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Journal articles on the topic 'Elevated right ventricular pressure'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Groh, Georgeann, Philip Levy, Mark Holland, Joshua Murphy, Timothy Sekarski, and Gautam Singh. "DOPPLER ECHOCARDIOGRAPHY INACCURATELY ESTIMATES RIGHT VENTRICULAR PRESSURE IN CHILDREN WITH ELEVATED RIGHT HEART PRESSURE." Journal of the American College of Cardiology 61, no. 10 (2013): E462. http://dx.doi.org/10.1016/s0735-1097(13)60462-3.

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2

Groh, Georgeann K., Philip T. Levy, Mark R. Holland, et al. "Doppler Echocardiography Inaccurately Estimates Right Ventricular Pressure in Children with Elevated Right Heart Pressure." Journal of the American Society of Echocardiography 27, no. 2 (2014): 163–71. http://dx.doi.org/10.1016/j.echo.2013.09.016.

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3

DeGroff, Curt G. "Doppler Echocardiography Inaccurately Estimates Right Ventricular Pressure in Children with Elevated Right Heart Pressure." Journal of the American Society of Echocardiography 27, no. 3 (2014): 342. http://dx.doi.org/10.1016/j.echo.2013.11.017.

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4

Ishihara, Satomi, Hidetaka Kioka, Tomohito Ohtani, et al. "Successful treatment of severe combined post- and pre-capillary pulmonary hypertension in a patient with idiopathic restrictive cardiomyopathy." Pulmonary Circulation 8, no. 3 (2018): 204589401877013. http://dx.doi.org/10.1177/2045894018770131.

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Restrictive cardiomyopathy (RCM) is a rare form of cardiomyopathy that is characterized by restrictive ventricular filling. Elevated filling pressure leads to pulmonary hypertension (PH), which often progresses to combined post- and pre-capillary PH (Cpc-PH) with increased diastolic pulmonary vascular pressure gradient (DPG) and pulmonary vascular resistance (PVR) caused by longstanding backward hemodynamic consequences of left heart disease (LHD) leading to morphological changes in the pulmonary vasculature. Patients with high PVR undergoing left ventricular assist device (LVAD) implantation

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5

Tai TC Huang, HP. "Echocardiographic assessment of right heart indices in dogs with elevated pulmonary artery pressure associated with chronic respiratory disorders, heartworm disease, and chronic degenerative mitral valvular disease." Veterinární Medicína 58, No. 12 (2013): 613–20. http://dx.doi.org/10.17221/7180-vetmed.

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The aim of this study was to evaluate right ventricular (RV) remodeling and right heart failure associated with different causes of elevated pulmonary arterial pressure (PAP) in dogs. In total, 169 client-owned dogs with tricuspid regurgitation (TR) and 40 client-owned clinically healthy dogs were included. Dogs with TR were further categorised as suffering from chronic respiratory disorders (CRD), heartworm disease (HWD), mild/moderate chronic degenerative mitral valvular disease (CDMD), and severe CDMD. Among the echocardiographic indices of the right heart, no significant difference in the

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6

Forrest, P. "Anaesthesia and Right Ventricular Failure." Anaesthesia and Intensive Care 37, no. 3 (2009): 370–85. http://dx.doi.org/10.1177/0310057x0903700314.

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Acute right ventricular (RV) failure has until recently received relatively little attention in the cardiology, critical care or anaesthesia literature. However, it is frequently encountered in cardiac surgical cases and is a significant cause of mortality in patients with severe pulmonary hypertension who undergo non-cardiac surgery. RV dysfunction may be primarily due to impaired RV contractility, or volume or pressure overload. In these patients, an increased pulmonary vascular resistance (PVR) or a decreased aortic root pressure may lead to RV ischaemia, resulting in a rapid, downward haem

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7

Srinivas, Arun, Madathil Ranjit, James L. Wilkinson, et al. "Hemodynamic and angiographic findings following arterial switch repair for complete transposition." Cardiology in the Young 6, no. 4 (1996): 298–307. http://dx.doi.org/10.1017/s1047951100003929.

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AbstractThe arterial switch operation is the treatment of choice for complete transposition, and for the Taussig-Bing anomaly, with good early and mid-term results. This retrospective study examined the findings obtained at routine follow-up cardiac catheterization after primary arterial switch repair. We catheterized 111 patients after a mean of 16.9 months after surgery. These included 67 patients with an intact ventricular septum, 33 with a ventricular septal defect, and 11 with the Taussig-Bing anomaly. Right ventricular pressures were mildly elevated (mean 33.9±10.2 mm Hg) in the overall

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8

Ketabchi, Farzaneh, Shirin Bajoovand, Mojtaba Adlband, Maryam Naseh, Ali A. Nekooeian, and Elaheh Mashghoolozekr. "Right ventricular pressure elevated in one-kidney, one clip Goldblatt hypertensive rats." Clinical and Experimental Hypertension 39, no. 4 (2017): 344–49. http://dx.doi.org/10.1080/10641963.2016.1259329.

