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1. Relationship Between Cardiac Structure and Function With Renal Function Trajectory and Outcomes in Patients With Heart Failure: Insights From the PARAGON-HF Trial

Author

Lu, Henri, Chatur, Safia, Lee, Sahmin, Inciardi, Riccardo M., Abanda, Martin, Mc Causland, Finnian R., Kalayci, Arzu, Taheri, Kimia Karimi, Shah, Amil M., Cikes, Maja, Claggett, Brian L., Prasad, Narayana, Lam, Carolyn S.P., O’Meara, Eileen, Wang, Xiaowen, McMurray, John J.V., Pfeffer, Marc A., Hegde, Sheila M., Solomon, Scott D., and Skali, Hicham

Published
2024
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2. Pharmacogenetics-guided dalcetrapib therapy after an acute coronary syndrome: the dal-GenE trial

Author

Tardif, Jean Claude, Pfeffer, Marc A, Kouz, Simon, Koenig, Wolfgang, Maggioni, Aldo P, McMurray, John JV, Mooser, Vincent, Waters, David D, Grégoire, Jean C, L’Allier, Philippe L, Jukema, J Wouter, White, Harvey D, Heinonen, Therese, Black, Donald M, Laghrissi-Thode, Fouzia, Levesque, Sylvie, Guertin, Marie Claude, Dubé, Marie Pierre, and Investigators, for the dal-GenE

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Clinical Trials and Supportive Activities, Clinical Research, Cardiovascular, Genetics, Heart Disease - Coronary Heart Disease, Heart Disease, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Acute Coronary Syndrome, Adenylyl Cyclases, Amides, Anticholesteremic Agents, Double-Blind Method, Esters, Heart Arrest, Humans, Myocardial Infarction, Pharmacogenetics, Retrospective Studies, Stroke, Sulfhydryl Compounds, Precision medicine, Atherosclerosis, Myocardial infarction, CETP, Adenylate cyclase type 9, dal-GenE Investigators, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

AimsIn a retrospective analysis of dal-Outcomes, the effect of dalcetrapib on cardiovascular events was influenced by an adenylate cyclase type 9 (ADCY9) gene polymorphism. The dal-GenE study was conducted to test this pharmacogenetic hypothesis.Methods and resultsdal-GenE was a double-blind trial in patients with an acute coronary syndrome within 1-3 months and the AA genotype at variant rs1967309 in the ADCY9 gene. A total of 6147 patients were randomly assigned to receive dalcetrapib 600 mg or placebo daily. The primary endpoint was the time from randomization to first occurrence of cardiovascular death, resuscitated cardiac arrest, non-fatal myocardial infarction, or non-fatal stroke. After a median follow-up of 39.9 months, the primary endpoint occurred in 292 (9.5%) of 3071 patients in the dalcetrapib group and 327 (10.6%) of 3076 patients in the placebo group [hazard ratio 0.88; 95% confidence interval (CI) 0.75-1.03; P = 0.12]. The hazard ratios for the components of the primary endpoint were 0.79 (95% CI 0.65-0.96) for myocardial infarction, 0.92 (95% CI 0.64-1.33) for stroke, 1.21 (95% CI 0.91-1.60) for death from cardiovascular causes, and 2.33 (95% CI 0.60-9.02) for resuscitated cardiac arrest. In a pre-specified on-treatment sensitivity analysis, the primary endpoint event rate was 7.8% (236/3015) in the dalcetrapib group and 9.3% (282/3031) in the placebo group (hazard ratio 0.83; 95% CI 0.70-0.98).ConclusionDalcetrapib did not significantly reduce the risk of occurrence of the primary endpoint of ischaemic cardiovascular events at end of study. A new trial would be needed to test the pharmacogenetic hypothesis that dalcetrapib improves the prognosis of patients with the AA genotype.Clinical trial registrationTrial registration dal-GenE ClinicalTrials.gov Identifier: NCT02525939.

Published
2022

5. Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis

Author

Reith, Christina, Preiss, David, Blackwell, Lisa, Emberson, Jonathan, Spata, Enti, Davies, Kelly, Halls, Heather, Harper, Charlie, Holland, Lisa, Wilson, Kate, Roddick, Alistair J, Cannon, Christopher P, Clarke, Robert, Colhoun, Helen M, Durrington, Paul N, Goto, Shinya, Hitman, Graham A, Hovingh, G Kees, Jukema, J Wouter, Koenig, Wolfgang, Marschner, Ian, Mihaylova, Borislava, Newman, Connie, Probsfield, Jeffrey L, Ridker, Paul M, Sabatine, Marc S, Sattar, Naveed, Schwartz, Gregory G, Tavazzi, Luigi, Tonkin, Andrew, Trompet, Stella, White, Harvey, Yusuf, Salim, Armitage, Jane, Keech, Anthony, Simes, John, Collins, Rory, Baigent, Colin, Barnes, Elizabeth, Fulcher, Jordan, Herrington, William G, Kirby, Adrienne, O'Connell, Rachel, Amarenco, Pierre, Arashi, Hiroyuki, Barter, Philip, Betteridge, D John, Blazing, Michael, Blauw, Gerard J, Bosch, Jackie, Bowman, Louise, Braunwald, Eugene, Bulbulia, Richard, Byington, Robert, Clearfield, Michael, Cobbe, Stuart, Dahlöf, Björn, Davis, Barry, de Lemos, James, Downs, John R, Fellström, Bengt, Flather, Marcus, Ford, Ian, Franzosi, Maria Grazia, Fuller, John, Furberg, Curt, Glynn, Robert, Goldbourt, Uri, Gordon, David, Gotto, Jr, Antonio, Grimm, Richard, Gupta, Ajay, Hawkins, C Morton, Haynes, Richard, Holdaas, Hallvard, Hopewell, Jemma, Jardine, Alan, Kastelein, John JP, Kean, Sharon, Kearney, Patricia, Kitas, George, Kjekshus, John, Knatterud, Genell, Knopp, Robert H, Koren, Michael, Krane, Vera, Landray, Martin, LaRosa, John, Latini, Roberto, Lonn, Eva, Lucci, Donata, MacFadyen, Jean, Macfarlane, Peter, MacMahon, Stephen, Maggioni, Aldo, Marchioli, Roberto, Moyé, Lemuel, Murphy, Sabina, Neil, Andrew, Nicolis, Enrico B, Packard, Chris, Parish, Sarah, Pedersen, Terje R, Peto, Richard, Pfeffer, Marc, Poulter, Neil, Pressel, Sara, Probstfield, Jeffrey, Rahman, Mahboob, Robertson, Michele, Sacks, Frank, Schmieder, Roland, Serruys, Patrick, Sever, Peter, Shaw, John, Shepherd, James, Simpson, Lara, Sleight, Peter, Smeeth, Liam, Tobert, Jonathan, Tognoni, Gianni, Varigos, John, Wanner, Christoph, Wedel, Hans, Weis, Stephen, Welch, K Michael, Wikstrand, John, Wilhelmsen, Lars, Wiviott, Stephen, Yamaguchi, Junichi, Young, Robin, and Zannad, Faiez

