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(Circulation. 1999;100:2312.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Comparative Effects of Low and High Doses of the Angiotensin-Converting Enzyme Inhibitor, Lisinopril, on Morbidity and Mortality in Chronic Heart Failure
From the College of Physicians and Surgeons (M.P.), Columbia University, New York, NY; Imperial College School of Medicine (P.A.P-W.), University of London, UK; University of Alberta (P.W.A.), Edmonton, Canada; University of Hull (J.G.F.C.), UK; University of Adelaide (J.H.), Australia; University of California (B.M.M.), San Francisco; Karolinska Institutet (L.R.), Stockholm, Sweden; Aarhus University Hospital (K.T.), Denmark; and University of Texas, Galveston (B.F.U).
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionAppendix 1References |
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Background—Angiotensin-converting enzyme (ACE) inhibitors are generally prescribed by physicians in doses lower than the large doses that have been shown to reduce morbidity and mortality in patients with heart failure. It is unclear, however, if low doses and high doses of ACE inhibitors have similar benefits.
Methods and Results—We randomly assigned 3164 patients with New
York Heart Association class II to IV heart failure and an ejection
fraction 
30% to double-blind treatment with either low doses (2.5 to
5.0 mg daily, n=1596) or high doses (32.5 to 35 mg daily, n=1568) of
the ACE inhibitor, lisinopril, for 39 to 58
months, while background therapy for heart failure was continued. When
compared with the low-dose group, patients in the high-dose group had a
nonsignificant 8% lower risk of death (P=0.128) but a
significant 12% lower risk of death or hospitalization for any reason
(P=0.002) and 24% fewer hospitalizations for heart
failure (P=0.002). Dizziness and renal insufficiency was
observed more frequently in the high-dose group, but the 2 groups were
similar in the number of patients requiring discontinuation of the
study medication.
Conclusions—These findings indicate that patients with heart failure should not generally be maintained on very low doses of an ACE inhibitor (unless these are the only doses that can be tolerated) and suggest that the difference in efficacy between intermediate and high doses of an ACE inhibitor (if any) is likely to be very small.
Key Words: heart failure • drugs • mortality • morbidity • trials
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Several treatment guidelines have made a strong recommendation to physicians that angiotensin-converting enzyme (ACE) inhibitors be used in all patients with heart failure resulting from left ventricular systolic dysfunction who can tolerate treatment with these drugs.1 2 Despite this guidance, a large proportion of patients with heart failure are not receiving ACE inhibitors,3 4 and when used, the doses prescribed are substantially smaller than the target doses used in the large-scale studies that established the utility of these drugs.5 This practice persists although there is little information about the efficacy of low doses of ACE inhibitors in the treatment of chronic heart failure.
The preference of physicians for low doses of ACE inhibitors may reflect the perception that low doses are as effective as high doses and are associated with a significantly lower risk of important side effects.5 Yet, the validity of these 2 assumptions has never been adequately tested in a controlled clinical trial, because most studies have been performed to determine if, not how, ACE inhibitors should be used in the treatment of heart failure. The few studies that have compared low and high doses of ACE inhibitors in heart failure have focused on their physiological and symptomatic effects6 7 8 9 10 and thus were too small to evaluate possible differences between low and high doses on the risk of major clinical events.
We conducted the Assessment of Treatment with Lisinopril and Survival (ATLAS) study to compare the efficacy and safety of low and high doses of ACE inhibition on the risk of death and hospitalization in chronic heart failure.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Patients were recruited into the ATLAS study if they had New York Heart Association (NYHA) class II, III, or IV symptoms of heart failure associated with a left ventricular ejection fraction
30% despite treatment with diuretics for 
2
months. Patients with class II symptoms were required to have received
treatment for heart failure in an emergency room or hospital within 6
months. Prior use of digitalis, ACE inhibitors, or
vasodilators was allowed but not mandated. Patients were excluded if
they had had an acute coronary ischemic event or
revascularization procedure within 2 months, had a
history of sustained or symptomatic ventricular
tachycardia, were known to be intolerant of ACE
inhibitors, had a serum creatinine >2.5 mg/dL,
or had any noncardiac disorder that could limit survival. The trial was
conducted in accordance with the Declaration of Helsinki; the protocol
was approved by the institutional review boards of all 287
participating hospitals in all 19 countries; written informed consent
was obtained from all patients.
