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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.

Exercise-Induced Human Coronary Collateral Function: Quantitative Assessment during Acute Coronary Occlusions

“…Consequently, it is a rather conservative estimate on the basis of our study that β-blockade tends to reduce effects of exercise on collateral function. This is in agreement with previous observations made in clinical [20, 27]but also in numerous experimental studies according to which exercise and other forms of stress are mediated as hyperemic stimulus by β-adrenergic receptor activation with vasodilatation of coronary collateral vessels [12, 28]. As an additional mechanism contributing to exercise-induced collateral vasomotion, flow-mediated, nitric oxide-dependent dilatation has been shown to play a role [13, 29].…”

Determinants of Preformed Collateral Vessels in the Human Heart without Coronary Artery Disease

“…Patients with previous percutaneous coronary intervention, coronary bypass grafting, previous myocardial infarction, or acute coronary syndrome were excluded from the study. Since beta-blockers have a known constrictive effect on coronary collaterals [13,14,15,16], an additional analysis in patients with and without beta-blockers was performed. All patients gave written informed consent to participate in the study.…”