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Serial changes in left and right ventricular systolic and diastolic dynamics during the first year after an index
K Hirose1, J E Reed, J A Rumberger
1Department of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
Insights
After heart attack, ventricular emptying and filling rates decrease but intrinsic contractility remains stable. Changes are linked to afterload from chamber enlargement, not reduced heart muscle performance.
Area of Science:
- Cardiology
- Cardiac Imaging
- Heart Failure Research
Background:
- Limited data exists on serial changes in ventricular dynamics post-myocardial infarction.
- Understanding these changes is crucial for managing post-infarction cardiac remodeling.
Purpose of the Study:
- To quantify serial biventricular emptying and filling dynamics after infarction.
- To correlate these dynamics with changes in ventricular volume, muscle mass, wall stress, and contractility.
Main Methods:
- Serial electron beam computed tomography (EBCT) in 40 infarction patients over one year.
- Quantification of global biventricular volumes, peak emptying/filling rates, and left ventricular muscle mass.
- Estimation of mid-left ventricular end-systolic wall stress and contractility indexes.
Main Results:
- Biventricular chamber volume increased 15-35% by 1 year post-infarction.
- Global emptying and filling rates decreased 20-30% but stabilized after 6 weeks.
- Despite increased wall stress, left ventricular contractility remained unchanged, suggesting adaptation to afterload.
Conclusions:
- Post-infarction ventricular function changes are primarily adaptive responses to increased afterload.
- Progressive chamber enlargement and limited hypertrophy influence left ventricular afterload.
- Intrinsic global left ventricular contractile performance is not altered by early post-infarction remodeling.
Objectives:
This study quantified serially biventricular emptying and filling after infarction and related these to changes in volume, muscle mass, wall stress and contractility.
Background:
There are limited data on serial changes in ventricular dynamics after infarction.
Methods:
Forty patients had serial electron beam computed tomographic examinations during the first year after index Q wave infarction (21 anterior, 19 inferior), and global biventricular volumes, peak rates of emptying and filling and left ventricular muscle masses were quantified. Mean mid-left ventricular end-systolic wall stresses, rate-corrected velocities of circumferential shortening and two indexes of left ventricular contractility--the end-systolic wall stress/volume ratio and the end-systolic wall stress/rate-corrected velocity of circumferential shortening relation--were estimated in each instance.
Results:
Patients with anterior infarction had an increase in biventricular chamber volume of 15% to 35% by 1 year. Global biventricular peak rates of emptying and filling were decreased by 20% to 30% from hospital discharge to 6 weeks but thereafter remained unchanged. Despite a significant increase in mean wall stresses, the end-systolic wall stress/volume ratio remained unchanged during the year. The rate-corrected velocities of circumferential shortening declined serially after anterior infarction but did so in proportion to the increase in mean wall stresses, consistent with no net change in left ventricular contractility. Patients with inferior infarction showed a trend toward similar changes, but the magnitudes did not reach significance.
Conclusions:
Left (and right) ventricular global peak rates of emptying and filling during the first year after infarction can be altered in the absence of additional ischemic injury but are more consistent with responses to changes in left ventricular afterload than changes in intrinsic ventricular performance or contractility. Serial changes in left ventricular afterload after infarction are largely due to progressive chamber enlargement and limited development of compensatory hypertrophy during the first year. Intrinsic global left ventricular contractile performance was not altered by postinfarction cardiac remodeling in the patients examined.