Study Design
Following an initial evaluation, all patients received
open-label lisinopril for 4 weeks to assess their ability
to tolerate the drug, as described previously.11 Those who
could tolerate 12.5 to 15 mg daily for 2 weeks were randomly assigned
(double-blind, 1:1 ratio) to either a low-dose or high-dose ACE
inhibitor strategy. The target dose of
lisinopril was 2.5 to 5.0 mg daily in the low-dose group
and 32.5 to 35 mg daily in the high-dose group. These doses were
selected on the basis of data indicating that doses of 2.5 to 5.0 mg of
lisinopril daily had favorable hemodynamic
effects5 8 and that doses of 20 to 40 mg daily were
comparable to the doses of ACE inhibitors used in clinical
trials that demonstrated a reduction in morbidity and
mortality.12 13 14 To achieve these targets, after
randomization all patients received a 2.5- or 5.0-mg tablet of
open-label lisinopril once daily (dose was selected by the
investigator); in addition, patients received up to three 10-mg tablets
of double-blind lisinopril (high-dose strategy) or matching
placebo (low-dose strategy). The study medications were continued at
the highest tolerated doses (along with the patient’s usual
medications for heart failure) for the remainder of the trial. Changes
in NYHA class and laboratory tests were evaluated every 3 to 6 months.
If the patient’s condition deteriorated, physicians could prescribe
open-label therapy with an ACE inhibitor, after which
dosing with the study medication could be maintained, reduced, or
discontinued at the discretion of the investigator. The study was to be
completed when the last patient randomized into the study had been
followed for a minimum of 3 years or until 1600 patients had died.
End Points
The primary end point was all-cause mortality, and the 4
secondary end points specified in the original protocol were
cardiovascular mortality,
cardiovascular hospitalizations, all-cause mortality
combined with cardiovascular hospitalizations, and
cardiovascular mortality combined with
cardiovascular hospitalizations. While the study was in
progress, and without knowledge of any interim results or treatment
assignments, the Steering Committee recognized that hospitalization for
any reason (rather than for a cardiovascular reason)
represented a less biased approach to the analysis
of morbidity and accordingly added (in March 1997) the combined risk of
all-cause mortality and hospitalization for any reason to the list of
end points. Because of concerns that the overall mortality rate in the
study was lower than expected, the Steering Committee considered
designating this new end point as the primary end point but instead
chose to designate it as a secondary end point with priority over all
others. The combined risk of fatal and nonfatal myocardial infarction
plus hospitalization for unstable angina was also added as a
prespecified analysis. All end points were adjudicated
according to prespecified criteria by an End Points Committee blinded
to the treatment assignment.
Statistical Analysis
A sample size of 3000 patients was selected on the basis of the
following assumptions: recruitment would be completed in 18 months with
the last patient followed for 36 months, the 1-year mortality rate in
the high-dose group would be 19%, and the study would have 90% power
to detect a 15% relative difference in mortality between the treatment
groups (
=0.05, 2-tailed). Because the use of high doses of ACE
inhibitors had been reported to reduce mortality by 16%
when compared with placebo,13 the protocol assumed that
low doses of ACE inhibitors would have little effect on the
risk of death. No allowance was made for the possibility that patients
might stop taking the double-blind study medication or commence
open-label therapy with an ACE inhibitor.
An independent Data and Safety Monitoring Board was prospectively constituted at the start of the study, periodically reviewed the blinded results, and was empowered to recommend early termination of the study if it observed a treatment effect that exceeded the prespecified boundaries. To protect against increasing a false-positive error rate due to repeated interim analyses, the Lan-DeMets procedure15 using an O’Brien-Fleming type boundary16 was used. Using this procedure, comparisons of the 2 treatments for all-cause mortality at the scheduled end of the trial were considered significant if P<0.0394 was attained; thus, 96.1% CIs were used for the hazard ratio for the primary end point. In contrast, secondary end points were assessed at the 0.05 level of significance, and 95% CIs were used to describe their hazard ratios.
