Publications

Observations on human and experimental atherosclerosis, biomarker studies, and now a large-scale clinical trial support the operation of immune and inflammatory pathways in this disease. The factors that incite innate and adaptive immune responses implicated in atherogenesis and in lesion complication include traditional risk factors such as protein and lipid components of native and modified low-density lipoprotein, angiotensin II, smoking, visceral adipose tissue, and dysmetabolism. Infectious processes and products of the endogenous microbiome might also modulate atherosclerosis and its complications either directly, or indirectly by eliciting local and systemic responses that potentiate disease expression. Trials with antibiotics have not reduced recurrent cardiovascular events, nor have vaccination strategies yet achieved clinical translation. However, anti-inflammatory interventions such as anticytokine therapy and colchicine have begun to show efficacy in this regard. Thus, inflammatory and immune mechanisms can link traditional and emerging risk factors to atherosclerosis, and offer novel avenues for therapeutic intervention.

BACKGROUND

Small studies have shown that adenosine is equivalent to regadenoson when obtaining coronary fractional flow reserve (FFR) measurements. A study that also evaluates time and safety of aminophylline reversal of regadenoson effects has not been presented.

HYPOTHESIS

Reversal of regadenoson with aminophylline is safe and equivalent to adenosine for FFR measurements.

METHODS

Forty-six consecutive patients who underwent clinically indicated FFRs at the time of coronary angiography were enrolled between 4/2012 and 5/2014. Each patient had FFR measured using adenosine 140 mcg/kg/min IV, and following return to baseline, FFR was measured using regadenoson 400 mcg IV, which then was reversed with aminophylline 150 mg IV. Time to baseline hemodynamics was measured. Agreement between the two assessments was compared using linear regression.

RESULTS

FFR results were similar with both agents (R = 0.935, P < 0.0001). Also, using the 0.80 cutoff for significantly depressed FFR, there was no divergence regarding studies' significance. After aminophylline reversal of regadenoson, hemodynamics returned to baseline in 111 ± 71 seconds. There were no unexpected side effects or complications.

CONCLUSIONS

For FFR measurement, regadenoson and adenosine are equivalent hyperemic agents. Regadenoson with aminophylline reversal may be considered as an alternative to adenosine for FFR measurements.