Measurement of transstenotic pressure gradient during percutaneous transluminal coronary angioplasty

Obstruction to blood flow is accompanied by a pressure gradient across the obstructed site. In certain clinical settings, magnitude of pressure gradient has been used to judge severity of obstruction, and gradient reduction to judge success of an interventional procedure. In percutaneous transluminal coronary angioplasty (PTCA) the relationships between transstenotic pressure gradient, diameter stenosis, and lesion length are imprecisely known. We therefore examined 4263 sets of measurements in patients who underwent PTCA on single, discrete coronary arterial lesions. Multivariate regression analysis demonstrated that pressure gradient was artifactually elevated by about 12 mm Hg at low values of diameter stenosis but increased by the 4th power of stenosis as expected from fluid dynamics models. Pressure gradient was dampened and relatively constant at values of diameter stenosis of 60% or higher, probably because of total or near-total occlusion of the artery. Lesion length was not found to influence pressure gradient. Reductions in diameter stenosis (delta D) and pressure gradient (delta G) were related nonlinearly, with delta D proportional to the square root of delta G, suggesting that a reduction in gradient is directly proportional to an increase in cross-sectional area of the stenosis. The predictive value of final post-PTCA pressure gradients was found: a final gradient of 15 mm Hg or less predicted a final post-PTCA diameter stenosis of 30% or less, with 75% sensitivity and 29% specificity (p less than .01). The results of this study suggest that (1) pressure gradient as currently measured during PTCA is related to diameter stenosis but not to lesion length (2) reductions in pressure gradient and diameter stenosis are nonlinearly related.(ABSTRACT TRUNCATED AT 250 WORDS)     

Implication of transstenotic coronary pressure gradient measurement during coronary angioplasty

The aim of this study was to establish a criterion for the success of an angioplasty based upon pressure gradients across coronary lesions. Sixty-two percutaneous transluminal coronary angioplasties (PTCA) in 56 patients with isolated left anterior descending artery disease were examined. Pressure gradients measured before and after PTCA were expressed as normalized mean pressure gradients (NMPG) computed by dividing mean pressure gradient by mean aortic or proximal coronary artery pressure. Angiographic severity was expressed as percentage area stenosis (AS) calculated from diastolic caliper measurements of diameter of each lesion and the nearest normal adjacent segment in at least two projections. The relationship between AS and NMPG was nonlinear with a steep increase in gradients beyond a critical value of AS of about 60%. This relationship was unaffected by angiographically visualized collaterals. All except one of 65 coronary stenotic lesions with NMPG of more than 0.32 had an AS of more than 60%. Only three of 57 coronary stenoses with NMPG of less than 0.32 had severe AS (p < 0.001). The results indicate that NMPG is a reliable, practical guide to the severity of coronary stenosis and is therefore a useful measurement for assessing either the success or the residual stenosis during PTCA.     

Phase variations in the left coronary transstenotic pressure gradient before and after dilatation by percutaneous coronary angioplasty

The concept of significant coronary stenosis may be approached by studying the effects of the narrowing not in absolute values of pressure and flow but by studying the mode of blood flow across the stenosis. Ten patients with isolated stenosis of the LAD were studied for phasic variations of the transstenotic pressure gradient before and after dilatation. The material used was a ST 3.7 catheter with a 0.12 inch guide. Instantaneous pressure recording throughout the cardiac cycle were obtained using a computer. After dilatation, the area of the stenosis minus the area of transverse section of the dilating catheter increased from 0.5 +/- 0.3 to 2.2 +/- 0.3 mm2, the average gradient between the aorta and the post stenotic LAD decreased from 75 +/- 10 to 12 +/- 8 mmHg, and the ratio between the mean diastolic gradient and mean gradient increased from 75 +/- 7 to 245 +/- 30% (p less than 0.01 for the 3 parameters, paired t test). These results show that the LAD transstenotic pressure gradient is not phasic in severe stenosis. It becomes phasic, only in diastole, after dilatation of the stenosis (slight residual stenosis due to the catheter). This difference may be due to the type of flow, continuous and dependent on the stenosis before dilatation, or phasic dependent on the distal coronary circulation after dilatation. Analysis of the phasic changes of coronary flow may be useful for the evaluation of the severity of left coronary stenosis in the absence of pressure measurements.     

