Jeffrey C. Trost
Johns Hopkins University
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Circulation | 2011
L. David Hillis; Peter K. Smith; John A. Bittl; Charles R. Bridges; John G. Byrne; Joaquin E. Cigarroa; Verdi J. DiSesa; Loren F. Hiratzka; Adolph M. Hutter; Michael E. Jessen; Ellen C. Keeley; Stephen J. Lahey; Richard A. Lange; Martin J. London; Michael J. Mack; Manesh R. Patel; John D. Puskas; Joseph F. Sabik; Ola A. Selnes; David M. Shahian; Jeffrey C. Trost; Michael D. Winniford; Alice K. Jacobs; Jeffrey L. Anderson; Nancy M. Albert; Mark A. Creager; Steven M. Ettinger; Robert A. Guyton; Jonathan L. Halperin; Judith S. Hochman
L. David Hillis, MD, FACC, Chair†; Peter K. Smith, MD, FACC, Vice Chair*†; Jeffrey L. Anderson, MD, FACC, FAHA*‡; John A. Bittl, MD, FACC§; Charles R. Bridges, MD, SCD, FACC, FAHA*†; John G. Byrne, MD, FACC†; Joaquin E. Cigarroa, MD, FACC†; Verdi J. DiSesa, MD, FACC†; Loren F. Hiratzka, MD, FACC, FAHA†; Adolph M. Hutter, Jr, MD, MACC, FAHA†; Michael E. Jessen, MD, FACC*†; Ellen C. Keeley, MD, MS†; Stephen J. Lahey, MD†; Richard A. Lange, MD, FACC, FAHA†§; Martin J. London, MD ; Michael J. Mack, MD, FACC*¶; Manesh R. Patel, MD, FACC†; John D. Puskas, MD, FACC*†; Joseph F. Sabik, MD, FACC*#; Ola Selnes, PhD†; David M. Shahian, MD, FACC, FAHA**; Jeffrey C. Trost, MD, FACC*†; Michael D. Winniford, MD, FACC†
Journal of the American College of Cardiology | 2011
L. David Hillis; Peter K. Smith; Jeffrey L. Anderson; John A. Bittl; Charles R. Bridges; John G. Byrne; Joaquin E. Cigarroa; Verdi J. DiSesa; Loren F. Hiratzka; Adolph M. Hutter; Michael E. Jessen; Ellen C. Keeley; Stephen J. Lahey; Richard A. Lange; Martin J. London; Michael J. Mack; Manesh R. Patel; John D. Puskas; Joseph F. Sabik; Ola A. Selnes; David M. Shahian; Jeffrey C. Trost; Michael D. Winniford; Alice K. Jacobs; Nancy M. Albert; Mark A. Creager; Steven M. Ettinger; Robert A. Guyton; Jonathan L. Halperin; Judith S. Hochman
Alice K. Jacobs, MD, FACC, FAHA, Chair Jeffrey L. Anderson, MD, FACC, FAHA, Chair-Elect Nancy Albert, PhD, CCNS, CCRN, FAHA Mark A. Creager, MD, FACC, FAHA Steven M. Ettinger, MD, FACC Robert A. Guyton, MD, FACC Jonathan L. Halperin, MD, FACC, FAHA Judith S. Hochman, MD, FACC, FAHA
The Journal of Thoracic and Cardiovascular Surgery | 2012
L. David Hillis; Peter K. Smith; Jeffrey L. Anderson; John A. Bittl; Charles R. Bridges; John G. Byrne; Joaquin E. Cigarroa; Verdi J. DiSesa; Loren F. Hiratzka; Adolph M. Hutter; Michael E. Jessen; Ellen C. Keeley; Stephen J. Lahey; Richard A. Lange; Martin J. London; Michael J. Mack; Manesh R. Patel; John D. Puskas; Joseph F. Sabik; Ola A. Selnes; David M. Shahian; Jeffrey C. Trost; Michael D. Winniford; Alice K. Jacobs; Nancy M. Albert; Mark A. Creager; Steven M. Ettinger; Robert A. Guyton; Jonathan L. Halperin; Judith S. Hochman
2011;58;2584-2614; originally published online Nov 7, 2011; J. Am. Coll. Cardiol. Winniford Joseph F. Sabik, Ola Selnes, David M. Shahian, Jeffrey C. Trost, and Michael D. A. Lange, Martin J. London, Michael J. Mack, Manesh R. Patel, John D. Puskas, Adolph M. Hutter, Jr, Michael E. Jessen, Ellen C. Keeley, Stephen J. Lahey, Richard Bridges, John G. Byrne, Joaquin E. Cigarroa, Verdi J. DiSesa, Loren F. Hiratzka, L. David Hillis, Peter K. Smith, Jeffrey L. Anderson, John A. Bittl, Charles R. Surgeons Surgery, Society of Cardiovascular Anesthesiologists, and Society of Thoracic Developed in Collaboration With the American Association for Thoracic Foundation/American Heart Association Task Force on Practice Guidelines Executive Summary: A Report of the American College of Cardiology 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: This information is current as of January 22, 2012 http://content.onlinejacc.org/cgi/content/full/58/24/2584 located on the World Wide Web at: The online version of this article, along with updated information and services, is
