Читать книгу Interventional Cardiology - Группа авторов - Страница 174

Non‐specific agents such as adenosine and papaverine are commonly used to induce maximal hyperemia for assessment of indices such as Coronary Flow Reserve (CFR), FFR and index of microcirculatory resistance (IMR). The dose of adenosine is usually 140 mcg/kg/min when given as a central venous infusion; ATP can be given as an alternative. The hyperemic effect is typically observed after 30 seconds and infusions should continue for 1–2 minutes to observe for stable hyperemia. Side‐effects include relative hypotension, a central chest discomfort or burning, dyspnea, and bronchospasm. Adenosine should be avoided in patients with severe brittle asthma. However, it has been used relatively safely in those with milder variants of asthma, albeit with full resuscitation facilities available. Other lung conditions such as chronic obstructive pulmonary disease can generally tolerate an adenosine infusion. Short‐lived atrio‐ventricular conduction delay is frequent; caution should be considered in those with established conduction disease.

For intracoronary dosing, clinical practice remains variable. Early validation work was all performed using considerably lower doses than found in clinical practice today. Accepted intracoronary doses of adenosine or ATP are 80–120 mcg in the left coronary system and 40 mcg in right coronary artery. Intracoronary adenosine typically achieves hyperemia lasting 5 to 10 seconds. Papaverine is an alternative intracoronary agent that achieves a longer lasting hyperemia between 30–60 seconds which may permit pullback assessments at the cost of transient QT prolongation and rare trigger ventricular tachycardia or torsarde de pointes. It is typically used where adenosine is not available (15–20mg in the left coronary artery; 10–12 mg in the right coronary artery).

Newer alternatives include Regadenoson, a selective A2A receptor agonist which has been approved for use in myocardial perfusion imaging. Given as a single bolus into a peripheral vein using a weight‐unadjusted dose (400 mcg over 10 seconds), regadenoson achieves a peak flow velocity after a minute and declines thereafter. The duration of hyperemia is variable between patients making pullback and multi‐vessel assessment unreliable. Side‐effects include adenosine‐like effects with hypotension, chest discomfort and flushing. Third‐degree heart block has also occurred.

Maximal hyperemia is believed to occur in two stages. Agents primarily achieve maximal hyperemia through their vasodilator action on microvascular smooth muscle cells (an endothelium‐independent response). The resultant increase in blood flow is thought to stimulate shear stress‐induced endothelial nitric oxide release, which promotes further vasodilatation of the microcirculation (flow‐mediated dilatation) and increase in blood flow (an endothelium‐dependent response). Therefore, the response to hyperemic agents will integrate a change in coronary blood flow and microvascular function but alone cannot distinguish between both components.