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2. Clinical and Coronary Plaque Predictors of Atherosclerotic Nonresponse to Statin Therapy

Author

Sophie E. van Rosendael, Inge J. van den Hoogen, Fay Y. Lin, Daniele Andreini, Mouaz H. Al-Mallah, Matthew J. Budoff, Filippo Cademartiri, Kavitha Chinnaiyan, Jung Hyun Choi, Edoardo Conte, Hugo Marques, Pedro de Araújo Gonçalves, Ilan Gottlieb, Martin Hadamitzky, Jonathon A. Leipsic, Erica Maffei, Gianluca Pontone, Gilbert L. Raff, Sanghoon Shin, Yong-Jin Kim, Byoung Kwon Lee, Eun Ju Chun, Ji Min Sung, Sang-Eun Lee, Renu Virmani, Habib Samady, Peter H. Stone, James K. Min, Jagat Narula, Leslee J. Shaw, Hyuk-Jae Chang, Alexander R. van Rosendael, and Jeroen J. Bax

Subjects
Radiology, Nuclear Medicine and imaging, Cardiology and Cardiovascular Medicine
Published
2023
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3. Risk factors based vessel‐specific prediction for stages of coronary artery disease using Bayesian quantile regression machine learning method: Results from the PARADIGM registry

Author

Hyung‐Bok Park, Jina Lee, Yongtaek Hong, So Byungchang, Wonse Kim, Byoung K. Lee, Fay Y. Lin, Martin Hadamitzky, Yong‐Jin Kim, Edoardo Conte, Daniele Andreini, Gianluca Pontone, Matthew J. Budoff, Ilan Gottlieb, Eun Ju Chun, Filippo Cademartiri, Erica Maffei, Hugo Marques, Pedro de A. Gonçalves, Jonathon A. Leipsic, Sanghoon Shin, Jung H. Choi, Renu Virmani, Habib Samady, Kavitha Chinnaiyan, Peter H. Stone, Daniel S. Berman, Jagat Narula, Leslee J. Shaw, Jeroen J. Bax, James K. Min, Woong Kook, and Hyuk‐Jae Chang

Subjects
cardiovascular risk factors, Prevention, Bayes Theorem, Coronary Artery Disease, General Medicine, Cardiorespiratory Medicine and Haematology, Coronary Angiography, Cardiovascular, Atherosclerosis, Coronary Vessels, Angina Pectoris, Machine Learning, Heart Disease, Cardiovascular System & Hematology, Risk Factors, Humans, Registries, Cardiology and Cardiovascular Medicine, Heart Disease - Coronary Heart Disease
Abstract

Background and hypothesisThe recently introduced Bayesian quantile regression (BQR) machine-learning method enables comprehensive analyzing the relationship among complex clinical variables. We analyzed the relationship between multiple cardiovascular (CV) risk factors and different stages of coronary artery disease (CAD) using the BQR model in a vessel-specific manner.MethodsFrom the data of 1,463 patients obtained from the PARADIGM (NCT02803411) registry, we analyzed the lumen diameter stenosis (DS) of the three vessels: left anterior descending (LAD), left circumflex (LCx), and right coronary artery (RCA). Two models for predicting DS and DS changes were developed. Baseline CV risk factors, symptoms, and laboratory test results were used as the inputs. The conditional 10%, 25%, 50%, 75%, and 90% quantile functions of the maximum DS and DS change of the three vessels were estimated using the BQR model.ResultsThe 90th percentiles of the DS of the three vessels and their maximum DS change were 41%-50% and 5.6%-7.3%, respectively. Typical anginal symptoms were associated with the highest quantile (90%) of DS in the LAD; diabetes with higher quantiles (75% and 90%) of DS in the LCx; dyslipidemia with the highest quantile (90%) of DS in the RCA; and shortness of breath showed some association with the LCx and RCA. Interestingly, High-density lipoprotein cholesterol showed a dynamic association along DS change in the per-patient analysis.ConclusionsThis study demonstrates the clinical utility of the BQR model for evaluating the comprehensive relationship between risk factors and baseline-grade CAD and its progression.

Published
2023
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4. Impact of statins based on high-risk plaque features on coronary plaque progression in mild stenosis lesions: results from the PARADIGM study

Author

Hyung-Bok Park, Reza Arsanjani, Ji Min Sung, Ran Heo, Byoung Kwon Lee, Fay Y Lin, Martin Hadamitzky, Yong-Jin Kim, Edoardo Conte, Daniele Andreini, Gianluca Pontone, Matthew J Budoff, Ilan Gottlieb, Eun Ju Chun, Filippo Cademartiri, Erica Maffei, Hugo Marques, Pedro de Araújo Gonçalves, Jonathon A Leipsic, Sang-Eun Lee, Sanghoon Shin, Jung Hyun Choi, Renu Virmani, Habib Samady, Kavitha Chinnaiyan, Peter H Stone, Daniel S Berman, Jagat Narula, Leslee J Shaw, Jeroen J Bax, James K Min, and Hyuk-Jae Chang

Subjects
Radiology, Nuclear Medicine and imaging, General Medicine, Cardiology and Cardiovascular Medicine
Abstract

Aims To investigate the impact of statins on plaque progression according to high-risk coronary atherosclerotic plaque (HRP) features and to identify predictive factors for rapid plaque progression in mild coronary artery disease (CAD) using serial coronary computed tomography angiography (CCTA). Methods and results We analyzed mild stenosis (25–49%) CAD, totaling 1432 lesions from 613 patients (mean age, 62.2 years, 63.9% male) and who underwent serial CCTA at a ≥2 year inter-scan interval using the Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging (NCT02803411) registry. The median inter-scan period was 3.5 ± 1.4 years; plaques were quantitatively assessed for annualized percent atheroma volume (PAV) and compositional plaque volume changes according to HRP features, and the rapid plaque progression was defined by the ≥90th percentile annual PAV. In mild stenotic lesions with ≥2 HRPs, statin therapy showed a 37% reduction in annual PAV (0.97 ± 2.02 vs. 1.55 ± 2.22, P = 0.038) with decreased necrotic core volume and increased dense calcium volume compared to non-statin recipient mild lesions. The key factors for rapid plaque progression were ≥2 HRPs [hazard ratio (HR), 1.89; 95% confidence interval (CI), 1.02–3.49; P = 0.042], current smoking (HR, 1.69; 95% CI 1.09–2.57; P = 0.017), and diabetes (HR, 1.55; 95% CI, 1.07–2.22; P = 0.020). Conclusion In mild CAD, statin treatment reduced plaque progression, particularly in lesions with a higher number of HRP features, which was also a strong predictor of rapid plaque progression. Therefore, aggressive statin therapy might be needed even in mild CAD with higher HRPs. Clinical trial registration ClinicalTrials.gov NCT02803411

Published
2023
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5. Relationship of Psychological Characteristics to Daily Life Ischemia: An Analysis From the National Heart, Lung, and Blood Institute Psychophysiological Investigations in Myocardial Ischemia

Author

Osama Dasa, Ahmed N. Mahmoud, Peter G. Kaufmann, Mark Ketterer, Kathleen C. Light, James Raczynski, David S. Sheps, Peter H. Stone, Eileen Handberg, and Carl J. Pepine

Subjects
Male, Myocardial Ischemia, Coronary Artery Disease, Anger, Middle Aged, United States, Article, Cohort Studies, Psychiatry and Mental health, Hostility, Ischemia, Humans, Female, National Heart, Lung, and Blood Institute (U.S.), Applied Psychology, Stress, Psychological
Abstract

Cardiac ischemia during daily life is associated with an increased risk of adverse outcomes. Mental stress is known to provoke cardiac ischemia and is related to psychological variables. In this multicenter cohort study, we assessed whether psychological characteristics were associated with ischemia in daily life.This study examined patients with clinically stable coronary artery disease (CAD) with documented cardiac ischemia during treadmill exercise (n = 196, mean [standard deviation] age = 62.64 [8.31] years; 13% women). Daily life ischemia (DLI) was assessed by 48-hour ambulatory electrocardiophic monitoring. Psychological characteristics were assessed using validated instruments to identify characteristics associated with ischemia occurring in daily life stress.High scores on anger and hostility were common in this sample of patients with CAD, and DLI was documented in 83 (42%) patients. However, the presence of DLI was associated with lower anger scores (odds ratio [OR] = 2.03; 95% confidence interval [CI] = 1.12-3.69), reduced anger expressiveness (OR = 2.04; 95% CI = 1.10-3.75), and increased ratio of anger control to total anger (OR = 2.33; 95% CI = 1.27-4.17). Increased risk of DLI was also associated with lower hostile attribution (OR = 2.22; 95% CI = 1.21-4.09), hostile affect (OR = 1.92; 95% CI = 1.03-3.58), and aggressive responding (OR = 2.26; 95% CI = 1.25-4.08). We observed weak inverse correlations between DLI episode frequency and anger expressiveness, total anger, and hostility scores. DLI was not associated with depression or anxiety measures. The combination of the constructs low anger expressiveness and low hostile attribution was independently associated with DLI (OR = = 2.59; 95% CI = 1.42-4.72).In clinically stable patients with CAD, the tendency to suppress angry and hostile feelings, particularly openly aggressive behavior, was associated with DLI. These findings warrant a study in larger cohorts, and intervention studies are needed to ascertain whether management strategies that modify these psychological characteristics improve outcomes.

Published
2023

6. Endothelial shear stress computed from coronary computed tomography angiography: A direct comparison to intravascular ultrasound

Author

Diaa Hakim, Ahmet U. Coskun, Charles Maynard, Zhongyue Pu, Deborah Rupert, Nicholas Cefalo, Michelle Cormier, Mona Ahmed, James Earls, Rob Jennings, Kevin Croce, Saima Mushtaq, Daniele Andreini, Edoardo Conte, David Molony, Habib Samady, James K. Min, and Peter H. Stone

Subjects
Radiology, Nuclear Medicine and imaging, Cardiology and Cardiovascular Medicine
Published
2023
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7. The Role of Shear Stress in Coronary Artery Disease

Author

Gerasimos Siasos, Vasiliki Tsigkou, Ahmet Umit Coskun, Evangelos Oikonomou, Marina Zaromitidou, Lilach O Lerman, Amir Lerman, and Peter H Stone

Subjects
Drug Discovery, General Medicine
Abstract

Abstract: Coronary artery disease is the leading cause of morbidity and mortality worldwide, especially in developed countries, with an increasing incidence in developing countries. Despite the ad-vances in cardiology, there are yet many unanswered questions about the natural history of cor-onary atherosclerosis. However, it has not been fully explained why some coronary artery plaques remain quiescent over time, whereas others evolve to a high-risk, “vulnerable” plaque with a predisposition to destabilize and induce a cardiac event. Furthermore, approximately half of the patients with acute coronary syndromes demonstrate no prior symptoms of ischemia or angiographically evident disease. Recent findings have indicated that apart from cardiovas-cular risk factors, genetics, and other unknown factors, local hemodynamic forces, such as en-dothelial shear stress, blood flow patterns, and endothelial dysfunction of the epicardial and microvascular coronary arteries, are associated with the progression of coronary plaque and the development of cardiovascular complications with complex interactions. In this review article, we summarize the mechanisms that affect coronary artery plaque progression, indicating the importance of endothelial shear stress, endothelial dysfunction of epicardial and microvascular vessels, inflammation, and their complex associations, underlying in parallel the clinical per-spectives of these findings.

