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Clinical characteristics of coronary artery spasm: electrocardiographic, hemodynamic and arteriographic assessment
Insights
Coronary artery spasm (CAS) correlates with ST segment deviation and fixed stenosis. Mechanical impairment precedes electrical changes during spasm, with left anterior descending artery spasm causing severe left ventricular dysfunction.
Area of Science:
- Cardiology
- Clinical Medicine
- Medical Research
Background:
- Angina pectoris can be associated with coronary artery spasm (CAS).
- Understanding the relationship between CAS, electrocardiographic changes, and hemodynamic alterations is crucial for patient management.
Purpose of the Study:
- To investigate the clinical characteristics of patients with angina pectoris and CAS.
- To determine the relationship between CAS, ST segment deviation, fixed stenosis, and hemodynamic changes during spastic events.
Main Methods:
- Simultaneous analysis of coronary arteriograms and multilead electrocardiograms in 170 CAS events.
- Assessment of hemodynamic alterations, including left ventricular (LV) filling pressure and LV dP/dt, during spastic events in 49 patients.
Main Results:
- A close correlation was found between the magnitude of CAS and ST segment deviation.
- CAS frequently occurred at sites of pre-existing fixed stenosis, though often non-significant.
- Mechanical impairment (reduced LV dP/dt) preceded electrical changes (ST deviation), with LAD spasm and ST elevation indicating severe LV dysfunction.
Conclusions:
- CAS is closely linked to fixed coronary stenosis, which may play a limited causative role.
- Mechanical dysfunction precedes electrical abnormalities in CAS.
- Left anterior descending artery spasm with ST elevation signifies the most severe left ventricular dysfunction.
Abstract:
We studied the clinical characteristics of 153 patients with angina pectoris associated with coronary artery spasm (CAS). The study was designed to investigate the relationship of CAS to ST segment deviation and to the site of fixed stenosis, and hemodynamic alteration during a spastic event. Analysis of coronary arteriograms and multilead electrocardiograms obtained simultaneously from 170 events of CAS by the use of radioluscent carbon-fiber electrodes resulted in 58 events with ST elevation which were related to total occlusion of major coronary arteries due to CAS; another 54 events with ST depression, in which the affected coronary arteries demonstrated severe but incomplete occlusion, or total occlusion but were visualized via collateral vessels; and remaining 58 events without ST deviation showing mild occlusion. The results indicate a close correlation between magnitude of CAS and ST segment deviation. CAS occurred at the site of pre-existing fixed stenosis including minor plaque defect in 133 patients and at apparently normal site in 20 patients. In the former group, only four patients had triple vessel disease, while 95 had nonsignificant fixed lesion. In the latter group, 10 patients had minor lesion distant from the site of CAS. Thus, CAS is closely related to fixed stenosis, which may have but a limited role as a cause of CAS. Hemodynamic measurements during spastic events were obtained from 49 patients including 41 events with spasm of the left anterior descending artery (LAD) and 21 events with spasm of the right coronary artery (RCA). The onset of an increase in left ventricular (LV) filling pressure and a reduction in LV dP/dt preceded ST segment deviation in all events. The first hemodynamic variable manifested in the spastic event was the reduction of LV contraction dP/dt in the majority of patients. The increase of LV filling pressure was greater in LAD spasm than RCA spasm (11 +/- 6 mmHg vs 7 +/- 4 mmHg, P less than 0.0125) and in events with ST elevation than with ST depression (11 +/- 5 mmHg vs 6 +/- 5 mmHg, p less than 0.001). Right ventricular functional impairment was mild in most patients during CAS. The study indicates that mechanical impairment precedes electrical impairment during CAS and that LAD spasm with ST elevation represents the most severe LV dysfunction.