Published
2024
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10. Role of Adenylate Cyclase 9 in the Pharmacogenomic Response to Dalcetrapib: Clinical Paradigm and Molecular Mechanisms in Precision Cardiovascular Medicine.

Author

Rhainds, David, Packard, Chris J, Brodeur, Mathieu R, Niesor, Eric J, Sacks, Frank M, Jukema, J Wouter, Wright, R Scott, Waters, David D, Heinonen, Therese, Black, Donald M, Laghrissi-Thode, Fouzia, Dubé, Marie-Pierre, Pfeffer, Marc A, and Tardif, Jean-Claude

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Rare Diseases, Clinical Research, Human Genome, Genetics, Cardiovascular, Good Health and Well Being, Adenylyl Cyclases, Amides, Biomarkers, Cardiovascular Diseases, Cholesterol, Cholesterol Ester Transfer Proteins, Esters, Genotype, Humans, Pharmacogenetics, Precision Medicine, Sulfhydryl Compounds, acute coronary syndrome, adenylate cyclase, dalcetrapib, macrophages, precision medicine, Medical Biotechnology, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

Following the neutral results of the dal-OUTCOMES trial, a genome-wide study identified the rs1967309 variant in the adenylate cyclase type 9 (ADCY9) gene on chromosome 16 as being associated with the risk of future cardiovascular events only in subjects taking dalcetrapib, a CETP (cholesterol ester transfer protein) modulator. Homozygotes for the minor A allele (AA) were protected from recurrent cardiovascular events when treated with dalcetrapib, while homozygotes for the major G allele (GG) had increased risk. Here, we present the current state of knowledge regarding the impact of rs1967309 in ADCY9 on clinical observations and biomarkers in dalcetrapib trials and the effects of mouse ADCY9 gene inactivation on cardiovascular physiology. Finally, we present our current model of the interaction between dalcetrapib and ADCY9 gene variants in the arterial wall macrophage, based on the intracellular role of CETP in the transfer of complex lipids from endoplasmic reticulum membranes to lipid droplets. Briefly, the concept is that dalcetrapib would inhibit CETP-mediated transfer of cholesteryl esters, resulting in a progressive inhibition of cholesteryl ester synthesis and free cholesterol accumulation in the endoplasmic reticulum. Reduced ADCY9 activity, by paradoxically leading to higher cyclic AMP levels and in turn increased cellular cholesterol efflux, could impart cardiovascular protection in rs1967309 AA patients. The ongoing dal-GenE trial recruited 6145 patients with the protective AA genotype and will provide a definitive answer to whether dalcetrapib will be protective in this population.

Published
2021

11. Pulmonary Congestion and Left Ventricular Dysfunction After Myocardial Infarction: Insights From the PARADISE-MI Trial

Author

Petrie, Mark C., Rouleau, Jean L., Claggett, Brian, Jering, Karola, van der Meer, Peter, Køber, Lars, Miao, Zi Michael, Lewis, Eldrin, Granger, Christopher, De Pasqulae, Carmine G., Mann, Douglas, Steg, Philippe Gabriel, Maggioni, Aldo, Amir, Offer, Lefkowitz, Marty, Braunwald, Eugene, Solomon, Scott D, McMurray, John J.V., and Pfeffer, Marc A.

Published
2024
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12. Right Ventricular Function and Pulmonary Coupling in Patients With Heart Failure and Preserved Ejection Fraction

Author

Inciardi, Riccardo M., Abanda, Martin, Shah, Amil M., Cikes, Maja, Claggett, Brian, Skali, Hicham, Vaduganathan, Muthiah, Prasad, Narayana, Litwin, Sheldon, Merkely, Bela, Kosztin, Annamaria, Nagy, Klaudia Vivien, Shah, Sanjiv J., Mullens, Wilfred, Zile, Michael R., Lam, Carolyn S.P., Pfeffer, Marc A., McMurray, John J.V., and Solomon, Scott D.

Published
2023
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15. Abstract 13828: Aptamer Proteomics for Biomarker Discovery in Heart Failure With Preserved Ejection Fraction: The PARADIGM-HF Proteomic Sub-Study

Author

Patel-Murray, Natasha, Zhang, Luqing, Claggett, Brian, Xu, Dongchu, Serrano-Fernandez, Pablo, Wandel, Simon, Xu, Huilei, Healey, Margaret, Turner, Gordon, Chen, Chien-Wei, Zhao, Faye, CHUTKOW, WILLIAM A, Yates, Denise, ODonnell, Christopher, Prescott, Margaret, Lefkowitz, Martin P, Gimpelewicz, Claudio R, Beste, Michael, Gou, Liangke, Desai, Akshay S, Jhund, Pardeep S, Packer, Milton, Pfeffer, Marc A, Redfield, Margaret M, Rouleau, Jean L, ZANNAD, Faiez, Zile, Michael R, McMurray, John J, Mendelson, Michael, Solomon, Scott D, and Cunningham, Jonathan

Published
2023
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16. Abstract 12701: Safety and Tolerability of Angiotensin Receptor Neprilysin Inhibitor Initiation in High-Risk Acute Myocardial Infarction Relative to Drug Initiation Setting: A Subgroup Analysis of the PARADISE-MI Trial

Author

De Pasquale, Carmine, Claggett, Brian, Jering, Karola, McMurray, John J, Mann, Douglas L, Granger, Christopher, Kober, Lars, Lewis, Eldrin F, Maggioni, Aldo Pietro P, Rouleau, Jean L, Solomon, Scott, Steg, Philippe G, van der meer, peter, Braunwald, Eugene, and Pfeffer, Marc A