Published
2023
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10. Initial Invasive or Conservative Strategy for Stable Coronary Disease

Author

Maron D. J., Hochman J. S., Reynolds H. R., Bangalore S., O'Brien S. M., Boden W. E., Chaitman B. R., Senior R., Lopez-Sendon J., Alexander K. P., Lopes R. D., Shaw L. J., Berger J. S., Newman J. D., Sidhu M. S., Goodman S. G., Ruzyllo W., Gosselin G., Maggioni A. P., White H. D., Bhargava B., Min J. K., John Mancini G. B., Berman D. S., Picard M. H., Kwong R. Y., Ali Z. A., Mark D. B., Spertus J. A., Krishnan M. N., Elghamaz A., Moorthy N., Hueb W. A., Demkow M., Mavromatis K., Bockeria O., Peteiro J., Miller T. D., Szwed H., Doerr R., Keltai M., Selvanayagam J. B., Gabriel Steg P., Held C., Kohsaka S., Mavromichalis S., Kirby R., Jeffries N. O., Harrell F. E., Rockhold F. W., Broderick S., Bruce Ferguson T., Williams D. O., Harrington R. A., Stone G. W., Rosenberg Y, ISCHEMIA Research Group: Joseph Ricci, A Tello Montoliu, A I Robero Aniorte, Abbey Mulder, Abhay A Laddu, Abhinav Goyal, Abhishek Dubey, Abhishek Goyal, Abigail Knighton, Abraham Oomman, Adam J Jaskowiak, Adam Kolodziej, Adam Witkowski, Adnan Hameed, Adriana Anesini, Afshan Hussain, Agne Juceviciene, Agne Urboniene, Agnes Jakal, Agnieszka Szramowska, Ahmad Khairuddin, Ahmed Abdel-Latif, Ahmed Adel, Ahmed Aljzeeri, Ahmed Kamal, Ahmed Talaat, Aimee Mann, Aira Contreras, Ajit Kumar, V K Kumar, Akemi Furukawa, Akshay Bagai, Akvile Smigelskaite, Alain Furber, Alain Rheault, Alaine Melanie Loehr, Alan Rosen, Albert Varga, Albertina Qelaj, Alberto Barioli, Aldo Russo, Alec Moorman, Alejandro Gisbert, Aleksandra Fratczak, Aleksandras Laucevicius, Alena Kuleshova, Alessandro Sionis, Alexander A Sirker, Alexander M Chernyavskiy, Alexandra Craft, Alexandra Vazquez, Alexandre Ciappina Hueb, Alexandre S Colafranseschi, Alexandre Schaan de Quadros, Alexandre Tognon, Ali Alghamdi, Alice Manica Muller, Aline Nogueira Rabaça, Aline Peixoto Deiro, Alison Hallam, Allegra Stone, Allison Schley, Almudena Castro, Alvaro Rabelo Ales, Amanda Germann, Amanda O'Malley, Amar Uxa, Amarachi Ojajuni, Amarino C Oliveira Jr, Amber B Hull, Ambuj Roy, Amer Zarka, Amir Janmohamed, Ammani Brown, Ammy Malinay, Amparo Martinez Monzonis, Amy J Richards, Amy Iskandrian, Amy Ollinger, Ana D Djordjevic-Dikic, Ana Fernández Martínez, Ana Gomes Almeida, Ana Paula Batista, Ana Rita Francisco, Ana S Mladenovic, Ana Santana, Anam Siddiqui, Anastasia M Kuzmina-Krutetskaya, Andras Vertes, Andre S Sousa, Andre Gabriel, André Schmidt, Andrea M Lundeen, Andrea Bartykowszki, Andrea Lorimer, Andrea Mortara, Andrea Pascual, Andreia Coelho, Andreia Rocha, Andrés García-Rincón, Andrew G Howarth, Andrew J Moriarty, Andrew Docherty, Andrew Starovoytov, Andrew Zurick, Andrzej Łabyk, Andrzej Swiatkowski, Andy Lam, Anelise Kawakami, Angela Hoye, Angela Kim, Angelique Smit, Angelo Nobre, Anil V Shah, Anja Ljubez, Anjali Anand, Ankush Sachdeva, Ann Greenberg, Ann Luyten, Ann Ostrander, Anna Di Donato, Anna Cichocka-Radwan, Anna Fojt, Anna Plachcinska, Anna Proietti, Anna Teresinska, Anne Marie Webb, Anne Cartwright, Anne Heath, Anne Mackin, Anong Amaritakomol, Anong Chaiyasri, Anoop Chauhan, Anoop Mathew, Anthony Gemignani, Anto Luigi Andres, Antonia Vega, Antonietta Hansen, Antonino Ginel Iglesias, Antonio Carlos Carvalho, Antonio Di Chiara, Antonio Serra Peñaranda, Antonio Carvalho, Antonio Colombo, Antonio Fiarresga, Anupama Rao, Aquiles Valdespino-Estrada, Araceli Boan, Areef Ishani, Ariel Diaz, Arijit Ghosh, Arintaya Prommintikul, Arline Roberts, Arnold H Seto, Arnold P Good, Arshed Quyyumi, Arthur J Labovitz, Arthur Kerner, Arturo S Campos-Santaolalla, Arunima Misra, Ashok Mukherjee, Ashok Seth, Ashraf Seedhom, Asim N Cheema, Asker Ahmed, Atul Mathur, Atul Verma, Audrey W Leong, Axel Åkerblom, Axelle Fuentes, Aynun Naher, Badhma Valaiyapathi, Baljeet Kaur, Bandula Guruge, Barbara Brzezińska, Barbara Nardi, Bartosz Czarniak, Bebek Singh, Begoña Igual, Bela Merkely, Belen Cid Alvarez, Benjamin J Spooner, Benjamin J W Chow, Benjamin Cheong, Benoy N Shah, Bernard de Bruyne, Bernardas Valecka, Bernhard Jäger, Beth A Archer, Beth Abramson, Beth Jorgenson, Bethany Harvey, Betsy O'Neal, Bev Atkinson, Bev Bozek, Bevin Lang, Bijulal Sasidharan, Bin Yang, Bin Zhang, Binoy Mannekkattukudy Kurian, Bjoern Goebel, Bob Hu, Bogdan A Popescu, Bogdan Crnokrak, Bolin Zhu, Bonnie J Kirby, Brandi D Zimbelman, Brandy Starks, Branko D Beleslin, Brenda Hart, Brian P Shapiro, Brian McCandless, Brianna Wisniewski, Brigham R Smith, Brooks Mirrer, Bruce McManus, Bruce Rutkin, Bruna Edilena Paulino, Bruna Maria Ascoli, Bryn Smith, Byron J Allen, C Michael Gibson, C Noel Bairey Merz, Calin Pop, Cameron Hague, Camila Thais de Ormundo, Candace Gopaul, Candice P Edillo, Carísi A Polanczyk, Carita Krannila, Carla Vicente, Carl-Éric Gagné, Carlo Briguori, Carlos Peña Gil, Carlos Alvarez, Carly Ohmart, Carmen C Beladan, Carmen Ginghina, Carol M Kartje, Caroline Alsweiler, Caroline Brown, Caroline Callison, Caroline Pinheiro, Caroline Rodgers, Caroline Spindler, Carolyn Corbett, Carrie Drum, Casey Riedberger, Catherine Bone, Catherine Fleming, Catherine Gordon, Catherine Jahrsdorfer, Catherine Lemay, Catherine Weick, Cathrine Patten, Cecilia Goletto, Cezary Kepka, Chandini Suvarna, Chang Xu, Chantale Mercure, Charle A Viljoen, Charlene Wiyarand, Charles Jia-Yin Hou, Charles Y Lui, Charles Cannan, Charles Cornet, Charlotte Pirro, Chataroon Rimsukcharoenchai, Chen Wang, Cheng-Ting Tsai, Chen-Yen Chien, Cheryl A Allardyce, Chester M Hedgepeth, Chetan Patel, Chiara Attanasio, Chih-Hsuan Yen, Chi-Ming Chow, Ching Min Er, Ching-Ching Ong, Cholenahally Nanjappa Manjunath, Chris Beck, Chris Buller, Christel Vassaliere, Christian Hamm, Christiano Caldeira, Christie Ballantyne, Christina Björklund, Christine R Hinton, Christine Bergeron, Christine Masson, Christine Roraff, Christine Shelley, Christophe Laure, Christophe Thuaire, Christopher Kinsey, Christopher McFarren, Christopher Spizzieri, Christopher Travill, Chun-Chieh Liu, Chung-Lieh Hung, Chunguang Li, Chun-Ho Yun, Chunli Xia, Ciarra Heard, Cidney Schultz, Clare Venn-Edmonds, Claudia P Hochberg, Claudia Wegmayr, Claudia Cortés, Claudia Escobar, Cláudia Freixo, Claudio T Mesquita, Clemens T Kadalie, Colin Berry, Constance Philander, Corine Thobois, Costantino Costantini, Courtney Page, Craig Atkinson, Craig Barr, Craig Paterson, Cristina Bare, Cynthia Baumann, Cynthia Burman, Dalisa Espinosa, Damien Collison, Dan Deleanu, Dan Elian, Dan Gao, Dana Oliver, Daniel P Vezina, Daniel O'Rourke, Daniele Komar, Danielle Schade, Darrel P Francis, Dastan Malaev, David A Bull, David E Winchester, David P Faxon, David Booth, David Cohen, David DeMets, David Foo, David Schlichting, David Taggart, David Waters, David Wohns, Davis Vo, Dawid Teodorczyk, Dawn Shelstad, Dawn Turnbull, Dayuan Li, Dean Kereiakes, Deborah O'Neill, Deborah Yip, Debra K Johnson, Debra Dees, Deepak L Bhatt, Deepika Gopal, Deepti Kumar, Deirdre Mattina, Deirdre Murphy, Delano R Small, Delsa K Rose, Dengke Jiang, Denis Carl Phaneuf, Denise Braganza, Denise Fine, Derek Cyr, Desiree Tobin, Diana Cukali, Diana Parra, Diane Camara, Diane Minshall Liu, Diego Adrián Vences, Diego Franca de Cunha, Dimitrios Stournaras, Dipti Patel, Dongze Li, Donna Exley, Dorit Grahl, Dragana Stanojevic, Duarte Cacela, Dwayne S G Conway, E Pinar Bermudez, Eapen Punnoose, Edgar L Tay, Edgar Karanjah, Edoardo Verna, Eduardo Hernandez-Rangel, Edward D Nicol, Edward O McFalls, Edward T Martin, Edyta Kaczmarska, Ekaterina I Lubinskaya, Elena A Demchenko, Elena Refoyo Salicio, Eli Feen, Elihú Durán-Cortés, Elisabeth M Janzen, Elise L Hannemann, Elise van Dongen, Elissa Restelli Piloto, Eliza Kaplan, Elizabeta Srbinovska Kostovska, Elizabeth Capasso-Gulve, Elizabeth Congdon, Elizabeth Ferguson, Elizaveta V Zbyshevskaya, Ellen Magedanz, Ellie Fridell, Ellis W Lader, Elvin Kedhi, Emanuela Racca, Emilie Tachot, Emily DeRosa, Encarnación Alonso-Álvarez, Eric Nicollet, Eric Peterson, Erick Alexánderson Rosas, Erick Donato Morales, Erin Orvis, Ermina Moga, Estelle Montpetit, Estevao Figueiredo, Eugene Passamani, Eugenia Nikolsky, Eunice Yeoh, Evgeniy I Kretov, Ewa Szczerba, Ewelina Wojtala, Expedito Eustáquio Ribeiro Silva, F Marin Ortuño, Fabio R Farias, Fabio Fimiani, Fabrizio Rolfo, Fa-Chang Yu, Fadi Hage, Fadi Matar, Fahim Haider Jafary, Fang Feng, Fang Liu, Fatima Ranjbaran, Fatima Rodriguez, Fausto J Pinto, Fauzia Rashid, Federica Ramani, Fei Wang, Fernanda Igansi, Filipa Silva, Filippo Ottani, Fiona Haines, Firas Al Solaiman, Flávia Egydio, Flavio Lyra, Florian Egger, Fran Farquharson, Frances Laube, Francesc Carreras Costa, Francesca de Micco, Francesca Bianchini, Francesca Pezzetta, Francesca Pietrucci, Francesco Orso, Francesco Pisano, Francis Burt, Francisca Patuleia Figueiras, Francisco Fernandez-Aviles, Francois Pierre Mongeon, Frans Van de Werf, Franziska Guenther, Fraser N Witherow, Fred Mohr, Frederico Dall'Orto, Fumiyuki Otsuka, G De La Morena, G Karthikeyan, Gabor Dekany, Gabor Kerecsen, Gabriel Galeote, Gabriel Grossmann, Gabriel Vorobiof, Gabriela Sanchez de Souza, Gabriela Guzman, Gabriela Zeballos, Gabriele Gabrielli, Gabriele Jakl-Kotauschek, Gail A Shammas, Gail Brandt, Gang Chen, Gary E Lane, Gary J Luckasen, Gautam Sharma, Gelmina Mikolaitiene, Gennie Yee, Georg Nickenig, George E Revtyak, George J Juang, Gerald Fletcher, Gerald Leonard, Gerard Patrick Devlin, Gerard Esposito, Gergely Ágoston, Gervasio Lamas, Geza Fontos, Ghada Mikhail, Gia Cobb, Gian Piero Perna, Gianpiero Leone, Giles Roditi, Gilles Barone-Rochette, Girish Mishra, Giuseppe Tarantini, Glenda Wong, Glenn S Hamroff, Glenn Rayos, Gong Cheng, Gonzalo Barge-Caballero, Goran Davidović, Goran Stankovic, Gordana Stevanovic, Grace Jingyan Wang, Grace M Young, Graceanne Wayser, Graciela Scaro, Graham S Hillis, Graham Wong, Grazyna Anna Szulczyk, Gregor Simonis, Gregory Kumkumian, Gretchen Ann Peichel, Grzegorz Gajos, Gudrun Steinmaurer, Guilherme G Rucatti, Guilherme Portugal, Guilhermina Cantinho Lopes, Guillem Pons Lladó, Gunnar Frostfelt, Gurpreet S Wander, Gurpreet Gulati, Gustavo Pucci, Hafidz Abd Hadi, Haibo Zhang, Haitao Wang, Halina Marciniak, Han Chen, Hanan Kerr, Hani Najm, Hanna Douglas, Hannah Phillips, Hao Dai, Haojian Dong, Haqeel Jamil, Harikrishnan Sivadasanpillai, Harry Suryapranata, Hassan Reda, Hayley Pomeroy, Heather Barrentine, Heather Golden, Heather Hurlburt, Heidi Wilson, Helen C Tucker, Helene Abergel, Hemalata Siddaram, Hermine Osseni, Herwig Schuchlenz, Hesong Zeng, Hicham Skali, Hilda Solomon, Hollie Horton, Holly Hetrick, Holly Little, Holly