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2. Baseline body mass index does not significantly affect outcomes after pulmonary thromboendarterectomy.

Author

Fernandes, Timothy M, Auger, William R, Fedullo, Peter F, Kim, Nick H, Poch, David S, Madani, Michael M, Pretorius, Victor G, Jamieson, Stuart W, and Kerr, Kim M

Subjects
Pulmonary Artery, Humans, Hypertension, Pulmonary, Pulmonary Embolism, Tomography, X-Ray Computed, Angiography, Body Mass Index, Treatment Outcome, Endarterectomy, Thrombectomy, Survival Rate, Risk Factors, Retrospective Studies, Follow-Up Studies, Middle Aged, California, Female, Male, Cardiac Catheterization, Lung, Patient Safety, Prevention, Clinical Research, Nutrition, Obesity, Clinical Trials and Supportive Activities, Cardiovascular, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Respiratory System
Abstract

BackgroundObesity is a common comorbidity of patients with chronic thromboembolic pulmonary hypertension referred for pulmonary thromboendarterectomy, yet the effect of obesity on pulmonary thromboendarterectomy outcomes has not been well described.MethodsWe conducted a retrospective cohort study in which 476 consecutive operations over a 3.5-year period were examined to determine the effects of obesity on outcomes. Patients were grouped into four categories based on body mass index (BMI): less than 22 kg/m2, 22 to 30 kg/m2, 30 to 40 kg/m2, and more than 40 kg/m2.ResultsThere were important differences in baseline pulmonary hemodynamics, with obese patients having significantly lower pulmonary vascular resistances than nonobese patients. All patients achieved a significant reduction in pulmonary vascular resistance, although the improvement was greatest in the lower BMI groups. The overall in-hospital mortality was 0.8%, and there were no differences in risk among BMI groups. Among the BMI groups, there were no differences in incidence of postoperative complications, including atrial fibrillation (overall 24.8%), reperfusion lung injury (overall 23.1%), and surgical site infection (overall 4.4%) or in median lengths of stay (including ventilator days, intensive care unit days, and postoperative length of stay).ConclusionsPulmonary thromboendarterectomy outcomes have continued to improve, and this surgery can safely be completed in obese patients, previously deemed to be at high risk for poor outcomes.

Published
2014

4. Pulmonary Endarterectomy

Author

Madani, Michael M., Jamieson, Stuart W., Yuan, Jason X. -J., editor, Garcia, Joe G.N., editor, West, John B., editor, Hales, Charles A., editor, Rich, Stuart, editor, and Archer, Stephen L., editor

Published
2011
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10. Contributors

