Utility of Continuous Measurement of Pulmonary Artery Oxygen Saturation During Episodic Myocardial Ischemia in Patients

The use of continuously monitored pulmonary artery oxygen saturation (PAOS)for the assessment of transient myocardial ischemia was examined in a controlled human model during coronary angioplasty, producing brief reversible episodes of myocardial ischemia. Clinical and anatomic variables were prospectively recorded and correlated with changes in continuous PAOS during repeated episodes of coronary artery occulsion. Forty-seven patients underwent left anterior descending (LAD, n = 43) or circumflex (n = 4) coronary balloon occlusion. Patients were subgrouped by PAOS responses: group 1, 22 patients with ± 10% drop in PAOS during balloon inflation and group 2, 25 patients in whom the PAOS signal was stable or only minimally affected during transient ischemia. Anatomical features analyzed included normal coronary diameter, location of lesion (e.g., proximal to the first septal branch) and extent of myocardium supplied by an occluded artery (LAD extending beyond the apex of the left ventricle [LV] or a large diagonal after the occlusion point). Left ventricular wall motion abnormalities, presence of other coronary artery disease, diabetes and hypertension were also analyzed. Groups were similar with respect to age (61 ± 13, 62 ± 10 years), LV ejection fraction, LV score, incidence of hypertension and diabetes or anatomic scores (2.2 ± 1.0, for group 1 vs 2.0 ± 0.9 for group 2), normal angiographic arterial diameter and presence of coronary collateral supply.
Although some episodes of myocardial ischemia in electively studied stable patients may be associated with significant reducitons in PAOS, the occurrence or degree of PAOS reduction is not predicted by coronary anatomy, LV function or other clinical variables. Use of PAOS to identify ischemic events in more critically ill patients is potentially useful, but must be assessed individually during the clinical situation. (J Interven Cardiol 1988:1:2)     

Intracoronary Nitrogylcerin and Regional Coronary Blood Flow Responses During Coronary Angioplasty in Patients

To examine the direct effects of nitroglycerin (NTG) on anterior regional coronary blòod flow, electrocardiographic and hemodynamic responses were measured immediately before, during, and after brief coronary occlusion in 17 patients undergoing left anterior descending coronary angioplasty (PTCA). Hemodynamic data and the time from the onset of coronary occlusion to 1.0 mm ST elevation or depression were compared for matched control and NTG occlusion periods. Ten seconds before the "NTG" occlusion, 200 μg of NTG was injected into the left coronary artery. Baseline and occlusion level great cardiac vein flow (thermodilution) was similar for both occlusion periods (93 ± 27 to 59 ± 23 mL/min for control; 95 ± 27 to 56 ± 22 mL/min for NTG occlusion). NTG reduced mean arterial pressure (91 ± 11 to 82 ± 15 mmHg, P < 0.05) during increased basal great vein flow (95 ± 27 to 127 ± 54 mL/min p < 0.01) immediately prior to occlusion. Great vein hyperemic flow after release of occlusion increased 21 ± 30% versus 36 ± 40% (P = ns) after control occlusion. There were no differences in heart rate or systolic-heart rate pressure products, time to ischemic ST-T wave changes or the maximal hyperemic responses from the control occlusion. These data suggest that during the initial minutes of coronary occlusion, the marked but transient coronary vasodilation induced by intracoronary NTG does not significantly modulate myocardial ischemia or regional coronary blood flow responses. The clinical benefits of NTG during PTCA most likely occur more through other mechanisms than direct myocardial flow augmentation. (J Interven Cardiol: 1988:1:1)     

The Effects of Coronary Angioplasty on Nitroglycerin-Induced Augmentation of Regional Myocardial Blood Flow

Percutaneous transluminal coronary angioplasty (PTCA) may improve coronary vasomotor responses after relief of flow limiting luminal narrowings. To evaluate the effects of PTCA on nitro-glycerin-induced augmentation of coronary blood flow, great cardiac vein (thermodilution) blood flow and systemic hemodynamic responses to low (50 meg) and high (200 meg) dose intracoronary nitroglycerin (NTG) before and after PTCA were measured in 20 patients undergoing left anterior descending artery (LAD) balloon dilatation. Before PTCA, low dose NTG increased great vein flow 44 ±31% (from 56 ± 21 to 81 ± 33 mL/min, P < 0.01). High dose NTG increased great vein flow 55 + 30% (56 ± 23 to 87 ± 38 mL/min, P < 0.01). PTCA reduced LAD stenosis (79 ± 13 to 20 ± 9%, P < 0.01) and translesional pressure gradient (49 ± 10 to 15 ± 13 mmHg, P < 0.01) increasing post-PTCA basal great vein flow 45% (56 ± 21 mL/min to 81 ±27 mL/min, P < 0.01).
After PTCA, low dose NTG increased great vein flow only 26 ± 23% (81 ± 27 to 101 ± 39mL/min, P < 0.01; P < 0.05 versus 44 ± 31% before PTCA). The high dose NTG-induced coronary hy-peremic responses were unchanged after PTCA (55 ± 30, 55 ± 34%, P = ns). When compared to dose related NTG hyperemic responses in 10 patients with normal LAD, the post-PTCA responses remained attenuated.
These data indicate that NTG-induced augmentation of coronary blood flow remains unchanged or attenuated and does not appear to be improved by PTCA. These findings should be considered when evaluating pharmacological coronary blood flow responses after PTCA. These data also suggest that epicardial coronary resistance plays a limited role in NTG-induced augmentation of coronary blood flow inpatients with atherosclerotic coronary disease. (J Interven Cardiol 1988:1:2)