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1. Neurohormones and oxidative stress in nonischemic cardiomyopathy: Relationship to survival and the effect of treatment with amlodipine

Author

Wijeysundera, H.C., Hansen, M.S., Stanton, E., Cropp, A.S., Hall, C., Dhalla, N.S., Ghali, J., and Rouleau, J.L.

Subjects
Heart diseases -- Research, Heart diseases -- Care and treatment, Oxidative stress -- Research, Oxidative stress -- Care and treatment, Neurohormones -- Research, Cardiomyopathy -- Research, Cardiomyopathy -- Care and treatment, Health
Published
2003

4. Baseline characteristics of patients with heart failure and preserved ejection fraction in the PARAGON-HF trial

Author

Solomon, S.D. Rizkala, A.R. Lefkowitz, M.P. Shi, V.C. Gong, J. Anavekar, N. Anker, S.D. Arango, J.L. Arenas, J.L. Atar, D. Ben-Gal, T. Boytsov, S.A. Chen, C.-H. Chopra, V.K. Cleland, J. Comin-Colet, J. Duengen, H.-D. Echeverría Correa, L.E. Filippatos, G. Flammer, A.J. Galinier, M. Godoy, A. Goncalvesova, E. Janssens, S. Katova, T. Køber, L. Lelonek, M. Linssen, G. Lund, L.H. O'Meara, E. Merkely, B. Milicic, D. Oh, B.-H. Perrone, S.V. Ranjith, N. Saito, Y. Saraiva, J.F. Shah, S. Seferovic, P.M. Senni, M. Sibulo, A.S. Sim, D. Sweitzer, N.K. Taurio, J. Vinereanu, D. Vrtovec, B. Widimský, J. Yilmaz, M.B. Zhou, J. Zweiker, R. Anand, I.S. Ge, J. Lam, C.S.P. Maggioni, A.P. Martinez, F. Packer, M. Pfeffer, M.A. Pieske, B. Redfield, M.M. Rouleau, J.L. Van Veldhuisen, D.J. Zannad, F. Zile, M.R. McMurray, J.J.V.

Abstract

Background: To describe the baseline characteristics of patients with heart failure and preserved left ventricular ejection fraction enrolled in the PARAGON-HF trial (Prospective Comparison of Angiotensin Receptor Neprilysin Inhibitor With Angiotensin Receptor Blocker Global Outcomes in HFpEF) comparing sacubitril/valsartan to valsartan in reducing morbidity and mortality. Methods and Results: We report key demographic, clinical, and laboratory findings, and baseline therapies, of 4822 patients randomized in PARAGON-HF, grouped by factors that influence criteria for study inclusion. We further compared baseline characteristics of patients enrolled in PARAGON-HF with those patients enrolled in other recent trials of heart failure with preserved ejection fraction (HFpEF). Among patients enrolled from various regions (16% Asia-Pacific, 37% Central Europe, 7% Latin America, 12% North America, 28% Western Europe), the mean age of patients enrolled in PARAGON-HF was 72.7±8.4 years, 52% of patients were female, and mean left ventricular ejection fraction was 57.5%, similar to other trials of HFpEF. Most patients were in New York Heart Association class II, and 38% had ≥1 hospitalizations for heart failure within the previous 9 months. Diabetes mellitus (43%) and chronic kidney disease (47%) were more prevalent than in previous trials of HFpEF. Many patients were prescribed angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (85%), β-blockers (80%), calcium channel blockers (36%), and mineralocorticoid receptor antagonists (24%). As specified in the protocol, virtually all patients were on diuretics, had elevated plasma concentrations of N-terminal pro-B-type natriuretic peptide (median, 911 pg/mL; interquartile range, 464-1610), and structural heart disease. Conclusions: PARAGON-HF represents a contemporary group of patients with HFpEF with similar age and sex distribution compared with prior HFpEF trials but higher prevalence of comorbidities. These findings provide insights into the impact of inclusion criteria on, and regional variation in, HFpEF patient characteristics. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01920711. © 2018 American Heart Association, Inc.

Published
2018

7. A PROSPECTIVE INVESTIGATION OF THE IMPACT OF AGTR1 A1166C ON THE NEUROHORMONAL AND HEMODYNAMIC EFFECTS OF CANDESARTAN IN HEART FAILURE PATIENTS

Author

de Denus, S., primary, Dubé, M.P., additional, Fouodjio, R., additional, Huynh, T., additional, Leblanc, M.H., additional, Lepage, S., additional, Sheppard, R., additional, Giannetti, N., additional, Lavoie, J., additional, Mansour, A., additional, Phillips, M.S., additional, Turgeon, J., additional, Provost, S., additional, Normand, V., additional, Mongrain, I., additional, Langlois, M., additional, O'Meara, E., additional, Ducharme, A., additional, Racine, N., additional, Guertin, M.C., additional, Tardif, J.C., additional, Rouleau, J.L., additional, and White, M., additional