Determinants of transstenotic gradients observed during angioplasty: An experimental model

Pressure gradient measurement across a stenosis is used during angiopiasty to aid catheter positioning and estimate dilatation efficacy. The angiopiasty catheter itself, however, further reduces lumen size, and therefore augments the transstenotic gradient. To more precisely define the catheter influence on gradient, we derived a theoretical expression relating the measured gradient with the angiopiasty catheter in situ to the “true” gradient; that is, the gradient in the absence of the angiopiasty catheter. We then tested this theoretical construct in a canine femoral artery angiopiasty model. Fifty-four measurements were performed using 23 separate, 3-mm-long, 40 to 70% stenoses. As predicted by the theoretic model, “true” gradient is compounded by the angiopiasty catheter principally as a function of the angiopiasty catheter diameter (Dc) and the stenosis diameter (Ds). The best-fit curve of data points relating “true” and compounded gradients to various Dc and Ds combinations can be expressed as: Measured GRADIENT = K × true gradient, where K = 0.25 (e)^4.47 (Dc÷Ds and e = 2.718. Thus, the transstenotic gradient measured at angiopiasty overestimates “true” resting gradient in a predictable manner, which is dependent on the ratio of Dc to Ds.     

The transstenotic pressure gradient trend as a predictor of acute complications after percutaneous transluminal coronary angioplasty

The transstenotic pressure gradient recorded during coronary angioplasty (PTCA) reflects the dynamic relationship that exists between coronary blood flow and the effective cross-sectional area of the arterial lumen. An apparent relationship between the dynamic behavior of the pressure gradient and subsequent acute vessel closure was observed in our catheterization laboratory. We therefore examined the usefulness of the pressure gradient trend in predicting acute complications after 463 attempted PTCA procedures. Two pressure gradient trend patterns were identified: (1) a rising trend pattern identified by an increasing pressure gradient in the interval after deflation of the angioplasty, and (2) a stable trend pattern identified by a constant or decreasing pressure gradient. The incidence of acute vessel closure (17% vs 4%, p = .0001), emergency CABG (5.6% versus 1%, p less than .05), and myocardial infarction (13% versus 2%, p less than .0001) after the PTCA procedure was significantly higher among patients with rising trend patterns when compared with patients with stable trend patterns. Multivariate analysis identified independent predictors for an acute closure event as rising trend pattern (p less than .001), post-PTCA gradient (p less than .05), and post-PTCA percent diameter stenosis (p less than .02). Independent predictors for emergency coronary artery bypass grafting and myocardial infarction were post-PTCA gradient (p less than .001) and a rising trend pattern (odds ratio = 2.91, p less than .001), respectively. The dynamic behavior of the gradient trend provides additional useful information about the results of dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of transstenotic coronary pressure gradient measurements during diagnostic catheterization

A difficult problem in coronary arteriography is the assessment of the hemodynamic significance of stenoses that appear angiographically to be of only moderate severity (25 to 75% diameter narrowing). This is particularly important in patients who may be candidates for invasive therapy, such as percutaneous transluminal coronary angioplasty (PTCA) or coronary bypass surgery. To determine the significance of such lesions, we measured transstenotic coronary pressure gradients in 15 patients with angiographically moderate stenoses. For comparison, similar measurements were made in 17 patients with severe stenoses (more than 75% diameter narrowing) being considered for PTCA. The transstenotic pressure gradients were measured with a 2.0Fr polyvinyl chloride catheter cleared of microbubbles of air by flushing with carbon dioxide and degassed saline solution and attached to a low-volume displacement transducer for optimal frequency response. Mean transstenotic pressure gradients greater than 10 mm Hg at rest or more than 20 mm Hg under conditions of high coronary blood flow, as induced by Renografin 76, appeared to be associated with objective evidence of myocardial ischemia and symptomatic relief from PTCA. Smaller pressure gradients occurred in patients whose symptoms probably were not ischemic in nature. Transstenotic pressure gradient determination performed at the time of diagnostic catheterization may provide assistance in clinical decision-making in selected patients with angiographically moderate stenoses.     

