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B P Kimball

Publications and source records attributed to B P Kimball.

15 recordsLinked to original sources

Comparison of acute elastic recoil after directional coronary atherectomy versus standard balloon angioplasty.

We evaluated intraprocedural "elastic recoil" in 25 patients (22 men and 3 women) undergoing directional coronary atherectomy (DCA) of left anterior descending stenoses, and compared these with 25 temporally-matched (14 men and 11 women) patients having balloon angioplasties (PTCA). Quantitative arteriography was performed using the Coronary Measurement System (Leiden, The Netherlands), with "elastic recoil" defined as the difference in maximum device or balloon size minus residual minimum diameter. In addition, we determined the effects of relative device size, specific anatomic location (proximal/mid artery), lesion length, eccentricity (symmetry index), and dystrophic calcification on acute "recoil" severity after both procedures. Although initial coronary stenoses were similar (minimum stenotic diameter, DCA = 0.59 +/- 0.20 mm versus PTCA = 0.55 +/- 0.23 mm, p = NS), less "elastic recoil" was observed after atherectomy (DCA = 0.83 +/- 0.57 mm versus PTCA = 1.26 +/- 0.56 mm, p < 0.01), and this was confirmed by absolute recoil/maximum device size ratios (DCA = 23.5 +/- 16.0% versus PTCA = 41.6 +/- 13.8%, p < 0.01). Acute "elastic recoil" was also influenced by maximum device size/"normal" coronary artery ratios [(ratio < 0.9, DCA = 0.26 +/- 0.10 mm versus PTCA = 0.84 +/- 0.13 mm, p < 0.01); (ratio 0.9 to 1.1, DCA = 0.69 +/- 0.41 mm versus PTCA 0.75 +/- 0.32 mm, p = NS); (ratio > 1.1, DCA = 1.09 +/- 0.64 mm versus PTCA = 1.59 +/- 0.48 mm, p < 0.05)].(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

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)

Adult

Acute outcome of directional coronary atherectomy vs standard balloon angioplasty in de novo left anterior descending stenoses.

To assess the immediate outcome of directional coronary atherectomy (DCA) versus standard balloon angioplasty (PTCA) in de novo left anterior descending coronary stenoses, 25 consecutive atherectomies (22 men, 3 women) performed at The Toronto Hospital, between July 1990 and March 1991 were compared with 25 (14 men, 11 women) temporally matched successful angioplasties. Coronary stenoses were analyzed by quantitative arteriography, using the Coronary Measurement System (Leiden, The Netherlands), with estimation of transstenotic hemodynamics by fluid dynamic equations. Before and after procedure qualitative blood flow (TIMI criteria) was also evaluated, as was intimal haziness and coronary dissection. In comparison to PTCA, coronary atherectomy produced less residual minimum stenotic diameter (DCA, 2.75 +/- 0.55 vs PTCA, 1.70 +/- 0.44 mm, p < 0.001), and relative percent diameter stenosis (DCA, 17.9 +/- 10.7 vs PTCA, 34.4 +/- 10.7 percent, p < 0.001), with less transstenotic obstructive gradient (DCA, 0.2 +/- 0.2 vs PTCA, 1.0 +/- 1.5 mm Hg, p < 0.05), and greater estimated stenotic flow reserve (DCA, 4.86 +/- 0.15 vs PTCA, 4.50 +/- 0.48 x baseline, p < 0.05). Coronary atherectomy "normalized" TIMI flow patterns in virtually all patients (DCA, 2.96 +/- 0.20 vs PTCA, 2.72 +/- 0.45, p < 0.05), while creating less intimal haziness (DCA, 10/25 [40 percent] vs PTCA, 23/25 [92 percent], p < 0.01), and coronary dissection (DCA, 6/25 [24 percent] vs PTCA, 16/25 [64 percent], p < 0.05). Therefore, when compared with standard balloon angioplasty, DCA produces less residual stenosis, better transstenotic hemodynamics, while decreasing the frequency of coronary artery damage, in de novo left anterior descending stenoses.

Adult

Directional coronary atherectomy at the Toronto and Mount Sinai Hospitals: report of the initial 120 procedures.

OBJECTIVE: To assess the procedural success and complication rates of the first 120 directional coronary atherectomy cases performed at two Toronto hospitals. DESIGN AND SETTING: Case series in tertiary referral centres. PATIENTS: One hundred and thirteen patients in whom 120 atherectomy procedures were attempted between July 1990 and April 1992. INTERVENTION: Directional coronary atherectomy. MAIN RESULTS: Angiographic success was obtained in 115 of 120 procedures (96%) involving 117 of 123 lesions (95%). Procedural success (angiographic success without death, myocardial infarction or coronary bypass surgery) was obtained in 110 of 120 procedures (92%). Adjunctive balloon angioplasty was required in 20 procedures (17%). There was one death at 36 h in an elderly patient who underwent an emergency procedure while in cardiogenic shock. Periprocedural non-Q wave myocardial infarction occurred in five patients. There were no Q wave myocardial infarctions. Three patients required coronary bypass surgery prior to discharge and vascular complications occurred in five patients. CONCLUSIONS: Directional coronary atherectomy can be performed with procedural success and complication rates comparable to conventional balloon angioplasty. Randomized trials are underway to determine if atherectomy results in a lower restenosis rate.