Published
2016
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9. Angiotensin receptor neprilysin inhibition compared with enalapril on the risk of clinical progression in surviving patients with heart failure

Author

Packer, M., McMurray, J.J., Desai, A.S., Gong, J., Lefkowitz, M.P., Rizkala, A.R., Rouleau, J.L., Shi, V.C., Solomon, S.D., Swedberg, K., Zile, M., Andersen, K., Arango, J.L., Arnold, J.M., Belohlavek, J., Bohm, M., Boytsov, S., Burgess, L.J., Cabrera, W., Calvo, C., Chen, C.H., Dukat, A., Duarte, Y.C., Erglis, A., Fu, M., Gomez, E., Gonzalez-Medina, A., Hagege, A.A., Huang, J., Katova, T., Kiatchoosakun, S., Kim, K.S., Kozan, O., Llamas, E.B., Martinez, F., Merkely, B., Mendoza, I., Mosterd, A., Negrusz-Kawecka, M., Peuhkurinen, K., Ramires, F.J., Refsgaard, J., Rosenthal, A., Senni, M., Sibulo, A.S., Jr., Silva-Cardoso, J., Squire, I.B., Starling, R.C., Teerlink, J.R., Vanhaecke, J., Vinereanu, D., Wong, R.C., Bellersen, L., et al., Packer, M., McMurray, J.J., Desai, A.S., Gong, J., Lefkowitz, M.P., Rizkala, A.R., Rouleau, J.L., Shi, V.C., Solomon, S.D., Swedberg, K., Zile, M., Andersen, K., Arango, J.L., Arnold, J.M., Belohlavek, J., Bohm, M., Boytsov, S., Burgess, L.J., Cabrera, W., Calvo, C., Chen, C.H., Dukat, A., Duarte, Y.C., Erglis, A., Fu, M., Gomez, E., Gonzalez-Medina, A., Hagege, A.A., Huang, J., Katova, T., Kiatchoosakun, S., Kim, K.S., Kozan, O., Llamas, E.B., Martinez, F., Merkely, B., Mendoza, I., Mosterd, A., Negrusz-Kawecka, M., Peuhkurinen, K., Ramires, F.J., Refsgaard, J., Rosenthal, A., Senni, M., Sibulo, A.S., Jr., Silva-Cardoso, J., Squire, I.B., Starling, R.C., Teerlink, J.R., Vanhaecke, J., Vinereanu, D., Wong, R.C., Bellersen, L., and et al.

Abstract

Item does not contain fulltext, BACKGROUND: Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. METHODS AND RESULTS: We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of medical treatment for heart failure (520 versus 604; hazard ratio, 0.84; 95% confidence interval, 0.74-0.94; P=0.003) or an emergency department visit for worsening heart failure (hazard ratio, 0.66; 95% confidence interval, 0.52-0.85; P=0.001). The patients in the LCZ696 group had 23% fewer hospitalizations for worsening heart failure (851 versus 1079; P<0.001) and were less likely to require intensive care (768 versus 879; 18% rate reduction, P=0.005), to receive intravenous positive inotropic agents (31% risk reduction, P<0.001), and to have implantation of a heart failure device or cardiac transplantation (22% risk reduction, P=0.07). The reduction in heart failure hospitalization with LCZ696 was evident within the first 30 days after randomization. Worsening of symptom scores in surviving patients was consistently more common in the enalapril group. LCZ696 led to an early and sustained reduction in biomarkers of myocardial wall stress and injury (N-terminal pro-B-type natriuretic peptide and troponin) versus enalapril. CONCLUSIONS: Angiotensin-neprilysin inhibition prevents the clinical progression of surviving patients with heart failure more effectively than angiotensin-converting enzyme inhibition. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifi