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9

Hoendermis, Elke S., and Joost P. van Melle. "Impaired right ventricular function and elevated pulmonary artery pressure: a lethal combination." European Journal of Heart Failure 15, no. 4 (2013): 363–65. http://dx.doi.org/10.1093/eurjhf/hft033.

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10

Fadel, Bahaa M., Khaled Al-Mulla, Bader Al-Mahdi, and Giovanni Di Salvo. "Elevated Right Ventricular End-Diastolic Pressure by Doppler Echocardiography-A Case Report." Echocardiography 31, no. 1 (2013): 117–19. http://dx.doi.org/10.1111/echo.12377.

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11

Marshall, William, Stephen Gee, Woobeen Lim, Lauren Hassen, and Saurabh Rajpal. "ECHOCARDIOGRAPHIC RISK STRATIFICATION OF PREGNANT WOMEN WITH ELEVATED RIGHT VENTRICULAR SYSTOLIC PRESSURE." Journal of the American College of Cardiology 77, no. 18 (2021): 1673. http://dx.doi.org/10.1016/s0735-1097(21)03029-1.

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12

Ha, B., C. L. Lucas, G. W. Henry, E. G. Frantz, J. I. Ferreiro, and B. R. Wilcox. "Effects of chronically elevated pulmonary arterial pressure and flow on right ventricular afterload." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 1 (1994): H155—H165. http://dx.doi.org/10.1152/ajpheart.1994.267.1.h155.

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The effects of pulsatile hemodynamics on right ventricle-pulmonary circulation interactions were studied in control lambs and in two lamb models of altered pulmonary hemodynamics induced at infancy: elevated pulmonary arterial pressure (PAP) was created by the infusion of monocrotaline pyrrole (MCTP), and elevated pulmonary arterial blood flow was obtained by the creation of an arteriovenous fistula (Shunt). High-fidelity PAP, midvessel Doppler blood velocity (PAV), and cardiac output (CO) were measured in open-chest, anesthetized lambs. PAV waveforms were normalized to match the measured CO.

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13

Werchan, P. M., W. R. Summer, A. M. Gerdes, and K. H. McDonough. "Right ventricular performance after monocrotaline-induced pulmonary hypertension." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (1989): H1328—H1336. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1328.

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Chronic pulmonary hypertension leads to a compensatory hypertrophy of the right ventricle (RV). Performance of the hypertrophied heart has been shown to vary depending on the type and severity of the overload, the species, age, and sex of the animal in which the hypertrophy is induced and the ventricle to which the overload is applied (left ventricle vs. right ventricle). In this study we employed two novel approaches to examine the performance of the hypertrophied right ventricle in male Sprague-Dawley rats. First, monocrotaline (MCT), a pyrrolizidine alkaloid isolated from the plant Crotalar

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14

Setty, Srinath, Xiaoming Bian, Johnathan D. Tune, and H. Fred Downey. "Endogenous nitric oxide modulates myocardial oxygen consumption in canine right ventricle." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 2 (2001): H831—H837. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h831.

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The role of endogenous nitric oxide (NO) in modulating myocardial oxygen consumption (MV˙o 2) is unclear, in part because of systemic and coronary hemodynamic effects of blocking NO release. This study evaluated the effect of NO on right ventricular MV˙o 2 under controlled hemodynamic conditions. In 12 open-chest dogs, N ω-nitro-l-arginine methyl ester (l-NAME, 150 μg/min), a NO synthase (NOS) blocker, was infused into the right coronary artery. Heart rate and mean aortic pressure were constant. Right coronary blood flow and right ventricular MV˙o 2 were measured at normal and elevated right c

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15

Harvey, Robert, Adrian Chong, John Hill, and Dariusz Korczyk. "Transiently elevated estimated pulmonary pressures in a patient with complete heart block undergoing permanent pacing: a case report." European Heart Journal - Case Reports 4, no. 3 (2020): 1–4. http://dx.doi.org/10.1093/ehjcr/ytaa072.