Park, Hongjie Chi, Hossam Mahrous, Howard A Levite, Hristo Pejkov, Huajun Li, Hugo Bloise-Adames, Hugo Marques, Hui Zhong, Hui-Min Zhang, Humayrah Hashim, Hung-I Yeh, Hussien El Fishawy, Ian Webb, Iftikhar Kullo, Igor O Grazhdankin, Ihab Hamzeh, Ikraam Hassan, Ikuko Ueda, Ileana L Pina, Ilona Tamasauskiene, Ilse Bouwhuis, Imran Arif, Ina Wenzelburger, Inês Zimbarra Cabrita, Ines Rodrigues, Inga H Robbins, Inga Soveri, Ingela Schnittger, Iqbal Karimullah, Ira M Dauber, Iram Rehman, Irena Peovska Mitevska, Irene Marthe Lang, Irina Subbotina, Irma Kalibataite-Rutkauskiene, Irni Yusnida, Isabel Estela Carvajal, Isabella C Palazzo, Isabelle Hogan, Isabelle Roy, Ishba Syed, Ishita Tejani, Ivan A Naryshkin, Ivana Jankovic, Iwona Niedzwiecka, J David Knight, Jacek Kusmierek, Jackie M White, Jackie Chow, Jacob Udell, Jacqueline E Tamis-Holland, Jacqueline Fannon, Jacquelyn A Quin, Jacquelyn Do, Jaekyeong Heo, Jakub Maksym, James E Davies, James H O'Keefe Jr, James J Jang, James Cha, James Harrison, James Hirsch, James Stafford, James Tatoulis, Jamie Rankin, Jan Henzel, Jan Orga, Jana Tancredi, Janaina Oliveira, Jane Burton, Jane Eckstein, Jane Marucci, Janet P Knight, Janet Blount, Janet Halliday, Janetta Kourzenkova, Janitha Raj, Jan-Malte Sinning, Jaqueline Pozzibon, Jaroslaw Drozdz, Jaroslaw Karwowski, Jason D Glover, Jason Loh Kwok, Jason T Call, Jason Linefsky, Jassira Gomes, Jati Anumpa, Javier J Garcia, Javier Courtis, Jay Meisner, K Jayakumar, Jayne Scales, Jean E Denaro, Jean Michel Juliard, Jean Ho, Jeanette K Stansborough, Jean-Michel Juliard, Jeanne Russo, Jeannette J M Schoep, Jeet Thambyrajah, Jeff Leimberger, Jeffery A Breall, Jeffrey A Kohn, Jeffrey C Milliken, Jeffrey Anderson, Jeffrey Blume, Jeffrey Kanters, Jeffrey Lorin, Jeffrey Moses, Jelena J Stepanovic, Jelena Celutkiene, Jelena Djokic, Jelena Stojkovic, Jenne M Jose, Jenne Manchery, Jennifer A Mull, Jennifer H Czerniak, Jennifer L Stanford, Jennifer Gillis, Jennifer Horst, Jennifer Isaacs, Jennifer Langdon, Jennifer Thomson, Jennifer Tomfohr, Jennifer White, Jen-Yuan Kuo, Jeremy Rautureau, Jerome Fleg, Jessica Berg, Jessica Rodriguez, Jessica Waldron, Jhina Patro, Jia Li, Jiajia Mao, Jiamin Liu, Jian'an Wang, Jianhua Li, Jianxin Zhang, Jie Qi, Jihyun Lyo, Jill Marcus, Jim Blankenship, Jing Zhang, Jingjing Liu, Jing-Yao Fan, Jiun-Yi Li, Jiwan Pradhan, Jiyan Chen, J M Rivera Caravaca, Jo Evans, Joan Garcia Picart, Joan Hecht, Joanna Jaroch, Joanna Zalewska, Joanne Kelly, Joanne Taaffe, João Reynaldo Abbud, João V Vitola, Joaquín V Peñafiel, Jocelyne Benatar, Jody Bindeman, Joe Sabik, Joel Klitch, Johann Christopher, Johannes Aspberg, John D Friedman, John F Beltrame, John F Heitner, John Joseph Graham, John R Davies, John Doan, John Kotter, John Kurian, John Mukai, John Pownall, Jolanta Sobolewska, Jon Kobashigawa, Jonathan L Goldberg, Jonathan W Bazeley, Jonathan Byrne, Jonathan Himmelfarb, Jonathan Leipsic, Jonean Thorsen, Jorge F Trejo Gutierrez, Jorge Escobedo, Jorik Timmer, José A Ortega-Ramírez, José Antonio Marin-Neto, Jose D Salas, Jose Enrique Castillo, Jose Francisco Saraiva, José J Cuenca-Castillo, Jose L Diez, José Luis Narro Villanueva, José Luiz da Vieira, José M Flores-Palacios, Jose Ramon Gonzalez, Jose Seijas Amigo, Jose Fragata, Josep Maria Padró, Josheph F X McGarvey Jr, Joseph Hannan, Joseph Sacco, Joseph Sweeny, Joseph Wiesel, Josephine D Abraham, Joshua P Loh, Joy Burkhardt, Joyce R White, Joyce Riestenberg-Smith, Judit Sebo, Judith L Meadows, Judith Wright, Judy Mae Foltz, Judy Hung, Judy Otis, Juergen Stumpf, Jui-Peng Tsai, Julia S Dionne, Julia de Aveiro Morata, Julie Bunke, Julie Morrow, Julio César Figal, Jun Fujita, Jun Jiang, Junhua Li, Junqing Yang, Juntima Euathrongchit, Jyotsna Garg, K Manjula Rani, K Preethi, Kaatje Goetschalckx, Kai Eggers, Kamalakar Surineni, Kanae Hirase, T R Kapilamoorthy, Karen Calfas, Karen Gratrix, Karen Hallett, Karen Hultberg, Karen Nugent, Karen Petrosyan, Karen Swan, Karolina Kryczka, Karolina Wojtczak-Soska, Karolina Wojtera, Karsten Lenk, Karthik Ramasamy, Katarzyna Łuczak, Katarzyna Malinowska, Kate Pointon, Kate Robb, Katherine Martin, Kathleen Claes, Kathryn Carruthers, Kathy E Siegel, Katia Drouin, Katie Fowler-Lehman, Kavita Rawat, Kay Rowe, Keiichi Fukuda, Keith A A Fox, Ken Mahaffey, Kendra Unterbrink, Kenneth Giedd, Kerrie Van Loo, Kerry Lee, Kerstin Bonin, Kevin R Bainey, Kevin T Harley, Kevin Anstrom, Kevin Chan, Kevin Croce, Kevin Landolfo, Kevin Marzo, Keyur Patel, Khaled Abdul-Nour, Khaled Alfakih, Khaled Dajani, Khaled Ziada, Khaula Baloch, Khrystyna Kushniriuk, Kian-Keong Poh, Kim F Ireland, Kim Holland, Kimberly Ann Byrne, Kimberly E Halverson, Kimberly Elmore, Kimberly Miller-Cox, Kiran Reddy, Kirsten J Quiles, Kirsty Abercrombie, Klaus Matschke, Konrad Szymczyk, Koo Hui Chan, Kotiboinna Preethi, Kozhaya Sokhon, Krissada Meemuk, Kristian Thygesen, Kristin M Salmi, Kristin Newby, Kristina Wippler, Kristine Arges, Kristine Teoh, Krystal Etherington, Krystyna Łoboz-Grudzień, Krzysztof W Reczuch, Krzysztof Bury, Krzysztof Drzymalski, Krzysztof Kukuła, Kuo-Tzu Sung, Kurt Huber, Ladda Douangvila, Lance Sullenberger, Larissa Miranda Trama, Laszlone Matics, Laura Drew, Laura Flint, Laura 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Luiz A Carvalho, Luyang Xiong, Lynette L Teo, Lynn M Neeson, Lynne Winstanley, M Barbara Srichai-Parsia, M Quintana Giner, M Sowjanya Reddy, M Valdés Chávarri, M Grazia Rossi, Maarten Simoons, Maayan Konigstein, Maciej Lesiak, Maciej Olsowka, Mafalda Selas, Magalie Corfias, Magdalena Madero Rovalo, Magdalena Łanocha, Magdalena Miller, Magdalena Misztal-Teodorczyk, Magdalena Rantinella, Magdy Abdelhamid, Magnolia Jimenez, Mahboob Alam, Mahevamma Mylarappa, Mahfouz El Shahawy, Mahmoud Mohamed, Mahmud Al-Bustami, Majo X Joseph, Malgorzata Frach, Małgorzta Celińska-Spodar, Malte Helm, Manas Chacko, Mandy Murphy, Manitha Vinod, Manjula Rani, Manu Dhawan, Manuela Mombelli, Marcel Weber, Marcello Galvani, Marcelo Jamus Rodrigues, Marcia F Dubin, Marcia F Werner Bayer, Marcin Szkopiak, Marco Antonio Monsalve, Marco Bizzaro Santos, Marco Magnoni, Marco Marini, Marco Sicuro, Marco Zenati, Marcos Valério Coimbra Resende, Marek Roik, Margalit Bentzvi, Margaret Gilsenan, Margaret Iraola, Margot C 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Hayes, Sebastian Sobczak, Senait Asier, Sergey A Sayganov, Seth I Sokol, Shaheen Pandie, Shaiful Azmi Yahaya, Shamir Mehta, Shao-Ping Nie, Sharad Chandra, Sharder Islam, Sharon Tai, Sheetal Rupesh Karwa, Sheri Ussery, Sheromani Bajaj, Sherron C Crook, Shigeyuki Nishimura, Shintaro Nakano, Shirin Heydari, Shiv Kumar Choudhary, Shivali Patel, Shobana Ganesan, Shruti Pandey, Shuyang Zhang, Shweta Hande, Siddharth Gadage, Sik-Yin V Tan, Silvia Zottis Poletti, Silvia Riera, Silvia Valbuena, Simon Walsh, Simona Maspoli, Simone Savaris, Si-Ting Feng, So Yang Cho, Solomon Yakubov, Songlin Zhu, Songtao Wang, Sonia Guerrero, Sonika Gupta, Sonja Salinger Martinovic, Sonya Brons, Sorin Brener, Sothinathan Gurunathan, Souheil Saba, Soundarya Nayak, Sowjanya Reddy, Srinivasa Potluri, Sriram Sudarshan, Srun Kuanprasert, Stacie Van Oosterhout, Stamatios Lerakis, Stanley E Cobos, Stefan C Bertog, Stefan M Simović, Stefan Weikl, Stefano Di Marco, Stefano Provasoli, Stephanie A Tirado, Stephanie C Boer, Stephanie M Lane, Stephanie Ferket, Stephanie Kelly, Stephanie Wasmiller, Stephen H McKellar, Stephen P Hoole, Stephen Fremes, Stephen Preston, Steve Leung, Steven A Fein, Steven J Lindsay, Steven P Sedlis, Steven Giovannone, Steven Michael, Steven Weitz, Stijn van Vugt, Subhash Banerjee, Sudhir Naik, Suellen Hosino, Sukie Desire, Sukit Yamwong, Suku T Thambar, Sulagna Mookherjee, Suman Singh, Sundeep Mishra, Sunil Kumar Verma, Supap Kulthawong, Supatchara Khwakhong, Surendra Naik, Suresh Babu, Surin Woragidpoonpol, Suryaprakash Narayanappa, Susan Derbyshire, Susan Gent, Susan Mathus, Susan Milbrandt, Susan Moore, Susan Regan, Susan Stinson, Susan Webber, Susana Silva, Susanna Stevens, Susanne Gruensfelder, Suthara Aramcharoen, Suvarna Kolhe, Suzana Tavares, Suzanne Arnold, Suzanne Welsh, Svetlana Apostolovic, Swapna Kunhunny, Ta-Chuan Hung, Taissa Zappernick, Tali Sharir, Talita Silva, Tamara Colaiácovo Soares, Tapan Umesh Pillay, Tarun K Mittal, Tatiana Trifonova, Tauane Bello Duarte, Tauqir Huk, Téodora Dutoiu, Terrance Chua, Terry Weyand, Thabitha Charles, Theodoros Kofidis, Theresa McCreary, Thierry Lefevre, Thippeekaa Arumairajah, Thitipong Tepsuwan, Thomas J Mulhearn, Thomas M Meyer, Thomas P Rocco, Thomas R Downes, Thomas Crain, Thomas Haldis, Thomas Mathew, Thomas Redick, Thounaojam Indira Devi, Thuraia Nageh, Tia Cauthren, Tiago Silva, Tiffany Little, Tijana Andric, Tina Harding, Titus Lau, Tiziana Formisano, Tiziano Moccetti, Tomasz Ciurus, Tomasz Mazurek, Tomasz Tarchalski, Toshiyuki Nagai, Tri Tran, Tricia Youn, Trish Tucker, Trudie Milner, Tuhina Bose, Tushar Kotecha, Udo Sechtem, Uma S Valeti, Umberto Cucchini, Umesh Badami, Upendra Kaul, V K Bahl, V S Narain, Valentina Casali, Valeria Godoy, Valerie Robesyn, Vamshi P Priya, Vandana Yadav, Vera McKinney, Veronica De Lenges, Veronica Tinnirello, Vicente Miro, Victor Navarro, Victoria Gumerova, Victoria Hernandez, Vidya Seeratan, Vijay Kumar, Vikentiy Y Kozulin, Viktoria Bulkley, Vilmar Veiga Jr, Vincent Setang, C P Vineeth, Virginai Pubull Nuñez, Virginia Fernández-Figares, Vitor Gomes, Viviana Gabriel, Viviane Dos Santos, Viviane Almeida, Vlad A Iliescu, Vladan Mudrenovic, Vladimir Dzavik, Vojislav L Giga, Walter Enrique Mogrovejo, Wan Xian Chan, Wanda C Marfori, Wanda Parker, Warangkana Mekara, Wassim Nona, Wayne Old, Wayne Pennachi, Weerachai Nawarawong, Wei Chen, Wei Su, Weibing Xing, Wei-Ren Lan, Wenda Crawford, Wendy L Stewart, Wendy Drewes, Wenhua Lin, William B Abernethy, William D Salerno, William F Fearon, William Vergoni, William Weintraub, Winnie C Sia, Wlodzimierz J Musial, Xacobe Flores-Ríos, Xavier Garcia-Moll Marimon, Xi Su, Xiang Ma, Xiangqiong Gu, Xiao Wang, Xiaomei Li, Xiaowei Yao, Xin Fu, Xin Su, Xin Zeng, Xinchun Yang, Xiuhong Li, Xuehua Fang, Xutong Wang, Yaming Geng, Yan Yan, Yanek Pépin-Dubois, Yanfu Wang, Yang Wang, Yanmeng Tian, Yaping Huang, Yechen Han, Yesenia Zambrano, Yi-Hsuan Yang, Ying Tung Sia, Yining Yang, Yitong Ma, Yolayfi Peralta, Yongjian Wu, Yu Kunwu, Yu Zhao, Yudong Peng, Yueh-Hung Lin, Yulan Zhao, Yumei Dong, Yunhai Zhao, Yutthaphan Wannasopha, Yvonne Taul, Zakir Sahul, Zalina Kudzoeva, Zbigniew Kalarus, Zeljko Z Markovic, Zhen Huang, Zheng Ji, Zhenyu Liu, Zhou Yue, Zhulin Zhang, Zhuxi Li, Zile Singh Meharwal, Ziliang Bai, Zixiang Yu, Zohra Huda, Zoltan Davidovits

