scholarly journals CT-Derived Pulmonary Artery Diameters to Preselect for Echocardiography in COPD Patients Eligible for Bronchoscopic Treatments

Respiration ◽  
2020 ◽  
Vol 99 (10) ◽  
pp. 846-852
Author(s):  
Marieke C. van der Molen ◽  
Jorine E. Hartman ◽  
Karin Klooster ◽  
Huib A.M. Kerstjens ◽  
Joost van Melle ◽  
...  

<b><i>Background:</i></b> Currently, patients with COPD who are evaluated for bronchoscopic treatments are routinely screened for pulmonary hypertension (PH) and systolic left ventricle dysfunction by echocardiography. <b><i>Objectives:</i></b> We evaluated the prevalence of PH and systolic left ventricle dysfunction in this patient group and investigated if the previously proposed CT-derived pulmonary artery to aorta (PA:A) ratio &#x3e;1 and PA diameter measurements can be used as alternative screening tools for PH. <b><i>Methods:</i></b> Two hundred fifty-five patients were included in this retrospective analysis (FEV<sub>1</sub> 25%pred, RV 237%pred). All patients received transthoracic echocardiography and chest CT scans on which diameters of the aorta and pulmonary artery were measured at the bifurcation and proximal to the bifurcation. <b><i>Results:</i></b> Following echocardiography, 3 patients (1.2%) had PH and 1 (0.4%) had systolic left ventricle dysfunction. Using a PA:A ratio &#x3e;1, only 10.3% of the patients with a right ventricular systolic pressure (RVSP) ≥35 mm Hg were detected and none of the patients with an RVSP &#x3e;50 mm Hg were detected. Patients with an RVSP ≥35 mm Hg had significantly higher PA diameters (29.5 vs. 27.5 mm; <i>p</i> = 0.02) but no significantly different PA:A ratios. All patients with an RVSP &#x3e;50 mm Hg had PA diameters &#x3e;30 mm. <b><i>Conclusions:</i></b> The prevalence of PH and systolic left ventricle dysfunction is low in this preselected cohort of patients with severe COPD. In this population, a PA:A ratio &#x3e;1 is not a useful cardiac screening tool for PH. A PA diameter &#x3e;30 mm could substitute for routinely performed echocardiography in the screening for PH in this patient group.

2016 ◽  
Vol 26 (7) ◽  
pp. 1406-1413
Author(s):  
Simon Lee ◽  
Irene D. Lytrivi ◽  
Zhanna Roytman ◽  
Hyun-Sook Helen Ko ◽  
Cheryl Vinograd ◽  
...  

AbstractIntroductionAgreement between echocardiography and right heart catheterisation-derived right ventricular systolic pressure is modest in the adult heart failure population, but is unknown in the paediatric cardiomyopathy population.MethodsAll patients at a single centre from 2001 to 2012 with a diagnosis of cardiomyopathy who underwent echocardiography and catheterisation within 30 days were included in this study. The correlation between tricuspid regurgitation gradient and catheterisation-derived right ventricular systolic pressure and mean pulmonary artery pressure was determined. Agreement between echocardiography and catheterisation-derived right ventricular systolic pressure was assessed using Bland–Altman plots. Analysis was repeated for patients who underwent both procedures within 7 days. Haemodynamic data from those with poor agreement and good agreement between echocardiography and catheterisation were compared.ResultsA total of 37 patients who underwent 48 catheterisation procedures were included in our study. The median age was 11.8 (0.1–20.6 years) with 22 males (58% total). There was a modest correlation (r=0.65) between echocardiography and catheterisation-derived right ventricular systolic pressure, but agreement was poor. Agreement between tricuspid regurgitation gradient and right ventricular systolic pressure showed wide 95% limits of agreement. There was a modest correlation between the tricuspid regurgitation gradient and mean pulmonary artery pressure (r=0.6). Shorter time interval between the two studies did not improve agreement. Those with poor agreement between echocardiography and catheterisation had higher right heart pressures, but this difference became insignificant after accounting for right atrial pressure.ConclusionTransthoracic echocardiography estimation of right ventricular systolic pressure shows modest correlation with right heart pressures, but has limited agreement and may underestimate the degree of pulmonary hypertension in paediatric cardiomyopathy patients.


CHEST Journal ◽  
2004 ◽  
Vol 126 (4) ◽  
pp. 884S
Author(s):  
Luis E. Santos-Martinez ◽  
Jose Gotes ◽  
Carlos Tena ◽  
Pedro Flores ◽  
Samuel Ramirez ◽  
...  