Adult

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)

Blood Flow Velocity

Preservation of left ventricular performance with reduced ischemic dysfunction by intravenous nisoldipine.

The effect of intravenous nisoldipine on cardiac performance was examined during pacing-induced ischemia in 14 patients with coronary artery disease. The relative contributions of afterload reduction or prevention of myocardial ischemia were assessed using load-independent global (peak-systolic pressure/end-systolic volume) and regional (peak-systolic pressure/end-systolic radial length) "contractile" indexes. Nisoldipine decreased aortic pressure (predrug, 109 +/- 14 vs postdrug, 88 +/- 13 mm Hg, p less than 0.01) and prevented elevation of left ventricular end-diastolic pressure during rapid atrial pacing (predrug, 7.9 +/- 5.7 vs postdrug, -0.5 +/- 4.9 mm Hg, p less than 0.001). Resting cardiac index (predrug, 3.3 +/- 0.6 vs postdrug, 4.2 +/- 0.7 liters/min/m2, p less than 0.05), and left ventricular ejection fraction (predrug, 68.1 +/- 9.0 vs postdrug, 74.2 +/- 9.4%, p less than 0.05) increased after nisoldipine, which also prevented the deterioration in left ventricular ejection fraction (predrug, -8.1 +/- 7.9 vs postdrug, -1.0 +/- 3.7%, p less than 0.05) and fractional radial shortening (predrug, -8.7 +/- 13.1 vs postdrug, 3.7 +/- 16.4%, p less than 0.01) during rapid atrial pacing. Under these conditions, nisoldipine preserved myocardial function, as determined by global peak-systolic pressure/end-systolic volume (predrug, -0.82 +/- 0.39 vs postdrug, 0.17 +/- 1.54 mm Hg/ml, p less than 0.05) and regional (peak-systolic pressure/end-systolic radial length, predrug, -23.8 +/- 36.1 vs postdrug, 12.7 +/- 36.3 mm Hg/cm, p less than 0.01) "contractile" indexes. Intravenous nisoldipine maintains ventricular performance during rapid atrial pacing via a combination of systemic vasodilation and amelioration of ischemic myocardial dysfunction.

Adult

Comparison of proximal left anterior descending and circumflex coronary artery dimensions in aortic valve stenosis and hypertrophic cardiomyopathy.

To examine the "adequacy" of basal coronary flow in ventricular hypertrophy, the relation between proximal coronary artery dimensions and regional ventricular mass in aortic valve stenosis (AS) and hypertrophic cardiomyopathy (HC) was evaluated. Coronary artery size was determined by quantitative coronary arteriography while global/regional ventricular mass was calculated using computer-processed biplane 2-dimensional echocardiography. In comparison to 18 "normal" subjects, left anterior descending coronary dimensions were significantly larger in those with hypertrophy (normal 3.32 +/- 0.54, AS 3.82 +/- 0.71, HC 4.72 +/- 0.81 mm, p less than 0.05), with progressive increases in left anterior descending/circumflex coronary diameter ratios (normal 1.04 +/- 0.14, AS 1.18 +/- 0.19, HC 1.25 +/- 0.31, p less than 0.01). Compared to the AS group, indexed anteroseptal mass was greater in the HC subjects (AS 40.9 +/- 8.9 vs HC 72.1 +/- 21 g/m2, p less than 0.001). Both septal width/left anterior descending coronary diameter ratios (AS 3.61 +/- 1.06 vs HC 4.85 +/- 1.17 mm/mm, p less than 0.05) and indexed anteroseptal mass/left anterior descending coronary diameter ratios (AS 11.2 +/- 3.0 vs HC 15.6 +/- 3.4 g/m2/mm, p less than 0.01) were greater in HC subjects. Increased coronary dimensions were observed in both AS and HC, with the greatest changes noted within the left anterior descending distribution in HC, but when analyzed with respect to regional ventricular mass, these subjects demonstrated relative "inadequate" enlargement in coronary artery diameters. Underdeveloped epicardial coronary arteries may contribute to anteroseptal myocardial ischemia, with resultant angina pectoris, increased ventricular ectopic activity and sudden death in HC.

Aged

Validation of left ventricular function parameters acquired with the non-imaging nuclear probe: comparison with tantalum marker cine-fluoroscopy.