Subjects
Male, Cardiac Catheterization, Computed Tomography Angiography, medicine.medical_treatment, Myocardial Ischemia, Coronary Disease, Coronary Artery Disease, Kaplan-Meier Estimate, 030204 cardiovascular system & hematology, Coronary Angiography, ISCHEMIA Research Group, law.invention, Angina, Coronary artery disease, 0302 clinical medicine, Randomized controlled trial, law, Cardiovascular Disease, Myocardial Revascularization, 030212 general & internal medicine, Coronary Artery Bypass, 11 Medical and Health Sciences, Cardiac catheterization, General Medicine, Middle Aged, humanities, Cardiovascular Diseases, Cardiology, Female, Human, medicine.medical_specialty, Ischemia, Article, 03 medical and health sciences, Geriatric cardiology, Percutaneous Coronary Intervention, General & Internal Medicine, Internal medicine, medicine, Humans, Angina, Unstable, Aged, business.industry, Coronary Artery Bypa, Percutaneous coronary intervention, Bayes Theorem, medicine.disease, Heart failure, Quality of Life, business
Abstract

BACKGROUND: Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS: We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS: Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, -1.8 percentage points; 95% CI, -4.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS: Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used. (Funded by the National Heart, Lung, and Blood Institute and others; ISCHEMIA ClinicalTrials.gov number, NCT01471522.).

Published
2020
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11. Measurement of compensatory arterial remodelling over time with serial coronary computed tomography angiography and 3D metrics

Author

Inge J van den Hoogen, Alexander R van Rosendael, Fay Y Lin, Umberto Gianni, Daniele Andreini, Mouaz H Al-Mallah, Matthew J Budoff, Filippo Cademartiri, Kavitha Chinnaiyan, Jung Hyun Choi, Edoardo Conte, Hugo Marques, Pedro de Araújo Gonçalves, Ilan Gottlieb, Martin Hadamitzky, Jonathon Leipsic, Erica Maffei, Gianluca Pontone, Sanghoon Shin, Yong Jin Kim, Byoung Kwon Lee, Eun Ju Chun, Ji Min Sung, Sang Eun Lee, Daniel S Berman, Renu Virmani, Habib Samady, Peter H Stone, Jagat Narula, Hyuk Jae Chang, James K Min, Leslee J Shaw, and Jeroen J Bax

Subjects
Male, Computed Tomography Angiography, Humans, Female, Radiology, Nuclear Medicine and imaging, Coronary Artery Disease, General Medicine, Middle Aged, Coronary Angiography, Cardiology and Cardiovascular Medicine, Coronary Vessels, Plaque, Atherosclerotic, Aged
Abstract

Aims The magnitude of alterations in which coronary arteries remodel and narrow over time is not well understood. We aimed to examine changes in coronary arterial remodelling and luminal narrowing by three-dimensional (3D) metrics from serial coronary computed tomography angiography (CCTA). Methods and results From a multicentre registry of patients with suspected coronary artery disease who underwent clinically indicated serial CCTA (median interscan interval = 3.3 years), we quantitatively measured coronary plaque, vessel, and lumen volumes on both scans. Primary outcome was the per-segment change in coronary vessel and lumen volume from a change in plaque volume, focusing on arterial remodelling. Multivariate generalized estimating equations including statins were calculated comparing associations between groups of baseline percent atheroma volume (PAV) and location within the coronary artery tree. From 1245 patients (mean age 61 ± 9 years, 39% women), a total of 5721 segments were analysed. For each 1.00 mm3 increase in plaque volume, the vessel volume increased by 0.71 mm3 [95% confidence interval (CI) 0.63 to 0.79 mm3, P < 0.001] with a corresponding reduction in lumen volume by 0.29 mm3 (95% CI −0.37 to −0.21 mm3, P < 0.001). Serial 3D arterial remodelling and luminal narrowing was similar in segments with low and high baseline PAV (P ≥ 0.496). No differences were observed between left main and non-left main segments, proximal and distal segments and side branch and non-side branch segments (P ≥ 0.281). Conclusions Over time, atherosclerotic coronary plaque reveals prominent outward arterial remodelling that co-occurs with modest luminal narrowing. These findings provide additional insight into the compensatory mechanisms involved in the progression of coronary atherosclerosis.

Published
2021
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14. Fundamental Pathobiology of Coronary Atherosclerosis and Clinical Implications for Chronic Ischemic Heart Disease Management—The Plaque Hypothesis

Author

Peter H, Stone, Peter, Libby, and William E, Boden

Subjects
Cardiology and Cardiovascular Medicine
Abstract

ImportanceRecent clinical and imaging studies underscore that major adverse cardiac events (MACE) outcomes are associated not solely with severe coronary obstructions (ischemia hypothesis or stenosis hypothesis), but with the plaque burden along the entire coronary tree. New research clarifies the pathobiologic mechanisms responsible for plaque development/progression/destabilization leading to MACE (plaque hypothesis), but the translation of these insights to clinical management strategies has lagged. This narrative review elaborates the plaque hypothesis and explicates the current understanding of underlying pathobiologic mechanisms, the provocative destabilizing influences, the diagnostic and therapeutic implications, and their actionable clinical management approaches to optimize the management of patients with chronic coronary disease.ObservationsClinical trials of management strategies for patients with chronic coronary artery disease demonstrate that while MACE rate increases progressively with the anatomic extent of coronary disease, revascularization of the ischemia-producing obstruction does not forestall MACE. Most severely obstructive coronary lesions often remain quiescent and seldom destabilize to cause a MACE. Coronary lesions that later provoke acute myocardial infarction often do not narrow the lumen critically. Invasive and noninvasive imaging can identify the plaque anatomic characteristics (plaque burden, plaque topography, lipid content) and local hemodynamic/biomechanical characteristics (endothelial shear stress, plaque structural stress, axial plaque stress) that can indicate the propensity of individual plaques to provoke a MACE.Conclusions and RelevanceThe pathobiologic construct concerning the culprit region of a plaque most likely to cause a MACE (plaque hypothesis), which incorporates multiple convergent plaque features, informs the evolution of a new management strategy capable of identifying the high-risk portion of plaque wherever it is located along the course of the coronary artery. Ongoing investigations of high-risk plaque features, coupled with technical advances to enable prognostic characterization in real time and at the point of care, will soon enable evaluation of the entire length of the atheromatous coronary artery and broaden the target(s) of our therapeutic intervention to include all regions of the plaque (both flow limiting and nonflow limiting).