Published
2015

11. Effect of Nesiritide in Patients with Acute Decompensated Heart Failure

Author

OConnor, C.M., Starling, R.C., Hernandez, A.F., Armstrong, P.W., Dickstein, K., Hasselblad, V., Heizer, G.M., Komajda, M., Massie, B.M., McMurray, J.J. V., Nieminen, M.S., Reist, C.J., Rouleau, J.L., Swedberg, K., Adams, K.F., Anker, S.D., Atar, D., Battler, A., Botero, R., Bohidar, N.R., Butler, J., Clausell, N., Corbalan, R., Costanzo, M.R., Dahlström, Ulf, Deckelbaum, L.I., Diaz, R., Dunlap, M.E., Ezekowitz, J.A., Feldman, D., Felker, G.M., Fonarow, G.C., Gennevois, D., Gottlieb, S.S., Hill, J.A., Hollander, J.E., Howlett, J.G., Hudson, M.P., Kociol, R.D., Krum, H., Laucevicius, A., Levy, W.C., Mendez, G.F., Metra, M., Mittal, S., Oh, B.-H., Pereira, N.L., Ponikowski, P., Wilson, W.H., Tanomsup, S., Teerlink, J.R., Triposkiadis, F., Troughton, R.W., Voors, A.A., Whellan, D.J., Zannad, F., Califf, R.M., OConnor, C.M., Starling, R.C., Hernandez, A.F., Armstrong, P.W., Dickstein, K., Hasselblad, V., Heizer, G.M., Komajda, M., Massie, B.M., McMurray, J.J. V., Nieminen, M.S., Reist, C.J., Rouleau, J.L., Swedberg, K., Adams, K.F., Anker, S.D., Atar, D., Battler, A., Botero, R., Bohidar, N.R., Butler, J., Clausell, N., Corbalan, R., Costanzo, M.R., Dahlström, Ulf, Deckelbaum, L.I., Diaz, R., Dunlap, M.E., Ezekowitz, J.A., Feldman, D., Felker, G.M., Fonarow, G.C., Gennevois, D., Gottlieb, S.S., Hill, J.A., Hollander, J.E., Howlett, J.G., Hudson, M.P., Kociol, R.D., Krum, H., Laucevicius, A., Levy, W.C., Mendez, G.F., Metra, M., Mittal, S., Oh, B.-H., Pereira, N.L., Ponikowski, P., Wilson, W.H., Tanomsup, S., Teerlink, J.R., Triposkiadis, F., Troughton, R.W., Voors, A.A., Whellan, D.J., Zannad, F., and Califf, R.M.

Abstract

Background Nesiritide is approved in the United States for early relief of dyspnea in patients with acute heart failure. Previous meta-analyses have raised questions regarding renal toxicity and the mortality associated with this agent. Methods We randomly assigned 7141 patients who were hospitalized with acute heart failure to receive either nesiritide or placebo for 24 to 168 hours in addition to standard care. Coprimary end points were the change in dyspnea at 6 and 24 hours, as measured on a 7-point Likert scale, and the composite end point of rehospitalization for heart failure or death within 30 days. Results Patients randomly assigned to nesiritide, as compared with those assigned to placebo, more frequently reported markedly or moderately improved dyspnea at 6 hours (44.5% vs. 42.1%, P = 0.03) and 24 hours (68.2% vs. 66.1%, P = 0.007), but the prespecified level for significance (P = 0.005 for both assessments or Pd less than= 0.0025 for either) was not met. The rate of rehospitalization for heart failure or death from any cause within 30 days was 9.4% in the nesiritide group versus 10.1% in the placebo group (absolute difference, -0.7 percentage points; 95% confidence interval [CI], -2.1 to 0.7; P = 0.31). There were no significant differences in rates of death from any cause at 30 days (3.6% with nesiritide vs. 4.0% with placebo; absolute difference, -0.4 percentage points; 95% CI, -1.3 to 0.5) or rates of worsening renal function, defined by more than a 25% decrease in the estimated glomerular filtration rate (31.4% vs. 29.5%; odds ratio, 1.09; 95% CI, 0.98 to 1.21; P = 0.11). Conclusions Nesiritide was not associated with an increase or a decrease in the rate of death and rehospitalization and had a small, nonsignificant effect on dyspnea when used in combination with other therapies. It was not associated with a worsening of renal function, but it was associated with an increase in rates of hypotension. On the basis of these results, nesiritide cannot b

Published
2011
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12. Results of a non-specific immunomodulation therapy on chronic heart failure (ACCLAIM trial): a placebo-controlled randomised trial

Author

Torre-Amione, G., Anker, S.D., Bourge, R.C., Colucci, W.S., Greenberg, B.H., Hildebrandt, P., Keren, A., Motro, M., Moye, L.A., Otterstad, J.E., Pratt, C.M., Ponikowski, P., Rouleau, J.L., Sestier, F., Winkelmann, B.R., Young, J.B., Torre-Amione, G., Anker, S.D., Bourge, R.C., Colucci, W.S., Greenberg, B.H., Hildebrandt, P., Keren, A., Motro, M., Moye, L.A., Otterstad, J.E., Pratt, C.M., Ponikowski, P., Rouleau, J.L., Sestier, F., Winkelmann, B.R., and Young, J.B.

