Carmen Pizarro

Effect of endobronchial valve therapy on pulmonary perfusion and ventilation distribution.

Introduction Endoscopic lung volume reduction (ELVR) is an emerging therapy for emphysematous COPD. However, any resulting changes in lung perfusion and ventilation remain undetermined. Here, we report ELVR-mediated adaptations in lung perfusion and ventilation, as investigated by means of pulmonary scintigraphy. Methods In this observational study, we enrolled 26 patients (64.9±9.4 yrs, 57.7% male) with COPD heterogeneous emphysema undergoing ELVR with endobronchial valves (Zephyr, Pulmonx, Inc.). Mean baseline FEV1 and RV were 32.9% and 253.8% predicted, respectively. Lung scintigraphy was conducted prior to ELVR and eight weeks thereafter. Analyses of perfusion and ventilation shifts were performed and complemented by correlation analyses between paired zones. Results After ELVR, target zone perfusion showed a mean relative reduction of 43.32% (p<0.001), which was associated with a significant decrease in target zone ventilation (p<0.001). Perfusion of the contralateral untreated zone and of the contralateral total lung exhibited significant increases post-ELVR (p = 0.002 and p = 0.005, respectively); both correlated significantly with the corresponding target zone perfusion adaptations. Likewise, changes in target zone ventilation correlated significantly with ventilatory changes in the contralateral untreated zone and the total contralateral lung (Pearson’s r: −0.42, p = 0.04 and Pearson’s r: −0.42, p = 0.03, respectively). These effects were observed in case of clinical responsiveness to ELVR, as assessed by changes in the six-minute walk test distance. Discussion ELVR induces a relevant decrease in perfusion and ventilation of the treated zone with compensatory perfusional and ventilatory redistribution to the contralateral lung, primarily to the non-concordant, contralateral zone.

Diagnostic value of speckle-tracking echocardiography in confirmed cardiac sarcoidosis

Sirs: Sarcoidosis is a chronic, non-caseating granulomatous disease of unknown origin that can affect any organ. Given the heterogeneity of sarcoidosis per se and cardiac sarcoidosis (CS), in particular [1, 2], major efforts are undertaken to identify cardiac sarcoid that may initially be clinically silent and may first manifest as sudden cardiac death. Since the use of advanced imaging modalities, such as positron emission tomography and cardiovascular magnetic resonance (CMR) imaging, is restricted due to their limited availability and costliness, alternative imaging techniques that allow for a reliable, and timely CS diagnosis demand attention. Two-dimensional (2D) speckletracking echocardiography facilitates the assessment of regional and global myocardial deformation properties [3]. Nonetheless, the question of its potential to visualize CSinduced myocardial dysfunction remains unresolved. To define its validity for the diagnosis of cardiac sarcoidal involvement, we performed speckle-tracking analysis of both CS-positive and CS-negative patients. Study population comprised 60 patients with histologically proven sarcoidosis of whom 19 patients suffered from cardiac sarcoid involvement, whereas the remaining 41 patients did not. CS-presence and CS-absence were defined on the basis of prior CMR results. At the time of CMR examination, patients underwent complementary 2D transthoracic echocardiography. Echocardiographic data were digitized and transferred to a commercially available medical workstation (TomTec Imaging Systems GmbH, Unterschleissheim, Germany). An apical four chamber view was offline speckle-tracking-analyzed. Regional strain evaluation was conducted by each ventricle’s segmentation into an apical, mid-ventricular, and basal region. Statistical analysis was performed using the SPSS Software Version 23.0 (Armonk, NY, USA). Bonferroni correction was applied for adjustment for multiple comparisons. Receiver operating characteristic (ROC) curve analysis was conducted to describe the predictive value of strain measurements. In ten consecutive patients, interobserver agreement and intra-observer agreement of strain measurement were tested by intraclass correlation coefficient; a coefficient [0.8 indicated a good reliability. A two-tailed p value of 0.05 was considered statistical significant. Table 1 summarizes the study populatiońs demographic, echocardiographic, and CMR characteristics. Evaluation of global and regional biventricular deformation properties derived from 2D longitudinal strain imaging revealed impairment of longitudinal performance in CS-positive patients as compared to CS-negative individuals. Specifically, the left ventricular (LV) global, medial septal, and apical septal longitudinal strain were significantly reduced in and correlated with CS-presence (p = 0.009, p = 0.007, p = 0.02, respectively; Table 1). After adjustment for multiple comparisons, the global and medial septal longitudinal strain persistently differed between groups, whereas the apical septal longitudinal strain did not (p = 0.04, p = 0.04, and p = 0.12, respectively). Comparative ROC analysis of the global and medial septal measures identified the LV global longitudinal strain to have the highest predicted value for the diagnosis of CS: the area under the curve was 0.72 (95 % CI: 0.56–0.87; p 0.01) and C. Pizarro and F. Kluenker contributed equally to this work.