Acute coronary occlusion during percutaneous transluminal coronary angioplasty

Two hundred and forty percutaneous transluminal coronary angioplasty procedures were performed in three centres over a two year period. Acute occlusion of the vessel undergoing angioplasty was seen on 20 (8%) occasions. The cause of occlusion was determined angiographically and in some cases confirmed at the time of emergency open heart surgery. The mechanism of coronary occlusion was arterial dissection in six cases, persisting coronary arterial spasm in seven, and coronary thrombosis in four. In three patients the mechanism could not be determined. Immediate reintroduction of a balloon dilatation catheter was attempted in 10 patients and resulted in restoration of adequate coronary flow in six. The remaining 14 patients underwent open heart surgery as an emergency procedure.     

Benign coronary perforation during percutaneous transluminal coronary angioplasty

In two patients percutaneous transluminal coronary angioplasty was complicated by coronary perforation. In both cases the complication was managed conservatively.     

Distal coronary hemoperfusion during percutaneous transluminal coronary angioplasty

Distal coronary hemoperfusion during percutaneous transluminal coronary angioplasty (PTCA)—with an autoperfusion balloon or active system—facilitates prolonged balloon inflation. Prolonged inflations may tack up intimal dissections and improve the primary angioplasty result in complex lesions. Additionally, distal perfusion may reduce the likelihood of cardiogenic shock during high-risk PTCA. Autoperfusion balloons are most frequently used to treat acute or threatened closure. There currently is no prospective clinical study showing that stent implantation for this complication is more successful and more cost-effective. The blood flow rates through autoperfusion balloons may not abolish myocardial ischemia, and higher flow rates can often be achieved with pumps. Therefore, during high-risk PTCA, pumps may be preferred to prevent hemodynamic collapse. Clinical application of perfusion pumps is hampered by the risk for mechanical hemolysis during prolonged perfusion and the high velocity of the bloodstream that exits the PTCA catheter, causing distal vessel wall trauma. © 1996 Wiley-Liss, Inc.     

Relation of coronary arterial occlusion pressure during percutaneous transluminal coronary angioplasty to presence of collaterals

To investigate the relation of the gradient across a coronary artery stenosis and the pressure distal to the stenosis after proximal occlusion during percutaneous transluminal coronary angioplasty to the amount of angiographically estimated collateral circulation, 63 patients (55 men, 8 women) were studied. All patients had 1-vessel disease (54 left anterior descending, 8 right coronary artery and 1 circumflex coronary artery). All patients had documented ischemia, and angioplasty was carried out within 4 weeks after the initial angiogram. The patients were separated into 4 groups: 0 = no collaterals (35 patients), +1 = just visible collaterals (8 patients), +2 = collaterals without reaching the contralateral vessel (10 patients), and +3 = filling of the contralateral vessel (10 patients). There was no difference in age among the 4 groups. There was a significant negative relation of the gradient vs the extent of collateral circulation, although the degree of stenosis increased significantly from group 0 to group +3. There was a significant positive relation of the occlusion pressure (in absolute terms and in percent of the proximal systolic pressure) vs the extent of collateral circulation. There was a significantly smaller change of the occlusion pressure vs the distal pressure before occlusion if good collaterals were present. The occlusion pressure remained constant during 1 occlusion up to 40 seconds and was reproducible in 3 successive occlusions. In conclusion, the pressure distal to a coronary artery stenosis is mainly dependent on the severity of the stenosis and on the collateral flow. If anterograde flow is eliminated by proximal occlusion the distal pressure is only dependent on the extent of collateral circulation.     