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Abstract Background Complete heart block (CHB) is a frequent cause for acute admission in older patients with significant cardiac conduction disease. Common presenting symptoms are syncope and dyspnoea. Some patients may exhibit clinical and radiological signs of left ventricular (LV) decompensation, despite preserved LV ejection fraction on transthoracic echocardiography (TTE) and absent pre-existing LV dysfunction. Case summary In this clinical report, we present a case of CHB associated with transient but severe elevation in pulmonary artery systolic pressure, measured as the equivalent rig

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16

Kothari, Shana, Michael Kalinowski, Natasha Shah, and Hareth Raddawi. "A Case of Idiopathic Non-Cirrhotic Portal Hypertension in a Patient With a Left Ventricular Assist Device." Journal of Investigative Medicine High Impact Case Reports 7 (January 2019): 232470961987833. http://dx.doi.org/10.1177/2324709619878337.

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Idiopathic non-cirrhotic portal hypertension is a rare diagnosis caused by an unknown etiology with elevated intrahepatic portal pressures in the absence of underlying liver disease. We present a unique case of a 57-year-old male with a left ventricular assist device and preserved right ventricular function that was found to have an elevated hepatic venous pressure gradient and sequelae of portal hypertension without underlying liver disease. There is limited treatment available as management is primarily aimed toward preventing complications of the disease. This case highlights the need for f

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17

Maddali, Madan Mohan, Sandip Waman Junghare, Pranav Subbaraya Kandachar, Hanan Shatayat Al-Ghanami, Zsolt Lajos Nagy, and Cheskey Manoj Jayatilaka. "An Unusual Cause for an Elevated Right Ventricular Pressure Following Bentall Procedure With Ventricular Septal Defect Closure." Journal of Cardiothoracic and Vascular Anesthesia 31, no. 1 (2017): 388–90. http://dx.doi.org/10.1053/j.jvca.2016.04.012.

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18

Manor, D., S. Williams, R. Ator, K. Bryant, and K. W. Scheel. "Left ventricular mechanics in arrested dog heart: effects of ventricular interaction and vascular volumes." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 5 (1995): H2125—H2132. http://dx.doi.org/10.1152/ajpheart.1995.268.5.h2125.

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The present study was designed to determine the effects of right heart pressure on the compliance of the left ventricle (LV). The studies were conducted on isolated, blood-perfused, potassium-arrested dog hearts with vasomotor tone either present (n = 5) or absent (n = 8). A balloon was used to control LV volume, whereas right heart (RHP) or coronary sinus (CSP) pressures were controlled via a column placed in the right heart or coronary sinus, respectively. Control of CSP independently of RHP allowed us to assess the relative contribution of coronary venous pressure to changes in LV complianc

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19

Maniar, Hersh S., Sunil M. Prasad, Sydney L. Gaynor, Celeste M. Chu, Paul Steendijk, and Marc R. Moon. "Impact of pericardial restraint on right atrial mechanics during acute right ventricular pressure load." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 1 (2003): H350—H357. http://dx.doi.org/10.1152/ajpheart.00444.2002.

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Optimization of right atrial (RA) mechanics is important for maintaining right ventricular (RV) filling and global cardiac output. However, the impact of pericardial restraint on RA function and the compensatory role of the right atrium to changes in RV afterload remain poorly characterized. In eight open-chest sheep, RA elastance (contractility) and chamber stiffness were measured (RA pressure-volume relations) at baseline and during partial pulmonary artery (PA) occlusion. Data were collected before and after pericardiotomy. With the pericardium intact and partial PA occlusion, RA elastance

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20

Sydykov, Akylbek, Abdirashit Maripov, Nadira Kushubakova, et al. "An Exaggerated Rise in Pulmonary Artery Pressure in a High-Altitude Dweller during the Cold Season." International Journal of Environmental Research and Public Health 18, no. 8 (2021): 3984. http://dx.doi.org/10.3390/ijerph18083984.

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Chronic hypoxia-induced sustained pulmonary vasoconstriction and vascular remodeling lead to mild-to-moderate elevation of pulmonary artery pressure in high-altitude residents. However, in some of them, severe pulmonary hypertension may develop. Besides hypoxia, high-altitude residents also face other environmental challenges such as low ambient temperatures. We describe a case of a 49-year-old woman of Kyrgyz ethnicity with abnormally increased pulmonary artery pressure, revealed by Doppler echocardiography. Significantly elevated pulmonary artery pressure was detected in late winter and this

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21

Emerson, Dominic A., Richard L. Amdur, Jason R. Morrissette, et al. "Using Cardiac Magnetic Resonance Imaging to Evaluate Cardiac Function and Predict Outcomes in Patients with Valvular Heart Disease." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 10, no. 1 (2015): 63–67. http://dx.doi.org/10.1097/imi.0000000000000119.

