New England Journal of Medicine December 21, 1995

A Clinical Trial of the Angiotensin-Converting-Enzyme Inhibitor Trandolapril in Patients with Left Ventricular Dysfunction after Myocardial Infarction

Lars Køber, Christian Torp-Pedersen, Jan E. Carlsen, et al.

Bottom Line

In patients with left ventricular systolic dysfunction following an acute myocardial infarction, the ACE inhibitor trandolapril significantly reduces all-cause mortality, cardiovascular death, and progression to severe heart failure.

Key Findings

1. Over a follow-up period of 24 to 50 months, 304 patients (34.7%) in the trandolapril group died from any cause, compared to 369 (42.3%) in the placebo group, representing a significant reduction in all-cause mortality (RR 0.78; 95% CI, 0.67 to 0.91; P=0.001).
2. Trandolapril significantly reduced the risk of death from cardiovascular causes (RR 0.75; 95% CI, 0.63 to 0.89; P=0.001).
3. The risk of sudden death was significantly lower in patients treated with trandolapril compared with placebo (RR 0.76; 95% CI, 0.59 to 0.98; P=0.03).
4. Progression to severe heart failure was notably less frequent in the trandolapril intervention arm (RR 0.71; 95% CI, 0.56 to 0.89; P=0.003).

Study Design

Design
RCT
Double-Blind
Sample
1,749
Patients
Duration
24-50 mo
Median
Setting
Multicenter, Denmark
Population Patients with a confirmed acute myocardial infarction and echocardiographic evidence of left ventricular systolic dysfunction (wall motion index ≤1.2, corresponding to LVEF ≤35%) evaluated 3 to 7 days post-infarction.
Intervention Oral trandolapril, initiated at a low test dose and titrated up to a target dose of 4 mg once daily.
Comparator Matching oral placebo.
Outcome All-cause mortality.

Study Limitations

The trial strictly enrolled patients with a depressed left ventricular ejection fraction (LVEF ≤35%), meaning the results cannot be reliably extrapolated to post-MI patients with preserved or mildly reduced ejection fractions.
Patients had to tolerate a test dose of the medication prior to randomization, which could introduce a degree of selection bias by excluding those most prone to early hypotensive or adverse effects.
Patients with severe uncontrolled diabetes or renal impairment (serum creatinine >2.3 mg/dL) were excluded, limiting generalizability to these more complex patient populations.

Clinical Significance

The TRACE trial established that early initiation of an ACE inhibitor (trandolapril) following a myocardial infarction in patients with left ventricular dysfunction provides a robust, long-term survival benefit. It reinforced the status of ACE inhibitors as a cornerstone, life-saving standard of care to prevent adverse remodeling and severe heart failure in this high-risk population.

Historical Context

Prior to TRACE, landmark trials such as SAVE (using captopril) and AIRE (using ramipril) had demonstrated mortality benefits for ACE inhibitors when started after a myocardial infarction in patients with LV dysfunction or clinical heart failure. TRACE (Trandolapril Cardiac Evaluation) corroborated these findings within a broad, consecutively screened population across Danish centers, helping solidify the robust 'class effect' of ACE inhibitors in reducing post-MI mortality.

Guided Discussion

High-yield insights from every perspective

Med Student
Medical Student

How does the inhibition of angiotensin-converting enzyme by trandolapril physiologically prevent the progression of left ventricular dysfunction after a myocardial infarction?

Key Response

ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, decreasing sympathetic activity, vasoconstriction, and aldosterone secretion. Crucially post-MI, this reduces afterload and inhibits maladaptive left ventricular remodeling (fibrosis and dilation), thereby preserving cardiac output and delaying heart failure.

Resident
Resident

Given the TRACE study findings, how should the timing of initiating an ACE inhibitor like trandolapril be managed in a hemodynamically stable patient newly diagnosed with an anterior STEMI and an ejection fraction of 30 percent?

Key Response

In TRACE, trandolapril was initiated 3 to 7 days post-MI, but current clinical practice, informed by this and subsequent trials (like ISIS-4 and GISSI-3), advocates for earlier initiation (within 24 hours) if the patient is hemodynamically stable, to maximize the prevention of early remodeling and sudden cardiac death.