Published
2023
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17. Abstract 12470: Sacubitril/Valsartan in Patients With Heart Failure and Deterioration of Kidney Function to Estimated Glomerular Filtration Rate Less Than 30ml/min/1.73m2: Insights From PARAGON-HF and PARADIGM-HF

Author

Chatur, Safia, Vaduganathan, Muthiah, Claggett, Brian L, McCausland, Finnian, Desai, Akshay S, Beldhuis, Iris, Rouleau, Jean L, Zile, Michael R, Packer, Milton, Pfeffer, Marc A, Lefkowitz, Martin P, McMurray, John J, and Solomon, Scott D

Published
2023
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19. Study design of Dal-GenE, a pharmacogenetic trial targeting reduction of cardiovascular events with dalcetrapib

Author

Tardif, Jean-Claude, Dubé, Marie-Pierre, Pfeffer, Marc A, Waters, David D, Koenig, Wolfgang, Maggioni, Aldo P, McMurray, John JV, Mooser, Vincent, White, Harvey D, Heinonen, Therese, Black, Donald M, Guertin, Marie-Claude, and Investigators, for the dal-GenE

Subjects
Genetics, Heart Disease - Coronary Heart Disease, Heart Disease, Cardiovascular, Prevention, Clinical Research, Clinical Trials and Supportive Activities, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Adenylyl Cyclases, Amides, Anticholesteremic Agents, Atherosclerosis, Dose-Response Relationship, Drug, Double-Blind Method, Esters, Female, Follow-Up Studies, Genetic Testing, Genome-Wide Association Study, Genotype, Global Health, Humans, Incidence, Male, Middle Aged, Pharmacogenetics, Polymorphism, Genetic, Precision Medicine, Prognosis, Prospective Studies, Retrospective Studies, Sulfhydryl Compounds, dal-GenE Investigators, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

The objectives of precision medicine are to better match patient characteristics with the therapeutic intervention to optimize the chances of beneficial actions while reducing the exposure to unneeded adverse drug experiences. In a retrospective genome-wide association study of the overall neutral placebo-controlled dal-Outcomes trial, the effect of the cholesteryl ester transfer protein (CETP) modulator dalcetrapib on the composite of cardiovascular death, myocardial infarction or stroke was found to be influenced by a polymorphism in the adenylate cyclase type 9 (ADCY9) gene. Whereas patients with the AA genotype at position rs1967309 experienced fewer cardiovascular events with dalcetrapib, those with the GG genotype had an increased rate and the heterozygous AG genotype exhibited no difference from placebo. Measurements of cholesterol efflux and C-reactive protein (CRP) offered directionally supportive genotype-specific findings. In a separate, smaller, placebo-controlled trial, regression of ultrasonography-determined carotid intimal-medial thickness was only observed in dalcetrapib-treated patients with the AA genotype. Collectively, these observations led to the hypothesis that the cardiovascular effects of dalcetrapib may be pharmacogenetically determined, with a favorable benefit-risk ratio only for patients with this specific genotype. We describe below the design of dal-GenE, a precision medicine, placebo-controlled clinical outcome trial of dalcetrapib in patients with a recent acute myocardial infarction with the unique feature of selecting only those with the AA genotype at rs1967309 in the ADCY9 gene.

Published
2020

22. Safety and Tolerability of Angiotensin Receptor-Neprilysin Inhibitor Initiation in High-Risk Acute Myocardial Infarction Relative to Care Setting: A Subgroup Analysis of the PARADISE-MI Trial

Author

De Pasquale, Carmine G., primary, Claggett, Brian, additional, Jering, Karola, additional, McMurray, John J.V., additional, Mann, Douglas, additional, Miao, Zi Michael, additional, Granger, Christopher B., additional, Køber, Lars, additional, Maggioni, Aldo P., additional, Rouleau, Jean-Lucien, additional, Solomon, Scott D., additional, Steg, Philippe Gabriel, additional, van der Meer, Peter, additional, Braunwald, Eugene, additional, and Pfeffer, Marc A., additional

Published
2024
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23. Cardiovascular-Kidney-Metabolic Overlap in Heart Failure with Mildly Reduced or Preserved Ejection Fraction: A Trial-Level Analysis

Author

Ostrominski, John W., primary, Claggett, Brian L., additional, Miao, Zi Michael, additional, Mc Causland, Finnian R., additional, Anand, Inder S., additional, Desai, Akshay S., additional, Jhund, Pardeep S., additional, Lam, Carolyn S.P., additional, Pfeffer, Marc A., additional, Pitt, Bertram, additional, Zannad, Faiez, additional, Zile, Michael R., additional, Bomfim Wirtz, Antonieta, additional, Lay-Flurrie, James, additional, Viswanathan, Prabhakar, additional, McMurray, John J.V., additional, Solomon, Scott D., additional, and Vaduganathan, Muthiah, additional

Published
2024
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25. Albuminuria and Allograft Failure, Cardiovascular Disease Events, and All-Cause Death in Stable Kidney Transplant Recipients: A Cohort Analysis of the FAVORIT Trial

Author

Weiner, Daniel E, Park, Meyeon, Tighiouart, Hocine, Joseph, Alin A, Carpenter, Myra A, Goyal, Nitender, House, Andrew A, Hsu, Chi-Yuan, Ix, Joachim H, Jacques, Paul F, Kew, Clifton E, Kim, S Joseph, Kusek, John W, Pesavento, Todd E, Pfeffer, Marc A, Smith, Stephen R, Weir, Matthew R, Levey, Andrew S, and Bostom, Andrew G

Subjects
Clinical Research, Transplantation, Kidney Disease, Organ Transplantation, Heart Disease, Prevention, Cardiovascular, Renal and urogenital, Good Health and Well Being, Albuminuria, Cardiovascular Diseases, Cause of Death, Cohort Studies, Creatinine, Double-Blind Method, Female, Graft Survival, Humans, Kidney Transplantation, Longitudinal Studies, Male, Middle Aged, Postoperative Complications, Risk Assessment, Treatment Outcome, allograft failure, biomarker, cardiovascular disease, death, end-stage renal disease, graft survival, kidney failure, kidney transplant outcomes, protein excretion, renal transplantation, urinary albumin-creatinine ratio, Clinical Sciences, Public Health and Health Services, Urology & Nephrology
Abstract