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Objective In valvular heart disease, elevated left atrial and pulmonary pressures contribute to right ventricular strain and, ultimately, right ventricle failure. Elevated pulmonary artery (PAP) and left ventricular end diastolic pressures are used as markers of right ventricle dysfunction and correlate with poor outcomes. Using cardiac magnetic resonance imaging (CMR), it is possible to directly quantify both left and right ventricular ejection function (LVEF and RVEF), and here, we compare CMR with traditional markers as outcome predictors. Methods A retrospective review of prospectively col

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22

Anversa, P., A. V. Loud, V. Levicky, and G. Guideri. "Left ventricular failure induced by myocardial infarction. I. Myocyte hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 6 (1985): H876—H882. http://dx.doi.org/10.1152/ajpheart.1985.248.6.h876.

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To determine whether left ventricular failure after acute myocardial infarction is associated with a growth response of the myocytes that tends to compensate for the loss of muscle mass and function, the left coronary artery in rats was ligated near its origin, and the animals were killed 3 days later. Elevated left ventricular end-diastolic pressure and decreased first derivative of left ventricular pressure and systolic arterial pressure indicated significant impairment of ventricular function. Absolute infarct size, determined morphometrically by measurement of the fraction of myocyte nucle

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23

Ozaki, Takefumi, Noritomo Ohnuma, Norihiro Shimizu, Atsushi Hasegawa, and Masashi Horimoto. "Cardiac Sarcoidosis Culminating in Severe Biventricular Failure." Case Reports in Medicine 2009 (2009): 1–3. http://dx.doi.org/10.1155/2009/856785.

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A 59-year-old woman with a history of lung sarcoidosis developed general edema and exertional dyspnea. An electrocardiogram showed first-degree atrioventricular block with complete right bundle branch block. Chest X-ray showed cardiomegaly. Echocardiography showed diffuse and severe hypokinesis of the left ventricle (LV) and biventricular enlargement with severe tricuspid regurgitation. Myocardial scintigraphy disclosed a perfusion defect at the ventricular septum and hypoperfusion at the posterior wall and the apex. On cardiac catheterization, pulmonary capillary wedge pressure, right ventric

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24

He, Yingke, John Ong, Thuan Tong Tan, Brian K. P. Goh, and Sharon G. K. Ong. "SIRS Triggered by Acute Right Ventricular Function, Mimicked Septic Shock." Journal of Critical Care Medicine 5, no. 4 (2019): 149–56. http://dx.doi.org/10.2478/jccm-2019-0022.

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Abstract Background The systemic inflammatory response syndrome (SIRS) is a complex immune response which can be precipitated by non-infectious aetiologies such as trauma, burns or pancreatitis. Addressing the underlying cause is crucial because it can be associated with increased mortality. Although the current literature associates chronic heart failure with SIRS, acute right ventricular dysfunction has not previously been reported to trigger SIRS. This case report describes the presentation of acute right ventricular dysfunction that triggered SIRS and mimicked septic shock. Case presentati

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25

Johnson, Shelsey W., Alison Witkin, Josanna Rodriguez-Lopez, and Richard Channick. "Room for improvement in pulmonary capillary wedge pressure reporting: a review of hemodynamic tracings at a large academic medical center." Pulmonary Circulation 10, no. 4 (2020): 204589402092915. http://dx.doi.org/10.1177/2045894020929157.

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To describe the frequency with which pulmonary capillary wedge pressure measurements, obtained during right heart catheterization, are falsely elevated and to educate operators on techniques to improve accuracy of pulmonary capillary wedge pressure reporting. Failure to completely occlude pulmonary artery branch vessels during balloon inflation can lead to falsely elevated, “incomplete” pulmonary capillary wedge pressures. Balloon deflation prior to catheter retraction may result in catheter advancement into smaller branch vessels, yielding an inadvertent but more accurate alternative pulmonar

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26

Shah, Saumil R., Sergio Waxman, and William H. Gaasch. "The Impact of an Atrial Septal Defect on Hemodynamics in Patients With Heart Failure." US Cardiology Review 11, no. 2 (2017): 72. http://dx.doi.org/10.15420/ucs.2017:9:2.

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In patients with left ventricular (LV) dysfunction, a large atrial septal defect (ASD) provides an alternate pathway for left atrial emptying and prevents abnormal elevation of left atrial and LV filling pressures. In such patients, closure of the ASD can cause an increase in LV diastolic pressure with pulmonary venous hypertension and congestion. The protective effect of an ASD is attenuated or abolished in the presence of right ventricular (RV) dysfunction. Thus, an elevated LV diastolic pressure in the presence of an ASD indicates dysfunction or failure of both ventricles. In this situation

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27

Yu, Ying, Johnathan D. Tune, and H. Fred Downey. "Elevated right atrial pressure does not reduce collateral blood flow to ischemic myocardium." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 5 (1997): H2296—H2303. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2296.