Author

Abbott, Brian G., primary, Abbott, J. Dawn, additional, Adams, David H., additional, Al-Atassi, Talal, additional, Al-Dameh, Ali, additional, Allen, Mark S., additional, Altorki, Nasser K., additional, Anand, Jatin, additional, Anderson, Robert H., additional, Anraku, Masaki, additional, Anyanwu, Anelechi C., additional, Arora, Amit, additional, Austin, Erle H., additional, Awtry, Eric H., additional, Bacha, Emile A., additional, Backhus, Leah M., additional, Bagai, Jayant, additional, Baillot, Richard, additional, Baird, Christopher W., additional, Barron, David J., additional, Bavaria, Joseph E., additional, Bernal, Jose M., additional, Bianco, Valentino J., additional, Bichell, David P., additional, Birgisson, Sigurbjorn, additional, Blackburn, Nick J.R., additional, Bonatti, Johannes, additional, Boodhwani, Munir, additional, Bove, Edward L., additional, Brawn, William J., additional, Brizard, Christian P., additional, Brothers, Julie A., additional, Brown, Lisa M., additional, Bryant, Ayesha S., additional, Burkhart, Harold M., additional, Caldarone, Christopher A., additional, Cannon, Jeremy W., additional, Carr, Justine M., additional, Castelvecchio, Serenella, additional, Castillo, Javier G., additional, Cecchin, Frank, additional, Cerfolio, Robert J., additional, Chahine, A. Alfred, additional, Chaikof, Elliot L., additional, Chan, Vincent, additional, Chaudhry, Sunit-Preet, additional, Chen, Frederick Y., additional, Chen, Stuart H., additional, Cheng, Aaron M., additional, Chien, Victor, additional, Chin, Alvin J., additional, Chin, Cynthia S., additional, Chiu, Peter, additional, Cleveland, Joseph C., additional, Cohn, Lawrence H., additional, Cohn, William E., additional, Colson, Yolonda L., additional, Colucci, Wilson S., additional, Cook, Andrew C., additional, Coselli, Joseph S., additional, Crawford, Todd C., additional, Culligan, Melissa, additional, Dagenais, François, additional, Damiano, Ralph J., additional, D'Amico, Thomas A., additional, Dartevelle, Philippe G., additional, David, Tirone E., additional, D'Cunha, Jonathan, additional, de la Cruz, Kim I., additional, Dearani, Joseph A., additional, DeArmond, Daniel T., additional, del Nido, Pedro J., additional, DeMeester, Tom R., additional, Demers, Philippe, additional, Demmy, Todd L., additional, Dexter, Elisabeth U., additional, Dhupar, Rajeev, additional, DiNardo, James A., additional, Doyle, Thomas P., additional, Ehsan, Afshin, additional, Khoury, Gebrine El, additional, Ellis, Ethan R., additional, Elmadhun, Nassrene Y., additional, Emani, Sitaram M., additional, Erasmus, Jeremy J., additional, Fauza, Dario O., additional, Fein, Adam S., additional, Fiedler, Amy G., additional, Foppa, Murilo, additional, Freeman, Rosario V., additional, Friedberg, Joseph, additional, Friscia, Michael, additional, Fynn-Thompson, Francis, additional, Gaynor, J. William, additional, Ge, Liang, additional, Geva, Tal, additional, Gheewala, Neil M., additional, Gillinov, A. Marc, additional, Glower, Donald D., additional, Goldstone, Andrew B., additional, Groth, Shawn S., additional, Grover, Frederick L., additional, Guccione, Julius, additional, Ha, Richard, additional, Hammon, John W., additional, Hanna, Jennifer M., additional, Harrison, David G., additional, Hauser, Thomas H., additional, Henn, Matthew C., additional, Hirsch-Romano, Jennifer C., additional, Hoang, Chuong D., additional, Hofstetter, Wayne L., additional, Honjo, Osami, additional, Huynh, Tam T., additional, Bravo, Carlos E., additional, Iturra, Sebastian, additional, Jacobs, Jeffrey P., additional, Jacobs, Marshall L., additional, Jaklitsch, Michael T., additional, Jamieson, Stuart W., additional, Jarrar, Doraid, additional, Jarrett, Craig M., additional, Jones, David R., additional, Josephson, Mark E., additional, Joventino, Lilian P., additional, Juraszek, Amy L., additional, Kachala, Stefan S., additional, Kaiser, Larry R., additional, Kanter, Kirk R., additional, Karamichalis, John M., additional, Kaza, Aditya K., additional, Kemp, Clinton D., additional, Kernstine, Kemp H., additional, Keshavamurthy, Suresh, additional, Keshavjee, Shaf, additional, Kozik, Deborah J., additional, Laham, Roger J., additional, Landzberg, Michael J., additional, Lawrance, Christopher P., additional, Lee, Lawrence S., additional, LeMaire, Scott A., additional, Levitsky, Sidney, additional, Levy, Jerrold