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Beta-adrenergic blockade decreases coronary collateral blood flow in patients with coronary artery disease
Z S Kyriakides1, T Kolettis, A Antoniadis
1Second Department of Cardiology, Onassis Cardiac Surgery Center, Athens, Greece. zskyr@otenet.gr, elbee@ath.forthnet.gr
Insights
Beta-adrenergic blockade, administered locally, reduces coronary collateral blood flow, potentially worsening ischemia. However, it also lessens myocardial ischemia during coronary angioplasty procedures.
Area of Science:
- Cardiology
- Pharmacology
Background:
- The impact of beta-adrenergic blockade on coronary collateral blood flow remains unclear.
- Coronary collateral circulation is vital for supplying blood to ischemic heart muscle.
Purpose of the Study:
- To investigate the acute effects of beta-adrenergic blockade on coronary collateral blood flow.
- To assess the influence of propranolol on myocardial ischemia during coronary angioplasty.
Main Methods:
- Fifteen patients with stable angina undergoing coronary angioplasty were studied (Part A).
- Intracoronary propranolol was administered, and collateral flow velocity was measured using a Doppler guidewire during balloon inflations.
- Ten controls received saline infusion.
- In Part B, the effect of intracoronary propranolol on coronary artery area was assessed in 10 patients.
Main Results:
- Intracoronary propranolol administration decreased heart rate, velocity time integral, and ST elevation during balloon inflations.
- These changes were not observed in the saline control group.
- Propranolol did not significantly alter coronary artery lumen area.
Conclusions:
- Intracoronary beta-adrenergic blockade reduces coronary collateral blood flow, potentially exacerbating the ischemic area.
- Despite reducing collateral flow, beta-adrenergic blockade ameliorates myocardial ischemia during coronary angioplasty.
Abstract:
The effect of beta-adrenergic blockade on coronary collateral blood flow has not been clarified. We examined the acute effects of beta-adrenergic blockade on coronary collateral blood flow. Fifteen patients (Part A) with stable angina were studied while undergoing coronary angioplasty. According to the protocol, all patients underwent a minimum of three balloon inflations. Collateral flow velocity was determined during balloon inflations using the Doppler flow guidewire positioned distally to the lesion. The two tested balloon inflations, the second and third, were maintained for the same length of time. Between the second and third balloon inflations, 1 mg of propranolol was administered IC into the treated artery. Ten controls were studied following saline infusion. In 10 other patients (Part B), the effect of 1 mg IC propranolol on the coronary artery area distal to the lesion was studied, and five patients served as controls. In the treated group, in Part A blood pressure remained stable during the balloon inflations tested. Heart rate decreased from 79 +/- 11 to 73 +/- 12 beats/min (P < .05), velocity time integral from 9.6 +/- 8.2 to 6.6 +/- 4.1 cm (P < .05), and ST elevation from 1.3 +/- .9 to .9 +/- 1.0 mV (P < .05) between the second and third balloon inflations. In the controls the variables examined did not change during the balloon inflations tested. In Part B, neither propranolol nor normal saline had any significant effect on coronary artery lumen area. Thus, IC administration of beta-adrenergic blockade decreases coronary collateral blood flow, and this potentially worsens the ischemic zone. However, beta-adrenergic blockade ameliorates myocardial ischemia during coronary angioplasty.