State-of-the-art pulmonary arterial imaging – Part 1

VASA ◽  
2018 ◽  
Vol 47 (5) ◽  
pp. 345-359 ◽  
Author(s):  
Yuki Tanabe ◽  
Luis Landeras ◽  
Abed Ghandour ◽  
Sasan Partovi ◽  
Prabhakar Rajiah
Keyword(s):  
State Of The Art ◽  
Pulmonary Arteries ◽  
Pulmonary Angiography ◽  
Imaging Modalities ◽  
Nuclear Medicine Imaging ◽  
Multiple State ◽  
Pulmonary Arterial ◽  
Magnetic Resonance Imaging Mri ◽  
Acquired Abnormalities ◽  
Arterial Imaging

Abstract. The pulmonary arteries are affected by a variety of congenital and acquired abnormalities. Multiple state-of-the art imaging modalities are available to evaluate these pulmonary arterial abnormalities, including computed tomography (CT), magnetic resonance imaging (MRI), echocardiography, nuclear medicine imaging and catheter pulmonary angiography. In part one of this two-part series on state-of-the art pulmonary arterial imaging, we review these imaging modalities, focusing particularly on CT and MRI. We also review the utility of these imaging modalities in the evaluation of pulmonary thromboembolism.

State-of-the-art pulmonary arterial imaging – Part 2

VASA ◽  
2018 ◽  
Vol 47 (5) ◽  
pp. 361-375 ◽  
Author(s):  
Harold Goerne ◽  
Abhishek Chaturvedi ◽  
Sasan Partovi ◽  
Prabhakar Rajiah
Keyword(s):  
Pulmonary Artery ◽  
State Of The Art ◽  
Therapy Monitoring ◽  
Pulmonary Arteries ◽  
Imaging Modalities ◽  
Cross Sectional ◽  
Multiple Imaging ◽  
Cross Sectional Imaging ◽  
Pulmonary Arterial ◽  
Arterial Imaging

Abstract. Although pulmonary embolism is the most common abnormality of the pulmonary artery, there is a broad spectrum of other congenital and acquired pulmonary arterial abnormalities. Multiple imaging modalities are now available to evaluate these abnormalities of the pulmonary arteries. CT and MRI are the most commonly used cross-sectional imaging modalities that provide comprehensive information on several aspects of these abnormalities, including morphology, function, risk-stratification and therapy-monitoring. In this article, we review the role of state-of-the-art pulmonary arterial imaging in the evaluation of non-thromboembolic disorders of pulmonary artery.

scholarly journals Effects of acute Rho kinase inhibition on chronic hypoxia-induced changes in proximal and distal pulmonary arterial structure and function

2011 ◽  
Vol 110 (1) ◽  
pp. 188-198 ◽  
Author(s):  
Rebecca R. Vanderpool ◽  
Ah Ram Kim ◽  
Robert Molthen ◽  
Naomi C. Chesler
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Rho Kinase ◽  
Pressure Flow ◽  
Kinase Inhibition ◽  
Pulmonary Vasoconstriction ◽  
Pulsatile Pressure ◽  
Arterial Structure ◽  
Pulmonary Arterial ◽  
Induced Changes

Hypoxic pulmonary hypertension (HPH) is initially a disease of the small pulmonary arteries. Its severity is usually quantified by pulmonary vascular resistance (PVR). Acute Rho kinase inhibition has been found to reduce PVR toward control values in animal models, suggesting that persistent pulmonary vasoconstriction is the dominant mechanism for increased PVR. However, HPH may also cause proximal arterial changes, which are relevant to right ventricular (RV) afterload. RV afterload can be quantified by pulmonary vascular impedance, which is obtained via spectral analysis of pulsatile pressure-flow relationships. To determine the effects of HPH independent of persistent pulmonary vasoconstriction in proximal and distal arteries, we quantified pulsatile pressure-flow relationships before and after acute Rho kinase inhibition and measured pulmonary arterial structure with microcomputed tomography. In control lungs, Rho kinase inhibition decreased 0 Hz impedance (Z0), which is equivalent to PVR, from 2.1 ± 0.4 to 1.5 ± 0.2 mmHg·min·ml−1 ( P < 0.05) and tended to increase characteristic impedance (ZC) from 0.21 ± 0.01 to 0.22 ± 0.01 mmHg·min·ml−1. In HPH lungs, Rho kinase inhibition decreased Z0 ( P < 0.05) without affecting ZC. Microcomputed tomography measurements performed on lungs after acute Rho kinase inhibition demonstrated that HPH significantly decreased the unstressed diameter of the main pulmonary artery (760 ± 60 vs. 650 ± 80 μm; P < 0.05), decreased right pulmonary artery compliance, and reduced the frequency of arteries of diameter 50–100 μm (both P < 0.05). These results demonstrate that acute Rho kinase inhibition reverses many but not all HPH-induced changes in distal pulmonary arteries but does not affect HPH-induced changes in the conduit arteries that impact RV afterload.