Rationale & objectiveCardiovascular disease (CVD) is common and overall graft survival is suboptimal among kidney transplant recipients. Although albuminuria is a known risk factor for adverse outcomes among persons with native chronic kidney disease, the relationship of albuminuria with cardiovascular and kidney outcomes in transplant recipients is uncertain.Study designPost hoc longitudinal cohort analysis of the Folic Acid for Vascular Outcomes Reduction in Transplantation (FAVORIT) Trial.Setting & participantsStable kidney transplant recipients with elevated homocysteine levels from 30 sites in the United States, Canada, and Brazil.PredictorUrine albumin-creatinine ratio (ACR) at randomization.OutcomesAllograft failure, CVD, and all-cause death.Analytical approachMultivariable Cox models adjusted for age; sex; race; randomized treatment allocation; country; systolic and diastolic blood pressure; history of CVD, diabetes, and hypertension; smoking; cholesterol; body mass index; estimated glomerular filtration rate (eGFR); donor type; transplant vintage; medications; and immunosuppression.ResultsAmong 3,511 participants with complete data, median ACR was 24 (Q1-Q3, 9-98) mg/g, mean eGFR was 49±18 (standard deviation) mL/min/1.73m2, mean age was 52±9 years, and median graft vintage was 4.1 (Q1-Q3, 1.7-7.4) years. There were 1,017 (29%) with ACR < 10mg/g, 912 (26%) with ACR of 10 to 29mg/g, 1,134 (32%) with ACR of 30 to 299mg/g, and 448 (13%) with ACR ≥ 300mg/g. During approximately 4 years, 282 allograft failure events, 497 CVD events, and 407 deaths occurred. Event rates were higher at both lower eGFRs and higher ACR. ACR of 30 to 299 and ≥300mg/g relative to ACR < 10mg/g were independently associated with graft failure (HRs of 3.40 [95% CI, 2.19-5.30] and 9.96 [95% CI, 6.35-15.62], respectively), CVD events (HRs of 1.25 [95% CI, 0.96-1.61] and 1.55 [95% CI, 1.13-2.11], respectively), and all-cause death (HRs of 1.65 [95% CI, 1.23-2.21] and 2.07 [95% CI, 1.46-2.94], respectively).LimitationsNo data for rejection; single ACR assessment.ConclusionsIn a large population of stable kidney transplant recipients, elevated baseline ACR is independently associated with allograft failure, CVD, and death. Future studies are needed to evaluate whether reducing albuminuria improves these outcomes.

Published
2019

26. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials

Author

Reith, Christina, Baigent, Colin, Blackwell, Lisa, Emberson, Jonathan, Spata, Enti, Davies, Kelly, Halls, Heather, Holland, Lisa, Wilson, Kate, Armitage, Jane, Harper, Charlie, Preiss, David, Roddick, Alistair, Keech, Anthony, Simes, John, Collins, Rory, Barnes, Elizabeth, Fulcher, Jordan, Herrington, William G, Kirby, Adrienne, Mihaylova, Borislava, O'Connell, Rachel, Amarenco, Pierre, Barter, Philip, Betteridge (deceased), D John, Blazing, Michael, Bosch, Jackie, Bowman, Louise, Braunwald, Eugene, Cannon, Christopher P, Clearfield, Michael, Cobbe, Stuart, Colhoun, Helen M, Dahlöf, Björn, Davis, Barry, de Lemos, James, Downs, John R, Durrington, Paul N, Fellström, Bengt, Ford, Ian, Franzosi, Maria Grazia, Fuller (deceased), John, Furberg, Curt, Glynn, Robert, Gordon, David, Gotto Jr, Antonio, Grimm, Richard, Gupta, Ajay, Hawkins, C Morton, Hitman, Graham A, Holdaas (deceased), Hallvard, Jardine, Alan, Jukema, J Wouter, Kastelein, John JP, Kean, Sharon, Kjekshus, John, Knatterud (deceased), Genell, Knopp (deceased), Robert H, Koenig, Wolfgang, Koren, Michael, Krane, Vera, Landray, Martin, LaRosa, John, Latini, Roberto, Lonn, Eva, Lucci, Donata, MacFadyen, Jean, Macfarlane, Peter, MacMahon, Stephen, Maggioni, Aldo, Marchioli, Roberto, Marschner, Ian, Moyé, Lemuel, Murphy, Sabina, Neil, Andrew, Nicolis, Enrico B, Packard, Chris, Parish, Sarah, Pedersen, Terje R, Peto, Richard, Pfeffer, Marc, Poulter, Neil, Pressel, Sara, Probstfield, Jeffrey, Rahman, Mahboob, Ridker, Paul M, Robertson, Michele, Sacks, Frank, Sattar, Naveed, Schmieder, Roland, Serruys, Patrick W, Sever, Peter, Shaw (deceased), John, Shepherd (deceased), James, Simpson, Lara, Sleight (deceased), Peter, Tavazzi, Luigi, Tognoni, Gianni, Tonkin, Andrew, Trompet, Stella, Wanner, Christoph, Wedel, Hans, Weis, Stephen, Welch, K Michael, White, Harvey, Wikstrand, John, Wilhelmsen, Lars, Wiviott, Stephen, Young, Robin, Yusuf, Salim, Zannad, Faiez, Arashi, Hiroyuki, Byington, Robert, Clarke, Robert, Flather, Marcus, Goldbourt, Uri, Goto, Shinya, Hopewell, Jemma, Hovingh, Kees, Kearney, Patricia, Kitas, George, Newman, Connie, Sabatine, Marc S, Schwartz, Greg, Smeeth, Liam, Tobert, Jonathan, Varigos, John, and Yamaguchi, Junichi

Published
2022
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33. Incidence of clinical outcomes in heart failure patients with and without advanced chronic kidney disease.