Abstract

Background Evidence suggests that inflammatory mediators contribute to development and progression of chronic heart failure. We therefore tested the hypothesis that immunomodulation might counteract this pathophysiological mechanism in patients. Methods We did a double-blind, placebo-controlled study of a device-based non-specific immunomodulation therapy (IMT) in patients with New York Heart Association (NYHA) functional class II-IV chronic heart failure, left ventricular (LV) systolic dysfunction, and hospitalisation for heart failure or intravenous drug therapy in an outpatient setting within the past 12 months. Patients were randomly assigned to receive IMT (n=1213) or placebo (n=1213) by intragluteal injection on days 1, 2, 14, and every 28 days thereafter. Primary endpoint was the composite of time to death from any cause or first hospitalisation for cardiovascular reasons. The study continued until 828 primary endpoint events had accrued and all study patients had been treated for at least 22 weeks. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00111969. Findings During a mean follow-up of 10 . 2 months, there were 399 primary events in the IMT group and 429 in the placebo group (hazard ratio 0 . 92; 95% CI 0 . 80-1.05; p=0 . 22). In two prespecified subgroups of patients-those with no history of previous myocardial infarction (n=919) and those with NYHA II heart failure (n=689)-IMT was associated with a 26% (0.74; 0 . 57-0 . 95; p=0.02) and a 39% (0.61; 95% CI 0 . 46-0.80; p=0 . 0003) reduction in the risk of primary endpoint events, respectively. Interpretation Non-specific immunomodulation may have a role as a potential treatment for a large segment of the heart failure population, which includes patients without a history of myocardial infarction (irrespective of their functional NYHA class) and patients within NYHA class II Udgivelsesdato: 2008/1/19

Published
2008

13. Effect of antecedent hypertension and follow-up blood pressure on outcomes after high-risk myocardial infarction

Author

Thune, J.J., Signorovitch, J., Velazquez, E.J., McMurray, J.J., Califf, R.M., Maggioni, A.P., Rouleau, J.L., Howlett, J., Zelenkofske, S., Pfeffer, M.A., Solomon, S.D., Køber, Lars Valeur, Thune, J.J., Signorovitch, J., Velazquez, E.J., McMurray, J.J., Califf, R.M., Maggioni, A.P., Rouleau, J.L., Howlett, J., Zelenkofske, S., Pfeffer, M.A., Solomon, S.D., and Køber, Lars Valeur

Abstract

The influence of blood pressure on outcomes after high-risk myocardial infarction is not well characterized. We studied the relationship between blood pressure and the risk of cardiovascular events in 14 703 patients with heart failure, left ventricular systolic dysfunction, or both after acute myocardial infarction in the Valsartan in Myocardial Infarction Trial. We assessed the relationship between antecedent hypertension and outcomes and the association between elevated (systolic: >140 mm Hg) or low blood pressure (systolic: <100 mm Hg) in 2 of 3 follow-up visits during the first 6 months and subsequent cardiovascular events over a median 24.7 months of follow-up. Antecedent hypertension independently increased the risk of heart failure (hazard ratio [HR]: 1.19; 95% CI: 1.08 to 1.32), stroke (HR: 1.27; 95% CI: 1.02 to 1.58), cardiovascular death (HR: 1.11; 95% CI: 1.01 to 1.22), and the composite of death, myocardial infarction, heart failure, stroke, or cardiac arrest (HR: 1.13; 95% CI: 1.06 to 1.21). While low blood pressure in the postmyocardial infarction period was associated with increased risk of adverse events, patients with elevated blood pressure (n=1226) were at significantly higher risk of stroke (adjusted HR: 1.64; 95% CI: 1.17 to 2.29) and combined cardiovascular events (adjusted HR: 1.14; 95% CI: 1.00 to 1.31). Six months after a high-risk myocardial infarction, elevated systolic blood pressure, a potentially modifiable risk factor, is associated with an increased risk of subsequent stroke and cardiovascular events. Whether aggressive antihypertensive treatment can reduce this risk remains unknown Udgivelsesdato: 2008/1

Published
2007

14. Endocardial-myocardial interaction

Author

De Keulenaer, Gilles, Andries, Luc J., Fransen, Paul, Mohan, P., Kaluza, G., Rouleau, J.L., Brutsaert, Dirk L., and Sys, Stanislas