Published
2023
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15. Abstract 13620: Comparison of Endothelial Shear Stress (ESS) Computation Utilizing Non-Invasive Coronary Computed Tomography Angiography (CCTA) vs Invasive Intravascular Ultrasound (IVUS) Imaging

Author

Diaa Hakim, Ahmet Coskun, Chuck Maynard, zhongyue pu, Deborah Rupert, Nicholas Cefalo, Michelle Cormier, Kevin Croce, james K min, James Earls, Rob Jennings, Daniele Andreini, Saima Mushtaq, Edoardo Conte, and Peter H Stone

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Introduction: Risk-stratification of individual coronary plaques is an important goal to detect high-risk plaques likely to progress/destabilize, which could inform preemptive intervention to prevent adverse cardiac events. IVUS imaging, the current gold standard to assess plaque risk, has shown that biomechanical variables, particularly local ESS, contributes critical synergistic prognostic insight when combined with anatomic high-risk plaque features. Non-invasive risk assessment of coronary plaques with CCTA would be invaluable to enable broad population risk screening, but it is unknown whether CCTA, which has less spatial resolution than IVUS, can adequately measure the critical local biomechanical and anatomic variables. Aim: To compare the accuracy of ESS computation of local ESS metrics by non-invasive CCTA vs invasive IVUS imaging. Methods: We analyzed 30 arteries (22 LAD, 4 LCx,4 RCA) from 30 patients selected from a registry of patients who underwent both IVUS and CCTA of the same artery for suspected CAD. CCTA images were acquired using a CCTA with either 64 or 256 detector rows. We segmented lumen, vessel, and plaque areas with both IVUS (manual segmentation) and CCTA (AI based software; Cleerly Inc, NY). Co-registration of IVUS and CCTA Images was performed using fiduciary anatomic landmarks. Images from IVUS and CCTA were used to generate a 3-D arterial reconstruction, and local ESS distribution was assessed by computational fluid dynamics and reported in consecutive 3-mm segments. Results: Table Conclusion: Compared to IVUS values, 256-slice is more accurate than 64-slice CCTA to measure lumen and vessel areas, but computation of detailed local ESS (average, low and high) is similar by both CCTA methods. Local ESS evaluation using non-invasive CCTA is feasible and comparable to invasive gold standard IVUS and is suitable to characterize the local flow patterns that play an important role in plaque development, progression, and destabilization

Published
2021
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16. Abstract 11768: Role of Endothelial Shear Stress and Endothelial Shear Stress Gradient in Plaques Associated With Acute Erosion vs. Stable Control Plaques and Relationship Between Plaque Slope and Localization of Plaque Erosion

Author

Diaa Hakim, Ahmet U Coskun, Charles Maynard, zhongyue pu, Deborah Rupert, Nicholas Cefalo, Tej Sheth, Natalia Pinilla-Echeverri, Kajander A Olli, Gerasimos Siasos, Michail I Papafaklis, Stefanu Kostas, Lampros K Michalis, Kevin Croce, and Peter H Stone

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Introduction: The role of endothelial shear stress (ESS) in the development of coronary plaque erosion is unknown. High ESS gradient (ESSG) has been hypothesized to promote plaque erosion, but no studies have included matched control stable plaques with the same minimal and reference lumen area (MLA, RLA, respectively). No studies examined the location of plaque erosion (proximal vs distal to MLA of the culprit plaque) related to the max magnitude of upslope vs downslope of the lumen obstruction. Aims: (1) to compare ESSG between plaques with erosion and similar control plaques that remained stable; (2) among erosion plaques, to study the effect of max slope steepness (Δ lumen area/frame) up- and down-stream from the culprit plaque MLA on thrombus location. Methods: We studied 46 patients from TOTAL and COMPLETE trials who underwent angiography and OCT imaging: 46 arteries: 27 LAD, 6 LCX, 13 RCA. Plaques were divided into Plaque Erosion (n=24) with OCT features of erosion before PCI (17 definite, 7 probable erosion) and matched coronary plaques from separate control patients (n=22) without plaque disruption. Orthogonal angiographic views were used to generate a 3-D arterial reconstruction, and angio centerline was combined with OCT centerline. Local ESS distribution was assessed by computational fluid dynamics and reported in consecutive 3-mm segments. Among the plaque erosions, we calculated the up- and down-slope (Δ lumen area/frame) of lumen obstruction for each culprit plaque. Results: See Table Conclusion: In plaques with similarly severe obstruction, plaque erosion is associated with higher max ESS and max ESSG vs plaques that remain stable. Proximal plaque erosion/thrombus is associated with steeper plaque upslope vs downslope, and distal plaque erosion/thrombus is associated with steeper plaque downslope vs upslope. Absolute ESSG is higher in downslope vs upslope erosions. These features may help prognosticate individual plaques at risk for future erosion.

Published
2021
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18. Percent atheroma volume: Optimal variable to report whole-heart atherosclerotic plaque burden with coronary CTA, the PARADIGM study

Author

Alexander R. van Rosendael, Fay Y. Lin, Xiaoyue Ma, Inge J. van den Hoogen, Umberto Gianni, Omar Al Hussein, Subhi J. Al'Aref, Jessica M. Peña, Daniele Andreini, Mouaz H. Al-Mallah, Matthew J. Budoff, Filippo Cademartiri, Kavitha Chinnaiyan, Jung Hyun Choi, Edoardo Conte, Hugo Marques, Pedro de Araújo Gonçalves, Ilan Gottlieb, Martin Hadamitzky, Jonathon A. Leipsic, Erica Maffei, Gianluca Pontone, Gilbert L. Raff, Sanghoon Shin, Yong-Jin Kim, Byoung Kwon Lee, Eun Ju Chun, Ji Min Sung, Sang-Eun Lee, Daniel S. Berman, Renu Virmani, Habib Samady, Peter H. Stone, Jagat Narula, Jeroen J. Bax, Leslee J. Shaw, James K. Min, and Hyuk-Jae Chang

Subjects
Male, Aging, Time Factors, Body Surface Area, Computed Tomography Angiography, Coronary CTA, Coronary Artery Disease, Cardiorespiratory Medicine and Haematology, 030204 cardiovascular system & hematology, Cardiovascular, Coronary Angiography, Severity of Illness Index, Imaging, 030218 nuclear medicine & medical imaging, 0302 clinical medicine, Medicine, Prospective Studies, Registries, Plaque, Atherosclerotic, Body surface area, education.field_of_study, Middle Aged, Coronary Vessels, Plaque, Atherosclerotic, Heart Disease, medicine.anatomical_structure, Quartile, Percent atheroma volume, Coronary vessel, Cardiology, Disease Progression, Biomedical Imaging, Female, Cardiology and Cardiovascular Medicine, Artery, medicine.medical_specialty, Clinical Sciences, Population, Lumen (anatomy), 03 medical and health sciences, Sex Factors, Clinical Research, Predictive Value of Tests, Internal medicine, Humans, Radiology, Nuclear Medicine and imaging, education, Heart Disease - Coronary Heart Disease, Coronary atherosclerosis, Aged, business.industry, Atherosclerosis, medicine.disease, Atheroma, Cardiovascular System & Hematology, business
Abstract

BACKGROUND AND AIMS:Different methodologies to report whole-heart atherosclerotic plaque on coronary computed tomography angiography (CCTA) have been utilized. We examined which of the three commonly used plaque burden definitions was least affected by differences in body surface area (BSA) and sex. METHODS:The PARADIGM study includes symptomatic patients with suspected coronary atherosclerosis who underwent serial CCTA >2 years apart. Coronary lumen, vessel, and plaque were quantified from the coronary tree on a 0.5mm cross-sectional basis by a core-lab, and summed to per-patient. Three quantitative methods of plaque burden were employed: (1) total plaque volume (PV) in mm3, (2) percent atheroma volume (PAV) in % [which equaled: PV/vessel volume * 100%], and (3) normalized total atheroma volume (TAVnorm) in mm3 [which equaled: PV/vessel length * mean population vessel length]. Only data from the baseline CCTA were used. PV, PAV, and TAVnorm were compared between patients in the top quartile of BSA vs the remaining, and between sexes. Associations between vessel volume, BSA, and the three plaque burden methodologies were assessed. RESULTS:The study population comprised 1479 patients (age 60.7±9.3 years, 58.4% male) who underwent CCTA. A total of 17,649 coronary artery segments were evaluated with a median of 12 (IQR 11-13) segments per-patient (from a 16-segment coronary tree). Patients with a large BSA (top quartile), compared with the remaining patients, had a larger PV and TAVnorm, but similar PAV. The relation between larger BSA and larger absolute plaque volume (PV and TAVnorm) was mediated by the coronary vessel volume. Independent from the atherosclerotic cardiovascular disease risk (ASCVD) score, vessel volume correlated with PV (P&nbsp

Published
2019

19. The Hazardous Longitudinal Heterogeneity of Plaques: A Complex Mountain Range, Not a Single Volcano

Author

Peter H, Stone

Subjects
MACE, major adverse cardiovascular event(s), PSS, plaque structural stress, intravascular imaging, Coronary Vessels, Plaque, Atherosclerotic, Article, PB, plaque burden, stomatognathic diseases, myocardial infarction, VH-IVUS, virtual histology intravascular ultrasonography, MLA, minimal luminal area, Humans, VH-TCFA, virtual histology thin-cap fibroatheroma, cardiovascular diseases, Prospective Studies, HI, heterogeneity index, FEA, finite element analysis, plaque structural stress, thin-cap fibroatheroma
Abstract

Objectives This study sought to determine if plaque structural stress (PSS) and other plaque stress parameters are increased in plaques that cause future major adverse cardiovascular event(s) (MACE) and if incorporating these parameters improves predictive capability of intravascular ultrasonography (IVUS). Background Less than 10% of coronary plaques identified as high-risk by intravascular imaging result in subsequent MACE. Thus, more specific measurements of plaque vulnerability are required for effective risk stratification. Methods Propensity score matching in the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study plaque cohort resulted in 35 nonculprit lesions (NCL) associated with future MACE and 66 matched NCL that remained clinically silent. PSS was calculated by finite element analysis as the mechanical loading within the plaque structure in the periluminal region. Results PSS was increased in the minimal luminal area (MLA) regions of NCL MACE versus no MACE plaques for all plaques (PSS: 112.1 ± 5.5 kPa vs. 90.4 ± 3.3 kPa, respectively; p = 0.001) and virtual histology thin-cap fibroatheromas (VH-TCFAs) (PSS: 119.2 ± 6.6 kPa vs. 95.8 ± 5.0 kPa, respectively; p = 0.005). However, PSS was heterogeneous over short segments, and PSS heterogeneity index (HI) was markedly greater in NCL MACE than in no-MACE VH-TCFAs (HI: 0.43 ± 0.05 vs. 0.29 ± 0.03, respectively; p = 0.01). Inclusion of PSS in plaque assessment improved the identification of NCLs that led to MACE, including in VH-TCFAs (p = 0.03) and plaques with MLA ≤4 mm2 (p = 0.03). Incorporation of an HI further improved the ability of PSS to identify MACE NCLs in a variety of plaque subtypes including VH-TCFA (p = 0.001) and plaques with MLA ≤4 mm2 (p = 0.002). Conclusions PSS and variations in PSS are increased in the peri-MLA regions of plaques that lead to MACE. Moreover, longitudinal heterogeneity in PSS is markedly increased in MACE plaques, especially VH-TCFAs, potentially predisposing to plaque rupture. Incorporation of PSS and heterogeneity in PSS may improve the ability of IVUS to predict MACE., Central Illustration

Published
2019

22. Role of Low Endothelial Shear Stress and Plaque Characteristics in the Prediction of Nonculprit Major Adverse Cardiac Events: The PROSPECT Study

Author

Peter H, Stone, Akiko, Maehara, Ahmet Umit, Coskun, Charles C, Maynard, Marina, Zaromytidou, Gerasimos, Siasos, Ioannis, Andreou, Dimitris, Fotiadis, Kostas, Stefanou, Michail, Papafaklis, Lampros, Michalis, Alexandra J, Lansky, Gary S, Mintz, Patrick W, Serruys, Charles L, Feldman, and Gregg W, Stone

Subjects
Time Factors, Pilot Projects, Coronary Artery Disease, Coronary Angiography, Coronary Vessels, Risk Assessment, Plaque, Atherosclerotic, United States, Europe, Percutaneous Coronary Intervention, Treatment Outcome, Predictive Value of Tests, Risk Factors, Coronary Circulation, Disease Progression, Humans, Endothelium, Vascular, Prospective Studies, Stress, Mechanical, Ultrasonography, Interventional
Abstract

This study sought to determine whether low endothelial shear stress (ESS) adds independent prognostication for future major adverse cardiac events (MACE) in coronary lesions in patients with high-risk acute coronary syndrome (ACS) from the United States and Europe.Low ESS is a proinflammatory, proatherogenic stimulus associated with coronary plaque development, progression, and destabilization in human-like animal models and in humans. Previous natural history studies including baseline ESS characterization investigated low-risk patients.In the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study, 697 patients with ACS underwent 3-vessel intracoronary imaging. Independent predictors of MACE attributable to untreated nonculprit (nc) coronary lesions during 3.4-year follow-up were large plaque burden (PB), small minimum lumen area (MLA), and thin-cap fibroatheroma (TCFA) morphology. In this analysis, baseline ESS of nc lesions leading to new MACE (nc-MACE lesions) and randomly selected control nc lesions without MACE (nc-non-MACE lesions) were calculated. A propensity score for ESS was constructed for each lesion, and the relationship between ESS and subsequent nc-MACE was examined.A total of 145 lesions were analyzed in 97 patients: 23 nc-MACE lesions (13 TCFAs, 10 thick-cap fibroatheromas [ThCFAs]), and 122 nc-non-MACE lesions (63 TCFAs, 59 ThCFAs). Low local ESS (1.3 Pa) was strongly associated with subsequent nc-MACE compared with physiological/high ESS (≥1.3 Pa) (23 of 101 [22.8%]) versus (0 of 44 [0%]). In propensity-adjusted Cox regression, low ESS was strongly associated with MACE (hazard ratio: 4.34; 95% confidence interval: 1.89 to 10.00; p 0.001). Categorizing plaques by anatomic risk (high risk: ≥2 high-risk characteristics PB ≥70%, MLA ≤4 mmLocal low ESS provides incremental risk stratification of untreated coronary lesions in high-risk patients, beyond measures of PB, MLA, and morphology.