Acute hypoxia increases intracellular [Ca2+] in pulmonary arterial smooth muscle by enhancing capacitative Ca2+ entry

2005 ◽  
Vol 288 (6) ◽  
pp. L1059-L1069 ◽  
Author(s):  
Jian Wang ◽  
Larissa A. Shimoda ◽  
Letitia Weigand ◽  
Wenqian Wang ◽  
Dejun Sun ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Primary Cultures ◽  
Fluorescent Microscopy ◽  
Pulmonary Arteries ◽  
Arterial Smooth Muscle ◽  
Fura 2 ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle

Hypoxic pulmonary vasoconstriction (HPV) requires influx of extracellular Ca2+ in pulmonary arterial smooth muscle cells (PASMCs). To determine whether capacitative Ca2+ entry (CCE) through store-operated Ca2+ channels (SOCCs) contributes to this influx, we used fluorescent microscopy and the Ca2+-sensitive dye fura-2 to measure effects of 4% O2 on intracellular [Ca2+] ([Ca2+]i) and CCE in primary cultures of PASMCs from rat distal pulmonary arteries. In PASMCs perfused with Ca2+-free Krebs Ringer bicarbonate solution (KRBS) containing cyclopiazonic acid to deplete Ca2+ stores in sarcoplasmic reticulum and nifedipine to prevent Ca2+ entry through L-type voltage-operated Ca2+ channels (VOCCs), hypoxia markedly enhanced both the increase in [Ca2+]i caused by restoration of extracellular [Ca2+] and the rate at which extracellular Mn2+ quenched fura-2 fluorescence. These effects, as well as the increased [Ca2+]i caused by hypoxia in PASMCs perfused with normal salt solutions, were blocked by the SOCC antagonists SKF-96365, NiCl2, and LaCl3 at concentrations that inhibited CCE >80% but did not alter [Ca2+]i responses to 60 mM KCl. In contrast, the VOCC antagonist nifedipine inhibited [Ca2+]i responses to hypoxia by only 50% at concentrations that completely blocked responses to KCl. The increased [Ca2+]i caused by hypoxia was completely reversed by perfusion with Ca2+-free KRBS. LaCl3 increased basal [Ca2+]i during normoxia, indicating effects other than inhibition of SOCCs. Our results suggest that acute hypoxia enhances CCE through SOCCs in distal PASMCs, leading to depolarization, secondary activation of VOCCs, and increased [Ca2+]i. SOCCs and CCE may play important roles in HPV.

Inhibition of hypoxic pulmonary vasoconstriction by antagonists of store-operated Ca2+ and nonselective cation channels

2005 ◽  
Vol 289 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Letitia Weigand ◽  
Joshua Foxson ◽  
Jian Wang ◽  
Larissa A. Shimoda ◽  
J. T. Sylvester
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Cation Channels ◽  
Pulmonary Vasoconstriction ◽  
Nonselective Cation Channels ◽  
Pressor Responses ◽  
Intracellular Ca ◽  
Pulmonary Arterial