Published
1997

15. Effect of Nesiritide in Patients with Acute Decompensated Heart Failure

Author

O'Connor, C.M., primary, Starling, R.C., additional, Hernandez, A.F., additional, Armstrong, P.W., additional, Dickstein, K., additional, Hasselblad, V., additional, Heizer, G.M., additional, Komajda, M., additional, Massie, B.M., additional, McMurray, J.J.V., additional, Nieminen, M.S., additional, Reist, C.J., additional, Rouleau, J.L., additional, Swedberg, K., additional, Adams, K.F., additional, Anker, S.D., additional, Atar, D., additional, Battler, A., additional, Botero, R., additional, Bohidar, N.R., additional, Butler, J., additional, Clausell, N., additional, Corbalán, R., additional, Costanzo, M.R., additional, Dahlstrom, U., additional, Deckelbaum, L.I., additional, Diaz, R., additional, Dunlap, M.E., additional, Ezekowitz, J.A., additional, Feldman, D., additional, Felker, G.M., additional, Fonarow, G.C., additional, Gennevois, D., additional, Gottlieb, S.S., additional, Hill, J.A., additional, Hollander, J.E., additional, Howlett, J.G., additional, Hudson, M.P., additional, Kociol, R.D., additional, Krum, H., additional, Laucevicius, A., additional, Levy, W.C., additional, Méndez, G.F., additional, Metra, M., additional, Mittal, S., additional, Oh, B.-H., additional, Pereira, N.L., additional, Ponikowski, P., additional, Tang, W.H.W., additional, Tanomsup, S., additional, Teerlink, J.R., additional, Triposkiadis, F., additional, Troughton, R.W., additional, Voors, A.A., additional, Whellan, D.J., additional, Zannad, F., additional, and Califf, R.M., additional

Published
2011
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22. Contemporary management of patients with left ventricular systolic dysfunction. Results from the Study of Patients Intolerant of Converting Enzyme Inhibitors (SPICE) Registry

Author

Bart, B.A., primary, Ertl, G., additional, Held, P., additional, Kuch, J., additional, Maggioni, A.P., additional, McMurray, J., additional, Michelson, E.L., additional, Rouleau, J.L., additional, Warner Stevenson, L., additional, Swedberg, K., additional, Young, J.B., additional, Yusuf, S., additional, Sellers, M.A., additional, Granger, C.B., additional, Califf, R.M., additional, and Pfeffer for the SPICE investigators, M.A., additional

Published
1999
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25. Post myocardial infarction (MI) management patterns of pattents in the survival and ventricular enlargement (SAVE) study at Canadian and US Centers

Author

Rouleau, J.L., primary, Arnold, J.M.O., additional, Bernstein, V., additional, Cuddy, T.E., additional, Dagenais, G.R., additional, Geltman, E.M., additional, Goldman, S., additional, Gordon, D., additional, Lamas, G., additional, McCans, J., additional, McEwan, P., additional, Menapace, F.J., additional, Parker, J.O., additional, Pfeffer, M.A., additional, Sestier, F., additional, and Sussexfor, B., additional

Published
1990
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26. Bradykinin metabolism and hypotensive transfusion reactions.

Author

Cyr, M., Eastlund, T., Blais, Jr, C., Rouleau, J.L., Adam, A., and Blais, C Jr

Subjects
ACE inhibitors, ANIMAL experimentation, BLOOD transfusion reaction, BLOOD coagulation factors, COMPARATIVE studies, HYPOTENSION, INFLAMMATORY mediators, RESEARCH methodology, MEDICAL cooperation, RESEARCH, VASODILATORS, EVALUATION research
Published
2001
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27. Glucose and insulin abnormalities relate to functional capacity in patients with congestive heart failure.

Author

Suskin, N, McKelvie, R.S, Burns, R.J, Latini, R, Pericak, D, Probstfield, J, Rouleau, J.L, Sigouin, C, Solymoss, C.B, Tsuyuki, R, White, M, and Yusuf, S

Abstract

Aims In addition to diabetes mellitus, less severe abnormalities of glucose and insulin metabolism may be related to functional status in patients with heart failure. We examined the relationship of hyperglycaemia (≥6·1mmol.l−1) and hyperinsulinaemia (≥11·2mU.l−1) to functional status and cardiac function in patients with heart failure.Methods and Results Fasting plasma glucose and insulin levels were obtained in 663 heart failure patients. The average left ventricular ejection fraction was 0·28±0·07, 63% were in New York Heart Association Functional Class (NYHA-FC) I/II and 37% were in NYHA-FC III/IV. Twenty seven percent had diabetes mellitus, but an additional 8% had undiagnosed diabetes mellitus (glucose ≥7mmol.l−1) and 9% had glucose levels between 6·1 and 7mmol.l−1, so that a total of 43% (287) of patients had elevated glucose levels (≥6·1mmol.l−1). In general, more diabetic patients had NYHA-FC III/IV symptoms, shorter 6min walk distances, but similar left ventricular ejection fractions compared to non-diabetic patients. The non-diabetic patients in NYHA-FC III/IV had higher glucose and insulin levels than patients in NYHA-FC I/II (6·3±0·2 vs 5·6±0·1mmol.l−1,P <0·001 and 19·6±2·3 vs 10·2±0·6mU.l−1, P<0·001). Non-diabetic patients with elevated glucose levels had shorter 6min walk distances compared to those with normal glucose levels (368·2±8m vs 389·±4m, P=0·02), however, left ventricular ejection fraction was similar.Conclusion Glucose abnormalities are extremely common in heart failure patients (43% of patients). Diabetes mellitus and hyperglycaemia or hyperlinsulinaemia in non-diabetic patients were related to worse symptomatic status but not worsening left ventricular ejection fraction compared to patients with normal glucose and insulin levels. [ABSTRACT FROM PUBLISHER]

Published
2000
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28. Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study.

