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Details

Autor(en) / Beteiligte
Titel
Changes in left ventricular mass and volumes in patients receiving angiotensin-converting enzyme inhibitor therapy for left ventricular dysfunction after Q-wave myocardial infarction
Ist Teil von
  • The American heart journal, 1998-08, Vol.136 (2), p.269-275
Ort / Verlag
New York, NY: Mosby, Inc
Erscheinungsjahr
1998
Quelle
Elsevier Journal Backfiles on ScienceDirect (DFG Nationallizenzen)
Beschreibungen/Notizen
  • Objectives We evaluated global and segmental left ventricular (LV) mass and LV mass/volume ratio in patients with LV dysfunction receiving angiotensin-converting enzyme (ACE) inhibitor therapy after acute myocardial infarction (MI). Background ACE inhibitors attenuate LV dilatation and compensatory hypertrophy after acute MI in animal models. However, LV remodeling in patients after acute MI has been largely defined on the basis of changes in chamber volume alone. Methods and Results Twenty-nine patients with LV ejection fraction <40% received the ACE inhibitor ramipril (range 2.5 to 20 mg/day) within 5 days of their first Q-wave MI. Magnetic resonance imaging was performed at baseline and at 3 months, providing global and regional LV volumes and mass from summated serial short-axis slices. Mean arterial blood pressure was unchanged from baseline to 3-month follow-up (89 ± 10 to 92 ± 17 mm Hg). LV mass decreased (90 ± 25 to 77 ± 21 gm/m2, p < 0.0005) as LV end-diastolic volumes increased (65 ± 13 to 73 ± 22 ml/m2, p < 0.01). Global LV mass to volume ratio decreased from 1.40 ± 0.28 to 1.08 ± 0.18 gm/ml (p < 0.0001), as did circumferential wall thickness to volume ratio of noninfarcted myocardium at the base of the LV (0.06 ± 0.02 to 0.05 ± 0.02 mm/ml, p < 0.001). LV ejection fraction increased from 35 ± 6 to 40 ± 9% (p < 0.001) in the presence of an increase in calculated end-systolic wall stress (185 ± 57 to 227 ± 54 gm/cm2, p < 0.01). Conclusions ACE inhibitor therapy was associated with improved LV function in the face of a decrease in mass to volume ratio of the LV as well as a decrease in wall thickness to volume ratio of noninfarcted myocardium. Whether ACE inhibitor therapy had direct or indirect effects on these changes in LV mass and function are open questions that require further investigation. (Am Heart J 1998;136:269-275.)

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