Author

Zahir Anjum, Deewa, Bonde, Anders N., Fosbol, Emil, Hartwell Garred, Caroline, Gislason, Gunnar, Elmegaard, Mariam, Knigge, Pauline, Torp‐Pedersen, Christian, Andersson, Charlotte, Pfeffer, Marc A., Jhund, Pardeep S., McMurray, John J.V., Petrie, Mark C., Kober, Lars, and Schou, Morten

Subjects
CHRONIC kidney failure, HEART failure patients, GLOMERULAR filtration rate, EPIDERMAL growth factor receptors, HEART failure
Abstract

Aims: Chronic kidney disease (CKD) is a well‐established risk factor for heart failure (HF); however, patients with an estimated glomerular filtration rate (eGFR) < 30 mL/min/1.73 m2 have been systematically excluded from clinical trials. This study investigated the incidence of HF and kidney outcomes in HF patients with and without advanced CKD, that is, eGFR < 30. Methods: From nationwide registries, HF patients were identified from 2014 to 2018 and categorized into three groups according to baseline eGFR (eGFR ≥ 60, 60 > eGFR ≥ 30 and eGFR < 30). The incidence of primary outcomes (all‐cause mortality, HF hospitalization, end‐stage kidney disease and sustained 50% eGFR decline) was estimated using cumulative incidence functions. Results: Of the 21 959 HF patients included, the median age was 73.9 years, and 30% of patients had an eGFR between 30 and 60 and 7% had an eGFR < 30. The 4 year incidence of all‐cause mortality was highest for patients with eGFR < 30 (28.3% for patients with eGFR ≥ 60, 51.6% for patients with 60 > eGFR ≥ 30 and 72.2% for patients with eGFR < 30). The 4 year incidence of HF hospitalization was comparable between the groups (25.8%, 29.8% and 26.1% for patients with eGFR ≥ 60, 60 > eGFR ≥ 30 and eGFR < 30, respectively). For patients with eGFR < 30, kidney outcomes were four times more often the first event than patients with eGFR > 30 (4 year incidence of kidney outcome as the first event was 5.0% for eGFR ≥ 60, 4.8% for 60 > eGFR ≥ 30 and 20.1% for eGFR < 30). Conclusions: Patients with advanced CKD had a higher incidence of mortality and poorer kidney outcomes than those without advanced CKD, but a similar incidence of HF hospitalizations. [ABSTRACT FROM AUTHOR]

Published
2024
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34. Cardiovascular‐kidney‐metabolic overlap in heart failure with preserved ejection fraction: Cardiac structure and function, clinical outcomes, and response to sacubitril/valsartan in PARAGON‐HF.

Author

Lassen, Mats C.H., Ostrominski, John W., Claggett, Brian L., Packer, Milton, Zile, Michael, Desai, Akshay S., Shah, Amil M., Cikes, Maja, Merkely, Bela, Gori, Mauro, Wang, Xiaowen, Hegde, Sheila M., Pfeffer, Marc A., Lefkowitz, Martin, McMurray, John J.V., Solomon, Scott D., and Vaduganathan, Muthiah

Subjects
GLOBAL longitudinal strain, HEART failure, TYPE 2 diabetes, GLOMERULAR filtration rate, CHRONIC kidney failure, ENTRESTO
Abstract

Aims: Cardiovascular‐kidney‐metabolic (CKM) multimorbidity is prevalent among individuals with heart failure (HF), but whether cardiac structure and function, clinical outcomes, and treatment response to sacubitril/valsartan vary in relation to CKM status is unknown. Methods and results: In this PARAGON‐HF post‐hoc analysis, we evaluated the impact of CKM multimorbidity (atherosclerotic cardiovascular [CV] disease, chronic kidney disease, and type 2 diabetes) on cardiac structure and function, clinical outcomes, and treatment effects of sacubitril/valsartan versus valsartan. The primary outcome was a composite of total HF hospitalizations and CV death. Secondary outcomes included the individual components of the primary outcome and a composite kidney outcome (sustained estimated glomerular filtration rate reduction of ≥50%, end‐stage kidney disease, or kidney‐related death). At baseline, 35.2% had one CKM condition, 33.3% had two, 15.9% had three, and only 15.6% had HF alone. CKM multimorbidity was associated with higher septal and posterior wall thickness, lower global longitudinal strain, higher E/e', and worse right ventricular function. Total HF hospitalizations or CV death increased with greater CKM multimorbidity, with the highest relative risk observed with three CKM conditions (rate ratio 3.06, 95% confidence interval 2.33–4.03), compared with HF alone. Treatment effects of sacubitril/valsartan were consistent irrespective of the number of CKM conditions for the primary endpoint (pinteraction = 0.75), CV death (pinteraction = 0.82), total HF hospitalizations (pinteraction = 0.67), and the composite kidney endpoint (pinteraction = 0.99). Conclusions: Cardiovascular‐kidney‐metabolic multimorbidity was common in PARAGON‐HF and associated with adverse changes in cardiac structure and function and with a stepwise increase in risk of clinical outcomes. Treatment effects of sacubitril/valsartan were consistent irrespective of CKM burden. Clinical Trial Registration: ClinicalTrials.gov NCT01920711. [ABSTRACT FROM AUTHOR]

Published
2024
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35. A pre-specified analysis of the Dapagliflozin and Prevention of Adverse Outcomes in Chronic Kidney Disease (DAPA-CKD) randomized controlled trial on the incidence of abrupt declines in kidney function