Published
2016

23. Abstract 16948: Local Low Endothelial Shear Stress (ESS) Provides Incremental Prediction of Non-culprit MACE in Addition to Plaque Burden, Minimal Lumen Area, and Plaque Morphology: The PROSPECT Study

Author

Peter H Stone, Akiko Maehara, Ahmet U Coskun, Charles C Maynard, Ioannis Andreou, Gerasimos Siasos, Marina Zaromitidou, Dimitris Fotiadis, Kostas Stefanou, Michail Papafaklis, Lampros Michalis, Alexandra J Lansky, Gary S Mintz, Patrick W Serruys, Charles L Feldman, and Gregg W Stone

Subjects
Physiology (medical), cardiovascular diseases, Cardiology and Cardiovascular Medicine
Abstract

Introduction: Low ESS, a pro-inflammatory stimulus, is an important predictor of coronary plaque development/progression. Whether low ESS adds incremental predictive value for future major adverse cardiac events (MACE) in untreated coronary lesions in high-risk patients with an acute coronary syndrome (ACS) is unknown. Methods: In the PROSPECT study, 697 patients with ACS underwent 3-vessel intracoronary imaging. Independent predictors of non-culprit (nc) lesion MACE from untreated coronary lesions in 3 year followup (f/u) were large plaque burden (PB), small minimum lumen area (MLA), and thin cap fibroatheroma (TCFA) morphology. In the present analysis, all nc-lesions leading to a new MACE in f/u (nc-MACE lesions, n=50) and ~4-fold randomly selected control nc-lesions without f/u MACE (nc-non-MACE lesions) were analyzed. Baseline ESS for each lesion was calculated using computational fluid dynamics. A propensity score for low ESS was determined accounting for PB, MLA, TCFA, artery and location in the artery. Local ESS (lowest ESS in 90 o arc around the artery) was then examined for incremental association with MACE. Results: Imaging was sufficient for analysis in 32 nc-MACE lesions. Two nc-MACE lesions were excluded due to unreliable lesion morphology. Non-fibroatheromas were too few for analysis and excluded. Final dataset included 145 lesions: 13 nc-MACE TCFA, 10 nc-MACE thick cap fibroatheroma (ThCFA), and 122 non-nc-MACE lesions (63 TCFA, 59 ThCFA). Cumulative frequency distribution shows lesions responsible for future nc-MACE frequently exhibited low ESS (Figure). In a propensity-adjusted multivariable model, low ESS was strongly associated with nc-MACE in f/u (odds ratio 0.16 [95% CI 0.06-0.40], p Conclusions: After accounting for large PB, small MLA, TCFA, and lesion location, low local ESS adds significant and substantial incremental predictive value to identify high-risk untreated lesions likely to cause MACE during 3 year followup.

Published
2015
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25. ST-Segment Analysis in Ambulatory ECG (AECG or Holter) Monitoring in Patients with Coronary Artery Disease: Clinical Significance and Analytic Techniques

Author

Peter H. Stone

Subjects
medicine.medical_specialty, Adrenergic beta-Antagonists, Coronary Artery Disease, Coronary artery disease, Diltiazem, Articles Honoring Bruce Delmar, Physiology (medical), Internal medicine, Humans, Medicine, ST segment, Clinical significance, In patient, Hypolipidemic Agents, Randomized Controlled Trials as Topic, business.industry, Cardiovascular Agents, Signal Processing, Computer-Assisted, General Medicine, Prognosis, medicine.disease, Ambulatory ECG, Treatment Outcome, Electrocardiography, Ambulatory, Cardiology, Drug Therapy, Combination, Amlodipine, Cardiology and Cardiovascular Medicine, business, Holter monitoring
Published
2005
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26. Abstract 17259: Differential Changes in Plaque Behind the Stent After Bare-Metal and Drug-Eluting Stent Implantation in Humans: Implications for In-Stent Restenosis?

Author

Ioannis Andreou, Koki Shishido, Antonios P Antoniadis, Saeko Takahashi, Masaya Tsuda, Michail I Papafaklis, Shigeru Saito, Ahmet U Coscun, Charles L Feldman, and Peter H Stone

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Background: The natural history and the role of the atherosclerotic plaque located behind the stent (PBS) are still poorly understood. We evaluated the serial changes in PBS following bare-metal (BMS) compared with first-generation drug-eluting stent (DES) implantation and the impact of these changes on in-stent neointimal hyperplasia (NIH). Methods: 3D coronary reconstruction by angiography and intravascular ultrasound were serially performed after intervention and at 6- to 10-month follow-up in 157 Japanese patients treated with BMS (n=90) and DES (n=98; 68 sirolimus-eluting and 30 paclitaxel-eluting stents) included in the PREDICTION Study. Each reconstructed stented coronary artery was divided into consecutive 1.5-mm segments. External elastic lamina, lumen, stent, and PBS area were measured for each segment at both baseline and follow-up. At follow-up NIH area was assessed. Due to the very low rate of events in our population we used significant NIH (defined as NIH area >50% of stent area) as a binary anatomic outcome. Results: Patient, lesion, and stent characteristics were comparable between BMS and DES. There was a significant decrease in PBS area after BMS (median relative change: -7.2%, IQR -19.3 to 5.2%, p Conclusions: The PBS significantly decreased 6 to 10 months after BMS implantation, whereas after DES it increased. The decrease in PBS area was significantly associated with the development of NIH at follow-up in both stent types. These findings raise the possibility of a communication between the lesion within the stent and the underlying native atherosclerotic plaque, and may have important implications regarding the pathobiology of in-stent restenosis.

Published
2014
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28. ACC/AHA guidelines for ambulatory electrocardiography

Author

Michael H Crawford, Steven J Bernstein, Prakash C Deedwania, John P DiMarco, Kevin J Ferrick, Arthur Garson, Lee A Green, H.Leon Greene, Michael J Silka, Peter H Stone, Cynthia M Tracy, Raymond J Gibbons, Joseph S Alpert, Kim A Eagle, Timothy J Gardner, Gabriel Gregoratos, Richard O Russell, Thomas J Ryan, and Sidney C Smith

Subjects
medicine.medical_specialty, medicine.diagnostic_test, Cardiac pacing, Task force, business.industry, Guideline, CARDIAC THERAPY, Internal medicine, medicine, Cardiology, business, Cardiology and Cardiovascular Medicine, Electrocardiography, Ambulatory electrocardiography
Published
1999
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29. Exercise Stress Testing for T Wave Alternans to Expose Latent Electrical Instability

Author

Richard L. Verrier and Peter H. Stone

Subjects
Exercise stress testing, medicine.medical_specialty, Communication, medicine.diagnostic_test, business.industry, T wave alternans, EXPOSE, Physiology (medical), Internal medicine, medicine, Cardiology, Electrical instability, Electrical conduction system of the heart, Cardiology and Cardiovascular Medicine, business, Electrocardiography
Published
1997
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30. Comparison of subgroups assigned to medical regimens used to suppress cardiac ischemia (the Asymptomatic Cardiac Ischemia Pilot [ACIP] study)

Author

Craig M. Pratt, Robert P. McMahon, Sidney Goldstein, Carl J. Pepine, Thomas C. Andrews, Ihor Dyrda, William H. Frishman, Nancy L. Geller, James A. Hill, Nancy A. Morgan, Peter H. Stone, Geneil L. Knatterud, George Sopko, C.Richard Conti, and null The ACIP Investigators

Subjects
Male, medicine.medical_specialty, Time Factors, Nifedipine, Myocardial Ischemia, Ischemia, Pilot Projects, Isosorbide Dinitrate, Angina Pectoris, Angina, Diltiazem, Heart Rate, Internal medicine, medicine, Humans, Prospective Studies, cardiovascular diseases, ST depression, Exercise Tolerance, business.industry, Middle Aged, medicine.disease, Atenolol, Case-Control Studies, Delayed-Action Preparations, Anesthesia, Ambulatory, Electrocardiography, Ambulatory, Exercise Test, Cardiology, Drug Therapy, Combination, Female, medicine.symptom, Isosorbide dinitrate, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

This report focuses on the subset of 235 patients from the Asymptomatic Cardiac Ischemia Pilot (ACIP) study receiving randomly assigned medical therapy to treat angina and suppress ischemia detected on ambulatory electrocardiography: 121 patients received the sequence of atenolol and nifedipine, and 114 diltiazem and isosorbide dinitrate. After 12 weeks of therapy, the primary end point (absence of ambulatory electrocardiographic (ECG) ischemia and no clinical events) was reached in 47% of atenolol/nifedipine- versus 31% of diltiazem/isosorbide dinitrate-treated patients (adjusted p = 0.03). A trend to increased exercise time to ST depression was seen in the atenolol and nifedipine versus diltiazem and isosorbide dinitrate regimens (median treadmill duration 5.8 vs 4.8 minutes; p = 0.04). However, when adjusted for baseline imbalances in ambulatory ECG ischemia, the 2 medical combinations were similar in suppression of ambulatory ECG ischemia. In both medication regimens, an association between mean heart rate and ischemia on ambulatory electrocardiography after 12 weeks of treatment was observed so that patients on either regimen with a mean heart rate80 beats/min had ischemia detectable almost twice as often as those with a mean heart rate70 beats/min (p0.001).

Published
1996
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31. T-Wave Alternans During Ambulatory Ischemia in Patients with Stable Coronary Disease

Author

Richard L. Verrier, B S Gail MacCallum, Peter H. Stone, and Bruce D. Hearing

Subjects
medicine.medical_specialty, business.industry, medicine.medical_treatment, Ischemia, General Medicine, T wave alternans, Placebo, medicine.disease, Sudden death, Angina, Physiology (medical), Internal medicine, Angioplasty, Anesthesia, Ambulatory, medicine, Cardiology, ST segment, Cardiology and Cardiovascular Medicine, business
Abstract

Background: T-wave alternans is a marker of vulnerability to ventricular tachyarrhythmias and has been documented during myocardial ischemia associated with angioplasty, bypass graft occlusion, and episodes of Prinzmetal's variant angina. We examined whether this phenomenon was present during ambulatory ischemia in ten patients randomly selected from the placebo phase of the Angina and Silent Ischemia Study [ASIS]. Methods: The eligibility criteria for participation in the ASIS study were stable coronary disease, a positive exercise stress test, and verified ischemic episodes during ambulatory ECG (AECG) monitoring. For each patient, one ischemic episode was analyzed which met the criteria of > 2-mm ST segment depression for > 3 minutes with a relatively stable ST segment baseline of > 1 hour preceding the index episode. T-wave alternans was measured using the spectral analytical technique of complex demodulation. Results: In the stable coronary patients of the ASIS trial, we found that T-wave alternans magnitude nearly tripled from 0.27 ± 0.02 mV × ms before ischemia onset to 0.77 ± 0.08 mV × ms (P 2 mm and the ischemia-induced increase in T-wave alternans. Conclusions: We conclude that T-wave alternans often occurs in association with ambulatory ischemia. Thus, risk assessment in stable coronary patients may be enhanced by monitoring both ST segment deviation and T-wave alternans as they measure relevant but fundamentally different electrophysiological properties.

Published
1996
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32. Frequency Response Characteristics Required for Detection of T-Wave Alternans During Ambulatory ECG Monitoring

Author

Bruce D. Hearing, Peter H. Stone, and Richard L. Verrier

Subjects
medicine.medical_specialty, Frequency response, business.industry, Ventricular Tachyarrhythmias, General Medicine, T wave alternans, Signal, Sudden death, Ambulatory ECG, Physiology (medical), Distortion, Internal medicine, medicine, Cardiology, Cardiology and Cardiovascular Medicine, business
Abstract

Background: T-wave alternans has been increasingly implicated as a potential marker of vulnerability to ventricular tachyarrhythmias in both experimental and clinical investigations. However, the suitability of ambulatory ECG (AECG) recorders for monitoring this parameter has not been systematically studied. Methods: We evaluated the frequency response characteristics and performance in monitoring a computer simulated alternans signal in three brands of amplitude-modulated (AM) and one frequency-modulated (FM) recorder and compared the results to those of the reference digital AECG unit. Results: A common feature of the AM recorders was distortion due to electronic head resonance, particularly at heart rates in the range of 60–100 beats/min. The maximum distortion of T-wave morphology by the AM units was —6% to +28%. Conclusions: We conclude that digital and FM recorders are preferable for AECG monitoring of T-wave alternans. AM recorders can be used if the distortion is not excessive.