H., additional, Linden, Philip A., additional, Liptay, Michael J., additional, Litle, Virginia R., additional, Rito, Mauro Lo, additional, Luketich, James D., additional, Lytle, Bruce W., additional, Madani, Michael, additional, Mahmood, Feroze, additional, Mallidi, Hari R., additional, Mangi, Abeel A., additional, Manning, Warren J., additional, Marom, Edith M., additional, Marshall, Audrey C., additional, Martinez, Mauricio Perez, additional, Mascio, Christopher E., additional, Mason, David P., additional, Mathisen, Douglas J., additional, Mattox, Kenneth L., additional, Matyal, Robina, additional, McCully, James D., additional, McKenna, Robert J., additional, McNamee, Ciaran, additional, McNeil, Jeffrey D., additional, Menicanti, Lorenzo, additional, Mestres, Carlos A., additional, Mettler, Bret A., additional, Meyers, Bryan Fitch, additional, Mick, Stephanie, additional, Mihaljevic, Tomislav, additional, Milano, Carmelo A., additional, Miller, D. Craig, additional, Miller, Daniel L., additional, Miller, Meagan M., additional, Mitchell, John D., additional, Montealegre-Gallegos, Mario, additional, Moores, Neal G., additional, Murphy, Charles E., additional, Murthy, Raghav A., additional, Murthy, Sudish C., additional, Mussot, Sacha, additional, Naka, Yoshifumi, additional, Nathan, Meena, additional, Newman, Kurt D., additional, Nwogu, Chukwumere, additional, Odegard, Kirsten C., additional, Oh, Daniel S., additional, Ohye, Richard G., additional, Onaitis, Mark W., additional, Ostojic, Aleksandra, additional, Ott, Harald C., additional, Ouzounian, Maral, additional, Owais, Khurram, additional, Padalino, Massimo, additional, Papadakis, Konstantinos, additional, Patterson, G.A., additional, Patz, Edward F., additional, Paul, Subroto, additional, Pennathur, Arjun, additional, Perry, Yaron, additional, Piana, Robert N., additional, Pigula, Frank A., additional, Pinto, Duane S., additional, Pomar, Jose L., additional, Preventza, Ourania, additional, Pua, Bradley, additional, Puri, Varun, additional, Quinonez, Luis, additional, Raja, Siva, additional, Ratcliffe, Mark, additional, Reardon, Michael J., additional, Reilly, John J., additional, Reyes, Karl G., additional, Rice, Thomas W., additional, Robbins, Robert C., additional, Rocco, Gaetano, additional, Rubens, Fraser D., additional, Ruel, Marc, additional, Rusch, Valerie W., additional, Sabe, Ashraf A., additional, Said, Sameh M., additional, Samson, Pamela P., additional, Sanders, Stephen P., additional, Sarin, Eric L., additional, Schaff, Hartzell V., additional, Schaheen, Lara W., additional, Seder, Christopher W., additional, Sellke, Frank W., additional, Sepesi, Boris, additional, Shahani, Rohit, additional, Shamberger, Robert C., additional, Shapira, Oz M., additional, Shay, Steven S., additional, Shrager, Joseph B., additional, Si, Ming-Sing, additional, Singh, Steve K., additional, Smith, Peter K., additional, Sodha, Neel R., additional, Solaro, R. John, additional, Soukiasian, Harmik J., additional, Spurlock, David, additional, Stellin, Giovanni, additional, Stiles, Brendon M., additional, Straznicka, Michaela, additional, Stump, David A., additional, Sugarbaker, David J., additional, Suuronen, Erik J., additional, Svensson, Lars G., additional, Swanson, Scott J., additional, Szeto, Wilson Y., additional, Taghavi, Sharven, additional, Takayama, Hiroo, additional, Takeda, Koji, additional, Thiagarajan, Ravi R., additional, Thistlethwaite, Patricia A., additional, Thourani, Vinod H., additional, Toeg, Hadi D., additional, Tong, Michael Z., additional, Truesdell, Alexander G., additional, Tsai, Peter I., additional, Urschel, Harold C., additional, Valente, Anne Marie, additional, Vallabhajosyula, Prashanth, additional, Velotta, Jeffrey B., additional, Vida, Vladimiro, additional, Vlahakes, Gus J., additional, Voisine, Pierre, additional, Wall, Matthew J., additional, Walsh, Garrett L., additional, Walters, Dustin M., additional, Wei, Benjamin, additional, Welsby, Ian J., additional, Westfall, Margaret V., additional, Wiener, Daniel C., additional, Wilcox, Benson R., additional, Williams, Judson B., additional, Wilson, Jay M., additional, Woo, Y. Joseph, additional, Wood, Douglas E., additional, Wylie, John V., additional, Yang, Stephen C., additional, Yendamuri, Sai, additional, Yeon, Susan B., additional, and Zimetbaum, Peter J., additional