Author

Vantrimpont, P., Rouleau, J.L., Ciampi, A., Harel, F., de Champlain, J., Bichet, D., Moyé, L.A., and Pfeffer, M.

Abstract

Aims To describe the temporal evolution of neurohumoral activation in survivors of myocardial infarction with left ventricular dysfunction who are initially asymptomatic and to relate this to prognosis.Methods and Results Patients in the neurohumoral substudy (n=534) of the Survival and Ventricular Enlargement (SAVE) study had their neurohormones measured at baseline, 3, 12 and 24 months post-infarction, were followed 38±7 months and had these values related to prognosis. All patients had a left ventricular ejection fraction ≤40% early post-infarction. Atrial natriuretic peptide, aldosterone, norepinephrine and plasma renin activity decreased progressively over time. Patients with events had a persistent increase in these neurohormones with those dying within the first 24 months of follow-up having the greatest increase. Treatment with captopril affected only plasma renin activity (increase) and aldosterone (decrease). For patients who remained asymptomatic for the first 3 months post-infarction (n=471), by multivariate analyses (all neurohormones together with non-neurohumoral risk factors), 3-month plasma atrial natriuretic peptide and aldosterone were the most closely related to the development of severe heart failure or to the combined end-points (cardiovascular death, myocardial infarction, or severe heart failure). No neurohormone was related to recurrent myocardial infarction or to cardiovascular mortality. When the last neurohormone measured prior to an event was considered along with non-neurohumoral risk factors (adjusted univariate), atrial natriuretic peptide, aldosterone, norepinephrine and epinephrine were associated with prognosis indicating that a time-dependent analysis identified a closer relationship between neurohormones and events than that identified by 3-month values. However, by multivariate analyses atrial natriuretic peptide was the only neurohormone associated with an event, being associated with the development of severe heart failure (P<0·001) and the combined end-points (P=0·022). However, when neurohormones were con-sidered as binary variables, activated or non-activated (defined as >1·96SD above the mean of age-matched controls), an association between activation of norepinephrine prior to recurrent myocardial infarction (P<0·001) and combined end-points (P<0·01) and between activation of aldosterone and severe heart failure (P<0·05) was identified.Conclusions Neurohumoral activation decreases pro-gressively post-infarction, but only in patients with a good prognosis. In patients with a left ventricular ejection fraction ≤40% and asymptomatic post-infarction plasma atrial natriuretic peptide at 3 months, aldosterone levels appeared to be the neurohormones most closely associated with prognosis. Increased levels of atrial natriuretic peptide, aldosterone and norepinephrine appear to be temporally most closely associated with events. [ABSTRACT FROM PUBLISHER]

Published
1998
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29. Short- and long-acting angiotensin-converting enzyme inhibitors: A randomized trial of lisinopril versus captopril in the treatment of congestive heart failure

Author

Giles, Thomas D., Katz, Richard, Sullivan, Jay M., Wolfson, Paul, Haugland, Mark, Kirlin, Philip, Powers, Eric, Rich, Stuart, Hackshaw, Barry, Chiaramida, Anthony, Rouleau, J.L., Fisher, Mary B., Pigeon, Joseph, and Rush, Janet E.

Abstract

A randomized, parallel, double-blind study was performed with lisinopril, a long-acting angiotensin-converting enzyme inhibitor, versus captopril, a shorter-acting angiotensin-converting enzyme inhibitor, in the treatment of congestive heart failure. All patients were in New York Heart Association class II, III or IV and had remained symptomatic despite therapy with digoxin and diuretics. After a 4 to 14 day placebo baseline period, patients were randomized to receive either lisinopril, 5 mg orally once per day (n = 94), or captopril, 12.5 mg orally three times per day (n = 95), in addition to continuation of digoxin and diuretics. The dose of study drug could be doubled at 4 week intervals for a total of 12 weeks of double-blind therapy. The maximal dose was 20 mg once per day of lisinopril or 50 mg three times per day of captopril.

Published
1989
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30. The cardiac endothelium: Functional morphology, development, and physiology

Author

Brutsaert, D.L., De Keulenaer, G.W., Fransen, P., Mohan, P., Kaluza, G.L., Andries, L.J., Rouleau, J.L., and Sys, S.U.