Author

Heerspink, Hiddo J.L., Wheeler, David C., Chertow, Glenn, Correa-Rotter, Ricardo, Greene, Tom, Hou, Fan Fan, McMurray, John, Rossing, Peter, Toto, Robert, Stefansson, Bergur, Langkilde, Anna Maria, Maffei, L.E., Raffaele, P., Solis, S.E., Arias, C.A., Aizenberg, D., Luquez, C., Zaidman, C., Cluigt, N., Mayer, M., Alvarisqueta, A., Wassermann, A., Maldonado, R., Bittar, J., Maurich, M., Gaite, L.E., Garcia, N., Sivak, L., Ramallo, P.O., Santos, J.C., Garcia Duran, R., Oddino, J.A., Maranon, A., Maia, L.N., Avila, D.D., Barros, E.J.G., Vidotti, M.H., Panarotto, D., Noronha, I.D.L., Turatti, L.A.A., Deboni, L., Canziani, M.E., Riella, M.C., Bacci, M.R., Paschoalin, R.P., Franco, R.J., Goldani, J.C., St-Amour, E., Steele, A.W., Goldenberg, R., Pandeya, S., Bajaj, H., Cherney, D., Kaiser, S.M., Conway, J.R., Chow, S.S., Bailey, G., Lafrance, J., Winterstein, J., Cournoyer, S., Gaudet, D., Madore, F., Houlden, R.L., Dowell, A., Langlois, M., Muirhead, N., Khandwala, H., Levin, A., Hou, F., Xue, Y., Zuo, L., Hao, C., Ni, Z., Xing, C., Chen, N., Dong, Y., Zhou, R., Xiao, X., Zou, Y., Wang, C., Liu, B., Chen, Q., Lin, M., Luo, Q., Zhang, D., Wang, J., Chen, M., Wang, X., Zhong, A., Dong, J., Zhu, C., Yan, T., Luo, P., Ren, Y., Pai, P., Li, D., Zhang, R., Zhang, J., Xu, M., Zhuang, Y., Kong, Y., Yao, X., Peng, X., Persson, F.I., Hansen, T.K., Borg, R., Pedersen Bjergaard, U., Hansen, D., Hornum, M., Haller, H., Klausmann, G., Tschope, D., Kruger, T., Gross, P., Hugo, C., Obermuller, N., Rose, L., Mertens, P., Zeller-Stefan, H., Fritsche, A., Renders, L., Muller, J., Budde, K., Schroppel, B., Wittmann, I., Voros, P., Dudas, M., Tabak, G.A., Kirschner, R., Letoha, A., Balku, I., Hermanyi, Z., Zakar, G., Mezei, I., Nagy, G.G., Lippai, J., Nemeth, A., Khullar, D., Gowdaiah, P.K., Fernando Mervin, E., Rao, V.A., Dewan, D., Goplani, K., Maddi, V.S.K., Vyawahare, M.S., Pulichikkat, R.K., Pandey, R., Sonkar, S.K., Gupta, V.K., Agarwal, S., Asirvatham, A.J., Ignatius, A., Chaubey, S., Melemadathil, S., Alva, H., Kadam, Y., Shimizu, H., Sueyoshi, A., Takeoka, H., Abe, Y., Imai, T., Onishi, Y., Fujita, Y., Tokita, Y., Oura, M., Makita, Y., Idogaki, A., Koyama, R., Kikuchi, H., Kashihara, N., Hayashi, T., Ando, Y., Tanaka, T., Shimizu, M., Hidaka, S., Gohda, T., Tamura, K., Abe, M., Kamijo, Y., Imasawa, T., Takahashi, Y., Nakayama, M., Tomita, M., Hirano, F., Fukushima, Y., Kiyosue, A., Kurioka, S., Imai, E., Kitagawa, K., Waki, M., Wada, J., Uehara, K., Iwatani, H., Ota, K., Shibazaki, S., Katayama, K., Narita, I., Iinuma, M., Matsueda, S., Sasaki, S., Yokochi, A., Tsukamoto, T., Yoshimura, T., Kang, S., Lee, S., Lim, C.S., Chin, H., Joo, K.W., Han, S.Y., Chang, T.I., Park, S., Park, H., Park, C.W., Han, B.G., Cha, D.R., Yoon, S.A., Kim, W., Kim, S.W., Ryu, D., Correa Rotter, R., Irizar Santana, S.S., Hernandez Llamas, G., Valdez Ortiz, R., Secchi Nicolas, N.C., Gonzalez Galvez, G., Lazcano Soto, J.R., Bochicchio Riccardelli, T., Bayram Llamas, E.A., Ramos Ibarra, D.R., Melo, M.G.S., Gonzalez Gonzalez, J.G., Sanchez Mijangos, J.H., Madero Robalo, M., Garcia Castillo, A., Manrique, H.A., Farfan, J.C., Vargas, R., Valdivia, A., Dextre, A., Escudero, E., Calderon Ticona, J.R., Gonzales, L., Villena, J., Leon, L., Molina, G., Saavedra, A., Garrido, E., Arbanil, H., Vargas Marquez, S., Rodriguez, J., Isidto, R., Villaflor, A.J., Gumba, M.A., Tirador, L., Comia, R.S., Sy, R.A., Guanzon, M.L.V.V., Aquitania, G., De Asis, N.C., Silva, A.A., Romero, C.M., Lim, M.E., Danguilan, R.A., Nowicki, M., Rudzki, H., Landa, K., Kucharczyk-Bauman, I., Gogola-Migdal, B., Golski, M., Olech-Cudzik, A., Stompor, T., Szczepanik, T., Miklaszewicz, B., Sciborski, R., Kuzniewski, M., Ciechanowski, K., Wronska, D., Klatko, W., Mazur, S., Popenda, G., Myslicki, M., Bolieva, L.Z., Berns, S., Galyavich, A., Abissova, T., Karpova, I., Platonov, D., Koziolova, N., Kvitkova, L., Nilk, R., Medina, T., Rebrov, A., Rossovskaya, M., Sinitsina, I., Vishneva, E., Zagidullin, N., Novikova, T., Krasnopeeva, N., Magnitskaya, O., Antropenko, N., Batiushin, M., Escudero Quesada, V., Barrios Barrea, C., Espinel Garauz, E., Cruzado Garrit, J.M., Morales Portillo, C., Gorriz Teruel, J.L., Cigarran Guldris, S., Praga Terente, M., Robles Perez-Monteoliva, N.R., Tinahones Madueno, F.J., Soto Gonzalez, A., Diaz Rodriguez, C., Furuland, H., Saeed, A., Dreja, K., Spaak, J., Bruchfeld, A., Kolesnyk, M., Levchenko, O., Pyvovarova, N., Stus, V., Doretskyy, V., Korobova, N., Horoshko, O., Katerenchuk, I., Mostovoy, Y.M., Orynchak, M., Legun, O., Dudar, I., Bilchenko, O., Andreychyn, S., Levchenko, A., Zub, L., Tereshchenko, N., Topchii, I., Ostapenko, T., Bezuglova, S., Kopytsya, M., Turenko, O., Mark, P., Barratt, J., Bhandari, S., Fraser, D., Kalra, P., Kon, S.P., Mccafferty, K., Mikhail, A., Alvarado, O.P., Anderson, R., Andrawis, N.S., Arif, A., Benjamin, S.A., Bueso, G., Busch, R.S., Carr, K.W., Crawford, P., Daboul, N., De La Calle, G.M., Delgado, B., Earl, J., El-Shahawy, M.A., Graf, R.J., Greenwood, G., Guevara, A., Wendland, E.M., Mayfield, R.K., Montero, M., Morin, D.J., Narayan, P., Numrungroad, V., Reddy, A.C., Reddy, R., Samson, M.B., Trejo, R., Butcher, M.B., Wise, J.K., Zemel, L.R., Raikhel, M., Weinstein, D., Hernandez, P., Wynne, A., Khan, B.V., Sterba, G.A., Jamal, A., Ross, D., Rovner, S.F., Tan, A., Ovalle, F., Patel, R.J., Talano, J., Patel, D.R., Burgner, A., Aslam, N., Elliott, M., Goral, S., Jovanovich, A., Manley, J.A., Umanath, K., Waguespack, D., Weiner, D., Yu, M., Schneider, L., Jalal, D., Le, T., Nguyen, N., Nguyen, H., Nguyen, D., Nguyen, V., Do, T., Chu, P., Ta, D., Tran, N., Pham, B., Pfeffer, Marc A., Pocock, Stuart, Swedberg, Karl, Rouleau, Jean L., Chaturvedi, Nishi, Ivanovich, Peter, Levey, Andrew S., Christ-Schmidt, Heidi, Held, Claes, Christersson, Christina, Mann, Johannes, Varenhorst, Christoph, Cherney, David, Postmus, Douwe, Stefánsson, Bergur V., Chertow, Glenn M., Dwyer, Jamie P., Kosiborod, Mikhail, McMurray, John J.V., Sjöström, C. David, and Toto, Robert D.

