Residual coronary stenoses and calculated transstenotic gradients after intravenous streptokinase versus tissue plasminogen activator.

To compare the relative success of intravenous streptokinase (STK) and tissue plasminogen activator (TPA) on the severity of residual infarct-related coronary stenoses, we evaluated 45 patients receiving thrombolytic therapy for acute myocardial infarction. Twenty-three patients (18 men and 5 women) received STK (1.5 million units), while 22 patients (18 men and 4 women) received TPA (100 mg) within 6 hours of chest discomfort. Cardiac catheterization was performed before hospital discharge (8 days) with quantitative coronary arteriography and estimation of transstenotic pressure gradients using fluid dynamic equations. Although angina pectoris was equally common (STK, 7 of 23 [30%] versus TPA, 5 of 22 [23%], p = NS), recurrent infarction (STK, 3 of 23 [13%] versus TPA, 7 of 22 [32%], p less than 0.05) and coronary angioplasty (STK, 2 of 23 [9%] versus TPA, 7 of 22 [32%], p less than 0.05) were more frequent in those receiving TPA. Infarct-related coronary patency was greater in TPA-treated subjects (STK, 15 of 23 [65%] versus TPA, 19 of 22 [86%], p less than 0.05), although minimum stenotic diameter (STK, 0.77 +/- 0.48 mm versus TPA, 0.57 +/- 0.38 mm, p less than 0.05), and calculated transstenotic pressure gradient (STK, 8.7 +/- 17.0 mm Hg versus TPA, 23.7 +/- 30.2 mm Hg, p less than 0.05) suggested severe residual stenosis. These effects were accentuated at elevated coronary flow velocities (8 to 20 cm/sec).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiographic features associated with acute coronary artery occlusion during elective angioplasty.

To examine the morphologic features of stenotic segments developing abrupt coronary occlusion during elective angioplasty, 36 cases occurring at the Toronto General Hospital between January 1985 and December 1989 were evaluated and compared with a temporally matched successful group. Quantitative arteriographic analysis was performed, including estimates of arterial tortuosity (proximal-stenotic axis deviation) and qualitative assessment for dystrophic calcification, residual lumen eccentricity and intimal irregularity. Acute occlusion occurred more frequently in the mid-arterial segment (success, mid 14 versus occlusion 21, P less than 0.05). Stenosis severity assessed by minimum stenotic diameter did not affect outcome (success 0.42 mm versus occlusion 0.37 mm, not significant or relative percentage diameter stenosis (success 86% versus occlusion 86%, not significant). Average stenotic length was equal (success 14.3 mm versus occlusion 13.6 mm, not significant), although coronary arterial tortuosity was increased in the acute occlusion group (success 27 degrees versus occlusion 34 degrees, P less than 0.05). Residual lumen eccentricity score was increased (success 1.66 versus occlusion 2.69, P less than 0.001), with greater dystrophic calcification in the occlusion group (success 0.31 versus occlusion 0.69, P less than 0.05). In addition, intimal irregularity was significantly greater (success 1.65 versus occlusion 2.5, P less than 0.001), although major arterial side branches failed to predict outcome (success 28% versus occlusion 36%, not significant). These data suggested that a mid-coronary anatomic location, arterial tortuosity, lumen eccentricity, dystrophic calcification and intimal irregularity increased the probability of acute occlusion during elective coronary angioplasty.

Changes in diameter of coronary narrowings and translesional hemodynamics after intracoronary nitroglycerin.

The effect of intracoronary nitroglycerin on coronary stenosis dimensions and translesional hemodynamics was evaluated in 38 subjects (74 stenoses) referred for diagnostic coronary arteriography. Quantitative coronary arteriography was performed with standard Newtonian fluid dynamic equations used to estimate transstenotic gradients. Since intracoronary nitroglycerin can induce significant myocardial hyperemia (increased flow velocity), with increased translesional pressure gradients and a decrease in distal intraluminal pressure, the potential effect on subendocardial flow distribution was also analyzed. Minimum stenotic diameter significantly increased postnitroglycerin (NTG) (preNTG 1.42 vs postNTG 1.82 mm, p less than 0.01), with a decrease in relative percent diameter stenosis (preNTG 45.7 vs postNTG 40.7%, p less than 0.05). When changes in minimum stenotic diameter were analyzed according to stenosis severity (quartiles), the greatest effect was noted in those lesions with the least severe stenosis (quartile no. 1, 0.49 vs quartile no. 4, 0.32 mm, p less than 0.05). If coronary blood flow velocity remains at baseline values (4 cm/s), intracoronary nitroglycerin was predicted to significantly decrease transstenotic pressure gradients (preNTG 1.01 vs postNTG 0.82 mm Hg, p less than 0.05), with the greatest change shown in severe lesions (quartile no. 4, preNTG 3.79 to postNTG 2.28 mm Hg, p less than 0.01). Accelerated coronary flow velocity (myocardial hyperemia) increased calculated translesional pressure gradients (4 cm/s, 0.82 mm Hg vs 20 cm/s, 8.00 mm Hg, p less than 0.01), despite simultaneous stenotic vasodilation. Hemodynamic obstruction was particularly dependent on coronary flow velocity in the most severe stenoses (quartile no. 4, 4 cm/s, 2.28 vs 20 cm/s, 28.78 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative evaluation of coronary stenoses using fluid dynamic equations and standard quantitative coronary arteriography.

Traditional quantitative coronary arteriographic measurements have largely ignored geometric variables, which may be important in determining the obstructive nature of coronary stenoses. To illustrate the relation between standard quantitative coronary arteriography and calculated transstenotic fluid dynamics, 25 patients with 1-vessel disease referred for coronary angioplasty were analyzed. Minimal lumen diameter and percent stenosis were measured and the values compared with calculations of pressure loss that used standard hydraulic formulas encompassing both frictional and separation components within the stenotic segments. Baseline flow velocity was assumed to equal 4 cm/s and normal hyperemic flow response was presumed to equal 5 times that of baseline. Fluid dynamic estimates suggested that initial translesional pressure gradients would develop at a minimal diameter of 0.6 mm (80% diameter), with an exponentially severe pressure differential beyond a minimal coronary diameter of 0.3 mm (92% diameter). Maximal velocities were calculated based upon an assumed normal hyperemic flow response of 5 times that of baseline, with the demonstration of early impairment of hyperemic flow reserve at minimal diameters of 1.2 mm (46% diameter). Furthermore, hyperemic flow reserve was completely abolished at a minimal diameter of 0.3 to 0.5 mm (89 to 92% diameter). Beyond a minimal diameter of 0.2 mm (93% diameter), resting hypoperfusion was anticipated with flow velocities below the initially assumed value (4 cm/s). Thus, it is feasible to estimate transstenotic pressure losses and maximal coronary flow velocity by applying Newtonian fluid dynamic equations to actual angiographic stenoses in man. These calculations generally correlate with traditional quantitative arteriographic estimates of stenosis severity, although other geometric parameters such as lesion length, "exit angle" and blood viscosity may alter transstenotic hemodynamics.