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Coronary hemodynamic responses during spontaneous angina in patients with and patients without coronary artery spasm
Insights
Spontaneous angina can occur in patients with severe coronary artery disease even without coronary artery spasm. Hemodynamic changes varied, indicating no single mechanism for this condition.
Area of Science:
- Cardiology
- Physiology
Background:
- Spontaneous angina, occurring at rest without provocation, presents a complex clinical challenge.
- Understanding the underlying mechanisms is crucial for effective patient management.
Purpose of the Study:
- To investigate the hemodynamic and angiographic mechanisms of spontaneous angina in patients.
- To differentiate between coronary spasm and other factors in the etiology of spontaneous angina.
Main Methods:
- Cardiac catheterization was performed on 13 patients experiencing spontaneous angina.
- Measurements included left ventricular and systemic hemodynamics, coronary venous flows (thermodilution), ECG, and coronary angiography during angina episodes.
- Patients were categorized into Group I (coronary spasm) and Group II (no coronary spasm).
Main Results:
- Group I (n=5) showed coronary spasm with ECG changes (ST elevation/peaked T waves) and reduced coronary flow.
- Group II (n=8) had multivessel coronary artery disease and exhibited variable hemodynamic responses without spasm.
- All patients experienced increased left ventricular end-diastolic pressure; Group II consistently showed transient ST depression.
Conclusions:
- Spontaneous angina can occur in severe coronary artery disease without angiographically evident coronary spasm.
- The mechanisms of spontaneous angina are diverse and not uniformly explained by coronary spasm alone.
- Further research is needed to elucidate the varied pathophysiological pathways involved.
Abstract:
The mechanisms of spontaneous angina were evaluated during cardiac catheterization in 13 patients who had angina occurring without provocation at rest. Left ventricular and systemic hemodynamics, coronary venous flows (thermodilution technique), electrocardiogram and coronary angiograms were recorded before and during spontaneous angina. Angiography during spontaneous angina showed that 5 patients had coronary spasm (group I) and 8 patients did not (group II). In group II there was a preponderance of multivessel coronary artery disease. Left ventricular end-diastolic pressure increased in all patients in both groups during spontaneous angina. In group I, 4 patients had transient ST elevation and 1 patient had peaked T waves during angina. Transient ST depression occurred during spontaneous angina in all group II patients. Group I patients had decreased coronary sinus flow (4 of 5 patients) or decreased regional flow (5 of 5) during spontaneous angina. Coronary resistance and ratio of double product to coronary blood flow increased in all patients. In group II, coronary hemodynamic responses during spontaneous angina varied. Coronary venous flows, coronary resistance and ratio of double product to coronary blood flow showed no uniform pattern. Thus, patients with severe coronary artery disease can have spontaneous angina without angiographic findings of coronary spasm. After analysis of angiograms and coronary hemodynamics in these patients, no apparent uniform mechanism for spontaneous angina was found.