Published
2016
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18. Notch3 signaling promotes the development of pulmonary arterial hypertension

Author

Li, Xiaodong, Zhang, Xiaoxue, Leathers, Robin, Makino, Ayako, Huang, Chengqun, Parsa, Pouria, Macias, Jesus, Yuan, Jason X.-J., Jamieson, Stuart W., and Thistlethwaite, Patricia A.

Subjects
Cell proliferation -- Research -- Genetic aspects -- Health aspects, Molecular genetics -- Research -- Health aspects -- Genetic aspects, Vascular smooth muscle -- Properties -- Health aspects -- Genetic aspects -- Research, Pulmonary hypertension -- Genetic aspects -- Development and progression -- Research, Biological sciences, Health
Abstract

Notch receptor signaling is implicated in controlling smooth muscle cell proliferation and in maintaining smooth muscle cells in an undifferentiated state. Pulmonary arterial hypertension is characterized by excessive vascular resistance, smooth muscle cell proliferation in small pulmonary arteries, leading to elevation of pulmonary vascular resistance, right ventricular failure and death. Here we show that human pulmonary hypertension is characterized by overexpression of NOTCH3 in small pulmonary artery smooth muscle cells and that the severity of disease in humans and rodents correlates with the amount of NOTCH3 protein in the lung. We further show that mice with homozygous deletion of Notch3 do not develop pulmonary hypertension in response to hypoxic stimulation and that pulmonary hypertension can be successfully treated in mice by administration of N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), a γy-secretase inhibitor that blocks activation of Notch3 in smooth muscle cells. We show a mechanistic link from NOTCH3 receptor signaling through the Hairy and enhancer of Split-5 (HES-5) protein to smooth muscle cell proliferation and a shift to an undifferentiated smooth muscle cell phenotype. These results suggest that the NOTCH3--HES-5 signaling pathway is crucial for the development of pulmonary arterial hypertension and provide a target pathway for therapeutic intervention., Changes in the structure, function and integrity of blood vessels are necessary to the pathogenesis of many diseases, including pulmonary arterial hypertension (PAH), atherosclerosis and neointimal repair. Adult vascular smooth [...]

Published
2009

19. Inhibition of mTOR attenuates store-operated [Ca.sup.2+] entry in cells from endarterectomized tissues of patients with chronic thromboembolic pulmonary hypertension

Author

Ogawa, Aiko, Firth, Amy L., Yao, Weijuan, Madani, Michael M., Kerr, Kim M., Auger, William R., Jamieson, Stuart W., Thistlethwaite, Patricia A., and Yuan, Jason X.-J.

Subjects
Pulmonary hypertension -- Care and treatment, Pulmonary hypertension -- Research, Rapamycin -- Dosage and administration, Rapamycin -- Research, Cell proliferation -- Research, Biological sciences
Abstract