Heart | 2010
Armin Arbab-Zadeh; John Texter; K. M. Ostbye; Kakuya Kitagawa; Jeffery Brinker; Richard T. George; Julie M. Miller; Jeffrey C. Trost; Richard A. Lange; Joăo A.C. Lima; Albert C. Lardo
Background Quantitative coronary angiography (QCA) has inherent limitations for displaying complex vascular anatomy, yet it remains the gold standard for stenosis quantification. Objective To investigate the accuracy of stenosis assessment by multi-detector computed tomography (MDCT) and QCA compared to known dimensions. Methods Nineteen acrylic coronary vessel phantoms with precisely drilled stenoses of mild (25%), moderate (50%) and severe (75%) grade were studied with 64-slice MDCT and digital flat panel angiography. Fifty-seven stenoses of circular and non-circular shape were imaged with simulated cardiac motion (60 bpm). Image acquisition was optimised for both imaging modalities, and stenoses were quantified by blinded expert readers using electronic callipers (for MDCT) or lumen contour detection software (for QCA). Results Average difference between true and measured per cent diameter stenosis for QCA was similar compared to MDCT: 7 (±6)% vs 7 (±5)% (p=0.78). While QCA performed better than MDCT in stenoses with circular lumen (mean error 4 (±3)% vs 7 (±6)%, p<0.01), MDCT was superior to QCA for evaluating stenoses with non-circular geometry (mean error 10 (±7)% vs 7 (±5)%, p<0.05). In such lesions, QCA underestimated the true diameter stenosis by >20% in 9 of 27 (33%) vs 1 of 29 (3%) in lumen with circular geometry. Conclusions QCA often underestimates diameter stenoses in lumen with non-circular geometry. Compared to QCA, MDCT yields mildly greater measurement errors in perfectly circular lumen but performs better in non-circular lesions. These findings have implications for using QCA as the gold standard for stenosis quantification by MDCT.
Critical Care Medicine | 2011
Jeffrey C. Trost; Richard A. Lange
Objective:Acute coronary syndrome is a common cause of morbidity and mortality, both in the United States and worldwide. The goal of this review is to familiarize clinicians with recent information regarding the diagnosis and treatment of acute coronary syndrome. Data Sources:PubMed search and review of the relevant medical literature. Summary:Acute coronary syndrome encompasses three clinical diagnoses: unstable angina, non-ST-segment elevation myocardial infarction), and ST-segment elevation myocardial infarction. The definition, pathophysiology, clinical presentation, diagnosis, and treatment of unstable angina/non-ST-segment elevation myocardial infarction are reviewed here. Diagnosing unstable angina/non-ST-segment elevation myocardial infarction is a significant challenge in critically ill patients not initially suspected of having acute coronary syndrome (i.e., noncardiac intensive care unit patients), and diagnostic and treatment strategies for these patients have not been clearly established. Conclusions:Patients with acute coronary syndrome benefit from intensive medical therapy, including antianginal, antiplatelet, antithrombotic, and statin agents. Depending on their risk for future cardiovascular events as well as their risk of bleeding complications, patients may benefit from either an early invasive treatment strategy, in which routine coronary revascularization is performed, or a conservative strategy, in which revascularization is reserved for patients with recurrent or provocable cardiac ischemia.