Thromboxane release during percutaneous transluminal coronary angioplasty

The reason for coronary artery occlusion following percutaneous transluminal angioplasty (PTCA) remains an enigma. We postulated that alterations in arachidonic acid metabolism might contribute to coronary artery occlusion, particularly if platelets are perturbed and release thromboxane because of mechanical stimuli during PTCA. We serially monitored coronary sinus and peripheral arterial plasma thromboxane (TX) and prostacyclin (by standard radioimmunoassay of the metabolites TXB2 and 6-keto-PFG1 alpha) during PTCA in 10 patients. TX and prostacyclin were unchanged from control in seven uncomplicated procedures. In one patient with vasospasm, no changes were found. In two patients with occlusion, marked increases were measured in coronary sinus plasma TX. Patient No. 1 increased from 390 to 1375 pg/ml. Patient No. 2 increased from 155 to 1425 pg/ml. Both required emergency bypass grafting. No change in 6-keto-PGF1 alpha was found. Uncomplicated PTCA does not alter arachidonic acid metabolism through cyclooxygenase. Vasospasm need not be associated with TX release, but coronary artery occlusion is. TX may play a role in coronary artery occlusion during PTCA because of (1) increased release and (2) unopposed physiologic effects because increases were not found in the physiologic antagonist prostacyclin.     

Myocardial protection during percutaneous transluminal coronary angioplasty

Coronary angioplasty results in transient coronary artery occlusion. This article reviews with systemic and regional methods aimed at preventing the electrophysiologic and hemodynamic consequences of regional myocardial ischemia.     

Distal hemoperfusion during percutaneous transluminal coronary angioplasty

During percutaneous transluminal coronary angioplasty (PTCA), the ability to maintain balloon inflations for 3 to 5 minutes, as opposed to the usual 30 to 60 seconds, may lead to improved early and late results. To determine the feasibility and clarify the advantages of distal hemoperfusion during PTCA, blood from the renal vein was manually sampled and then reinjected through the pressure port of the coronary balloon catheter during sustained balloon inflations in 3 patients. By supplying the periphery of the left anterior descending coronary artery with flows of 30 to 50 ml/min, ischemic manifestations were suppressed in all 3 cases. Hemoperfusion was performed without complications for as long as 5 minutes, using a maximum of 225 ml of blood. This new technique represents a major step toward the long-sought goal of extracorporeal coronary circulation during PTCA.     

Two-dimensional echocardiography during percutaneous transluminal coronary angioplasty

In order to study myocardial and clinical events during transient coronary occlusion in humans, two-dimensional echocardiography was continuously performed in 15 patients undergoing 49 balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). Transient segmental asynergy developed in all patients 8 +/- 3 seconds after balloon inflation and returned to baseline 19 +/- 8 seconds after balloon deflation. Segmental dyskinesis was seen in only 8 of 11 patients undergoing PTCA of the left anterior descending artery (LAD). A wall motion score, based on degree of asynergy of 13 segments of the left ventricle, was significantly higher during LAD than during right coronary artery inflation (7.9 +/- 1.3 vs 4.0 +/- 1.4, p less than 0.01). Left ventricular size index increased significantly during balloon inflation, from 179 +/- 9 to 196 +/- 10 mm (p less than 0.01). Four patients developed transient ST segment changes in the extremity leads of the ECG and five patients had angina pectoris. The very first sign of ischemia in three patients, who developed all of these symptoms together, was consistently asynergy, followed by ECG changes, and last, angina pectoris. Thus during PTCA, transient asynergy and left ventricular dilatation develop, which are often clinically silent.     

