre-CMR to minimize interference with the electromagnetic fields. Devices were interrogated pre-CMR and post-CMR and after 3 months. Troponin I levels were measured pre-CMR and post-CMR; image quality (IQ) and DV of CMR were assessed. RESULTS: All devices could be reprogrammed normally post-CMR. No significant changes of pacing capture threshold, lead impedance, and troponin I were observed. Image quality in patients with right-sided devices (RSD) was better compared with that in patients with left-sided devices (LSD) (P < .05), and less myocardial segments were affected by device-related artefacts (P < .05). Diagnostic value was rated as sufficiently high, allowing for diagnosis, or better in 12 (100%) of 12 patients with RSD, and only in 7 (35%) of 20 patients with LSD. CONCLUSIONS: Cardiac MR may be performed safely when limiting specific absorption rate, appropriately monitoring patients, and following device reprogramming. Cardiac MR delivers good IQ and DV in patients with RSD. Cardiac MR in patients with RSD may therefore be performed with an acceptable risk/benefit ratio, whereas the risk/benefit ratio is rather unfavorable in patients with LSD.

Carotid strain measurement in patients with pseudoxanthoma elasticum - Hint for a different pathomechanism?

Pseudoxanthoma Elasticum (PXE), caused by autosomal-recessive mutations in the ATP-binding cassette transporter (ABCC6) gene, is known for high prevalence of atherosclerosis. A novel method investigating elastic properties of arteries in atherosclerotic patients is vascular strain analysis. We compared 44 PXE patients with peripheral artery disease (PXE+PAD group) with 50 control patients, each 25 without (control group) and with PAD (PAD group). All participants underwent an angiological examination including ankle-brachial index (ABI) and were examined with speckle-tracking based vascular strain analysis of common carotid arteries, measuring radial displacement (r.Dis), radial velocity (r.Vel), radial strain (r.Str), circumferential strain (c.Str), radial strainrate (r.SR) and circumferential strainrate (c.SR). We found significant lower ABI in patients with PXE compared to all other groups (each p < 0.01). The vascular strain analysis resulted in significantly decreased values in the PAD group compared to PXE with PAD (each p ≤ 0.01) and controls without PAD (each p ≤ 0.05), whereas no significant difference could be found between PXE+PAD and controls without PAD. We found significant negative correlations between low strain values and a higher prevalence of PAD in non-PXE patients (r.Str r = -0.34; c.Str r = -0.35; r.SR: r = -0.51; c.SR: r = -0.53). In conclusion, PXE patients had similar values for arterial stiffness compared to controls without PAD in vascular strain analysis. In this group, arterial stiffness parameters were significantly higher compared to non-PXE PAD patients. It is worth to discuss whether PAD-like manifestations in PXE are a different kind of disease and might need another strategy in diagnostics and therapy.

High prevalence of COPD in atherosclerosis patients.

Atherosclerosis and COPD are both systemic inflammatory diseases that may influence each other. The aim of the present study was to determine the prevalence of COPD in patients with cerebral and/or peripheral artery disease and to assess factors associated with the presence of COPD. Following the diagnosis of cerebral and/or peripheral artery disease by means of duplex sonography, 166 consecutive patients underwent body plethysmography with capillary blood gas analysis. Thereafter, blood tests with determination of different parameters such as lipid profile, inflammatory and coagulation markers were conducted in remaining 136 patients who fulfilled inclusion criteria of the study. Thirty-six out of 136 patients suffered from COPD, mostly in early stages of the disease. Residual volume indicating emphysema was increased (162.9%±55.9% vs 124.5%±37.0%, p<0.05) and diffusion capacity was decreased (55.1%±19.5% vs 75.3%±18.6%, p<0.05) in COPD patients vs non-COPD group. In capillary blood gas analysis, COPD patients had lower partial pressure of oxygen (70.9±11.5 vs 75.2±11.0 mmHg, p<0.05) and higher partial pressure of carbon dioxide (36.8±7.5 vs 34.4±4.4 mmHg, p<0.05) compared with non-COPD individuals. Presence of COPD was associated with predominance of diabetes mellitus, interleukin-8-related systemic neutrophilic inflammation and anemia. In conclusion, COPD is highly prevalent in patients with atherosclerotic artery disease.

Asthma is associated with atherosclerotic artery changes.