Fellow
Fellow

The TRACE trial specifically utilized the wall-motion index via echocardiography to screen consecutive patients for LV dysfunction, distinguishing it from trials like SAVE and AIRE. How does this screening method impact the trial's applicability to the modern heart failure phenotype we see today?

Key Response

By systematically screening all MI patients with echo, TRACE captured a broader population including those with asymptomatic LV dysfunction, whereas AIRE required clinical signs of heart failure. This supports the modern concept of Stage B heart failure, reinforcing that structural heart disease warrants neurohormonal blockade even before overt clinical symptoms manifest.

Attending
Attending

How do the long-term mortality benefits of trandolapril observed in TRACE inform our discussions with post-MI patients who express a desire to stop their ACE inhibitor therapy once their clinical heart failure symptoms have resolved?

Key Response

TRACE demonstrated sustained reductions in all-cause mortality and sudden death, independent of symptomatic status. The teaching point is that ACE inhibitors in this setting are disease-modifying, anti-remodeling agents, not merely symptom-relievers, and lifelong continuation is recommended to maintain these mortality benefits.

Scholarly Review

Critical appraisal through the lens of expert reviewers and guideline development

PhD
PhD

TRACE utilized a highly specific echocardiographic core laboratory to ensure consistency in measuring the wall-motion index for inclusion. In the design of modern multicenter cardiovascular outcome trials, how does the trade-off between centralized core lab adjudication versus site-investigator reported ejection fraction affect statistical power and external validity?

Key Response

Using a core lab (like in TRACE) reduces measurement noise and increases internal validity, requiring a smaller sample size to achieve statistical power. However, site-reported measures might better reflect real-world practice, enhancing external validity. A PhD researcher must balance precision against generalizability when designing inclusion criteria for heart failure trials.

Journal Editor
Journal Editor

A notable aspect of the TRACE trial is that concurrent therapies standard today, such as primary PCI, dual antiplatelet therapy, and early beta-blocker use, were not universally applied. As an editor evaluating a contemporary post-MI neurohormonal blockade trial, how would you require authors to address the background therapy effect when interpreting survival benefits?

Key Response

The absolute risk reduction observed in older trials like TRACE may be attenuated in modern populations due to the cumulative benefit of contemporary background therapies (the ceiling effect). Editors demand that modern trials power their studies based on current event rates and stratify outcomes by optimal medical therapy compliance to ensure the intervention adds incremental value.

Guideline Committee
Guideline Committee

Based on the findings of TRACE combined with SAVE and AIRE, what is the current ACC/AHA guideline recommendation regarding the class and level of evidence for ACE inhibitor use in post-MI patients with reduced ejection fraction, and does the choice of specific ACE inhibitor agent matter?

Key Response

Current ACC/AHA guidelines give a Class 1, Level of Evidence A recommendation for ACE inhibitors in patients with a recent MI and LVEF less than or equal to 40 percent to prevent symptomatic heart failure and reduce mortality. While TRACE used trandolapril, the guidelines generally consider the benefit a class effect, though agents specifically studied in these landmark post-MI trials are often preferred in clinical pathways.

Clinical Landscape

Noteworthy Related Trials

1992

SAVE Trial

n = 2,231 · NEJM

Tested

Captopril 50 mg TID

Population

Patients with LVEF <= 40% 3 to 16 days post-MI

Comparator

Placebo

Endpoint

All-cause mortality

Key result: Captopril significantly reduced all-cause mortality by 19% and cardiovascular mortality by 21% compared to placebo.
1993

AIRE Trial

n = 2,000 · Lancet

Tested

Ramipril 5 mg BID

Population

Patients with clinical evidence of heart failure 3 to 10 days post-MI

Comparator

Placebo

Endpoint

All-cause mortality

Key result: Ramipril significantly reduced all-cause mortality by 27% and the risk of severe heart failure compared to placebo.
2003

VALIANT Trial

n = 14,703 · NEJM

Tested

Valsartan 160 mg BID, Captopril 50 mg TID, or both

Population

Patients with heart failure or left ventricular dysfunction post-MI

Comparator

Captopril (active control)

Endpoint

All-cause mortality

Key result: Valsartan was non-inferior to captopril in reducing all-cause mortality, and combination therapy offered no additional survival benefit but increased adverse events.

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