Published
2022
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36. High-sensitivity C-reactive protein in heart failure with preserved ejection fraction: Findings from TOPCAT

Author

Ferreira, João Pedro, primary, Claggett, Brian L., additional, Liu, Jiankang, additional, Sharma, Abhinav, additional, Desai, Akshay S., additional, Anand, Inder S., additional, O'Meara, Eileen, additional, Rouleau, Jean L., additional, De Denus, Simon, additional, Pitt, Bertram, additional, Pfeffer, Marc A., additional, Zannad, Faiez, additional, and Solomon, Scott D., additional

Published
2024
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37. Age-stratified and blood-pressure-stratified effects of blood-pressure-lowering pharmacotherapy for the prevention of cardiovascular disease and death: an individual participant-level data meta-analysis

Author

Rahimi, Kazem, Bidel, Zeinab, Nazarzadeh, Milad, Copland, Emma, Canoy, Dexter, Wamil, Malgorzata, Majert, Jeannette, McManus, Richard, Adler, Amanda, Agodoa, Larry, Algra, Ale, Asselbergs, Folkert W, Beckett, Nigel S, Berge, Eivind, Black, Henry, Boersma, Eric, Brouwers, Frank P J, Brown, Morris, Brugts, Jasper J, Bulpitt, Christopher J, Byington, Robert P, Cushman, William C, Cutler, Jeffrey, Devereaux, Richard B, Dwyer, Jamie P, Estacio, Ray, Fagard, Robert, Fox, Kim, Fukui, Tsuguya, Gupta, Ajay K, Holman, Rury R, Imai, Yutaka, Ishii, Masao, Julius, Stevo, Kanno, Yoshihiko, Kjeldsen, Sverre E, Kostis, John, Kuramoto, Kizuku, Lanke, Jan, Lewis, Edmund, Lewis, Julia B, Lievre, Michel, Lindholm, Lars H, Lueders, Stephan, MacMahon, Stephen, Mancia, Giuseppe, Matsuzaki, Masunori, Mehlum, Maria H, Nissen, Steven, Ogawa, Hiroshi, Ogihara, Toshio, Ohkubo, Takayoshi, Palmer, Christopher R, Patel, Anushka, Pfeffer, Marc Allan, Pitt, Bertram, Poulter, Neil R, Rakugi, Hiromi, Reboldi, Gianpaolo, Reid, Christopher, Remuzzi, Giuseppe, Ruggenenti, Piero, Saruta, Takao, Schrader, Joachim, Schrier, Robert, Sever, Peter, Sleight, Peter, Staessen, Jan A, Suzuki, Hiromichi, Thijs, Lutgarde, Ueshima, Kenji, Umemoto, Seiji, van Gilst, Wiek H, Verdecchia, Paolo, Wachtell, Kristian, Whelton, Paul, Wing, Lindon, Woodward, Mark, Yui, Yoshiki, Yusuf, Salim, Zanchetti, Alberto, Zhang, Zhen-Yu, Anderson, Craig, Baigent, Colin, Brenner, Barry Morton, Collins, Rory, de Zeeuw, Dick, Lubsen, Jacobus, Malacco, Ettore, Neal, Bruce, Perkovic, Vlado, Rodgers, Anthony, Rothwell, Peter, Salimi-Khorshidi, Gholamreza, Sundström, Johan, Turnbull, Fiona, Viberti, Giancarlo, Wang, Jiguang, Chalmers, John, Davis, Barry R, Pepine, Carl J, and Teo, Koon K

Published
2021
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40. The Effects of Angiotensin Receptor-Neprilysin Inhibition on Major Coronary Events in Patients With Acute Myocardial Infarction: Insights From the PARADISE-MI Trial

Author

Mehran, Roxana, Steg, Philippe Gabriel, Pfeffer, Marc A., Jering, Karola, Claggett, Brian, Lewis, Eldrin F., Granger, Christopher, Køber, Lars, Maggioni, Aldo, Mann, Douglas L., McMurray, John J.V., Rouleau, Jean-Lucien, Solomon, Scott D., Ducrocq, Gregory, Berwanger, Otavio, De Pasquale, Carmine G., Landmesser, Ulf, Petrie, Mark, Leng, David Sim Kheng, van der Meer, Peter, Lefkowitz, Martin, Zhou, Yinong, and Braunwald, Eugene

Published
2022
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45. Incidence and Outcomes of Pneumonia in Patients With Heart Failure

Author

Shen, Li, Jhund, Pardeep S., Anand, Inder S., Bhatt, Ankeet S., Desai, Akshay S., Maggioni, Aldo P., Martinez, Felipe A., Pfeffer, Marc A., Rizkala, Adel R., Rouleau, Jean L., Swedberg, Karl, Vaduganathan, Muthiah, Vardeny, Orly, van Veldhuisen, Dirk J., Zannad, Faiez, Zile, Michael R., Packer, Milton, Solomon, Scott D., and McMurray, John J.V.