Previous studies indicated that acute hypoxia increased intracellular Ca2+ concentration ([Ca2+]i), Ca2+ influx, and capacitative Ca2+ entry (CCE) through store-operated Ca2+ channels (SOCC) in smooth muscle cells from distal pulmonary arteries (PASMC), which are thought to be a major locus of hypoxic pulmonary vasoconstriction (HPV). Moreover, these effects were blocked by Ca2+-free conditions and antagonists of SOCC and nonselective cation channels (NSCC). To test the hypothesis that in vivo HPV requires CCE, we measured the effects of SOCC/NSCC antagonists (SKF-96365, NiCl2, and LaCl3) on pulmonary arterial pressor responses to 2% O2 and high-KCl concentrations in isolated rat lungs. At concentrations that blocked CCE and [Ca2+]i responses to hypoxia in PASMC, SKF-96365 and NiCl2 prevented and reversed HPV but did not alter pressor responses to KCl. At 10 μM, LaCl3 had similar effects, but higher concentrations (30 and 100 μM) caused vasoconstriction during normoxia and potentiated HPV, indicating actions other than SOCC blockade. Ca2+-free perfusate and the voltage-operated Ca2+ channel (VOCC) antagonist nifedipine were potent inhibitors of pressor responses to both hypoxia and KCl. We conclude that HPV required influx of Ca2+ through both SOCC and VOCC. This dual requirement and virtual abolition of HPV by either SOCC or VOCC antagonists suggests that neither channel provided enough Ca2+ on its own to trigger PASMC contraction and/or that during hypoxia, SOCC-dependent depolarization caused secondary activation of VOCC.

Diameter and flow velocity changes in small pulmonary vessels due to microembolization

1988 ◽  
Vol 65 (1) ◽  
pp. 288-296 ◽  
Author(s):  
M. Shirai ◽  
K. Sada ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Volume Flow ◽  
Internal Diameter ◽  
Vascular Bed ◽  
Small Doses ◽  
Mechanical Factors ◽  
Pulmonary Arterial ◽  
Velocity Changes

The pulmonary vascular bed was embolized with glass beads in small doses that induced no significant changes in pulmonary arterial pressure in anesthetized cats. We analyzed changes in internal diameter (ID), flow velocity, and volume flow of embolized and nonembolized arteries simultaneously with ID changes of small veins. In embolized arteries, with 180-, 300-, and 500-microns beads, ID constricted maximally in just proximal portions of the plug by 22, 23, and 17%, respectively, but with 840-microns beads, no ID constriction occurred. With 50-microns beads, the maximum ID constriction occurred in arteries of 200-300 microns but not in those of 100-200 microns. The constriction decreased in the upstream larger arteries and disappeared in those greater than 800 microns ID. In the nonembolized arteries no ID change occurred. Veins constricted slightly compared with arteries. By heparin pretreatment, ID constriction was slightly attenuated in arteries and was almost abolished in veins, whereas it was not affected with hexamethonium bromide. At a branching site, volume flow to an embolized artery decreased because of a decrease in ID and flow velocity, whereas volume flow to a nonembolized artery increased because of an increase in flow velocity. We concluded that pulmonary microembolization induced a vasoconstriction chiefly in small pulmonary arteries upstream to the plug. After embolization, blood flow was locally redistributed from an embolized to a nonembolized artery at a branching site. Arterial vasoconstriction may be mediated chiefly by local mechanical factors.

Bone Metastases: Assessment of Therapeutic Response through Radiological and Nuclear Medicine Imaging Modalities

2011 ◽  
Vol 23 (9) ◽  
pp. 632-645 ◽  
Author(s):  
V. Vassiliou ◽  
D. Andreopoulos ◽  
S. Frangos ◽  
N. Tselis ◽  
E. Giannopoulou ◽  
...  
Keyword(s):  
Nuclear Medicine ◽  
Bone Metastases ◽  
Therapeutic Response ◽  
Imaging Modalities ◽  
Nuclear Medicine Imaging

scholarly journals Vulvar Lipoma: A Case Report

2018 ◽  
Vol 40 (10) ◽  
pp. 647-649
Author(s):  
Ahmed Reda ◽  
Ihab Gomaa
Keyword(s):  
Magnetic Resonance Imaging ◽  
Case Report ◽  
Magnetic Resonance ◽  
Histopathological Examination ◽  
Surgical Excision ◽  
Imaging Modalities ◽  
Resonance Imaging ◽  
Rare Site ◽  
Magnetic Resonance Imaging Mri ◽  
Vulvar Mass

