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Asynchronous left ventricular wall motion early after coronary thrombosis
Insights
Early acute myocardial infarction shows asynchronous wall motion, not just hypokinesis or dyskinesis. This suggests residual heart muscle activity persists for hours after coronary thrombosis symptoms begin.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Myocardial Infarction Research
Background:
- Acute myocardial infarction (AMI) diagnosis relies on detecting regional wall motion abnormalities.
- Early detection of these changes is crucial for timely intervention and improved patient outcomes.
Purpose of the Study:
- To investigate early regional wall motion changes in acute myocardial infarction (AMI) using left ventriculography.
- To differentiate between various patterns of wall motion abnormalities and their relation to coronary artery thrombosis.
Main Methods:
- Left ventriculograms from 24 patients within 3.5 hours of chest pain onset were analyzed frame-by-frame.
- Digital image processing generated isometric and contour plots to assess regional wall motion.
- Coronary angiography identified underlying stenosis and thrombosis in 19 patients.
Main Results:
- Global left ventricular function indices were mostly normal, but end-systolic volume was elevated.
- Asynchronous wall motion was more common than simple hypokinesis or dyskinesis in acute coronary thrombosis.
- Specific patterns of wall motion abnormalities correlated with the location of coronary artery thrombosis (anterior descending, right, or circumflex).
Conclusions:
- Early acute myocardial infarction is characterized by asynchronous regional wall motion, often preceding or accompanying hypokinesis/dyskinesis.
- The observed patterns suggest residual myocardial contractile activity can persist for up to six hours post-symptom onset in coronary thrombosis.
- Coronary artery disease complexity influences wall motion patterns, highlighting the need for detailed regional analysis.
Abstract:
To study regional wall motion early in the development of acute myocardial infarction, left ventriculograms performed in 24 patients before thrombolysis and within 3.5(1.2) (mean (SD] hours of the onset of pain were digitised frame by frame. Isometric and contour plots of regional wall motion were constructed. In 19 patients (seven with anterior descending, eight with right, and four with circumflex disease) thrombosis was demonstrated on an underlying stenosis. In 10 patients the two remaining coronary arteries were normal, and in nine, one or both showed important disease. Mean values of global indices of left ventricular function, including end diastolic volume, ejection fraction, peak ejection and filling rates, and cavity shape changes were all within normal limits, though end systolic volume was significantly raised. Total systolic amplitude of wall motion was normal in the affected area in all but seven patients (four with anterior descending, two with right, and one with circumflex thrombosis). Dyskinesis of more than 2 mm was seen in only three patients, all with thrombosis of the anterior anterior descending coronary artery, and hyperkinesis was present in four. The commonest abnormality of wall motion was hypokinesis during ejection followed by prolonged inward motion during isovolumic relaxation, which was seen in four patients with anterior descending, seven with right, and three with circumflex artery thrombosis. This was preceded by outward motion during isovolumic contraction and delayed inward motion during ejection in eight with right or circumflex thrombosis. Five of six patients without thrombosis had simple hypokinesis or dyskinesis without asynchrony. Disease of other coronary arteries did not affect the pattern of wall motion seen after right or circumflex coronary artery occlusion but it reduced the incidence of delayed inward motion along the free wall after thrombosis of anterior descending artery. Thus early after acute coronary thrombosis asynchronous wall motion is commoner than simple hypokinesis or dyskinesis. Its persistence suggests that in the setting of coronary artery thrombosis in man, residual contractile activity may persist for up to six hours after the onset of symptoms.