Pharmacological Achievement of Hyperaemia in the Catheter Laboratory for the Assessment of Fractional Flow Reserve

Abstract

The coronary microcirculation is a key regulator of myocardial blood flow. Through alterations in microvascular resistance, the microcirculation controls the delivery of blood to the myocardium over a wide range of perfusion pressures and myocardial oxygen demand through the process of autoregulation.1 In humans, coronary blood flow can increase up to five times basal flow to meet increased demand.2 Such an increase in blood flow is referred to as a hyperaemic response, and in humans is commonly observed in response to ischaemia and exercise.3,4 Quantifying the hyperaemic response is a critical step in understanding the coronary circulation and is applied in most physiological assessments of myocardial blood flow. In particular, the attainment of maximal hyperaemia is essential for an accurate assessment of fractional flow reserve (FFR).

Support
The publication of this information was supported by St. Jude Medical.
Received date
22 September 2014
Accepted date
22 September 2014
Citation
RadcliffeCardiology.com, October 2014

Pages

Introduction
The coronary microcirculation is a key regulator of myocardial blood flow. Through alterations in microvascular resistance, the microcirculation controls the delivery of blood to the myocardium over a wide range of perfusion pressures and myocardial oxygen demand through the process of autoregulation.1 In humans, coronary blood flow can increase up to five times basal flow to meet increased demand.2 Such an increase in blood flow is referred to as a hyperaemic response, and in humans is commonly observed in response to ischaemia and exercise.3,4 Quantifying the hyperaemic response is a critical step in understanding the coronary circulation and is applied in most physiological assessments of myocardial blood flow. In particular, the attainment of maximal hyperaemia is essential for an accurate assessment of fractional flow reserve (FFR).

In the catheter laboratory the attainment of a hyperaemic response is limited. Coronary occlusion to produce ischaemia (and thus reactive hyperaemia)5 is a method used in animal models but is not practical or safe to be used in humans who are not undergoing percutaneous intervention due to the inherent risk of vessel injury. Exercise is also not practical for most patients undergoing invasive coronary assessment. Thus, pharmacologically induced hyperaemia is the main method of producing hyperaemia in the catheter laboratory setting.

Anatomy of Hyperaemia
In the absence of hyperaemia, the arteriolar vessels are the primary components determining resistance.6 In the presence of hyperaemia following adenosine, total resistance decreases by approximately 68 %; arteriolar resistance and venous resistance reduced by 86 % and 98 %, respectively.6 However, capillary hydrostatic pressure changes very little as a result of a similar fall in arteriolar and venous resistances. Thus, the capillaries are the main determinant of microvascular resistance at hyperaemia, and hyperaemic indices will reflect capillary structure as well as arteriolar function.7 See Figures 1 and 2.


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References
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