Background: Ischemia, left ventricular dysfunction, endothelial damage and hemodynamic changes during percutaneous coronary intervention can lead to neurohumoral activation. This may partly explain the frequent episodes of coronary spasm, hypotension and bradycardia which occur during the procedure. Rotastenting, by employing the two basic mechanisms for coronary interventions-debulking and dilatation-epitomizes percutaneous coronary interventions in general. We sought to investigate the neurohumoral changes during and immediately following coronary rotastenting.
Methods and results: Eighteen patients undergoing elective rotablator atherectomy followed by balloon predilatation and stenting for chronic stable angina were studied. Four femoral vein blood samples were drawn from each patient at the start of the intervention (baseline), and 2 (postdebulking-2), 10 (postdebulking-10) and 60 (postdebulking-60) minutes. respectively, after the first complete passage of the rotablation burr across the whole length of lesion. Levels of 10 neurohormones, namely, endothelin-1, bradykinin, arginine vasopressin, norepinephrine, dopamine, epinephrine, angiotensin II, serum angiotensin-converting enzyme activity. atrial natriuretic peptide and kininogen were estimated in each sample. Endothelin-1 and bradykinin attained their peak levels in the postdebulking-2 samples. and the rise from 0.34+/-0.07 pmol/ml and 235.8+/-17.7 pg/ml to 0.42+/-0.06 pmol/ml and 337.2+/-41.0 pg/ml, respectively, was statistically significant (p<0.05). The level of arginine vasopressin showed a significant (p<0.05) rise from baseline (108.5+/-31.8 pg/ml) to postdebulking-60 samples (136.5+/-39.4 pg/ml). The other neurohormones did not show significant changes.
Conclusions: The results suggest a definite but differential neurohumoral activation during and immediately following rotastenting. These neurohumoral changes may have a role in untoward intra- and postprocedural vasomotor and hemodynamic effects. This study establishes the concept of neurohumoral activation during percutaneous coronary interventions.