Relation between coronary pressure derived collateral flow, myocardial perfusion grade, and outcome in left ventricular function after rescue percutaneous coronary intervention

冠状动脉压力衍生侧支循环、心肌灌注分级与经皮冠状动脉介入治疗后左心室功能预后的关系

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Abstract

OBJECTIVE: To evaluate the relation between pressure derived coronary collateral flow (PDCF) index and angiographic TIMI (thrombolysis in myocardial infarction) myocardial perfusion (TMP) grade, angiographic collateral grade, and subsequent recovery of left ventricular function after rescue percutaneous coronary intervention (PCI) for failed reperfusion in acute myocardial infarction. METHODS: The pressure wire was used as the guidewire in 38 consecutive patients who underwent rescue PCI between December 2000 and March 2002. Follow up angiography was performed at six months. Baseline and follow up single plane ventriculograms were analysed off line by an automated edge detection technique. A linear model was fitted to assess the relation between 0.1 unit increase in PDCF and change in left ventricular regional wall motion. RESULTS: Patients with TMP 0 grade had significantly higher mean (SD) PDCF than patients with TMP 1-3 (0.30 (0.11) v 0.15 (0.07), p < 0.0001, r = -0.5). A similar relation was observed between TMP grade and coronary wedge pressure (mean (SD) 28 (16) mm Hg with TMP 0 v 9 (7) mm Hg with TMP 1-3, p = 0.001, r = -0.4). Higher PDCF was associated with increased left ventricular end diastolic pressures (0.28 (0.14) with end diastolic pressure > 20 mm Hg v 0.22 (0.09) with end diastolic pressure < 20 mm Hg, p = 0.08, r = 0.2). No correlation was observed between PDCF and Rentrops collateral grade (0.26 (0.13) with grade 0 v 0.25 (0.11) with grades 1-3, p = 0.4, r = -0.06). No linear relation existed between changes in PDCF and changes in left ventricular regional wall motion. CONCLUSION: PDCF in the setting of rescue PCI for failed reperfusion after thrombolysis does not predict improvement in left ventricular function. Increased PDCF and coronary wedge pressure in acute myocardial infarction reflect a dysfunctional microcirculation rather than good collateral protection.

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