Invasive coronary angiography in patients with acute exacerbated COPD and elevated plasma troponin

Background In acute exacerbation of COPD, increased plasma levels of cardiac troponin are frequent and associated with increased mortality. Thus, we aimed at prospectively determining the diagnostic value of coronary angiography in patients with exacerbated COPD and concomitantly elevated cardiac troponin. Patients and methods A total of 88 patients (mean age 72.9±9.2 years, 56.8% male) hospitalized for acute exacerbation of COPD with elevated plasma troponin were included. All patients underwent coronary angiography within 72 hours after hospitalization. Complementary 12-lead electrocardiogram, transthoracic echocardiography, pulmonary function, and angiological testing were performed. Results Coronary angiography objectified the presence of ischemic heart disease (IHD) in 59 patients (67.0%), of whom 34 patients (38.6% of total study population) underwent percutaneous coronary intervention. Among these 34 intervened patients, the vast majority (n=26, 76.5%) had no previously known IHD, whereas only eight out of 34 patients (23.5%) presented an IHD history. Patients requiring coronary intervention showed significantly reduced left ventricular ejection fraction (45.8%±13.1% vs 55.1%±13.3%, P=0.01) and a significantly more frequent electrocardiographic ST-segment depression (20.6% vs 7.4%, P=0.01). Neither additional laboratory parameters for inflammation and myocardial injury nor lung functional measurements differed significantly between the groups. Conclusion Angiographically confirmed IHD that required revascularization occurred in 38.6% of exacerbated COPD patients with elevated cardiac troponin. In this considerable portion of patients, coronary angiography emerged to be of diagnostic and therapeutic value.

Impact of endoscopic lung volume reduction on right ventricular myocardial function.

Introduction Endoscopic lung volume reduction (ELVR) provides a minimally invasive therapy for patients with severe lung emphysema. As its impact on right ventricular (RtV) function is undefined, we examined the extent of RtV functional changes following ELVR, as assessed by use of speckle tracking-based RtV deformation analysis. Methods We enrolled 32 patients with severe emphysematous COPD scheduled for bronchoscopic LVR using endobronchial valves (Zephyr, PulmonX, Inc.), comprising 16 matched clinical responders and 16 non-responders. Echocardiography was conducted one day prior to ELVR and at an eight-week postprocedural interval. Results Patients were predominantly of late middle-age (65.8±8.7yrs), male (62.5%) and presented advanced COPD emphysema (means FEV1 and RV: 32.6% and 239.1% of predicted, respectively). After ELVR, RtV apical longitudinal strain improved significantly in the total study cohort (-7.96±7.02% vs. -13.35±11.48%, p=0.04), whereas there were no significant changes in other parameters of RtV function such as RtV global longitudinal strain, TAPSE or pulmonary arterial systolic pressure. In responding patients, 6MWT-improvement correlated with a decrease in NT-proBNP (Pearson´s r: -0.53, p=0.03). However, clinical non-responders did not exhibit any RtV functional improvement. Discussion ELVR beneficially impacts RtV functional parameters. Speckle tracking-based RtV apical longitudinal strain analysis allows early determination of RtV contractile gain and identification of clinical responsiveness.

