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Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Left ventricular diastolic function in normotensive subjects 2 months after acute myocardial infarction is related to
Abdul-Majeed Salmasi1, Peter Frost, Mark Dancy
1Cardiology Department, Central Middlesex Hospital, London, United Kingdom. majeed.salmasi@nwlh.nhs.uk
Background:
Both glucose intolerance and myocardial infarction are independently associated with impaired left ventricular (LV) function. This study was carried out to relate LV diastolic function in normotensive subjects 2 months after acute myocardial infarction (AMI) to glucose tolerance status.
Methods:
Left ventricular ejection fraction (LVEF), LV mass index, peak velocity of the early phase/atrial contraction wave, deceleration time of E wave, and isovolumic relaxation time were measured during echocardiograph/Doppler cardiography in 200 normotensive patients 2 months after AMI. Twenty-nine patients were known to be diabetic on admission with AMI. Glucose tolerance test was carried out in the 171 patients who are not known to be diabetic.
Results:
Independent of LVEF, restrictive LV filling (peak velocity of the early phase/atrial contraction wave > 1 but < 2 associated with deceleration time of E wave < or = 140 milliseconds) was found in 72% of the known-diabetic patients, 70% of the 20 preclinical diabetic patients, 23% of the 35 patients with impaired glucose tolerance, 13% of the 15 patients with stress hyperglycemia, and 7% of the euglycemic patients (P < .01). In the rest of these patients, LV filling was nonrestrictive. No significant difference was observed in LVEF and LV mass index between patient groups.
Conclusion:
Independent of LVEF, the pattern of abnormal LV filling in normotensive subjects 2 months after AMI is a function of the severity of glucose intolerance, restrictive in the majority of the diabetic patients and nonrestrictive in the majority of the euglycemic patients, impaired glucose tolerance, and stress hyperglycemia. After AMI, abnormal LV filling occurs even in the absence of detectable systolic dysfunction or left ventricular hypertrophy.
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