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Right atrial pressure (RAP) may become substantially elevated during heart failure and has been reported to reduce collateral flow to the ischemic myocardium of isolated hearts. The effect of elevated RAP on blood flow to collateral-dependent and normal myocardium of in situ hearts was studied in 20 open-chest anesthetized dogs with acute occlusion of the left anterior descending coronary artery. Regional myocardial blood flow was measured with radioactive microspheres while RAP was elevated by restricting right ventricular (RV) outflow with constant aortic pressure. Increasing RAP from 3.8 ±

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28

Capasso, J. M., P. Li, and P. Anversa. "Cytosolic calcium transients in myocytes isolated from rats with ischemic heart failure." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (1993): H1953—H1964. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h1953.

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Mechanical performance and cytosolic Ca2+ dynamics were characterized in myocytes isolated from left and right ventricles of rats with ischemic heart failure. Seven days after coronary artery narrowing (CAN) in rats filling pressures were elevated, whereas systolic pressures and ejection of blood were depressed. Left ventricular myocytes increased 18% in length and 19% in width, whereas right myocytes expanded longitudinally by 23% and transversely by 24%. Contractile behavior of myocytes displayed reductions in myocyte shortening and velocity of shortening, despite prolongation of time to pea

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29

Hickey, Tyler B. M., Ginjeet Gina K. Gill, Michael A. Seidman, and Douglas L. Webber. "CPR-associated right ventricular rupture in the setting of pulmonary embolism." CJEM 18, no. 6 (2016): 484–87. http://dx.doi.org/10.1017/cem.2016.327.

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AbstractCardiopulmonary resuscitation (CPR) is an inherently traumatic procedure. Successful resuscitations are often complicated by iatrogenic injuries to structures of the neck, thorax, or abdomen. Rib and sternal fractures are the most frequently induced injuries. However, rare and life-threatening trauma to vital organs such as the heart may also occur during CPR. We describe a novel case of CPR-associated right ventricular rupture in a woman with acute-on-chronic pulmonary embolism and no known pre-existing cardiac disease. We propose that chest compressions in the setting of elevated rig

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30

Lamberts, Regis R., Eric Caldenhoven, Mirian Lansink, et al. "Preservation of diastolic function in monocrotaline-induced right ventricular hypertrophy in rats." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (2007): H1869—H1876. http://dx.doi.org/10.1152/ajpheart.00294.2007.

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During ischemic heart diseases and when heart failure progresses depletion of myocardial energy stores occurs. d-Ribose (R) has been shown to improve cardiac function and energy status after ischemia. Folic acid (FA) is an essential cofactor in the formation of adenine nucleotides. Therefore, we assessed whether chronic R-FA administration during the development of hypertrophy resulted in an improved cardiac function and energy status. In Wistar rats ( n = 40) compensatory right ventricular (RV) hypertrophy was induced by monocrotaline (30 mg/kg; MCT), whereas saline served as control. Both gr

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31

Cody, R. J., S. H. Kubo, J. H. Laragh, and S. A. Atlas. "Cardiac secretion of atrial natriuretic factor with exercise in chronic congestive heart failure patients." Journal of Applied Physiology 73, no. 4 (1992): 1637–43. http://dx.doi.org/10.1152/jappl.1992.73.4.1637.

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We have previously reported a fivefold increase of plasma atrial natriuretic factor (ANF) in patients with congestive heart failure (CHF) compared with normal subjects. However, given the marked increase of ANF under basal conditions, the extent to which ANF secretion can further increase under physiological stress is not been clarified in CHF. We therefore evaluated ANF secretion during ergometric exercise in 11 patients with CHF, with peripheral venous ANF samples obtained at rest and peak exercise. In seven patients, simultaneous peripheral venous and right ventricular ANF samples were obta

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32

D. Peter, ID Igoche, MustafaO Asani, IIbrahim Aliyu, and PatienceN Obiagwu. "Elevated mean pulmonary artery pressure and right ventricular dysfunction in children with chronic kidney disease." Journal of Cardiovascular Echography 28, no. 2 (2018): 109. http://dx.doi.org/10.4103/jcecho.jcecho_56_17.

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33

Mirea, Oana, Oana M. Corîci, Octavian Istrătoaie, Ionuț Donoiu, Maria Iancău, and Constantin Militaru. "Left and right ventricular morphology and function in athletes with elevated pulmonary systolic arterial pressure." Echocardiography 35, no. 6 (2018): 769–76. http://dx.doi.org/10.1111/echo.14016.

