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Contrast injection bradycardia during coronary angiography: effects in the denervated human heart
Insights
Bradycardia during contrast coronary angiography is a neurally mediated phenomenon. Heart transplant patients lacking cardiac innervation showed no bradycardia, suggesting a role for cardiac nerves.
Area of Science:
- Cardiology
- Neuroscience
Background:
- Bradycardia can occur during contrast coronary angiography.
- The underlying mechanisms, particularly the role of cardiac innervation, are not fully understood.
Purpose of the Study:
- To investigate the contribution of cardiac innervation to bradycardia during contrast coronary angiography.
- To compare heart rate responses in different patient groups.
Main Methods:
- Compared heart rate (HR) responses before and after contrast coronary angiography.
- Measured longest P-P interval beat-to-beat in four groups: heart transplant patients, normal controls, coronary artery disease (CAD) patients, and congestive cardiomyopathy patients.
- Analyzed differences in HR response based on cardiac innervation status.
Main Results:
- Heart rate significantly decreased (HR1 vs. HR2, p<0.05) in control and CAD groups, but not in transplant or cardiomyopathy groups.
- The percentage decrease in HR was significantly less in transplant patients compared to cardiomyopathy patients.
- Contrast injection bradycardia was absent in denervated heart transplant patients.
Conclusions:
- Bradycardia during contrast coronary angiography is likely a neurally mediated phenomenon.
- Diminished vasodepressor reflexes in cardiomyopathy patients may contribute to a blunted bradycardia response.
- Cardiac innervation plays a crucial role in the bradycardia response observed during this procedure.
Abstract:
To assess the contribution of cardiac innervation toward understanding the mechanisms of bradycardia during contrast coronary angiography, heart rate (HR) responses in eight patients after heart transplantation were compared with 10 normal patients (control), 10 patients with coronary artery disease (CAD) and normal ventricular function, and 10 patients with congestive cardiomyopathy and normal coronary arteries. The longest P-P interval was measured beat to beat before (HR 1) and after (HR 2) coronary angiography. The coronary vessel perfusing the sinus node did not influence HR 2 responses within each group. HR 1 was significantly different from HR 2 (p less than 0.05) in the control and CAD groups but was not different in the transplant and cardiomyopathy groups. Compared with the control group, the percent decrease in HR was significantly less in transplant patients than in patients with cardiomyopathy. Thus contrast injection bradycardia is absent in denervated patients after heart transplant, and this response is markedly blunted in cardiomyopathy patients who are known to have diminished vasodepressor reflexes. These findings suggest that the bradycardia response is probably a neurally mediated phenomenon.