Coronary hemodynamics during percutaneous transluminal coronary angioplasty

The hemodynamic consequences of multiple transient occlusions (9.8 ± 3.7 seconds) of the left anterior descending coronary artery were assessed in 15 conscious patients during percutaneous transluminal coronary angioplasty. Thermodilution coronary venous blood flow, measured in the great cardiac vein, decreased from control values of 75.9 ± 24 ml/min to 50.9 ± 21.9 with coronary occlusion (probability [p] < 0.00001) and increased to 101.6 ± 34.3 after release of occlusion (p < 0.00001). Changes in coronary sinus blood flow, measured simultaneously, reflected the alterations in the great cardiac vein. Restoration of postocclusion blood flow to control values occurred in 18.2 ± 6.7 seconds, and is compatible with reactive hyperemia rather than sustained improvement in resting coronary blood flow. Flow repayment during reactive hyperemia exceeded flow debt incurred during coronary occlusion by 288.4 ± 106 percent (p < 0.05). The increase in reactive hyperemic flow after initial coronary occlusion (24.2 ± 15.7 ml/min) was less than that after final occlusion (42.2 ± 10.1, p < 0.05). This suggests an initial limitation of reactive hyperemia by persistent coronary stenosis. In all patients, reactive hyperemia accentuated the trans-stenotic coronary ostial to distal coronary arterial pressure gradient. Compared with a control value of 53.5 ± 7.7 percent, the great cardiac vein oxygen saturation transiently decreased to 49.3 ± 7.0 percent (p < 0.001) on release of the occlusion and then increased to 62.5 ± 5.2 percent (p < 0.001) during reactive hyperemia. A small reduction in aortic pressure from 96.4 ± 10.2 mm Hg to 89.9 ± 10.9 mm Hg(p < 0.00001) was observed during occlusion. A reduction in first derivative of left ventricular pressure (dP/dt) during coronary occlusion, in three patients in whom it was measured, suggests that the decrease in systemic pressure is due to transient ischemic myocardial dysfunction rather than to peripheral arteriolar vasodilation. These observations are relevant to the performance of coronary angioplasty, and to the understanding of the physiology of transient coronary occlusion in conscious patients.     

Coronary pacing during percutaneous transluminal coronary angioplasty

To avoid venous puncture, a new concept for standby cardiac pacing during percutaneous transluminal coronary angioplasty (PTCA) and diagnostic cardiac catheterization was developed. It uses an arterial guidewire as a unipolar pacing electrode with the second electrode attached to the skin. The system was tested in 25 coronary arteries of 22 patients undergoing PTCA and in the left ventricles of 10 patients undergoing diagnostic cardiac catheterization. Coronary pacing via the guidewire used for directing the balloon catheter was possible in all patients and in 24 of the 25 coronary arteries attempted. Maximum duration of pacing was 8 min. Threshold currents ranged from 1 to 15 mA (mean 5.7). Left ventricular pacing via the same wires or standard wires used for introduction of diagnostic or guiding catheters was possible in all patients and was maintained for up to 10 min. Threshold currents ranged from 1 to 7 mA (mean 3.9). Neither method for pacing produced adverse effects during these short applications. The setup for coronary pacing also allowed recording of an intracoronary electrocardiogram during PTCA. The presented system provides backup for the rare event of sustained bradycardia during PTCA or diagnostic cardiac catheterization. If applied cautiously, it may safely and reliably replace the standby of a conventional transvenous pacing catheter.     

Distal coronary power injection during percutaneous transluminal coronary angioplasty

A modification of the standard percutaneous transluminal coronary angioplasty (PTCA) procedure is described using a power injector instead of a hand-held syringe for distal coronary contrast injections. This system was used in 215 dilatations without complications related to the power injector. We found this system to simplify the PTCA procedure and allowed for improved distal visualization even with the steerable PTCA catheters containing an intraluminal guide wire.     

Acute coronary occlusion during percutaneous transluminal coronary angioplasty.

Two hundred and forty percutaneous transluminal coronary angioplasty procedures were performed in three centres over a two year period. Acute occlusion of the vessel undergoing angioplasty was seen on 20 (8%) occasions. The cause of occlusion was determined angiographically and in some cases confirmed at the time of emergency open heart surgery. The mechanism of coronary occlusion was arterial dissection in six cases, persisting coronary arterial spasm in seven, and coronary thrombosis in four. In three patients the mechanism could not be determined. Immediate reintroduction of a balloon dilatation catheter was attempted in 10 patients and resulted in restoration of adequate coronary flow in six. The remaining 14 patients underwent open heart surgery as an emergency procedure.