Cumulative survival curves were constructed as time-to-first-event plots by Kaplan-Meier survivorship methods, and differences between the curves were tested for significance by both the log-rank statistic and a Cox proportional hazard regression model, adjusted (as protocol-specified) for NYHA class and ejection fraction. The analyses included all randomized patients, and all events were assigned to the patient’s randomized treatment group (according to the intention-to-treat principle). According to the original protocol, the occurrence of cardiac transplantation was classified as a cardiovascular death. Between-group differences in postrandomization events were analyzed by the Wilcoxon rank sum test, and between-group differences in laboratory values were evaluated by ANCOVA using baseline values as the covariate.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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The ATLAS Trial began on October 13, 1992 and completed follow-up of all patients at midnight on September 14, 1997. Of the 3793 patients who entered the initial open-label tolerability phase, 629 were not deemed eligible for randomization: 55 patients died or had worsening heart failure, 176 patients were withdrawn for possible side effects when the dose of lisinopril was increased toward 12.5 to 15 mg, and 398 patients did not fulfill the criteria for participation in the study or did not participate for administrative or other reasons. The remaining 3164 patients were randomized to double-blind therapy: 1596 to the low-dose strategy and 1568 to the high-dose strategy.
The 2 groups were similar with respect to all pretreatment
characteristics (Table 1
).11
After randomization, target doses were achieved in 92.7% of the
patients in the low-dose group and 91.3% of the patients in the
high-dose group. At the end of dose titration following randomization,
patients received an average of 4.5±1.1 mg daily of
lisinopril in the low-dose group and 33.2±5.4 mg daily of
lisinopril in the high-dose group. During the course of the
study, 30.6% of the patients in the low-dose group and 27.2% of the
patients in the high-dose group stopped taking the study medications.
Moreover, 22.1% of the patients in the low-dose group and 18.3% of
the patients in the high-dose group were started on open-label therapy
with an ACE inhibitor other than the study drug. The
duration of follow-up in surviving patients ranged from 39 to 58 months
(median 45.7). No patient was lost to follow-up with respect to vital
status.
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Effect on Mortality
Patients in the high-dose group had an 8% lower risk of all-cause
mortality (P=0.128; Figure 1) and a 10% lower risk of
cardiovascular mortality (P=0.073) than
those in the low-dose group; neither difference was statistically
significant. The number of cardiac transplants was small and similar in
the 2 groups (20 in the low-dose group and 19 in the high-dose group);
inclusion or exclusion of the transplants did not affect the results.
The effect on mortality in subgroups was not different from the overall
effect (Figure 2).
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Effect on the Risk of Death and Hospitalization and on Total
Hospitalizations
The combined risk of morbidity and mortality was significantly
lower in the high-dose group than in the low-dose group regardless of
whether a comprehensive or cause-specific definition was used. For the
prioritized analysis of death or hospitalization for any
reason, patients in the high-dose group had a 12% lower risk than
those in the low-dose group, P=0.002 (Table 2 and Figure 3). The reduction in risk was similar
regardless of age, sex, cause of heart failure, ejection fraction, or
NYHA class (Figure 2
). A significant reduction in the combined
risk of death and hospitalization also was observed in the high-dose
group in all combined analyses of morbidity and mortality that
used a cause-specific definition of death or hospitalization (Table 2). However, the 8% lower risk of fatal and nonfatal myocardial
infarction and hospitalization for unstable angina in the high-dose
group was not statistically significant.
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When the total number of hospitalizations was analyzed
(including first and recurrent), the high-dose group experienced 13%
fewer hospitalizations for any reason (P=0.021), 16% fewer
hospitalizations for a cardiovascular reason
(P=0.05), and 24% fewer hospitalizations for heart failure
(P=0.002), Table 3. There were
no differences in NYHA functional class between the 2 treatment groups
at any time during the study.
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Safety
Of the 3793 patients who received open-label therapy with
lisinopril, 176 patients experienced adverse effects or
were found to have laboratory abnormalities (at a dose of 15 mg
daily) that prevented their randomization to double-blind therapy.
These included cough in 13 patients, hypotension/dizziness in 43
patients, renal insufficiency in 68 patients, and abnormal values for
serum potassium in 6 patients.
Three months after randomization, systolic blood pressure had decreased 4.4±0.6 mm Hg more and diastolic blood pressure had declined 2.3±0.4 mm Hg more in the high-dose group compared with the low-dose group (P<0.001), but the 2 groups showed little change in heart rate. At 3 months, the increase in serum creatinine in the high-dose group was slightly greater than in the low-dose group (P<0.001), but the number of patients with major increases in serum creatinine (>1 mg/dL) was not different.