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Szilvassy, Z., P. Ferdinandy, P. Bor, I. Jakab, J. Lonovics, and M. Koltai. "Ventricular overdrive pacing-induced anti-ischemic effect: a conscious rabbit model of preconditioning." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 5 (1994): H2033—H2041. http://dx.doi.org/10.1152/ajpheart.1994.266.5.h2033.

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To study whether ventricular overdrive pacing (VOP) induces preconditioning, rabbits were equipped with right ventricular electrode catheters for pacing and intracavital recording and polyethylene cannulas in the left ventricle and right carotid artery to measure intraventricular pressure and blood pressure. One week after surgery in conscious animals, VOP at 500 beats/min over 2, 5, or 10 min resulted in an intracavital S-T segment elevation, shortening of ventricular effective refractory period, decrease in maximum rate of pressure development and blood pressure, and increase in left ventric

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Hofmann, Nina P., Hassan Abdel-Aty, Stefan Siebert, Hugo A. Katus, and Grigorios Korosoglou. "Giant Dilatation of the Right Coronary Aortic Bulb with Compression of the Right Ventricular Outflow Tract Mimicking a Ventricular Septal Defect: Diagnostic workup Using Echocardiography, Heart Catheterization, and Cardiac Computed Tomography." Case Reports in Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/524526.

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Annuloaortic ectasia is a relatively rare diagnosis. Herein, we report an unusual case of an annuloaortic ectasia with asymmetric dilatation of the right coronary bulb mimicking a membranous ventricular septal defect (VSD) with Eisenmenger reaction by transthoracic echocardiography. Aortic angiography showed a dilated aortic root and moderate aortic regurgitation. Right cardiac catheterization, on the other hand, exhibited normal pulmonary artery blood pressure and normal pulmonary resistance, whereas normal venous gas values were measured throughout the caval vein and the right atrium, exclud

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Markel, Troy A., Paul R. Crisostomo, Meijing Wang, Jeremy L. Herrmann, Aaron M. Abarbanell, and Daniel R. Meldrum. "Right ventricular TNF resistance during endotoxemia: the differential effects on ventricular function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (2007): R1893—R1897. http://dx.doi.org/10.1152/ajpregu.00359.2007.

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Right and left ventricular myocytes originate from different cellular progenitors; however, it is unknown whether these cells differ in their response to endotoxemia. We hypothesized that 1) the percentage of endotoxemic functional depression within the right ventricle (RV) would be smaller than that of the left ventricle; and 2) that better RV function would correlate with lower levels of right ventricular TNF production. Adult Sprague-Dawley rats were divided into right and left control and endotoxin groups. Controls received vehicle, while endotoxin groups received LPS at 20 mg/kg ip. Heart

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37

Gray, Michael Patrick, Olivia Onyeador, and Joel A. Wirth. "Update on the PHA Pulmonary Hypertension Care Center Network: Early Experience With the National Accreditation Program." Advances in Pulmonary Hypertension 16, no. 4 (2018): 179–84. http://dx.doi.org/10.21693/1933-088x-16.4.179.

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World Health Organization (WHO) Group 1 pulmonary hypertension (PH) (PAH, pulmonary arterial hypertension) and WHO Group 4 PH (CTEPH, chronic thromboembolic pulmonary hypertension) are rare diseases of the pulmonary vascular system characterized by elevated pulmonary artery pressure and pulmonary vascular resistance in the absence of elevated left ventricular filling pressures, which may progress to right heart failure and death.1 Left untreated, the median survival for idiopathic (IPAH) and heritable (HPAH) disease is about 2.8 years from diagnosis.2 Adherence to expert consensus guidelines o

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Vaidyanathan, Swaminathan, Sivakumar Kothandam, Rajesh Kumar, Sujatha Desai Indrajith, and Ravi Agarwal. "Cavopulmonary Anastomosis in a Patient With Arrhythmogenic Right Ventricular Cardiomyopathy With Severe Right Ventricular Dysfunction." World Journal for Pediatric and Congenital Heart Surgery 11, no. 4 (2017): NP60—NP62. http://dx.doi.org/10.1177/2150135117707459.

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A 26-year-old lady presented with exertional dyspnea, palpitations, central cyanosis, and oxygen saturations of 80% in room air. Her electrocardiogram, echocardiogram, and cardiac magnetic resonance were diagnostic of arrhythmogenic right ventricular dysplasia. There was no documented ventricular arrhythmia or syncopal episodes and Holter recordings were repeatedly normal. Cardiac hemodynamics showed right to left shunt through atrial septal defect, low pulmonary blood flow, normal atrial pressures, and minimally elevated right ventricular end-diastolic pressures. Since her presenting symptoms

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Wiputra, Hadi, Ching Kit Chen, Elias Talbi, et al. "Human fetal hearts with tetralogy of Fallot have altered fluid dynamics and forces." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (2018): H1649—H1659. http://dx.doi.org/10.1152/ajpheart.00235.2018.

