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October 2, 2001Circulation562 citations

Reduction of Cardiovascular Risk by Regression of Electrocardiographic Markers of Left Ventricular Hypertrophy by the Angiotensin-Converting Enzyme Inhibitor Ramipril

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JMJames MathewPSPeter SleightELEva Lonn

Key Result

Ramipril reduced the development and persistence of ECG-LVH compared to placebo (8.1% vs 9.8%, P=0.007), and LVH regression was associated with a lower risk of cardiovascular death, MI, or stroke.

Key Points

  • This research investigates whether ramipril prevents the development and promotes regression of left ventricular hypertrophy (LVH) and its association with prognosis.
  • Patients at high risk were randomly assigned to receive ramipril or placebo in the HOPE study for 4.5 years.
  • Electrocardiograms (ECGs) were recorded at baseline and study end to evaluate LVH.
  • Outcomes related to cardiovascular events were measured and compared between groups.
  • In the ramipril group, 8.1% had development/persistence of LVH versus 9.8% in the placebo group (P=0.007).
  • 91.9% in the ramipril group had regression/prevention of LVH compared to 90.2% in the placebo group.
  • Patients with LVH regression in the ramipril group demonstrated a lower risk of combined cardiovascular events (12.3% vs. 15.8%, P=0.006).

Study Design

Type

RCT (n=8,281)

PICO

P
Population
High cardiovascular risk (n=8,281)
I
Intervention / Comparator
Ramipril vs Placebo
O
Primary Outcome
development/persistence of LVH, p=0.007

Main Result

Absolute Event Rate: 8.1% vs 9.8%

p-value: p=0.007

Abstract

BACKGROUND: Electrocardiographic markers of left ventricular hypertrophy (LVH) predict poor prognosis. We determined whether the ACE inhibitor ramipril prevents the development and causes regression of ECG-LVH and whether these changes are associated with improved prognosis independent of blood pressure reduction. METHODS AND RESULTS: In the Heart Outcomes Prevention Evaluation (HOPE) study, patients at high risk were randomly assigned to ramipril or placebo and followed for 4.5years. ECGs were recorded at baseline and at study end. We compared prevention/regression and development/persistence of ECG-LVH in the two groups and related these changes to outcomes. At baseline, 676 patients had LVH (321 in the ramipril group and 355 in the placebo group) and 7605 patients did not have LVH (3814 in the ramipril group and 3791 in the placebo group). By study end, 336 patients in the ramipril group (8.1%) compared with 406 in the placebo group (9.8%) had development/persistence of LVH; in contrast, 3799 patients in the ramipril group (91.9%) compared with 3740 in the placebo group (90.2%) had regression/prevention of LVH (P=0.007). The effect of ramipril on LVH was independent of blood pressure changes. Patients who had regression/prevention of LVH had a lower risk of the predefined primary outcome (cardiovascular death, myocardial infarction, or stroke) compared with those who had development/persistence of LVH (12.3% versus 15.8%, P=0.006) and of congestive heart failure (9.3% versus 15.4%, P<0.0001). CONCLUSIONS: The ACE inhibitor ramipril decreases the development and causes regression of ECG-LVH independent of blood pressure reduction, and these changes are associated with reduced risk of death, myocardial infarction, stroke, and congestive heart failure.

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Cite This Study

Mathew et al. (2001) conducted an RCT in High cardiovascular risk (n=8,281). Ramipril vs. Placebo was evaluated on development/persistence of LVH (p=0.007). Ramipril reduced the development and persistence of ECG-LVH compared to placebo (8.1% vs 9.8%, P=0.007), and LVH regression was associated with a lower risk of cardiovascular death, MI, or stroke.

synapsesocial.com/papers/6a1573f879ff98d0de4ea6d3https://doi.org/10.1161/hc3901.096700
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