Pulmonary vascular remodeling occurs in patients with chronic thromboembolic pulmonary hypertension (CTEPH). One factor contributing to this vascular wall thickening is the proliferation of pulmonary artery smooth muscle cells (PASMC). Store-operated [Ca.sup.2+] entry (SOCE) and cytosolic free [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.cyt]) in PASMC are known to be important in cell proliferation and vascular remodeling in pulmonary hypertension. Rapamycin is widely known for its antiproliferative effects in injured coronary arteries. Although several reports have suggested favorable effects of rapamycin in animal models of pulmonary hypertension, no reports have been published to date in human tissues. Here we report that rapamycin has an inhibitory effect on SOCE and an antiproliferative effect on PASMC derived from endarterectomized tissues of CTEPH patients. Cells were isolated from endarterectomized tissues obtained from patients undergoing pulmonary thromboendarterectomy (PTE). Immunohistochemical analysis indicated high deposition of platelet-derived growth factor (PDGF) in tissue sections from PTE tissues and increased PDGF receptor expression. PDGF transiently phosphorylated Akt, mammalian target of rapamycin (mTOR), and p70S6 kinase in CTEPH cells from CTEPH patients. Acute treatment (30 min) with rapamycin (10 nM) slightly increased cyclopiazonic acid (10 [micro]M)-induced [Ca.sup.2+] mobilization and significantly reduced SOCE. Chronic treatment (24 h) with rapamycin reduced [Ca.sup.2+] mobilization and markedly inhibited SOCE. The inhibitory effects of rapamycin on SOCE were less prominent in control cells. Rapamycin also significantly reduced PDGF-stimulated cell proliferation. In conclusion, the data from this study indicate the importance of the mTOR pathway in the development of pulmonary vascular remodeling in CTEPH and suggest a potential therapeutic benefit of rapamycin (or inhibition of mTOR) in these patients. proliferation; rapamycin; therapy doi: 10.1152/ajplung.90548.2008

Published
2009

20. Identification of putative endothelial progenitor cells ([CD34.sup.+] [CD133.sup.+][Flk-1.sup.+]) in endarterectomized tissue of patients with chronic thromboembolic pulmonary hypertension

Author

Yao, Weijuan, Firth, Amy L., Sacks, Richard S., Ogawa, Aiko, Auger, William R., Fedullo, Peter F., Madani, Michael M., Lin, Grace Y., Sakakibara, Naohide, Thistlethwaite, Patricia A., Jamieson, Stuart W., Rubin, Lewis J., and Yuan, Jason X.- J.

Subjects
Endothelium -- Physiological aspects, Endothelium -- Research, Endarterectomy -- Health aspects, Pulmonary hypertension -- Risk factors, Pulmonary hypertension -- Care and treatment, Pulmonary hypertension -- Research, Vascular resistance -- Physiological aspects, Vascular resistance -- Research, Biological sciences
Abstract

Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by a fibrotic thrombus persisting and obliterating the lumen of pulmonary arteries; its pathogenesis remains poorly defined. This study investigates a potential contribution for progenitor cell types in the development of vascular obliteration and remodeling in CTEPH patients. Endarterectomized tissue from patients undergoing pulmonary thromboendarterectomy was collected and examined for the structure and cellular composition. Our data show an organized fibrin network structure in unresolved thromboemboli and intimal remodeling in vascular wall tissues, characterized by smooth muscle [alpha]-actin (SM-[alpha]A)-positive cell proliferation in proximal regions (adjacent to thromboemboli) and neoangiogenesis/recanalization in distal regions (downstream from thromboemboli). Cells that are positively stained with CD34 and fetal liver kinase-1 (Flk-1) ([CD34.sup.+][Flk-1.sup.+]) were identified in both the proximal and distal vascular tissues; a subpopulation of [CD34.sup.+][Flk-1.sup.+][CD133.sup.+] cells were further identified by immunostaining. Triple-positive cells are indicative of a population of putative endothelial progenitor cells or potential colony-forming units of endothelial cells. In addition, inflammatory cells ([CD45.sup.+]) and collagen-secreting cells ([procollagen-1.sup.+]) were detected in the proximal vascular wall. Some of the [CD34.sup.+] cells in CTEPH cells isolated from proximal regions were also positive for SM-otA. Our data indicate that putative progenitor cell types are present in the neointima of occluded vessels of CTEPH patients. It is possible that the microenvironment provided by thromboemboli may promote these putative progenitor cells to differentiate and enhance intimal remodeling. pulmonary embolism; endarterectomy; vascular remodeling