As expected, patients in the high-dose group experienced dizziness,
hypotension, worsening renal function, more frequent
hyperkalemia, and less frequent hypokalemia than those
in the low-dose group (Table 4). However,
these side effects did not lead patients to stop the study medication
more frequently in the high-dose group than in the low-dose group
(17.0% versus 18.0%). Compared with the low-dose group, fewer
patients in the high-dose group experienced cough or reported worsening
heart failure as an adverse reaction.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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The results of the ATLAS study indicate that the use of high doses instead of low doses of the ACE inhibitor lisinopril reduces the risk of major clinical events in patients with chronic heart failure. This finding is consistent with earlier clinical studies, which suggested that high doses of ACE inhibitors produce greater hemodynamic and symptomatic benefits than low doses,9 10 and experimental studies, which indicated that high doses produce a larger reduction in mortality than low doses.17 Although high doses of enalapril were not superior to low doses in an earlier multicenter trial in heart failure,18 that study treated patients for only 6 months and recorded only 53 deaths and 90 hospitalizations for heart failure. In contrast, the ATLAS trial recorded nearly 1400 deaths and >8200 hospitalizations during a treatment period up to 5 years, and thus had sufficient power to detect small but meaningful differences in long-term outcome.
Nevertheless, the present study did not observe a significant difference between the 2 treatment groups in the risk of death, the primary end point of the study. This observation may represent the lack of a true difference or a smaller than anticipated treatment effect. When the protocol was first developed in 1992, we assumed that low doses of lisinopril would not decrease mortality rates. Hence, in calculating the sample size, we presumed that the difference in mortality risk between high doses and low doses in this study would be nearly identical to the observed difference in mortality risk between high doses of ACE inhibitors and placebo in the SOLVD trial,13 which enrolled similar types of patients. Yet, low doses of ACE inhibitors might favorably affect survival. In addition, the original calculations of sample size assumed that the annual mortality rate would be 19%, and they made no allowances for the possibility that patients randomized to high doses of ACE inhibitors might stop taking their study medication or that patients randomized to low doses of ACE inhibitors might start taking high doses of these drugs. Yet the observed annual mortality rate in the trial was only 15%, and many patients were not maintained on their assigned study medications.
It is noteworthy that patients receiving high doses did not experience a greater improvement in NYHA class than those who received low doses. The lack of a difference suggests that changes in symptoms cannot be used as a guide to the selection of a dose of an ACE inhibitor for clinical use, because an increase in dose may reduce the risk of death and hospitalization even if there is no improvement in functional status.5
As expected, adverse effects characteristic of ACE inhibitors were seen more frequently in the high-dose than in the low-dose group. More patients assigned to high doses experienced dizziness, hypotension, worsening renal function, and hyperkalemia, compared with those assigned to low doses. However, these adverse reactions could generally be managed by changes in the dose of lisinopril or concomitant medications, so that the number of patients who discontinued double-blind therapy because of these adverse reactions was small. Furthermore, consistent with the observed reduction in the frequency of hospitalizations, patients assigned to high doses reported fewer episodes of heart failure. Lessening of pulmonary congestion could also explain the lower incidence of cough observed in the high-dose group, even though cough is a side effect commonly associated with ACE inhibition. All of these observations should be viewed in the context that most patients (nearly 90%) had tolerated some dose of an ACE inhibitor before entering the study, and 4% of patients were excluded from participation because they could not tolerate intermediate doses of the drug.
Although we observed that high doses were more effective than low doses of ACE inhibitors in reducing the risk of death and hospitalization, our results cannot predict what we might have observed if low doses of ACE inhibitors had been compared with placebo or if high doses of ACE inhibitors had been compared with intermediate doses of these drugs. However, it is noteworthy that when compared with the low-dose group, the high-dose group had an 8% lower risk of death (rather than the 16% lower risk seen when high doses were compared with placebo in the SOLVD study)13 and a 15% lower risk of death or hospitalization for heart failure (compared with the 26% lower risk seen when high doses were compared with placebo in the SOLVD study).13 These observations suggest that low doses of ACE inhibitors may provide approximately half of the benefits associated with the use of high doses of these drugs. In the absence of an unusual dose-response relation, we would anticipate that differences in efficacy between high doses and intermediate doses would be even smaller than the small differences in efficacy between high doses and low doses observed in the present trial.
