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[Mechanical and electrocardiographic sequence of coronary artery occlusion: an echocardiographic study during
T Akasaka1, J Yoshikawa, K Yoshida
1Department of Cardiology, Kobe General Hospital, Japan.
Insights
Regional myocardial dysfunction in humans, detected via echocardiography during coronary artery interruptions, precedes electrocardiographic changes. Wall motion abnormalities recover after reperfusion before ECG normalization.
Area of Science:
- Cardiology
- Physiology
Context:
- Detecting regional myocardial dysfunction in humans has been challenging.
- Percutaneous transluminal coronary angioplasty (PTCA) offers a unique model to study acute ischemic events.
- Previous studies were limited to animal models or spontaneous/exercise-induced ischemia.
Purpose:
- To investigate the temporal relationship between left ventricular wall motion abnormalities and electrocardiographic (ECG) changes during acute coronary occlusion.
- To assess the recovery of myocardial function and ECG changes after reperfusion.
Summary:
- Echocardiograms and ECGs were recorded during 21 PTCA procedures in 11 patients with single coronary artery stenosis.
- Regional asynergy (hypokinesis, akinesis, or dyskinesis) appeared within seconds of balloon inflation, preceding ECG changes.
- Myocardial dysfunction began to normalize after balloon deflation, preceding ECG recovery.
Impact:
- Demonstrates that left ventricular wall motion abnormalities occur before ECG changes during acute ischemia in humans.
- Highlights the utility of PTCA as a model for studying acute myocardial dysfunction.
- Provides insights into the sequence of events during myocardial ischemia and reperfusion.
Abstract:
The detection of regional myocardial dysfunction due to acute ischemic event has been limited almost entirely to experimental animal models. In human subjects, it has been limited to the observations during spontaneously-occurring or exercise-induced ischemic events. Recently, percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to study such dysfunction as the result of repeated interruptions of coronary blood flow. Echocardiograms and electrocardiograms were simultaneously recorded immediately before, during, and after 21 episodes of complete interruptions of coronary blood flow by PTCA in 11 patients. No patient had asynergy of the left ventricle either by two-dimensional echocardiography (2DE) or angiography. All patients had isolated single coronary artery stenosis including the left anterior descending artery in nine, left circumflex artery in one and right coronary artery in one. Recordings of M-mode and 2DE were successfully obtained in 10 patients. After balloon inflation, regional asynergy in the distribution of the instrumented coronary artery appeared in all 10 patients. Hypokinesis developed 9 +/- 3 (means +/- SD) sec after balloon inflation and progressed rapidly to akinesis or dyskinesis. At the same time, decreased systolic thickening of the left ventricular wall appeared in some patients in relation to the development of regional asynergy. However, systolic thinning of the left ventricular wall was not noted in all. The regional asynergy preceded ischemic electrocardiographic changes and had no relation to chest pain. Left ventricular wall motion began to normalize 12 +/- 3 sec after balloon deflation. Thereafter, transient hyperkinesis of the left ventricle developed. The first ischemic electrocardiographic change was a negative U wave which appeared 13 +/- 7 sec after coronary occlusion and remained 3 to 4 sec. Tall T waves were recorded at 28 +/- 12 sec and significant ST elevations developed 31 +/- 11 sec, after balloon inflation. These electrocardiographic changes invariably occurred only after the onset of wall motion abnormalities. Normalization of T waves was recognized at 17 +/- 16 sec and ST segment deviation were no longer present at 18 +/- 10 sec, after reperfusion. These electrocardiographic changes also preceded normalization of regional myocardial dysfunction. In conclusion, left ventricular wall motion abnormalities after coronary occlusion invariably precede the electrocardiographic changes, and begin to normalize after reperfusion prior to the electrocardiographic recovery.