Published
2009

23. Contributors

Author

Adi, Ahmad, primary, Akhtar, Shamsuddin, additional, Arica, Koray, additional, Augoustides, John G., additional, Bailey, James M., additional, Bainbridge, Daniel, additional, Banks, Dalia A., additional, Barash, Paul G., additional, Baum, Victor C., additional, Bennett-Guerrero, Elliott, additional, Berkowitz, Dan E., additional, Body, Simon C., additional, Bowdle, T. Andrew, additional, Cahalan, Michael K., additional, Casta, Alfonso, additional, Chambers, Charles E., additional, Chaney, Mark A., additional, Chapital, Alyssa B., additional, Cheng, Alan, additional, Cheng, Davy C.H., additional, Cheung, Albert T., additional, Chikwe, Joanna, additional, Cook, David J., additional, De Souza, Duncan G., additional, Domino, Karen B., additional, Durieux, Marcel E., additional, Edmonds, Harvey L., additional, Edwards, Mark, additional, Enriquez, Liza J., additional, Fischer, Gregory W., additional, Fleisher, Lee A., additional, Fuster, Valentin, additional, Garcia, Mario J., additional, Gaztanaga, Juan, additional, Giacobbe, Dean T., additional, Groban, Leanne, additional, Grocott, Hilary P., additional, Grogan, Kelly, additional, Groom, Robert C., additional, Grosshans, David W., additional, Hayashi, Masao, additional, Hessel, Eugene A., additional, Hibbert, Benjamin, additional, Higgins, Thomas L., additional, Hogue, Charles W., additional, Horak, Jiri, additional, Horrow, Jay, additional, Housmans, Philippe R., additional, Jamieson, Stuart W., additional, Jones-Haywood, Mandisa-Maia, additional, Kahn, Ronald A., additional, Kaplan, Joel A., additional, Kerr, Jack F., additional, Kerr, Kim M., additional, Klimkina, Oksana, additional, Koch, Colleen, additional, Konstadt, Steven N., additional, Kozak, Mark, additional, Lerner, Adam B., additional, Levy, Jerrold H., additional, London, Martin J., additional, Love, Barry A., additional, Mahmood, Feroze, additional, Manecke, Gerard R., additional, Mora Mangano, Christina T., additional, Matei, Veronica, additional, Mauermann, William J., additional, Maus, Timothy M., additional, Mitter, Nanhi, additional, Mittnacht, Alexander J.C., additional, Mohler, Emile R., additional, Murkin, John M., additional, Murray, Andrew W., additional, Murray, Michael J., additional, Nathan, Howard J., additional, Nuttall, Gregory A., additional, Nyhan, Daniel, additional, O'brien, Edward R.M., additional, Oliver, William C., additional, Pagel, Paul S., additional, Pantin, Enrique J., additional, Quinlan, Joseph J., additional, Ramsay, James G., additional, Rehfeldt, Kent H., additional, Reich, David L., additional, Royster, Roger L., additional, Rozner, Marc A., additional, Savino, Joseph S., additional, Schwartz, Alan Jay, additional, Shah, Ashish, additional, Shanewise, Jack S., additional, Sharma, Sonal, additional, Shernan, Stanton K., additional, Shore-Lesserson, Linda, additional, Skubas, Nikolaos J., additional, Slaughter, Thomas F., additional, Spiess, Bruce D., additional, Stafford-Smith, Mark, additional, Stammers, Alfred H., additional, Stone, Marc E., additional, Tanaka, Kenichi, additional, Weiner, Menachem, additional, Weiss, Stuart J., additional, and Yared, Jean-Pierre, additional

Published
2011
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24. Signaling molecules in nonfamilial pulmonary hypertension

Author

Du, Lingling, Sullivan, Christopher C., Chu, Danny, Cho, Augustine J., Kido, Masakuni, Wolf, Paul L., Yuan, Jason X.-J., Deutsch, Reena, Jamieson, Stuart W., and Thistlethwaite, Patricia A.