Our observations suggest that patients with heart failure should not be maintained on very low doses of an ACE inhibitor unless these are the only doses that can be tolerated. It is less clear, however, if patients should be titrated to the high doses used in the present study. Although the ATLAS trial did not compare the efficacy and safety of intermediate and high doses of an ACE inhibitor, it is likely that differences between such doses (if any) are very small.
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Acknowledgments |
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This study was supported by a grant from Zeneca Pharmaceuticals, Macclesfield, UK.
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Footnotes |
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Reprint requests to Dr M. Packer, Division of Circulatory Physiology, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032.
1 A list of the ATLAS Study Investigators and Coordinators appears in the Appendix. 
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Steering Committee
M. Packer (chair), P. Armstrong, J. Cleland, J. Horowitz, B. Massie, P. Poole-Wilson, L. Rydén.
Data and Safety Monitoring Board
J. Kjekshus (chair), A. Castaigne, A. Dunning, C. Furberg, H.
Wedel.
End Point Committee
K. Thygesen, B. Uretsky.
Principal Investigators
Australia: P. Aylward, E. Barin, A. Broughton, M.
Dooris, A. Hamer, J. Horowitz, G. Lane, G. Leitl, P. Macdonald, A.
Tonkin. Austria: H. Glogar, W. Klein, O. Pachinger.
Belgium: I. Bekaert, J. Beys, J. Col, J. Creplet, X. Dalle,
M. De Myttenaere, D. de Waele, J. Debaisieux, Y. Devaleriola, G.
Jouret, B. Marchandise, J. Melchior, K. Mitri, R. Ranquin, R.
Rozberg, P. Surmont, A. Van Dorpe, W. Van Mieghem, U. Van Walleghem, J.
Van Welden, A. Van Wylick, J. Vincke, R. Zenner. Canada: J.
Arnold, T. Cuddy, R. Davies, L. Finkelstein, W. Hui, M. Khouri, P.
Klinke, C. Koilpillai, W. Kostuk, C. Maranda, H. Mizgala, G. Moe, Y.
Morin, A. Pasternak, D. Phaneuf, N. Robitaille, F. Sestier, P. Tanser,
J. Warnica. Czech Republic: J. Bultas, V. Cepelak, I.
Dvorak, P. Havranek, F. Kolbel, J. Marek, V. Stanek, M. Stejfa, P.
Widimsky, J. Vortel. Denmark: P. Grande, T. Haghfelt, G.
Jensen, E. Madsen, J. Nielsen, P. Nielsen, O. Pedersen, T. Pindborg, T.
Svendsen, A. Thomassen. Finland: M. Harkonen, K.
Peuhkurinen, P. Portsi, L. Voipio-Pulkki. France: G.
Baradat, B. Citron, J. Clementy, D. Colonna, P. Cornaert, J. Davy, G.
Dussarat, D. Flammang, A. Gerbe, D. Herpin, J. Hirsch, M. Komajda, J.
Mallion, M. Mansour, M. Martelet, A. Monnier, J. Normand, J. Ollivier,
J. Pony, M. Rauscher, A. Rifaï, P. Sagnol, M. Toussaint, J.
Touze, J. Weber, P. Webert. Hungary: C. Farsang, A. Janosi,
E. Kekes, L. Matos, K. Pader. Netherlands: J. Deppenbroek,
G. Kan, J. Kingma, J. Kragten, C. Peels, J. Ruiter, A. Schelling, H.
Spierenburg, F. Van Bemmel, D. van den Berg. Norway: T.
Hole, J. Erikssen, J. Haerem, A. Mangschou, J. Otterstad, D. Torvik, T.
Wessel-Aas. Portugal: S. Gomes, J. Maciel, T. Martins, A.
Sales Luis. Republic of Ireland: J. Barton, P. Crean, W.
Fennell, M. Laher, B. Maurer, D. Murray, T. Pierce, D. Sugrue, P.
Sullivan. Slovak Republic: P. Jonas, E. Vilcikova.
Spain: E. Algeria Esquerra, A. Bethencourt Gonzalez, A.
Cortina Llosa, M. Garcia Moll, J. Gonzalez Juanatey, F. Malpartida de
Torres, J. Marques Defez, F. Perez Casar, F. Rodriguez Rodrigo, F.
Valles Belsue. Sweden: M. Ali, L. Engquist, L. Erhardt, T.