Abstract

Cardiac endothelial cells, regardless of whether they are from endocardial or from coronary (micro)vascular origin, directly modulate performance of the subjacent cardiomyocytes, resulting in control of the onset of ventricular relaxation and rapid filling of the heart. This review summarizes major features of the morphology, embryology, and comparative physiology of cardiac endothelial cells as well as the experimental observations on how cardiac endothelial cells affect the mechanical performance of the heart. As for the underlying mechanisms of the interaction between cardiac endothelial cells and cardiomyocytes, two working hypotheses have been postulated over the past years; (1) interaction mediated through a trans-endothelial physicochemical gradient for various ions (active blood-heart barrier), and (2) interaction mediated through the release by the cardiac endothelial cells of various cardioactive substances, eg, nitric oxide, endothelin, and prostacyclin. These two mechanisms may act in concert or in parallel.

Published
1996
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31. Absence of a deleterious effect of calcium channel blockers in patients with left ventricular dysfunction after myocardial infarction: The SAVE study experience

Author

Hager, W., Davis, B.R., Riba, A., Moye, L.A., Wun, C.C., Rouleau, J.L., Lamas, G.A., and Pfeffer, M.A.

Abstract

Background As a result of randomized controlled trials with calcium channel blockers after myocardial infarction, concern has developed that these agents are associated with an increased risk of cardiovascular events, particularly in the presence of left ventricular dysfunction. Methods To test the hypothesis that calcium channel blockers increase cardiovascular events in such patients, the incidence of all-cause mortality, cardiovascular death, severe heart failure, and recurrent infarction was examined in 940 patients taking calcium channel blockers and 1180 not taking them 24 hours before randomization to placebo or captopril in the Survival and Ventricular Enlargement (SAVE) Trial. All patients had an ejection fraction @?40%. Relative risks for calcium channel blocker users versus nonusers and the 95% confidence intervals were computed with univariate and multivariate Cox regressions. Adjustments were made for differences in baseline covariates. Results For all causes of mortality, the relative risk for calcium channel blocker users versus nonusers was 0.96, with the 95% confidence interval of 0.78 to 1.17. In the SAVE placebo and captopril groups, the relative risks for the development of severe heart failure among the calcium channel block users versus nonusers were 0.95 and 1.23, with the 95% confidence interval of 0.72 to 1.25 and 0.88 to 1.71, respectively. A similar neutral result held for patients with and without a history of hypertension. Furthermore, calcium channel blockers did not alter the benefit of the angiotensin converting enzyme inhibitor, captopril. Conclusions This analysis of the nonrandomized clinical use of calcium channel blockers in the postmyocardial infarction population with left ventricular dysfunction did not identify either a clinical deterioration or improvement with respect to subsequent cardiovascular events. (Am Heart J 1998;135:406-13.)

Published
1998
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41. Pulse pressure and the risk of heart failure hospitalization after acute myocardial infarction: insights from the SAVE trial

Author

Valencia-Serrano, F., Lamas, G.A., Mitchell, G.F., Flaker, G.C., Rouleau, J.L., Braunwald, E., Solomon, S.D., and Pfeffer, M.A.

Subjects
HEART failure risk factors, MYOCARDIAL infarction
Abstract

An abstract of the article "Pulse pressure and the risk of heart failure hospitalization after acute myocardial infarction: insights from the SAVE trial," by F. Valencia-Serrano and colleagues is presented.

Published
2008
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45. Angiotensin–Neprilysin Inhibition in Heart Failure with Preserved Ejection Fraction

Author

Hans-Dirk Düngen, Margaret M. Redfield, Jean L. Rouleau, Brian Claggett, Faiez Zannad, Aldo P. Maggioni, Junbo Ge, Eva Goncalvesova, Marc A. Pfeffer, Béla Merkely, Inder S. Anand, Jianjian Gong, Sergey Boytsov, Felipe Martinez, José Francisco Kerr Saraiva, Victor Shi, Małgorzata Lelonek, Milton Packer, Martin Lefkowitz, Dirk J. van Veldhuisen, Adel R. Rizkala, Scott D. Solomon, Burkert Pieske, John G.F. Cleland, Akshay S. Desai, Michael R. Zile, Michele Senni, Jingmin Zhou, Sanjiv J. Shah, Tzvetana Katova, Pardeep S. Jhund, Carolyn S.P. Lam, Josep Comín-Colet, John J.V. McMurray, Solomon, S, Mcmurray, J, Anand, I, Ge, J, Lam, C, Maggioni, A, Martinez, F, Packer, M, Pfeffer, M, Pieske, B, Redfield, M, Rouleau, J, van Veldhuisen, D, Zannad, F, Zile, M, Desai, A, Claggett, B, Jhund, P, Boytsov, S, Comin-Colet, J, Cleland, J, Düngen, H, Goncalvesova, E, Katova, T, Kerr Saraiva, J, Lelonek, M, Merkely, B, Senni, M, Shah, S, Zhou, J, Rizkala, A, Gong, J, Shi, V, Lefkowitz, M, PARAGON-HF Investigators and, C, Cardiovascular Centre (CVC), Solomon S.D., McMurray J.J.V., Anand I.S., Ge J., Lam C.S.P., Maggioni A.P., Martinez F., Packer M., Pfeffer M.A., Pieske B., Redfield M.M., Rouleau J.L., Van Veldhuisen D.J., Zannad F., Zile M.R., Desai A.S., Claggett B., Jhund P.S., Boytsov S.A., Comin-Colet J., Cleland J., Dungen H.-D., Goncalvesova E., Katova T., Kerr Saraiva J.F., Lelonek M., Merkely B., Senni M., Shah S.J., Zhou J., Rizkala A.R., Gong J., Shi V.C., Lefkowitz M.P., and Borghi C