Subjects
Pulmonary hypertension -- Causes of, Pulmonary hypertension -- Physiological aspects
Abstract

Both familial and non-familial pulmonary hypertension may be caused by defects in signaling pathways governed by angiopoietin-1, its endothelial receptor TIE2, and bone morphogenetic protein receptor types 1A and 2. This may cause the excessive buildup of muscle tissue in patients with pulmonary hypertension, which is characterized by high blood pressure in the lungs.

Published
2003

28. Contributors

Author

Abtin, Fereidoun, primary, Afshar, Kamyar, additional, Auger, William R., additional, Balfe, David, additional, Barack, Bruce M., additional, Bremner, Ross, additional, Brown, Kathleen, additional, Chaux, George E., additional, Chen, Steve C., additional, Cheng, Wen, additional, Cho, John, additional, Colt, Henri G., additional, Conlan, Allan, additional, Tom Cooke, David, additional, Cutler, Jennifer, additional, Deslauriers, Jean, additional, Elsayegh, Ashraf, additional, Falk, Jeremy A., additional, Fedullo, Peter F., additional, Feins, Richard H., additional, Ferguson, Mark K., additional, Fortes, Daniel L., additional, Fréchette, Éric, additional, Fuller, Clark, additional, Ghandehari, Sara, additional, Greaves, S. Melanie, additional, Green, Leland, additional, Hackner, Dani, additional, Haithcock, Benjamin E., additional, Hakim, Alex, additional, Halkos, Michael E., additional, Heffner, John E., additional, Hermes, Kay E., additional, Jaklitsch, Michael T., additional, Jamieson, Stuart W., additional, Jones, Heather D., additional, Jordan, Stanley C., additional, Julien, Peter J., additional, Kamangar, Nader, additional, Kanaan, Samer, additional, Kass, Robert M., additional, Khan, Steven S., additional, Lee, C. Joyce, additional, Lewis, Michael I., additional, Liberman, Moishe, additional, Limsukon, Atikun, additional, Luketich, James D., additional, Madani, Michael M., additional, Mahtabifard, Ali, additional, Marchevsky, Alberto M., additional, Margulies, Daniel R., additional, Mathisen, Douglas J., additional, McKenna, Robert J., additional, McNamee, Ciaran, additional, Mehran, Reza J., additional, Miller, Joseph I., additional, Mirhadi, Amin J., additional, Mitchell, John D., additional, Morse, Christopher R., additional, Mosenifar, Zab, additional, Mountain, Clifton F., additional, Naik, Tej, additional, Natale, Ronald, additional, Ng, Tina T., additional, Nichols, Francis C., additional, Nuthakki, Vijay K., additional, Oh, Scott, additional, Ozawa, Yoko, additional, Parsons, Alden M., additional, Pedraza, Isabel, additional, Pezner, Richard D., additional, Pickens, Allan, additional, Rakovich, George, additional, Reddy, Hari, additional, Reece, T. Brett, additional, Sather, Curtis, additional, Simsir, Sinan, additional, Smethurst, Peter, additional, Soukiasian, Harmik J., additional, Suh, Robert D., additional, Symbas, John D., additional, Symbas, Panagiotis N., additional, Toyoda, Mieko, additional, Tzung, Brian, additional, Vo, Ashley A., additional, Waxman, Alan, additional, Wu, Carol C., additional, and Zakowski, Phillip, additional

Published
2010
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29. Contributors