Flodin, M. Freitag, S. Hansen, J. Herlitz, C. Hofman-Bang, J.
Jonsson, U. Rosenqvist, A. Stjerna, K. Tolagen, C. Wettervik, B.
Widgren. Switzerland: W. Vetter, P. Willimann. United
Kingdom: A. Adgey, S. Ball, P. Barnes, T. Callaghan, M. Davies, F.
Dunn, R. Greenbaum, A. Harley, S. Joseph, G. Kaye, M. Lye, A. McLeod,
C. Morley, W. Penny, L. Ramsay, P. Richardson, R. Smith, A. Struthers,
C. Sykes, L. Tan, D. Waller, J. Webster, R. Wray. United
States: B. Abramowitz, K. Adams, I. Anand, E. Anderson, G.
Andreae, M. Arif, R. Bahler, C. Baird, Jr, T. Berndt, K. Bescak, R.
Bies, M. Brottman, J. Burnett, S. Butman, P. Callaham, P. Carson,
D. Chinoy, L. Christie, Jr, S. Chrysant, J. Cobler, S. Cohen, C.
Corder, J. Doherty, D. Donovan, J. Douglas, K. Dowd, R. DuBroff, T.
Dudley, J. Farmer, D. Farnham, H. Fesniak, R. Fowles, B. Fuhs, J.
Ghali, E. Giardina, T. Giles, J. Glode, S. Goldman, D. Goldscher, D.
Gottlieb, W. Graettinger, W. Hager, J. Heinsimer, W. Herndon, C.
Hughes, M. Hussain, B. Iteld, K. Kadel, M. Karetzky, H. Karunaratne, H.
Kennedy, D. Kereiakes, H. Kimmerling, B. Kosowsky, W. Lee, W. Lewis, I.
Loh, D. Mann, T. Marbury, B. Massie, F. McBarron, H. Meilman, E.
Miller, D. Miller, W. Miller, S. Murali, R. Nelson, G. Neuberg, A.
Niederman, R. Oatfield, P. Pande, T. Paul, Jr, P. Perlman, I. Pina, H.
Reddy, D. Rothrock, P. Schmidt, D. Schmidt, C. Schulman, S. Sedlis, S.
Sharma, R. Sher, R. Siegel, L. Smith, J. Sorensen, J. Stafford, T.
Stern, J. Suh, J. Svinarich, Y. Szlachcic, G. Timmis, F. Tobis, S.
Turner, S. Ung, J. Van Gilder, C. Vander Ark, K. Vaska, N. Vijay, M.
Wilson, D. Wohns, J. Work, D. Zwicke.
Received October 11, 1999; revision received October 21, 1999; accepted October 21, 1999.
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W. Doehner, M. Rauchhaus, P. Ponikowski, I. F. Godsland, S. von Haehling, D. O. Okonko, F. Leyva, A. J. Proudler, A. J.S. Coats, and S. D. Anker Impaired Insulin Sensitivity as an Independent Risk Factor for Mortality in Patients With Stable Chronic Heart Failure J. Am. Coll. Cardiol., September 20, 2005; 46(6): 1019 - 1026. [Abstract] [Full Text] [PDF]
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K. Sliwa, G. R. Norton, N. Kone, G. Candy, J. Kachope, A. J. Woodiwiss, C. Libhaber, P. Sareli, and R. Essop Impact of initiating carvedilol before angiotensin-converting enzyme inhibitor therapy on cardiac function in newly diagnosed heart failure J. Am. Coll. Cardiol., November 2, 2004; 44(9): 1825 - 1830. [Abstract] [Full Text] [PDF]
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M. Azizi, A. Bissery, M. Lamarre-Cliche, and J. Menard Integrating Drug Pharmacokinetics for Phenotyping Individual Renin Response to Angiotensin II Blockade in Humans Hypertension, April 1, 2004; 43(4): 785 - 790. [Abstract] [Full Text] [PDF]
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M. Packer Should B-Type Natriuretic Peptide Be Measured Routinely to Guide the Diagnosis and Management of Chronic Heart Failure? Circulation, December 16, 2003; 108(24): 2950 - 2953. [Full Text] [PDF]
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D. B. Petitti New hope for hormone replacement and the heart? J. Am. Coll. Cardiol., October 1, 2003; 42(7): 1246 - 1248. [Full Text] [PDF]
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S. Stewart, L. Blue, A. Walker, C. Morrison, and J.J.V. Mcmurray An economic analysis of specialist heart failure nurse management in the U.K. Can we afford not to implement it? Eur. Heart J., September 1, 2002; 23(17): 1369 - 1378. [Abstract] [Full Text] [PDF]
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T. Elung-Jensen, J. Heisterberg, A.-L. Kamper, J. Sonne, S. Strandgaard, and N. E. Larsen High serum enalaprilat in chronic renal failure Journal of Renin-Angiotensin-Aldosterone System, December 1, 2001; 2(4): 240 - 245. [Abstract] [PDF]