Published
1996
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33. Abstract 347: Early Drug-Induced Inhibition of Proatherogenic Genes in Coronary Regions of Low Endothelial Shear Stress in Diabetic Hyperlipidemic Juvenile Swine

Author

Michail I Papafaklis, Konstantinos C Koskinas, Galina K Sukhova, Aaron B Baker, Antonios P Antoniadis, Ahmet U Coskun, Joseph W Franses, Saeko Takahashi, Elazer R Edelman, Peter H Stone, and Charles L Feldman

Subjects
Cardiology and Cardiovascular Medicine
Abstract

Introduction: Low endothelial shear stress (ESS) activates pro-inflammatory pathways and is a powerful instigator of atherogenesis. Angiotensin receptor blockers and statins have been associated with anti-inflammatory actions in advanced plaques. However, their effect on the earliest pathobiologic manifestations of atherosclerosis has not been studied. We tested the hypothesis that valsartan (V) or V plus simvastatin (V/S) exerts an early vasculoprotective effect in coronary regions exposed to low ESS in a porcine model of human-like atherosclerosis. Methods: Twelve diabetic-hyperlipidemic swine (age: 3 mo) were grouped into controls (n=4), and those treated with V (320 mg; n=4) or V/S (320/40 mg; n=4). 3D reconstruction of coronary arteries by angiography and intravascular ultrasound was performed in vivo at 4 (baseline) and 8 (follow-up) wks post-induction. Baseline local ESS was calculated by computational fluid dynamics and 3 mm segments with low (≤1.2 Pa; n=46) or higher (>1.2 Pa; n=66) ESS were identified. Coronary arteries were harvested at follow-up. qRT-PCR was used for assessing the expression of intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), LDL receptor and lipoprotein-associated phospholipase-A 2 (LpPLA 2 ). Results: The upregulation of ICAM-1, MCP-1, LDL receptor (p2 (p Conclusion: V and V/S attenuate the proatherogenic effects of low ESS within only 8 wks. These results suggest a drug-induced mechanism of regional atheroprotection early in the natural history of coronary artery disease.

Published
2012
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34. Abstract 515: Increased Adventitial Inflammation Occurs in Regions of Low Endothelial Shear Stress in a Swine Model of Coronary Atherosclerosis

Author

Antonios P Antoniadis, Michail I Papafaklis, Yiannis S Chatzizisis, Galina K Sukhova, Saeko Takahashi, Masaya Tsuda, Ahmet U Coskun, Peter H Stone, and Charles L Feldman

Subjects
Cardiology and Cardiovascular Medicine
Abstract

Introduction: Plaque inflammation is a critical step in the initiation and progression of atherosclerosis. Such inflammation is thought to originate from the luminal surface of plaque and infiltrate the intima-media in advanced lesions. Low endothelial shear stress (ESS) is known to induce intima-media inflammation and plaque growth. In this study we investigated in-vivo the hypothesis that low ESS induces also adventitial inflammation. Methods: We studied 11 swine at 23 (baseline) and 30 (followup) weeks after the induction of diabetes and hyperlipidemia. Using angiography and intravascular ultrasound data, we performed 3D coronary reconstruction of coronary arteries and calculated the ESS with computational fluid dynamics. In 56 segments, we assessed the adventitial inflammatory (CD45) and antigen-presenting (MHC-II) cell content at followup with immunohistochemistry. Segments were classified as low (≤ 1 Pa) or higher (>1 Pa) ESS. Results: MHC-II content in the adventitia (1.3±0.3%) was higher than in the media (0.3±0.1%, p Conclusion: Although total inflammation is not dependent on ESS, low ESS induces higher adventitial activated inflammatory cell content, as assessed by MHC-II immunostaining. This, in conjunction with the higher MHC-II content in the adventitia than in the media and the presence of an intact IEL suggests an additional source of inflammation in low-ESS plaque regions, originating from the vessel outer wall. The induction of neovascularization possibly accounts for this phenomenon.

Published
2012
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35. Management of the Patient with Asymptomatic Aortic Stenosis

Author

Peter H. Stone

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, Time Factors, medicine.medical_treatment, Population, Disease, Asymptomatic, Sudden death, Aortic valve replacement, Valve replacement, Internal medicine, medicine, Humans, Age of Onset, education, Aged, education.field_of_study, business.industry, Aortic Valve Stenosis, Middle Aged, medicine.disease, Stenosis, Heart Valve Prosthesis, Etiology, Cardiology, Surgery, medicine.symptom, Cardiology and Cardiovascular Medicine, business
Abstract

The etiology of acquired aortic stenosis (AS) has changed dramatically as socioeconomic and hygienic conditions have improved and as the general population lives to an older age. Rheumatic disease was responsible for most cases of AS until a few decades ago, whereas now most are due to calcific degenerative or bicuspid etiologies. There is a long latency period from the initial discovery of a murmur and first onset of symptoms. In studies representing clinical experience prior to the 1960s, the mean age at symptomatic presentation was 48 years, while in series representing experience up the 1980s, it was 61 years. The changing etiology of AS has Important implications for following patients with AS, and monitoring those who are discovered to have significant AS in the absence of symptoms. AS has become more a disease of the elderly, and it is the elderly patient with AS, especially those with calcific degenerative AS, who develop the most rapid and significant progression of their disease, present with symptoms of left ventricular (LV) failure, and are most likely to have critical outflow tract obstruction at the time of their presentation. Once symptoms develop, the outcome of patients with AS is quite poor: in early studies approximately 50% of such patients were dead at 5 years and 90% were dead at 10 years. Symptoms that represent LV failure, e.g., dyspnea, are associated with a worse survival (average survival 2 years) compared to symptoms that represent LV hypertrophy, e.g., angina or outflow obstruction, syncope (average survival 3 years). There is uniform agreement that once symptoms develop, patients with Significant AS should undergo valve replacement. Management of the asymptomatic patient with moderate-to-severe AS has been more problematic. Early studies suggested that sudden death could occur in even asymptomatic patients with severe AS, and recommended that prophylactic valve replacement be considered in this group. More recent studies, however, confirm that in the absence of symptoms, overall survival of patients with AS is similar to that predicted for age- and gender-matched control subjects. Although cardiac death occurs in approximately 2% to 4% of these patients, symptoms of AS have developed approximately 1 to 3 months before death in each documented case. The mortality associated with prophylactic aortic valve replacement is higher than the mortality associated with medical management of asymptomatic AS. In conclusion, aortic valve replacement should be deferred in patients with asymptomatic AS until the onset of symptoms. Patients with calcific degenerative AS and elderly patients with AS may have particularly rapid progression of AS and should have close follow-up. Since the interval between the onset of AS symptoms and cardiac death may be quite brief, all asymptomatic patients with significant AS should be followed closely for the onset of symptoms. (J Card Surg 1994;9[Suppl]:139–144)

Published
1994
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38. Contributors

Author

Joseph S. Alpert, Con Aroney, Philip L.G. Aylward, Sameer Bansilal, Gust H. Bardy, Philip Barter, George A. Beller, Rinaldo Bellomo, Tandeep Bhatti, Stefan Blankenberg, David Blythe, Pamela J. Bradshaw, David Brieger, Tom Briffa, Terence J. Campbell, Matthew A. Cavender, Derek P. Chew, Sharon Chih, Philip Cooke, Samir Damani, Timothy Davis, Rajinder K. Dhamija, Geoffrey A. Donnan, John T. Dowling, Jorge E. Echeverri, Hooi C. Ee, John W. Eikelboom, Nabil El-Sherif, Maros Elsik, Judith Finn, Keith A.A. Fox, Valentin Fuster, Alexander Gallus, Bernard J. Gersh, Ilan Goldenberg, Jonathan Golledge, Cindy L. Grines, Michel Haïssaguerre, Ian Hamilton-Craig, David L. Hare, Harvey S. Hecht, Siobhan Hickling, David Hillman, Kwok M. Ho, John D. Horowitz, Joseph Hung, Luan Tan Huynh, Ian Jacobs, Allan S. Jaffe, Konrad Jamrozik, Michael Jelinek, Nils P. Johnson, Desmond Julian, David Kaye, Till Keller, Anne M. Keogh, Leonard Kritharides, Henry Krum, Ashok Kumar, K. Lance Gould, Paul Langton, Mark J. Lennon, Harry Lowe, Peter Macdonald, Micha T. Maeder, Andrew Maiorana, Thomas H. Marwick, Jane McCrohon, Harry G. Mond, Arthur J. Moss, David Mountain, David Muller, Mark Newman, Mark Nidorf, E. Magnus Ohman, Bertram Pitt, Bradley M. Power, Abhiram Prasad, David Richards, James Robinson, David L. Ross, Karin Schenck-Gustafsson, Marion A. Simpson, Peter R. Sinnaeve, Graeme Sloman, Paul D. Stein, Paul Stobie, Peter H. Stone, Rajesh Subbiah, David Taggart, Angus G. Thompson, Peter L. Thompson, Kristian Thygesen, Mark N. Toogood, Eric J. Topol, Luke Torre, Frans Van de Werf, Rukshen Weerasooriya, Harvey White, Alexander B. Willson, and Ian F. Yusoff

Published
2011
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41. In vivo assessment of local intravascular hemodynamics and arterial morphology to investigate vascular outcomes: a growing field coming of age

Author

Peter H, Stone and Charles L, Feldman

Subjects
Sirolimus, Hemodynamics, Cardiovascular Agents, Drug-Eluting Stents, Arteries, Coronary Angiography, Prosthesis Design, Coronary Vessels, Carotid Arteries, Treatment Outcome, Metals, Predictive Value of Tests, Coronary Circulation, Image Interpretation, Computer-Assisted, Humans, Stents, Everolimus, Angioplasty, Balloon, Coronary, Ultrasonography, Interventional
Published
2010

42. Ischemia detected on continuous electrocardiography after acute coronary syndrome: observations from the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction 36) trial

Author

Benjamin M, Scirica, David A, Morrow, Andrzej, Budaj, Anthony J, Dalby, Satishkumar, Mohanavelu, Jie, Qin, Julian, Aroesty, Chester M, Hedgepeth, Peter H, Stone, and Eugene, Braunwald

Subjects
Male, Myocardial Infarction, Middle Aged, Risk Assessment, Piperazines, Treatment Outcome, Ranolazine, Risk Factors, Electrocardiography, Ambulatory, Humans, Acetanilides, Female, Acute Coronary Syndrome, Aged
Abstract

The purpose of this study was to assess the relationship between ischemia detected on continuous electrocardiographic (cECG) recording and cardiovascular outcomes after acute coronary syndrome (ACS).The small size of prior studies evaluating cECG prevented full evaluation of the risk associated with ischemia across subpopulations and compared with other methods of risk stratification. Ranolazine, a new antianginal agent, reduces ischemic symptoms in patients with chronic angina and after ACS but the anti-ischemic effect, as detected by cECG, is not known.In all, 6,560 patients hospitalized with non-ST-segment elevation ACS were randomly assigned to ranolazine or placebo in the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction 36) trial. The cECG was performed for 7 days after randomization. Outcomes were followed for a median of 348 days. Clinical events that occurred during cECG recording were excluded from analysis.A total of 6,355 (97%) patients had cECG recordings evaluable for ischemia analysis. Patients withor=1 episode of ischemia on cECG (n = 1,271, 20%) were at increased risk of cardiovascular death (7.7% vs. 2.7%, p0.001), MI (9.4% vs. 5.0%, p0.001), and recurrent ischemia (17.5% vs. 12.3%, p0.001). The relationship with cardiovascular death was independent of baseline characteristics or elevated biomarkers (adjusted hazard ratio: 2.46, p0.001). Ischemia on cECG was associated with significantly worse outcomes in several subgroups. Ranolazine did not reduce the rate of ischemia detected on cECG (19.9% vs. 21.0%, hazard ratio: 0.93, p = 0.21).In more than 6,300 patients with ACS, ischemia detected on cECG occurred frequently and was strongly and independently associated with poor cardiovascular outcomes, including cardiovascular death. Continuous ECG monitoring to detect ischemia after ACS may help to identify patients at increased risk. (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST Elevation Acute Coronary Syndromes [MERLIN]; NCT00099788).