American Journal of Cardiology | 2010
Drew E. Baldwin; J. Dawn Abbott; Jeffrey C. Trost; Helen Vlachos; Faith Selzer; Ruchira Glaser; Robert L. Wilensky; James Slater; Serge Doucet; Srihari S. Naidu; Herbert D. Aronow; David O. Williams
The effectiveness and safety of drug-eluting stents (DES) compared with bare-metal stents (BMS) in saphenous vein graft (SVG) disease remains unclear. In particular, there is a paucity of data on long-term outcomes. In this study, 395 patients enrolled in the National Heart, Lung, and Blood Institute Dynamic Registry who underwent stenting of SVG lesions with BMS (n = 192) from 1999 to 2006 or DES (n = 203) from 2004 to 2006 were analyzed. Patients were followed prospectively for the occurrence of cardiovascular events and death at 3 years. Patients treated with DES were more likely to have diabetes mellitus and other co-morbidities and previous percutaneous coronary intervention. Treated lesions in DES patients were more complex than those in BMS patients. At 3 years of follow-up, the adjusted risk for target vessel revascularization (hazard ratio 1.03, 95% confidence interval 0.65 to 1.62, p = 0.91) and death or myocardial infarction (hazard ratio 0.72, 95% confidence interval 0.49 to 1.04, p = 0.08) was similar in patients treated with DES and those treated with BMS. The combined outcome of death, myocardial infarction, or target vessel revascularization excluding periprocedural myocardial infarction was also similar (adjusted hazard ratio 0.82, 95% confidence interval 0.62 to 1.09, p = 0.16). In conclusion, this multicenter nonrandomized study of unselected patients showed no benefit of DES in SVG lesions, including no reduction in target vessel revascularization, compared with BMS at 3 years. An adequately powered randomized controlled trial is needed to determine the optimal stent type for SVG percutaneous coronary intervention.
The Cardiology | 2009
Armin Arbab-Zadeh; Benjamin D. Levine; Jeffrey C. Trost; Richard A. Lange; Ellen C. Keeley; L. David Hillis; Joaquin E. Cigarroa
Objectives: To assess the influence of acute hypoxemia on the dimensions of diseased and nondiseased coronary arterial segments in humans. Methods: In 18 subjects (age 53 ± 8 years) with known or suspected coronary artery disease, quantitative coronary angiography was performed before and after being randomly assigned to breathing (1) an inspired oxygen concentration (fraction of inspired oxygen, FIO2) of 21% (room air, RA) for 20 min (n = 4, controls) or (2) an FIO2 of 15 and 10% for 10 min each (corresponding to altitudes of 2,500 and 5,500 m, respectively; n = 14). Results: In the control subjects, no hemodynamic, oximetric or angiographic variable changed. In the 14 study subjects, the arterial partial pressure of oxygen averaged 85 ± 13 mm Hg on RA, 65 ± 15 mm Hg on 15% FIO2 and 44 ± 13 mm Hg on 10% FIO2. Average arterial segment diameter was 2.52 ± 0.63 mm on RA, 2.55 ± 0.62 mm on 15% FIO2 (not significant vs. RA) and 2.66 ± 0.66 mm on 10% FIO2 (p < 0.001 vs. RA). The increase in coronary arterial diameter with 10% FIO2 occurred only in normal segments (2.74 ± 0.64 vs. 2.97 ± 0.64 mm; p < 0.001), but not in diseased segments (2.34 ± 0.57 vs. 2.38 ± 0.55 mm; not significant). Conclusions: In humans, severe hypoxemia induces vasodilation of angiographically normal coronary arterial segments, whereas it causes no change in diseased segments.