AbstractThe present study is a case report of vulvar lipoma. The vulva is a rare site for the development of lipomas, and the aim of the study is to determine if the current imaging modalities can diagnose lipomas correctly. A 43-year-old patient presented with a painless, slowly progressive, oval, mobile and non-tender right vulvar mass compressing the vagina and totally covering the introitus. Both the ultrasonography and magnetic resonance imaging (MRI) exams suggested the diagnosis of lipoma. Surgical excision was performed, and the histopathological examination of the mass confirmed a lipoma.

scholarly journals Imaging of Fibrosis in Chronic Pancreatitis

2022 ◽  
Vol 12 ◽  
Author(s):  
Yasunobu Yamashita ◽  
Reiko Ashida ◽  
Masayuki Kitano
Keyword(s):  
Chronic Pancreatitis ◽  
Magnetic Resonance ◽  
Imaging Modality ◽  
Magnetic Resonance Cholangiopancreatography ◽  
Imaging Modalities ◽  
Diagnostic Tools ◽  
Diagnostic Modality ◽  
Magnetic Resonance Imaging Mri ◽  
Initial Imaging ◽  
Eus Elastography

Chronic pancreatitis (CP) describes long-standing inflammation of the pancreas, which leads to irreversible and progressive inflammation of the pancreas with fibrosis. CP also leads to abdominal pain, malnutrition, and permanent impairment of exocrine/endocrine functions. However, it is difficult to assess CP pathologically, and imaging modalities therefore play an important role in the diagnosis and assessment of CP. There are four modalities typically used to assess CP. Pancreatic duct features are assessed with magnetic resonance cholangiopancreatography (MRCP) and endoscopic retrograde cholangiopancreatography (ERCP). However, ERCP is a rather invasive diagnostic modality for CP, and can result in adverse events such as post-ERCP pancreatitis. Computed tomography (CT) is often the most appropriate initial imaging modality for patients with suspected CP, and has high diagnostic specificity. However, CT findings typically only appear in advanced stages of CP, and it is difficult to detect early CP. Endoscopic ultrasonography (EUS) provides superior spatial resolution compared with other imaging modalities such as CT and magnetic resonance imaging (MRI), and is considered the most reliable and efficient diagnostic modality for pancreatic diseases. The EUS-based Rosemont classification plays an important role in diagnosing CP in clinical practice. Evaluation of tissue stiffness can be another option to assess the diagnosis and progression of CP, and MRI and EUS can be used to assess CP not only with imaging, but also with elasticity measurement. MR and EUS elastography are expected to provide new alternative diagnostic tools for assessment of fibrosis in CP, which is difficult to evaluate pathologically.

scholarly journals Risk stratification in PAH

2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
Paul A Corris
Keyword(s):  
Heart Failure ◽  
Pulmonary Arteries ◽  
Right Heart Failure ◽  
Response To Therapy ◽  
Pulmonary Vasculature ◽  
Short Term ◽  
Right Heart ◽  
Term Survival ◽  
Pulmonary Arterial ◽  
Short Term Survival

[No abstract. Showing first paragraph of article]Pulmonary arterial hypertension (PAH) is a chronic disease of the pulmonary vasculature characterized by progressive narrowing of the pulmonary arteries leading to increased pulmonary vascular resistance, right heart failure, and ultimately premature death.There has been a significant improvement in the available medical therapeutic options in this field that have impacted the short-term survival and morbidity in these patients. However, the median survival post-diagnosis remains unacceptable at 7 years.Physicians’ ability to predict PAH disease progression and risk allows them to determine the patient’s prognosis, make informed adjustments to therapy, and monitor his or her response to therapy . If widely adopted, risk prediction can enhance the consistency of treatment approaches and improve the timeliness of referral for lung transplantation. This approach should lead optimal, directed care that ultimately reduces morbidity and improves mortality in patients with PAH.

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