Published
2008

43. Abstract 2850: Morphological Variability: A New Electrocardiographic Technique for Risk Stratification After NSTEACS

Author

Zeeshan Syed, Collin M Stultz, Benjamin M Scirica, Christopher P Cannon, Khaled Attia, Irina O Stebletsova, Satishkumar Mohanavelu, Peter H Stone, and John V Guttag

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Background : ECG parameters such as low heart rate variability (HRV) identify patients at high risk post-ACS. We recently developed morphological variability (MV), a novel technique that quantifies differences in the morphology of entire beats using a dynamic time-warping algorithm. MV incorporates strictly more information than HRV, potentially offering a more complete evaluation of the ECG. We assessed the relationship among MV, HRV, and outcomes after NSTEACS. Methods: MV and HRV were calculated in 863 pts from the DISPERSE2 trial using the first 24 hrs of continuous ECG (CECG) after randomization for NSTEACS. Using each measure, pts were split into high and low variability groups (cutpoint for HRV (SDNN)= 75ms and for MV=0.7). Ischemia on CECG was defined as ≥1mm ST dep lasting ≥1min. Results: A total of 144 (16.7%) pts had high MV and 58 (6.7%) had low HRV. Pts with high MV experienced higher rates of death, death/MI/severe recurrent ischemia (SRI), and ischemia detected on CECG compared to low MV. (Table-Figure ) This relationship remained consistent in pts with no ischemia on CECG (hazard ratio for D/MI/SRI =2.5, p=0.016). There was no difference in mortality or ischemia on CECG in pts with low HRV v high HRV, but pts with low HRV did have higher rates of death/MI/SRI. (Table) Conclusions: MV correlates significantly with poor cardiovascular outcomes, including death, after NSTEACS, even after controlling for other high risk features and even among pts without electrocardiographic evidence of ischemia. MV may offer a new non-invasive measure for risk stratification after ACS.

Published
2007
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44. Abstract 123: Role of Valsartan (V) Alone or in Combination with Simvastatin (S) in Reducing Inflammation of Thin Cap Fibroatheromas

Author

Yiannis S Chatzizisis, Michael Jonas, Ahmet U Coskun, Roy Beigel, Benjamin V Stone, Charles Maynard, Ross G Gerrity, William Daley, Campbell Rogers, Elazer R Edelman, Charles L Feldman, and Peter H Stone

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Objectives: We investigated the role of V alone or in combination with S on the histomorphologic characteristics of thin cap fibroatheromas (TCFAs), and tested the hypothesis that V or VS attenuate the proinflammatory effect of low endothelial shear stress (ESS). We used vascular profiling of swine coronary arteries for in vivo assessment of ESS to prospectively identify these low ESS areas that are prone to develop TCFAs. Methods: 12 diabetic hyperlipidemic swine were allocated into 3 treatment groups: placebo (P, n=4), V (n=4) and VS (n=4). Blood pressure, serum cholesterol and glucose were similar between the treatment groups. IVUS-based geometrically correct 3D reconstruction of the coronary arteries was performed at baseline (wk 23) and follow up (wk 30). Baseline ESS was calculated using computational fluid dynamics and plaque-free subsegments of interest were identified (n=109). Coronary arteries (n=31) were harvested at follow up, cryosectioned at the subsegments of interest and stained histologically. Intima/media ratio and inflammation (CD45) were quantified. Lesions were classified into atheromas without evidence of fibrous cap (n=82) and TCFAs (n=60). Results: V alone or in combination with S reduced the amount of plaque inflammation, particularly in TCFAs (Fig A ). V and VS attenuated the proinflammatory effect of local low ESS compared to P (Fig B ). Conclusion: V alone or in combination with S exerts a stabilizing effect of reducing plaque inflammation, even in high-risk regions with low ESS. These results suggest a mechanism of regional atheroprotection associated with V or VS.

Published
2007
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46. Antianginal efficacy of ranolazine when added to treatment with amlodipine: the ERICA (Efficacy of Ranolazine in Chronic Angina) trial

Author

Peter H, Stone, Nikolay A, Gratsiansky, Alexey, Blokhin, I-Zu, Huang, and Lixin, Meng

Subjects
Male, Incidence, Vasodilator Agents, Coronary Disease, Middle Aged, Piperazines, Angina Pectoris, Nitroglycerin, Treatment Outcome, Double-Blind Method, Ranolazine, Chronic Disease, Humans, Acetanilides, Drug Therapy, Combination, Female, Amlodipine, Aged
Abstract

The purpose of this study was to determine if ranolazine improves angina in stable coronary patients with persisting symptoms despite maximum recommended dose of amlodipine.Ranolazine is a unique antianginal agent that has been effective in stable angina, but it has not been studied in the setting of maximum recommended doses of conventional antianginal agents.Stable patients with coronary disease andor =3 anginal attacks per week despite maximum recommended dosage of amlodipine (10 mg/day) were randomized to 1,000 mg ranolazine or placebo twice a day for 6 weeks. Primary end point was the frequency of angina episodes per week during the double-blind treatment phase. Efficacy was also assessed by nitroglycerin consumption per week and the Seattle Angina Questionnaire (SAQ). Adjustment for multiple testing of secondary end points used a hierarchic closed testing procedure. Efficacy was assessed in subgroups based on baseline angina frequency, concomitant long-acting nitrate use, gender, and age. Safety was assessed by adverse events and electrocardiogram evaluations.A total of 565 patients were randomized: 281 patients to ranolazine and 284 patients to placebo. Baseline characteristics were similar between treatment groups. At baseline, angina frequency averaged 5.63 +/- 0.18 episodes/week, and nitroglycerin consumption averaged 4.72 +/- 0.21 tablets/week. Compared with placebo, ranolazine significantly reduced frequency of angina episodes (2.88 +/- 0.19 on ranolazine vs. 3.31 +/- 0.22 on placebo; p = 0.028) and nitroglycerin consumption (2.03 +/- 0.20 on ranolazine vs. 2.68 +/- 0.22; p = 0.014), with treatment effect that appeared consistent across subgroups. The median angina weekly episode rate at baseline was 4.5 per week. Subgroup analysis showed statistically significant reductions of angina frequency, nitroglycerin use, and SAQ angina frequency for patients with a baseline frequency4.5 per week but only of angina frequency for those with baseline frequencyor =4.5 per week. Patients with more frequent angina appeared to have a more pronounced treatment effect. No hemodynamic changes were observed. Ranolazine was well tolerated.Ranolazine significantly reduced frequency of angina and nitroglycerin consumption compared with placebo and was well tolerated. (The ERICA [Efficacy of Ranolazine In Chronic Angina] Trial; http://clinicaltrials.gov; NCT00091429).

Published
2006

47. A randomized trial to evaluate the relative protection against post-percutaneous coronary intervention microvascular dysfunction, ischemia, and inflammation among antiplatelet and antithrombotic agents: the PROTECT-TIMI-30 trial

Author

C Michael, Gibson, David A, Morrow, Sabina A, Murphy, Theresa M, Palabrica, Lisa K, Jennings, Peter H, Stone, Henry H, Lui, Thomas, Bulle, Nasser, Lakkis, Richard, Kovach, David J, Cohen, Polly, Fish, Carolyn H, McCabe, and Eugene, Braunwald

Subjects
Inflammation, Male, Heparin, Myocardial Infarction, Myocardial Ischemia, Eptifibatide, Platelet Glycoprotein GPIIb-IIIa Complex, Syndrome, Hirudins, Middle Aged, Postoperative Hemorrhage, Antithrombins, Peptide Fragments, Recombinant Proteins, Postoperative Complications, Fibrinolytic Agents, Acute Disease, Humans, Drug Therapy, Combination, Female, Angina, Unstable, Angioplasty, Balloon, Coronary, Enoxaparin, Peptides
Abstract

The goal of this study was to evaluate glycoprotein IIb/IIIa inhibition with eptifibatide when administered with indirect thrombin inhibition as compared with monotherapy with direct thrombin inhibition with bivalirudin among patients with non-ST-segment elevation acute coronary syndromes (ACS).The optimal combination of antiplatelet and antithrombin regimens that maximizes efficacy and minimizes bleeding among patients with non-ST-segment elevation ACS undergoing percutaneous coronary intervention (PCI) is unclear.A total of 857 patients with non-ST-segment elevation ACS were assigned randomly to eptifibatide + reduced dose unfractionated heparin (n = 298), eptifibatide + reduced-dose enoxaparin (n = 275), or bivalirudin monotherapy (n = 284).Among angiographically evaluable patients (n = 754), the primary end point of post-PCI coronary flow reserve was significantly greater with bivalirudin (1.43 vs. 1.33 for pooled eptifibatide arms, p = 0.036). Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade more often was normal with eptifibatide treatment compared with bivalirudin (57.9% vs. 50.9%, p = 0.048). The duration of ischemia on continuous Holter monitoring after PCI was significantly longer among patients treated with bivalirudin (169 vs. 36 min, p = 0.013). There was no excess of TIMI major bleeding among patients treated with eptifibatide compared with bivalirudin (0.7%, n = 4 vs. 0%, p = NS), but TIMI minor bleeding was increased (2.5% vs. 0.4%, p = 0.027) as was transfusion (4.4% to 0.4%, p0.001).Among moderate- to high-risk patients with ACS undergoing PCI, coronary flow reserve was greater with bivalirudin than eptifibatide. Eptifibatide improved myocardial perfusion and reduced the duration of post-PCI ischemia but was associated with higher minor bleeding and transfusion rates. Ischemic events and biomarkers for myonecrosis, inflammation, and thrombin generation did not differ between agents.

Published
2005

48. Effect of reducing interns' weekly work hours on sleep and attentional failures

Author

Steven W, Lockley, John W, Cronin, Erin E, Evans, Brian E, Cade, Clark J, Lee, Christopher P, Landrigan, Jeffrey M, Rothschild, Joel T, Katz, Craig M, Lilly, Peter H, Stone, Daniel, Aeschbach, Charles A, Czeisler, and C A, Czeisler

Subjects
Gerontology, Adult, Male, medicine.medical_specialty, Polysomnography, education, Graduate medical education, Personnel Staffing and Scheduling, Workload, Work hours, law.invention, law, Intensive care, Work Schedule Tolerance, medicine, Internal Medicine, Humans, Attention, health care economics and organizations, Accreditation, medicine.diagnostic_test, business.industry, Obstetrics and Gynecology, Internship and Residency, General Medicine, Intensive care unit, humanities, Schedule (workplace), Sleep deprivation, Intensive Care Units, Family medicine, Physical therapy, Sleep Deprivation, Female, Sleep (system call), medicine.symptom, business, Sleep
Abstract

background Knowledge of the physiological effects of extended (24 hours or more) work shifts in postgraduate medical training is limited. We aimed to quantify work hours, sleep, and attentional failures among first-year residents (postgraduate year 1) during a traditional rotation schedule that included extended work shifts and during an intervention schedule that limited scheduled work hours to 16 or fewer consecutive hours. methods Twenty interns were studied during two three-week rotations in intensive care units, each during both the traditional and the intervention schedule. Subjects completed daily sleep logs that were validated with regular weekly episodes (72 to 96 hours) of continuous polysomnography (r=0.94) and work logs that were validated by means of direct observation by study staff (r=0.98). results Seventeen of 20 interns worked more than 80 hours per week during the traditional schedule (mean, 84.9; range, 74.2 to 92.1). All interns worked less than 80 hours per week during the intervention schedule (mean, 65.4; range, 57.6 to 76.3). On average, interns worked 19.5 hours per week less (P

Published
2004

50. Optimizing ambulatory ECG monitoring of T-wave alternans for arrhythmia risk assessment

Author

Richard L, Verrier, Bruce D, Nearing, and Peter H, Stone

Subjects
Practice Guidelines as Topic, Electrocardiography, Ambulatory, Humans, Arrhythmias, Cardiac, Risk Assessment
Abstract

Considerable scientific data support the potential value of T-wave alternans (TWA) as an index of vulnerability to ventricular fibrillation. This chapter summarizes our state of knowledge regarding the use of routine ambulatory ECGs to evaluate TWA and discusses recent methodologic approaches designed to optimize AECG-based TWA analysis for arrhythmia risk stratification. Newer methods, including the nonspectral technique of Modified Moving Average analysis, appear promising in detecting TWA during the changing conditions associated with daily activities. The Modified Moving Average approach does not require specialized electrodes and is not encumbered by the need to achieve target heart rates, as is the case for conventional spectral-based methods. Guidelines are provided for evaluating latent cardiac electrical instability using AECG-based TWA testing. These recent developments make possible the TWA analysis of ambulatory ECGs not only in prospective trials but also in vast stores of archival data.

Published
2002

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