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Studies have suggested the effect of blood flow forces in pathogenesis and progression of some congenital heart malformations. It is therefore of interest to study the fluid mechanic environment of the malformed prenatal heart, such as the tetralogy of Fallot (TOF), especially when little is known about fetal TOF. In this study, we performed patient-specific ultrasound-based flow simulations of three TOF and seven normal human fetal hearts. TOF right ventricles (RVs) had smaller end-diastolic volumes (EDVs) but similar stroke volumes (SVs), whereas TOF left ventricles (LVs) had similar EDVs bu

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Abdelmoneim, Sahar S., Mathieu Bernier, Christopher G. Scott, et al. "Safety of Contrast Agent Use During Stress Echocardiography in Patients With Elevated Right Ventricular Systolic Pressure." Circulation: Cardiovascular Imaging 3, no. 3 (2010): 240–48. http://dx.doi.org/10.1161/circimaging.109.895029.

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Nagel, Christian, Alberto M. Marra, Nicola Benjamin, et al. "Reduced Right Ventricular Output Reserve in Patients With Systemic Sclerosis and Mildly Elevated Pulmonary Artery Pressure." Arthritis & Rheumatology 71, no. 5 (2019): 805–16. http://dx.doi.org/10.1002/art.40814.

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Jayasekera, Geeshath, Kathryn S. Wilson, Hanna Buist, et al. "Understanding longitudinal biventricular structural and functional changes in a pulmonary hypertension Sugen–hypoxia rat model by cardiac magnetic resonance imaging." Pulmonary Circulation 10, no. 1 (2020): 204589401989751. http://dx.doi.org/10.1177/2045894019897513.

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Cardiac magnetic resonance-derived ventricular variables are predictive of mortality in pulmonary arterial hypertension. Rodent models which emphasize ventricular function, allowing serial monitoring, are needed to identify pathophysiological features and novel therapies for pulmonary arterial hypertension. We investigated longitudinal changes in the Sugen–hypoxia model during disease progression. Sprague Dawley rats ( n = 32) were divided into two groups. (1) Sugen–hypoxia: a dose of subcutaneous Sugen-5416 and placed in hypobaric hypoxia for two weeks followed by normoxia for three weeks. (2

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Zuckerman, B. D., E. C. Orton, K. R. Stenmark, et al. "Alteration of the pulsatile load in the high-altitude calf model of pulmonary hypertension." Journal of Applied Physiology 70, no. 2 (1991): 859–68. http://dx.doi.org/10.1152/jappl.1991.70.2.859.

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We compared main pulmonary arterial elasticity and global pulmonary arterial compliance in control and high-altitude (HA) calves to determine whether 1) changes in pulmonary arterial elasticity are contributing to an increase in the oscillatory load of the right ventricle in this model of pulmonary hypertension and 2) measured changes in stiffness of the HA calves' arterial wall are the result of both an increase in pressure and an alteration of the material properties of the HA calves' arterial wall. Newborn calves were placed at 4,300 m simulated altitude for 14 days, and control calves were

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Haque, Mostashirul, Tunaggina Afrin Khan, Md Rasul Amin, et al. "Stage IV Sarcoidosis with Cor pulmonale: A Case Report." Bangladesh Heart Journal 30, no. 1 (2016): 37–42. http://dx.doi.org/10.3329/bhj.v30i1.28136.

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Sarcoidosis is a well known systemic disorder that invariably involves lungs. However, pulmonary hypertension and cor-pulmanle are not common due to pulmonary involvement of sarcoidosis. We report a case of pulmonary hypertension leading to corpulmonale due to sarcoidosis. An elderly female suffering from hypertension & sarcoidosis developed complications and arrived at the diagnosis by correlating various investigations. X-ray chest (P/A) showed cardiomegaly (right ventricular type), reticulo-nodular shadow involving both mid and lower zone; characteristic high resolution CT (HRCT) scan a

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Yamazaki, Ryo, Osamu Nishiyama, Kazuya Yoshikawa, et al. "HFpEF without elevated right ventricular systolic pressure is a favorable prognostic indicator in patients with IPF requiring hospitalization for heart failure." PLOS ONE 16, no. 1 (2021): e0245778. http://dx.doi.org/10.1371/journal.pone.0245778.