Asthma is a chronic airway inflammation with a potential systemic impact. Atherosclerosis is a chronic inflammatory artery disease. The aim of our study was to prove if there is a correlation between the occurrence of asthma and increased atherosclerotic vessel disorders. Vessel status was compared between mild-to-moderate, severe allergic asthma and matched controls. Measurements of artery stiffness were calculated by central pulse wave velocity, ultrasonographic strain imaging and ankle-brachial index. Atherosclerotic plaque burden was assessed by colour-coded duplex sonography. Additionally, analysis of cardiovascular and asthma blood markers was conducted. Arterial stiffness expressed as an increased central pulse wave velocity and decreased circumferential and radial strains as well as the prevalence of media sclerosis were significantly higher among asthma patients compared to controls. Atherosclerotic plaque burden was relevantly increased in asthma groups vs. controls (severe asthma: 43.1%, mild-to-moderate asthma: 25.0%, control: 14.3% of study participants). Except for the elevated IgE and fibrinogen concentrations as well as leukocyte number there were no relevant differences in the blood parameters between the groups. Allergic asthma is associated with distinct atherosclerotic artery changes compared to the respectively matched control collective. The severity of asthma correlates with more pronounced pathological vessel alternations.

Lower extremity and carotid artery disease in COPD.

In view of their common chronic inflammatory process, we sought to determine the linkage between peripheral artery disease and chronic obstructive pulmonary disease (COPD). 107 COPD patients (mean±sd age 64.6±10.4 years, 52.2% male) and 22 control smokers without previously diagnosed peripheral artery disease underwent standardised angiological examination for lower extremity artery disease (LEAD) and carotid artery disease. LEAD was significantly more prevalent in COPD patients than in controls (80.4% versus 54.5%, p=0.002). Among COPD patients, 57.0%, 12.2%, 10.3% and 0.9% were found to be in Fontaine stages I, IIA, IIB and III, respectively. As with carotid artery disease, its frequency increased from 36.4% in controls to 58.9% in COPD patients (p=0.003). Carotid plaque burden, LEAD Fontaine degrees as well as pulse wave index and ankle-brachial index manifested significant impairment over percentage predicted forced expiratory volume in 1 s (FEV1 % pred) (p=0.02, p<0.001, p=0.01 and p<0.001, respectively). Multivariate analysis revealed that COPD Global Initiative for Chronic Obstructive Lung Disease status was the strongest independent predictor for the presence of plaque in lower extremity arteries (odds ratio 1.63, 95% CI 1.19-2.25, p=0.003) and carotids (odds ratio 1.66, 95% CI 1.14-2.44, p=0.009). As compared with control smokers, peripheral artery disease is diagnosed in a sizeable proportion of COPD patients and exhibits significant distributive differences over FEV1 % pred that exceed the susceptibility conferred by common cardiovascular stressors.

Routine Endovascular Treatment With a Stent Graft for Access-Site and Access-Related Vascular Injury in Transfemoral Transcatheter Aortic Valve Implantation.

BACKGROUND: Access-site and access-related vascular injury (ASARVI) is still a major limiting factor in transcatheter aortic valve implantation and affects the outcome of patients. Management strategies for ASARVI include manual compression, stent grafts, and vascular surgery. We hypothesized that the standard use of a self-expanding stent graft for the management of ASARVI is feasible and safe. METHODS AND RESULTS: Of 407 patients treated by transfemoral transcatheter aortic valve implantation, 110 experienced ASARVI (27.0%). Of these, 96 (87.3%) were managed by the implantation of a self-expanding nitinol stent graft. In the majority of patients, minor vascular complications triggered the implantation of a stent graft (86.5%), mainly because of bleeding (90.6%) and dissection (5.2%) of the common femoral artery with high rates of primary treatment success (97.9%). Patients receiving stent grafts were more often female (62.2 versus 45.6%, P<0.01), had higher body mass indices (27.8±6.7 versus 25.7±4.7, P=0.01), and suffered more often from diabetes mellitus (34.4 versus 24.5%, P=0.04). Angiographic assessment after a median follow-up of 345 days (interquartile range, 23-745 days) revealed only one patient with moderate, asymptomatic instent-stenosis (1.0%). Compared with a propensity score-matched cohort of patients without ASARVI, stented patients had comparable long-term mortality, despite the occurrence of a vascular complication (1-year mortality: 17.7% versus 26.6%; stent versus matched cohort, respectively; P=0.1). CONCLUSIONS: Routine use of a self-expanding nitinol stent graft in selected patients experiencing ASARVI after transcatheter aortic valve implantation is feasible, safe, and associated with favorable short- and midterm clinical outcome.

Pre-Procedural Hemodynamic Status Improves the Discriminatory Value of the Aortic Regurgitation Index in Patients Undergoing Transcatheter Aortic Valve Replacement.

