Page 58 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 3
explains the decreased CFVR in our study because no difference in baseline flow velocity was measured from 1-week to 6-month follow-up, when bulging of the nonischemic area is expected to be present at 1 week. Increased minimal microvascular resistance in non-IRAs during AMI changed over time in the same direction as minimal microvascular resistance in IRAs, suggesting an impaired vasodilation capacity in the remote microvascular bed, although obstruction (e.g., through activation of thrombocytes and leukocytes) cannot be excluded in our study. The combination of a decreased corrected baseline microvascular resistance and increased minimal microvascular resistance at the time of AMI suggests disturbed autoregulation, probably due to neurohumoral activation in areas remote from the infarction. Although minimal microvascular resistance in non-IRAs reaches a stable level at 1-week follow-up and thus sooner than in IRAs, the variable arteriolar resistance index (variable and corrected variable arteriolar resistance indexes) is lower at 1-week than at 6-month follow-up, indicating that the autoregulatory capacity in the non-IRA is not yet normalized at 1 week after MI. Although speculative, pharmacologic adjunctive measures that decrease minimal microvascular resistance might improve clinical outcome. Our observations, i.e., neurohumoral activation influences microvascular resistance, may guide therapeutic measurements for hemodynamic improvement during the acute phase of MI in remote territories.
Several potential limitations of this study should be considered when interpreting these data. Pressure in the right atrium was not measured in all patients. Therefore, the transvascular pressure gradient used for resistance calculations may have varied slightly. Left ventricular end-diastolic pressure was not measured. High end-diastolic pressure may affect subendocardial microvascular resistance. Although this may have a role in the mechanistic explanation of the study outcome, it does not influence outcome itself. The bolus of adenosine given to induce hyperemia has varied in the recent literature. Because the adenosine boluses were similar at every time point, higher dosages of adenosine likely did not affect the trend in our results. Although diabetes mellitus may alter microvascular function, diabetic patients were not excluded from the protocol and the study population included 3 patients with diabetes. Post hoc analysis showed no difference in outcome when these 3 patients were omitted. At the time of the study, ticlopidine or clopidogrel was prescribed for 1 month. It is unknown whether a longer duration of administration would affect the time course of microvascular resistance.
56