Published
2021
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48. Sacubitril/valsartan compared to ramipril in high-risk post-myocardial infarction patients stratified according to use of mineralocorticoid receptor antagonists:insight from the PARADISE MI trial

Author

Schou, Morten, Claggett, Brian, Miao, Zi Michael, Fernandez, Alberto, Filippatos, Gerasimos, Granger, Christopher, Jering, Karola, Maggioni, Aldo P., McCausland, Finnian, Villota, Julio Nuñez, Rouleau, Jean Lucien, Mody, Freny Vaghaiwalla, van der Meer, Peter, Vinereanu, Dragos, McGrath, Martina, Zhou, Yinong, Mann, Douglas L., Solomon, Scott D., Steg, Philippe Gabriel, Braunwald, Eugene, McMurray, John J.V., Pfeffer, Marc A., Køber, Lars, Schou, Morten, Claggett, Brian, Miao, Zi Michael, Fernandez, Alberto, Filippatos, Gerasimos, Granger, Christopher, Jering, Karola, Maggioni, Aldo P., McCausland, Finnian, Villota, Julio Nuñez, Rouleau, Jean Lucien, Mody, Freny Vaghaiwalla, van der Meer, Peter, Vinereanu, Dragos, McGrath, Martina, Zhou, Yinong, Mann, Douglas L., Solomon, Scott D., Steg, Philippe Gabriel, Braunwald, Eugene, McMurray, John J.V., Pfeffer, Marc A., and Køber, Lars

Abstract

Aim It is unknown whether safety and clinical endpoints by use of sacubitril/valsartan (an angiotensin receptor–neprilysin inhibitor [ARNI]) are affected by mineralocorticoid receptor antagonists (MRA) in high-risk myocardial infarction (MI) patients. The aim of this study was to examine whether MRA modifies safety and clinical endpoints by use of sacubitril/valsartan in patients with a MI and left ventricular systolic dysfunction (LVSD) and/or pulmonary congestion. Methods and results Patients (n = 5661) included in the PARADISE MI trial (Prospective ARNI vs. ACE Inhibitor Trial to Determine Superiority in Reducing Heart Failure Events After MI) were stratified according to MRA. Primary outcomes in this substudy were worsening heart failure or cardiovascular death. Safety was defined as symptomatic hypotension, hyperkalaemia >5.5 mmol/L, or permanent drug discontinuation. A total of 2338 patients (41%) were treated with MRA. Safety of ARNI compared to ramipril was not altered significantly by ± MRA, and both groups had similar increase in symptomatic hypotension with ARNI. In patients taking MRA, the risk of hyperkalaemia or permanent drug discontinuation was not significantly altered by ARNI (p > 0.05 for all comparisons). The effect of ARNI compared with ramipril was similar in those who were and were not taking MRA (hazard ratio [HR]MRA 0.96, 95% confidence interval [CI] 0.77–1.19 and HRMRA– 0.87, 95% CI 0.71–1.05, for the primary endpoint; p = 0.51 for interaction [Clinical Endpoint Committee adjudicated]); similar findings were observed if investigator-reported endpoints were evaluated (p = 0.61 for interaction). Conclusions Use of a MRA did not modify safety or clinical endpoints related to initiation of ARNI compared to ramipril in the post-MI setting in patients with LVSD and/or congestion., Aim: It is unknown whether safety and clinical endpoints by use of sacubitril/valsartan (an angiotensin receptor–neprilysin inhibitor [ARNI]) are affected by mineralocorticoid receptor antagonists (MRA) in high-risk myocardial infarction (MI) patients. The aim of this study was to examine whether MRA modifies safety and clinical endpoints by use of sacubitril/valsartan in patients with a MI and left ventricular systolic dysfunction (LVSD) and/or pulmonary congestion. Methods and results: Patients (n = 5661) included in the PARADISE MI trial (Prospective ARNI vs. ACE Inhibitor Trial to Determine Superiority in Reducing Heart Failure Events After MI) were stratified according to MRA. Primary outcomes in this substudy were worsening heart failure or cardiovascular death. Safety was defined as symptomatic hypotension, hyperkalaemia >5.5 mmol/L, or permanent drug discontinuation. A total of 2338 patients (41%) were treated with MRA. Safety of ARNI compared to ramipril was not altered significantly by ± MRA, and both groups had similar increase in symptomatic hypotension with ARNI. In patients taking MRA, the risk of hyperkalaemia or permanent drug discontinuation was not significantly altered by ARNI (p > 0.05 for all comparisons). The effect of ARNI compared with ramipril was similar in those who were and were not taking MRA (hazard ratio [HR]MRA 0.96, 95% confidence interval [CI] 0.77–1.19 and HRMRA– 0.87, 95% CI 0.71–1.05, for the primary endpoint; p = 0.51 for interaction [Clinical Endpoint Committee adjudicated]); similar findings were observed if investigator-reported endpoints were evaluated (p = 0.61 for interaction). Conclusions: Use of a MRA did not modify safety or clinical endpoints related to initiation of ARNI compared to ramipril in the post-MI setting in patients with LVSD and/or congestion.

Published
2024

49. Pulmonary Congestion and Left Ventricular Dysfunction after Myocardial Infarction:Insights from the PARADISE-MI Trial

Author

Petrie, Mark C., Rouleau, Jean L., Claggett, Brian, Jering, Karola, Van Der Meer, Peter, Køber, Lars, Miao, Zi Michael, Lewis, Eldrin, Granger, Christopher, De Pasqulae, Carmine G., Mann, Douglas, Steg, Philippe Gabriel, Maggioni, Aldo, Amir, Offer, Lefkowitz, Marty, Braunwald, Eugene, Solomon, Scott D., McMurray, John J.V., Pfeffer, Marc A., Petrie, Mark C., Rouleau, Jean L., Claggett, Brian, Jering, Karola, Van Der Meer, Peter, Køber, Lars, Miao, Zi Michael, Lewis, Eldrin, Granger, Christopher, De Pasqulae, Carmine G., Mann, Douglas, Steg, Philippe Gabriel, Maggioni, Aldo, Amir, Offer, Lefkowitz, Marty, Braunwald, Eugene, Solomon, Scott D., McMurray, John J.V., and Pfeffer, Marc A.

Published
2024

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