Subjects
Male, MIDRANGE, MIDDLE CHILD, Tetrazoles, Insuficiència cardíaca, Sex Factor, 030204 cardiovascular system & hematology, Hospital patients, 0302 clinical medicine, Cardiovascular Disease, Single-Blind Method, 030212 general & internal medicine, Neprilysin, Tetrazole, Angiotensin Receptor Antagonists, Aminobutyrates, Angiotensin Receptor Antagonist, IMPAIRED SYSTOLIC FUNCTION, General Medicine, Stroke volume, Middle Aged, SPIRONOLACTONE, Hospitalization, Drug Combinations, HIPOTENSÃO, Valsartan, Cardiovascular Diseases, Cardiology, Female, Hypotension, medicine.drug, Human, Angiotensines, medicine.medical_specialty, Angiotensins, Aminobutyrate, Aged, Angioedema, Double-Blind Method, Follow-Up Studies, Heart Failure, Humans, Quality of Life, Sex Factors, Stroke Volume, Heart failure, Follow-Up Studie, 03 medical and health sciences, Internal medicine, Renin–angiotensin system, medicine, Mortalitat, Mortality, Malalts hospitalitzats, business.industry, fungi, medicine.disease, business, Heart failure with preserved ejection fraction, Sacubitril, Valsartan
Abstract

Background: \ud The angiotensin receptor–neprilysin inhibitor sacubitril–valsartan led to a reduced risk of hospitalization for heart failure or death from cardiovascular causes among patients with heart failure and reduced ejection fraction. The effect of angiotensin receptor–neprilysin inhibition in patients with heart failure with preserved ejection fraction is unclear.\ud \ud Methods: \ud We randomly assigned 4822 patients with New York Heart Association (NYHA) class II to IV heart failure, ejection fraction of 45% or higher, elevated level of natriuretic peptides, and structural heart disease to receive sacubitril–valsartan (target dose, 97 mg of sacubitril with 103 mg of valsartan twice daily) or valsartan (target dose, 160 mg twice daily). The primary outcome was a composite of total hospitalizations for heart failure and death from cardiovascular causes. Primary outcome components, secondary outcomes (including NYHA class change, worsening renal function, and change in Kansas City Cardiomyopathy Questionnaire [KCCQ] clinical summary score [scale, 0 to 100, with higher scores indicating fewer symptoms and physical limitations]), and safety were also assessed.\ud \ud Results: \ud There were 894 primary events in 526 patients in the sacubitril–valsartan group and 1009 primary events in 557 patients in the valsartan group (rate ratio, 0.87; 95% confidence interval [CI], 0.75 to 1.01; P=0.06). The incidence of death from cardiovascular causes was 8.5% in the sacubitril–valsartan group and 8.9% in the valsartan group (hazard ratio, 0.95; 95% CI, 0.79 to 1.16); there were 690 and 797 total hospitalizations for heart failure, respectively (rate ratio, 0.85; 95% CI, 0.72 to 1.00). NYHA class improved in 15.0% of the patients in the sacubitril–valsartan group and in 12.6% of those in the valsartan group (odds ratio, 1.45; 95% CI, 1.13 to 1.86); renal function worsened in 1.4% and 2.7%, respectively (hazard ratio, 0.50; 95% CI, 0.33 to 0.77). The mean change in the KCCQ clinical summary score at 8 months was 1.0 point (95% CI, 0.0 to 2.1) higher in the sacubitril–valsartan group. Patients in the sacubitril–valsartan group had a higher incidence of hypotension and angioedema and a lower incidence of hyperkalemia. Among 12 prespecified subgroups, there was suggestion of heterogeneity with possible benefit with sacubitril–valsartan in patients with lower ejection fraction and in women.\ud \ud Conclusions: \ud Sacubitril–valsartan did not result in a significantly lower rate of total hospitalizations for heart failure and death from cardiovascular causes among patients with heart failure and an ejection fraction of 45% or higher. (Funded by Novartis; PARAGON-HF ClinicalTrials.gov number, NCT01920711.)

Published
2019
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