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Background Some patients with idiopathic pulmonary fibrosis (IPF) must be hospitalized because of heart failure (HF), including HF with preserved ejection fraction (HFpEF) and HF with reduced EF (HFrEF). The association between IPF and HF has not been clarified. We retrospectively investigated the clinical features and outcomes of patients with IPF who required nonelective hospitalization because of HF. Methods We examined data from IPF patients who required nonelective hospitalization for HF at the Kindai University Hospital from January 2008 to December 2018. We divided the patients into 3 g

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Shifren, Adrian, Anthony G. Durmowicz, Russell H. Knutsen, Gilles Faury, and Robert P. Mecham. "Elastin insufficiency predisposes to elevated pulmonary circulatory pressures through changes in elastic artery structure." Journal of Applied Physiology 105, no. 5 (2008): 1610–19. http://dx.doi.org/10.1152/japplphysiol.90563.2008.

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Elastin is a major structural component of large elastic arteries and a principal determinant of arterial biomechanical properties. Elastin loss-of-function mutations in humans have been linked to the autosomal-dominant disease supravalvular aortic stenosis, which is characterized by stenotic lesions in both the systemic and pulmonary circulations. To better understand how elastin insufficiency influences the pulmonary circulation, we evaluated pulmonary cardiovascular physiology in a unique set of transgenic and knockout mice with graded vascular elastin dosage (range 45–120% of wild type). T

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Akazawa, Yohei, Kenichi Okumura, Ryo Ishii, et al. "Pulmonary artery banding is a relevant model to study the right ventricular remodeling and dysfunction that occurs in pulmonary arterial hypertension." Journal of Applied Physiology 129, no. 2 (2020): 238–46. http://dx.doi.org/10.1152/japplphysiol.00148.2020.

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Although animal models of pulmonary arterial hypertension and pressure loading are important to study right ventricular (RV) pathophysiology, pulmonary arterial hypertension models cannot interrogate RV responses independent of pulmonary vascular effects. Comparing three commonly used rat models under similar elevated RV pressure, we found that all models resulted in comparable maladaptive RV remodeling and dysfunction. Thus, these findings suggest that the pulmonary artery banding model can be used to investigate mechanisms of RV dysfunction in RV pressure overload and the effect of potential

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Bozkurt, Selim. "Computational Simulation of Cardiac Function and Blood Flow in the Circulatory System under Continuous Flow Left Ventricular Assist Device Support during Atrial Fibrillation." Applied Sciences 10, no. 3 (2020): 876. http://dx.doi.org/10.3390/app10030876.

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Prevalence of atrial fibrillation (AF) is high in heart failure patients supported by a continuous flow left ventricular assist device (CF-LVAD); however, the long term effects remain unclear. In this study, a computational model simulating effects of AF on cardiac function and blood flow for heart failure and CF-LVAD support is presented. The computational model describes left and right heart, systemic and pulmonary circulations and cerebral circulation, and utilises patient-derived RR interval series for normal sinus rhythm (SR). Moreover, AF was simulated using patient-derived unimodal and

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Ioffe, S., A. H. Jansen, and V. Chernick. "Fetal respiratory neuronal activity during REM and NREM sleep." Journal of Applied Physiology 75, no. 1 (1993): 191–97. http://dx.doi.org/10.1152/jappl.1993.75.1.191.

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Elevated plasma atrial natriuretic peptide (ANP) levels have been shown to blunt pulmonary hemodynamic responses to chronic hypoxia, but whether elevated circulating ANP levels negatively feedback on cardiac expression of the ANP gene is unknown. Using a recently developed strain of transgenic mouse (TTR-ANF) that expresses a transthyretin promoter-ANP fusion gene in the liver, we studied the effect of chronically elevated plasma ANP levels on cardiac hypertrophic and pulmonary hemodynamic responses and expression of the endogenous cardiac ANP gene during chronic hypoxia. Plasma ANP levels wer

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Klinger, J. R., R. D. Petit, L. A. Curtin, et al. "Cardiopulmonary responses to chronic hypoxia in transgenic mice that overexpress ANP." Journal of Applied Physiology 75, no. 1 (1993): 198–205. http://dx.doi.org/10.1152/jappl.1993.75.1.198.

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Elevated plasma atrial natriuretic peptide (ANP) levels have been shown to blunt pulmonary hemodynamic responses to chronic hypoxia, but whether elevated circulating ANP levels negatively feedback on cardiac expression of the ANP gene is unknown. Using a recently developed strain of transgenic mouse (TTR-ANF) that expresses a transthyretin promoter-ANP fusion gene in the liver, we studied the effect of chronically elevated plasma ANP levels on cardiac hypertrophic and pulmonary hemodynamic responses and expression of the endogenous cardiac ANP gene during chronic hypoxia. Plasma ANP levels wer

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