American Journal of Physiology-heart and Circulatory Physiology | 2012
Harry A. Silber; Jeffrey C. Trost; Peter V. Johnston; W. Lowell Maughan; Nae Yuh Wang; Edward K. Kasper; Thomas R. Aversano; David E. Bush
It is often challenging to assess cardiac filling pressure clinically. An improved system for detecting or ruling out elevated cardiac filling pressure may help reduce hospitalizations for heart failure. The blood pressure response to the Valsalva maneuver reflects left heart filling pressure, but its underuse clinically may be due in part to lack of continuous blood pressure recording along with lack of standardization of expiratory effort. In this study, we tested whether Valsalva-induced changes in the pulse amplitude of finger photoplethysmography (PPG), a technology already widely available in medical settings, correlate with invasively measured left ventricular end-diastolic pressure (LVEDP). We tested 33 subjects before clinically scheduled cardiac catheterizations. A finger photoplethysmography waveform was recorded during a Valsalva effort of 20 mmHg expiratory pressure sustained for 10 s, an effort most patients can achieve. Pulse amplitude ratio (PAR) was calculated as the PPG waveform amplitude just before release of expiratory effort divided by the waveform amplitude at baseline. PAR was well correlated with LVEDP (r = 0.68; P < 0.0001). For identifying LVEDP > 15 mmHG, PAR > 0.4 was 85% sensitive [95% confidence interval (95CI): 54-97%] and 80% specific (95CI: 56-93%). In conclusion, finger PPG, a technology already ubiquitous in medical centers, may be useful for assessing clinically meaningful categories of left heart filling pressure, using simple analysis of the waveform after a Valsalva maneuver effort that most patients can achieve.
Circulation | 2018
John W. McEvoy; Khalil Ibrahim; Thomas S. Kickler; William Clarke; Rani K. Hasan; Matthew J. Czarny; Ali R. Keramati; Rakesh R. Goli; Travis P. Gratton; Jeffrey A. Brinker; Matthews Chacko; Chao-Wei Hwang; Peter V. Johnston; Julie M. Miller; Jeffrey C. Trost; William R. Herzog; Roger S. Blumenthal; David R. Thiemann; Jon R. Resar; Steven P. Schulman
Fentanyl is a potent opiate commonly administered during cardiac catheterization procedures in North America.1 The question of whether fentanyl could have adverse consequences in patients undergoing percutaneous coronary intervention (PCI) is raised by recent research demonstrating that intravenous morphine significantly delays the absorption of oral P2Y12 platelet inhibitors.2 The presumed mechanism is slowed gastric emptying. The single-center PACIFY trial (Platelet Aggregation With Ticagrelor Inhibition and Fentanyl; ClinicalTrials.gov. Unique identifier: NCT02683707) randomized adults undergoing clinically indicated elective coronary angiography to receive the procedure with or without intravenous fentanyl.3 The study was approved by the Johns Hopkins Medicine Institutional Review Board, and all participants provided written informed consent. Eligible adults had not received P2Y12 inhibitors for 14 days before enrollment. Other exclusion criteria included preprocedural treatment with oral anticoagulants or opiates, platelet count <100 000/mm3, and impaired renal or hepatic function. All participants received subcutaneous lidocaine and intravenous midazolam at the start of the catheterization procedure and as needed thereafter. Doses of all drugs were at the discretion of treating providers. Patients and outcomes assessors were blinded; treating providers were not. Participants who required PCI received an oral dose of 180 mg ticagrelor at the conclusion of diagnostic angiography. Blood samples were collected at baseline and 0.5, 1, 2, 4, and 24 hours after the …
Critical Care Medicine | 2012
Jeffrey C. Trost; Richard A. Lange
Objective:Familiarize clinicians with recent information regarding the diagnosis and treatment of ST-segment elevation myocardial infarction. Data Sources:PubMed search and review of relevant medical literature. Summary:Definition, pathophysiology, clinical presentation, diagnosis, and treatment of ST-segment elevation myocardial infarction are reviewed. Conclusions:Patients with ST-segment elevation myocardial infarction benefit from prompt reperfusion therapy. Adjunctive antianginal, antiplatelet, antithrombotic, beta blocker, angiotensin-converting enzyme inhibitor, and statin agents minimize ongoing cardiac ischemia, prevent thrombus propagation, and reduce the risk of recurrent cardiovascular events.