OBJECTIVES: The aims of this study were to increase the discriminatory value of the aortic regurgitation index (ARI) for the assessment of paravalvular regurgitation (PVR) and to further elucidate the association between aortic regurgitation severity and mortality after transcatheter aortic valve replacement (TAVR). BACKGROUND: Hemodynamic parameters such as the ARI complement predominantly angiographically guided TAVR. However, the ARI depends on several baseline and periprocedural characteristics. METHODS: The ARI was prospectively calculated before and after TAVR in 600 patients. The severity of PVR was assessed in all patients by angiography and echocardiography according to a 3-class scheme. To account for pre-procedural hemodynamic status, the ARI ratio was calculated as post- over pre-procedural ARI. RESULTS: Apart from the degree of PVR (ß = -0.396, p < 0.001), pre-procedural hemodynamic status in the form of the ARI before TAVR (ß = 0.227, p < 0.001) was associated with post-procedural ARI in multivariate regression analysis. The ARI ratio increased the specificity of post-procedural ARI alone for the prediction of both more than mild PVR and 1-year mortality from 75.1% to 93.2% and from 75.0% to 93.3%, respectively. Patients with post-procedural ARI values <25 after TAVR had significantly increased 1-year mortality only when the ARI ratio was <0.60 (50.0% vs. 26.3%, p = 0.001). CONCLUSIONS: The ARI ratio integrating pre- and post-procedural hemodynamic status increases the discriminatory value of post-procedural ARI. The ARI ratio, which reflects acute hemodynamic changes after TAVR, is useful to identify patients with negative outcomes.

Pseudoxanthoma Elasticum - Also a Lung Disease? The Respiratory Affection of Patients with Pseudoxanthoma Elasticum.

BACKGROUND: Pseudoxanthoma elasticum (PXE) is an autosomal-recessive mineralisation disorder caused by loss of function mutations in the ABCC6 Gen. Histological findings and data of an autopsy of a PXE-patient suggest a possible pulmonal calcification. So far, there exists no clinical data whether PXE patients actually are at high risk of developing pulmonary disorder. METHODS: In a cross-sectional study, 35 PXE patients and 15 healthy controls underwent a pulmonary function testing, including spirometry, body plethysmography and carbon monoxide diffusing test. Additionally, PXE patients completed a COPD-Assessment-Test (CAT). RESULTS: We observed in PXE patients normal values for predicted vital capacity (VC%; 96.0±13.0%), predicted total lung capacity (TLC%; 98.2±12.0%) and predicted forced expiration volume (FEV1%; 102.5±15.6%), whereas compared to healthy controls the PXE group showed significant diminished values for carbon monoxide diffusing capacity (DLCO, 7.2 ±1.4mmol/min/kPa vs. 8.6 ±1.5 mmol/min/kPa; p = 0.008) and predicted carbon monoxide diffusing capacity (DLCO%; 79.7±11.5% vs. 87.2±6.6%; p = 0.008). 11/35 (31.4%) PXE patients showed pathological DLCO% values under 75% (68.5%±5.4%). CONCLUSION: PXE patients demonstrated a regular lung function testing, but nevertheless they had impaired CO diffusing parameters, which might be associated with a preclinical state of an interstitial lung disease and a risk for restrictive ventilation disorders.

Thrombin inhibition by dabigatran attenuates atherosclerosis in ApoE deficient mice.

INTRODUCTION: Atherosclerosis is a chronic inflammatory disease characterized by endothelial cell damage, infiltration, proliferation and accumulation of macrophages, lymphocytes and transformed vascular smooth muscle cells within the vascular wall and procoagulation processes involving activation of plasmatic coagulation events and platelets. Numerous studies suggested a close interaction between thrombin action and atherogenesis, but possibly underlying mechanisms are multiple and specific treatment options were missing until now. MATERIAL AND METHODS: Atherosclerosis prone 12 weeks old ApoE(-/-) mice were fed a cholesterol rich diet for 4 weeks and were concomitantly treated orally with placebo or the thrombin inhibitor dabigatran (1.2 g/kg/day). RESULTS: The thrombin time (HEMOCLOT(®)) was significant extended in dabigatran treated animals. Vascular oxidative stress was significantly reduced during thrombin inhibition, as assessed by L012 chemiluminescence in aortic segments (212 ±84 vs. 69 ±21 RLU/s/mg dry weight, p = 0.048). Organ chamber experiments of isolated aortic rings showed that dabigatran treatment significantly improved endothelium-derived vasorelaxation (p < 0.001). Dabigatran treated mice developed less atherosclerotic lesions (6.2 ±0.2% vs. 9 ±1.1%, p = 0.037) and showed less infiltration of atherosclerotic lesions with macrophages (2.59 ±0.3% vs. 5.14 ±0.7%, p = 0.0046), as determined by systematic histological and immunohistological analyses of the aortic root. Blood pressure, body weight and food intake were not altered by the treatment. CONCLUSIONS: The thrombin inhibitor dabigatran reduces vascular oxidative stress and inflammation, improves endothelial function and decreases atherosclerosis in mice.