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M.C. Petrie, C. Berry, S. Stewart, and J.J.V. McMurray Failing ageing hearts Eur. Heart J., November 1, 2001; 22(21): 1978 - 1990. [PDF]
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D. P. Holst, D. Kaye, M. Richardson, H. Krum, D. Prior, A. Aggarwal, R. Wolfe, and P. Bergin Improved outcomes from a comprehensive management system for heart failure Eur J Heart Fail, October 1, 2001; 3(5): 619 - 625. [Abstract] [Full Text] [PDF]
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P. Bovet, F. Paccaud, H. L. McLeod, F. A. Masoudi, E. P. Havranek, E. Ofili, J. Flack, G. Gibbons, D. V. Exner, M. J. Domanski, et al. Race and Responsiveness to Drugs for Heart Failure N. Engl. J. Med., September 6, 2001; 345(10): 766 - 768. [Full Text] [PDF]
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Task Force for the Diagnosis and Treatment of Chro, W. J. Remme, and K. Swedberg Guidelines for the diagnosis and treatment of chronic heart failure Eur. Heart J., September 1, 2001; 22(17): 1527 - 1560. [PDF]
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E. Weil and J. V. Tu Quality of congestive heart failure treatment at a Canadian teaching hospital Can. Med. Assoc. J., August 1, 2001; 165(3): 284 - 287. [Abstract] [Full Text] [PDF]
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N. Giannetti Management of congestive heart failure: How well are we doing? Can. Med. Assoc. J., August 1, 2001; 165(3): 305 - 306. [Full Text] [PDF]
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J. McMurray, A. Cohen-Solal, R. Dietz, E. Eichhorn, L. Erhardt, R. Hobbs, A. Maggioni, I. Pina, J. Soler-Soler, and K. Swedberg Practical recommendations for the use of ACE inhibitors, beta-blockers and spironolactone in heart failure: putting guidelines into practice Eur J Heart Fail, August 1, 2001; 3(4): 495 - 502. [Abstract] [Full Text] [PDF]
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C. Iribarren, A. J. Karter, A. S. Go, A. Ferrara, J. Y. Liu, S. Sidney, and J. V. Selby Glycemic Control and Heart Failure Among Adult Patients With Diabetes Circulation, June 5, 2001; 103(22): 2668 - 2673. [Abstract] [Full Text] [PDF]
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M. E. Khalil, A. W. Basher, E. J. Brown Jr, and I. A. Alhaddad A remarkable medical story: benefits of angiotensin-converting enzyme inhibitors in cardiac patients J. Am. Coll. Cardiol., June 1, 2001; 37(7): 1757 - 1764. [Abstract] [Full Text] [PDF]
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C. Berry, D. R. Murdoch, and J. J.V. McMurray Economics of chronic heart failure Eur J Heart Fail, June 1, 2001; 3(3): 283 - 291. [Abstract] [Full Text] [PDF]
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D. V. Exner, D. L. Dries, M. J. Domanski, and J. N. Cohn Lesser Response to Angiotensin-Converting-Enzyme Inhibitor Therapy in Black as Compared with White Patients with Left Ventricular Dysfunction N. Engl. J. Med., May 3, 2001; 344(18): 1351 - 1357. [Abstract] [Full Text] [PDF]
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F. H. H. Leenen and B. Yuan Prevention of Hypertension by Irbesartan in Dahl S Rats Relates to Central Angiotensin II Type 1 Receptor Blockade Hypertension, March 1, 2001; 37(3): 981 - 984. [Abstract] [Full Text] [PDF]
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M. W. Rich Heart Failure in the 21st Century: A Cardiogeriatric Syndrome J. Gerontol. A Biol. Sci. Med. Sci., February 1, 2001; 56(2): 88M - 96. [Abstract] [Full Text]
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