Author

Abbott, Brian G., primary, Adams, David H., additional, Aklog, Lishan, additional, Agnihotri, Arvind K., additional, Aquila Allen, Louise A., additional, Allen, Mark S., additional, Altorki, Nasser K., additional, Anderson, Robert H., additional, Anraku, Masaki, additional, Anyanwu, Anelechi C., additional, Ashiku, Simon K., additional, Austin, Erle H., additional, Awtry, Eric H., additional, Bacha, Emile A., additional, Baillott, Richard, additional, Baim, Donald S., additional, Balsam, Leora B., additional, Barner, Hendrick B., additional, Barron, David J., additional, Bavaria, Joseph E., additional, Bichell, David P., additional, Bove, Edward L., additional, Brawn, William J., additional, Brizard, Christian P., additional, Brothers, Julie A., additional, Brown, Morgan L., additional, Bryant, Ayesha S., additional, Burkhart, Harold M., additional, Caldarone, Christopher A., additional, Califf, Robert M., additional, Cantu, Edward, additional, Carr, Justine M., additional, Carrozza, Joseph P., additional, Cecchin, Frank, additional, Cerfolio, Robert J., additional, Chacko, Riya S., additional, Chahine, Alfred, additional, Chan, Vincent, additional, Chen, Frederick Y., additional, Chin, Alvin J., additional, Chin, Cynthia S., additional, Chikwe, Joanna, additional, Chitwood, W. Randolph, additional, Christian, Karla G., additional, Christie, Neil A., additional, Cleveland, Joseph C., additional, Cohn, Lawrence H., additional, Cohn, William E., additional, Colson, Yolanda L., additional, Colucci, Wilson S., additional, Cook, Andrew C., additional, Cooper, Joel D., additional, Copeland, Jack G., additional, Cowan, Scott, additional, Culligan, Melissa, additional, Dagenais, Francois, additional, Damiano, Ralph J., additional, D'Amico, Thomas A., additional, Daniel, Jonathan, additional, Dartevelle, Philippe G., additional, David, Tirone E., additional, D'Cunha, Jonathan, additional, Dearani, Joseph A., additional, DeArmond, Daniel T., additional, del Nido, Pedro J., additional, DeMeester, Tom R., additional, Demers, Philippe, additional, Demmy, Todd L., additional, Devaney, Eric J., additional, Dexter, Elisabeth U., additional, Di Donato, Marisa, additional, Ducko, Christopher T., additional, Duncan, Brian W., additional, Duran, Carlos M.G., additional, Edwards, Fred H., additional, Emani, Sitaram M., additional, Erasmus, Jeremy J., additional, Fauza, Dario O., additional, Fernandez, Felix G., additional, Fernando, Hiran C., additional, Filsoufi, Farzan, additional, Fischbein, Michael P., additional, Freeman, Rosario V., additional, Friedberg, Joseph, additional, Fullerton, David A., additional, Fynn-Thompson, Francis, additional, Garcia, Lawrence A., additional, Gaynor, J. William, additional, Geva, Tal, additional, Gilbert, Sébastien, additional, Gillinov, A. 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Published
2010
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38. Early expression of angiogenesis factors in acute myocardial ischemia and infarction

Author

Lee, Sang H., Wolf, Paul L., Escudero, Ryan, Deutsch, Reena, Jamieson, Stuart W., and Thistlethwaite, Patricia A.

Subjects
Growth factors -- Research, Ischemia -- Physiological aspects, Heart attack -- Physiological aspects
Abstract

Hypoxia-inducible factor 1 (HIF-1) is one of the first substances produced by the body in response to low oxygen levels, a condition called hypoxia. HIF-1 in turn activates genes that produce vascular endothelial growth factor (VEGF), a substance that causes blood vessels to grow. Researchers tested heart biopsy specimens from 37 patients having coronary bypass surgery for the presence of HIF-1 and VEGF. HIF-1 occurred in samples taken from patients in the early stages of a heart attack. VEGF only occurred in patients in the later stages of a heart attack.

Published
2000

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