Hypertension ◽  
2020 ◽  
Vol 75 (5) ◽  
pp. 1305-1314 ◽  
Author(s):  
Joshua M. Oakes ◽  
Jiaxi Xu ◽  
Tamara M. Morris ◽  
Nicholas D. Fried ◽  
Charlotte S. Pearson ◽  
...  

Cigarette smoking is the single most important risk factor for the development of cardiovascular and pulmonary diseases; however, the role of nicotine in the pathogenesis of these diseases is incompletely understood. The purpose of this study was to examine the effects of chronic nicotine inhalation on the development of cardiovascular and pulmonary disease with a focus on blood pressure and cardiac remodeling. Male C57BL6/J mice were exposed to air (control) or nicotine vapor (daily, 12 hour on/12 hour off) for 8 weeks. Systemic blood pressure was recorded weekly by radio-telemetry, and cardiac remodeling was monitored by echocardiography. At the end of the 8 weeks, mice were subjected to right heart catheterization to measure right ventricular systolic pressure. Nicotine-exposed mice exhibited elevated systemic blood pressure from weeks 1 to 3, which then returned to baseline from weeks 4 to 8, indicating development of tolerance to nicotine. At 8 weeks, significantly increased right ventricular systolic pressure was detected in nicotine-exposed mice compared with the air controls. Echocardiography showed that 8-week nicotine inhalation resulted in right ventricular (RV) hypertrophy with increased RV free wall thickness and a trend of increase in RV internal diameter. In contrast, there were no significant structural or functional changes in the left ventricle following nicotine exposure. Mechanistically, we observed increased expression of angiotensin-converting enzyme and enhanced activation of mitogen-activated protein kinase pathways in the RV but not in the left ventricle. We conclude that chronic nicotine inhalation alters both systemic and pulmonary blood pressure with the latter accompanied by RV remodeling, possibly leading to progressive and persistent pulmonary hypertension.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.


1982 ◽  
Vol 53 (4) ◽  
pp. 908-913 ◽  
Author(s):  
J. E. Whinnery ◽  
M. H. Laughlin

Measurements of right ventricular pressure in miniature swine were made at +Gz levels from +1 through +9 Gz. Polyethylene catheters were chronically placed in the cranial vena cava of five 2-yr-old female miniature swine (35–50 kg). The catheters were large enough to allow the introduction of a Millar pressure transducer into the venous system for placement in the right heart. The animals were fitted with an abdominal anti-G suit, restrained in a fiberglass couch, and exposed to the various +Gz levels on a centrifuge while fully conscious and unanesthetized. Right ventricular pressure and heart rate were measured during and for 2 min following 30-s exposures to each level of +Gz stress. The maximum right ventricular systolic pressure observed during +Gz was 200 Torr at +5 Gz with the maximum diastolic pressure being 88 Torr observed at +5 Gz. Mean heart rates were 200–210 beats/min at all levels of +Gz greater than or equal to +3 Gz when the animal remained stable. Mean maximum right ventricular pressures during +Gz stress were observed to increase through +5 Gz (85 Torr) and to decrease at higher levels of +Gz, indicating that through +5 Gz there is at least a partial compensation during acceleration stress. Decompensation in response to the stress began to occur during acceleration above +5 Gz with all animals decompensating during +9 Gz.


2012 ◽  
Vol 90 (10) ◽  
pp. 1364-1371
Author(s):  
Vicki N. Wang ◽  
Mavra Ahmed ◽  
Amelia Ciofani ◽  
Zion Sasson ◽  
John T. Granton ◽  
...  

We evaluated the effect of endogenous estrogen levels on exercise-related changes in right ventricular systolic pressure (RVSP) of healthy, eumenorrheic, sedentary women. Volunteers were studied at two separates phases of the menstrual cycle (LO and HI estrogen phases), exercised on a semi-supine ergometer with escalating workload and monitored continuously by 12-lead ECG and automated blood pressure cuff. At each exercise stage, Doppler echocardiography measurements were obtained and analyzed to determine RVSP. Fourteen subjects (age 24 ± 5) were studied. Exercise duration was significantly higher on the HI estrogen day, but no significant differences in hemodynamic response to exercise were found between the two study days. There were also no significant differences with respect to heart rate (HR) acceleration during early exercise, as well as resting and peak RVSP, HR, blood pressure, and rate pressure product. Doppler-estimated RVSP demonstrated a linear relationship to HR at a ratio of 1 mm Hg (1 mm Hg = 133.3224 Pa) for every 5 bpm (beats per minute) increase in HR. There were no differences in the slope of this relationship between HI and LO estrogen phases of the menstrual cycle. Our findings did not demonstrate any effect of endogenous estrogen levels on the modulation of the pulmonary vascular response to exercise in healthy women.


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