What is the clinical evidence from this study?

Study design: Cohort. Population: First anterior myocardial infarction (n=52). Intervention: Late post-infarction period (1 year) vs. Early post-infarction period (3 weeks). Primary outcome: End-diastolic volume (ml) (p=0.01).

What question did this study set out to answer?

To characterize the structural and geometric mechanisms responsible for late left ventricular volume enlargement in the first year following a first anterior myocardial infarction.

August 26, 2026Journal of the American College of Cardiology272 citationsOpen Access

Left ventricular remodeling in the year after first anterior myocardial infarction: A quantitative analysis of contractile segment lengths and ventricular shape

GMGary F. Mitchell GLGervasio A. Lamas DVDouglas E. Vaughan

Key Result

Late ventricular enlargement after anterior infarction (end-diastolic volume increasing from 230 to 244 ml, p=0.01) results from increased contractile segment length and geometry changes.

Key Points

To characterize the structural and geometric mechanisms responsible for late left ventricular volume enlargement in the first year following a first anterior myocardial infarction.
Evaluated 52 patients via biplane left ventriculography at 3 weeks and 1 year after a first anterior myocardial infarction.
Measured biplane diastolic circumference, contractile and noncontractile segment lengths, endocardial curvature, and ventricular sphericity index.
End-diastolic volume enlarged from 230 ± 42 to 244 ± 55 ml (p = 0.01), driven by increased contractile segment length (34 ± 5 to 37 ± 5 cm, p < 0.001) and sphericity index (0.74 ± 0.07 to 0.76 ± 0.08, p < 0.001), while noncontractile length decreased (15 ± 6 to 12 ± 6 cm, p < 0.005).
Patients with late enlargement (>20 ml increase, n = 19) exhibited increased sphericity (0.75 ± 0.05 to 0.80 ± 0.08, p < 0.005) and contractile segment elongation (32 ± 4 to 36 ± 4 cm, p = 0.001), which was attenuated by captopril therapy in high-risk patients.

Study Design

Type

Cohort (n=52)

PICO

Population

52 patients evaluated 3 weeks and 1 year after a first anterior myocardial infarction to assess ventricular remodeling.

Exposure / Comparator

Late post-infarction period (1 year) vs Early post-infarction period (3 weeks)

Primary Outcome

End-diastolic volume (ml), p=0.01

Main Result

Absolute Event Rate: 244% vs 230%

p-value: p=0.01

Abstract

Infarct expansion after myocardial infarction results in early ventricular enlargement and distortion of ventricular geometry. To characterize the components of late volume enlargement, biplane left ventriculography was performed in 52 patients 3 weeks and 1 year after a first anterior myocardial infarction. Biplane diastolic circumference and contractile and noncontractile segment lengths were measured. Global geometry was evaluated by using a sphericity index (angiographic volume of the ventricle divided by the volume of a sphere with the same circumference). Regional geometry was assessed by measurement of endocardial curvature, an important determinant of wall tension. End-diastolic volume was enlarged at baseline and increased at 1 year (230 +/- 42 to 244 +/- 55 ml, p = 0.01) as a result of increases in contractile segment length (34 +/- 5 to 37 +/- 5 cm, p less than 0.001) and sphericity index (0.74 +/- 0.07 to 0.76 +/- 0.08, p less than 0.001), whereas the noncontractile segment length decreased (15 +/- 6 to 12 +/- 6 cm, p less than 0.005). Curvature analysis revealed a flattening of presumably high tension concavity at the anterobasal (-6.0 +/- 4.0 to -4.5 +/- 3.7, p less than 0.01) and inferior (-4.5 +/- 2.0 to -3.6 +/- 2.1, p less than 0.005) margins of the infarct and less bulging of the anterior wall (9.4 +/- 2.5 to 8.2 +/- 2.3, p less than 0.001). Patients selected for late enlargement (diastolic volume increase greater than 20 ml, n = 19) had an increase in sphericity (0.75 +/- 0.05 to 0.80 +/- 0.08, p less than 0.005) and in diastolic circumference (54 +/- 3 to 56 +/- 4 cm, p less than 0.001) secondary to elongation of the contractile segment (32 +/- 4 to 36 +/- 4 cm, p = 0.001) at 1 year. Thus, late ventricular enlargement after anterior infarction results from an increase in contractile segment length and a change in ventricular geometry and is not a result of progressive infarct expansion. In the group of patients at high risk for late ventricular enlargement because of persistent occlusion of the infarct-related vessel, captopril therapy attenuated late volume enlargement by preventing these changes in contractile segment length and chamber geometry.

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