Volumetric and scintigraphic changes following endoscopic lung volume reduction

Bronchoscopic treatment of emphysema represents an emerging therapeutic modality for advanced emphysematous lung destruction in chronic obstructive pulmonary disease (COPD). Within the proposed techniques for endoscopic lung volume reduction (ELVR), a significant amount of experience exists for the placement of endobronchial valves (EBV) (Zephyr® valves; Pulmonx, Inc., Redwood City, CA, USA) targeting atelectasis of the treated, emphysematous lobe [1, 2]. However, post-procedural clinical improvement has also been documented in patients lacking lobar exclusion 3. While volumetric and density adaptations following ELVR have repeatedly been a focus [3, 4], the interaction of volume and perfusional/ventilatory changes remains unclear. In this observational study, we defined the extent of interdependency of ELVR-mediated volumetric and scintigraphic adaptations. EBV treatment reduces target lobe volume, ventilation and perfusion with consistent redistributive pattern http://ow.ly/C95Ue

Cardiovascular magnetic resonance imaging and clinical performance of somatostatin receptor positron emission tomography in cardiac sarcoidosis: CMR and SSTR PET in cardiac sarcoidosis

Cardiac affection constitutes a major limiting condition in systemic sarcoidosis. The primary objective of this study was to investigate the persistence rate of cardiac sarcoid involvement by cardiovascular magnetic resonance (CMR) imaging in patients diagnosed with cardiac sarcoidosis (CS). Moreover, we examined the additional insights into myocardial damages characteristics gained by somatostatin receptor scintigraphy.

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±10.4u2005years, 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 1u2005s (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. Undiagnosed lower extremity and carotid artery disease is common in COPD and aggravates over COPD GOLD stages http://ow.ly/w96f303lHTu

Nitinol stent insertion in tracheomalacia

A 69-year-old man was admitted to our hospital with progressive dyspnoea accompanied by inspiratory stridor. He presented a history of surgical aortic valve replacement 3u2005years previously, complicated by prolonged postoperative mechanical ventilation requiring percutaneous tracheostomy. Presently, bronchoscopy evidenced tracheomalacia (TM) with subtotal tracheal stenosis. CT scan confirmed long segment narrowing >20u2005mm of the upper trachea (figure 1). Operative retracheostomy resulted in repeated tube dislocation …

Pulmonary arterial hypertension is associated with increased T1 relaxation times and decreased left ventricular performance in spite of preserved left ventricular function

Background Pulmonary arterial hypertension (PAH) mainly affects the right (RV). Due to ventricular interdependence, PAH may also affect the left ventricle (LV) leading to opposite adaptive changes with an LV-atrophy and diffuse fibrosis. Strain analysis detects ventricular dysfunction even in patients with preserved ventricular function. Cardiac magnetic resonance (CMR) mapping techniques with determination of T1 and T2 relaxation times (T1 resp T2) may allow for discrimination between healthy myocardium and diffuse fibrosis in PAH patients. This study was performed to evaluate the association between myocardial changes assessed by strain analysis, and by native T1 and T2 map in patients with PAH.

Heart Rate Variability and Arrhythmic Burden in Pulmonary Hypertension

A growing body of evidence indicates that sudden cardiac death constitutes a major cause of mortality in pulmonary hypertension (PH). As validated method to evaluate cardiac autonomic system dysfunction, alterations in heart rate variability (HRV) are predictive of arrhythmic events, particularly in left ventricular disease. Here, we sought to determine the clinical value of HRV assessment in PH. Sixty-four patients were allocated to different PH-subgroups in this prospectively conducted trial: 25 patients with pulmonary arterial hypertension (PAH), 11 patients with chronic thromboembolic PH (CTEPH), and 28 patients with COPD-induced PH. All patients underwent 24-h Holter electrocardiogram for HRV assessment by time- and frequency-domain analysis. Arrhythmic burden was evaluated by manual analysis and complementary automatic measurement of premature atrial and ventricular contractions. The results were compared to 31 healthy controls. The PAH patients offered a significantly higher mean heart rate (78.6u2009±u200910.4xa0bpm vs. 70.1u2009±u200910.3xa0bpm, pu2009=u20090.04), a higher burden of premature ventricular contractions (pu2009<u20090.01), and decreases in HRV (SDNN: pu2009<u20090.01; SDANN: pu2009<u20090.01; very low frequency: pu2009<u20090.01; low frequency/high frequency ratio: pu2009<u20090.01; total power: pu2009=u20090.02). In CTEPH patients, only the amount of premature ventricular contractions differed from controls (pu2009<u20090.01), whereas in COPD both premature atrial contraction count and frequency-domain-based HRV manifested significant differences. In conclusion, PAH appears to be primarily affected by HRV alterations and ventricular arrhythmic burden, indicating a high risk for malignant arrhythmic events.