We evaluated the accuracy of the non-imaging nuclear probe for measuring various parameters of left ventricular function by comparing these with simultaneous measurements acquired via tantalum marker cine-fluoroscopy. Eight patients with surgically implanted mid-myocardial tantalum markers were studied during cardiac catheterization. High temporal resolution tantalum marker-derived volume/time curves were generated and calibrated to absolute endocardial volumes by comparison with contrast left ventricular angiography. Left ventricular function parameters were acquired at baseline and during atrial pacing, nitroprusside infusion and volume loading. Simultaneous measurements obtained with the nuclear probe and via tantalum marker cine-fluoroscopy were compared. The following correlation coefficients were obtained: ejection fraction, r = 0.49, P less than 0.001; peak ejection rate, r = 0.41, P less than 0.01; mean ejection rate, r = 0.62, P less than 0.001; time to peak ejection, r = 0.73, P less than 0.001; peak filling rate, r = 0.73, P less than 0.001; time to peak filling, r = 0.58, P less than 0.001. Relative changes in end-diastolic volume were accurately tracked by the nuclear probe in six of seven patients (r values 0.77-0.93). These results suggest that measurements of certain left ventricular volume parameters with the nuclear probe may not accurately reflect true volume changes as measured by tantalum marker cine-fluoroscopy. Although, the probe may be useful in tracking relative changes in end-diastolic volume, we would advise caution in using this instrument for studies requiring accurate measurements of ejection and filling parameters.

Cardiac Catheterization

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.

Adult

Effect of intracoronary nifedipine on coronary bloodflow and myocardial metabolism during pacing-induced ischemia.

The effects of intracoronary nifedipine on coronary bloodflow, its regional distribution, myocardial oxygen consumption and lactate metabolism during pacing-induced angina were evaluated in 15 subjects. These responses were directly compared to 10 subjects who received an alcohol-based control solvent. Myocardial bloodflow was measured by thermodilution, with changes in regional coronary flow assessed using a dual radiolabelled (technetium-99m and indium-111) intracoronary microsphere technique and single photon emission tomography. Neither intracoronary nifedipine (100 micrograms) or the control solvent produced changes in systemic arterial pressure (nifedipine -2 mmHg and control +2 mmHg, both not significant). Intracoronary nifedipine markedly increased left ventricular end diastolic pressure (pre-nifedipine 13.0 mmHg versus post nifedipine 20.1, P less than 0.05), while increasing total coronary sinus bloodflow (pre-nifedipine 134 mL/min versus post nifedipine 189, P less than 0.05): Regional coronary bloodflow increased in all myocardial segments, regardless of the severity of coronary stenosis (64 to 132% baseline, all P less than 0.05). In addition, intracoronary nifedipine increased myocardial oxygen consumption (pre-nifedipine 12.3 mL/min versus post nifedipine 15.7, P less than 0.05), with a trend towards improved lactate extraction (pre-nifedipine 0.24 mg/mL versus post nifedipine 0.12, not significant). Although decreased ventricular afterload (left ventricular systolic wall stress) may contribute to nifedipine's antianginal properties, a primary increase in regional coronary bloodflow also appears to be an important factor in the alleviation of myocardial ischemia.

Adult

Quantitative arteriographic responses to ergonovine provocation in subjects with atypical chest pain.

To evaluate the nonspecific vasoconstrictor response to intravenous ergonovine, and identify patient-related factors that systematically alter changes in coronary dimensions, 33 subjects (22 women, 11 men), mean age 54 years (range 39 to 70) were studied using a standardized ergonovine provocation test (Stanford protocol). Clinical responses, systemic hemodynamics and electrocardiographic changes were determined, with quantitative arteriography used for sequential measurement of proximal right coronary dimensions. A progressive decrease in proximal right coronary diameter was observed, with average control values and final diameters equaling 3.25 +/- 0.49 and 2.56 +/- 0.49 mm, respectively, thus representing an overall -21.2% change from baseline. No significant differences existed in control dimensions when analyzed with respect to gender (3.20 +/- 0.59 vs 3.40 +/- 0.72 mm, women vs men, difference not significant), although women demonstrated a greater decrease from baseline values (0.80 +/- 0.30 vs 0.50 +/- 0.24 mm, women vs men, p less than 0.05). The presence of minor atherosclerotic disease, as determined by the presence of minor (less than 30% diameter) luminal irregularities within the right coronary artery, failed to alter control dimensions (3.30 +/- 0.48 vs 3.20 +/- 0.51 mm, normal vs atherosclerotic persons, difference not significant), but was associated with more ergonovine-induced coronary vasospasm (0.41 +/- 0.27 vs 0.84 +/- 0.21 mm, normal vs atherosclerotic persons, p less than 0.01). Therefore, sequential intravenous ergonovine maleate infusion resulted in progressive, nonspecific reductions in proximal right coronary artery dimensions in subjects without a history compatible with vasospastic angina. This nonspecific vasoconstrictor effect was accentuated in women and subjects with intimal irregularities suggestive of minor atherosclerotic coronary disease.

Adult

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.

Blood Flow Velocity

Persistent ventricular adaptations in postoperative coarctation of the aorta.

To evaluate ventricular performance and myocardial contractility after surgical correction of congenital coarctation of the aorta, we studied 25 patients (16 men and 9 women, mean age 26.1 years [range 19 to 34]), an average of 10.6 years (range 2 to 25) after repair. Radionuclide ventriculography at rest and exercise and digitized, quantitative two-dimensional echocardiography were performed. Data from derived, high resolution time-activity curves by radionuclide ventriculography, combined with noninvasive hemodynamic/ventricular volume data, were compared with values in an age- and sex-matched normal population. Despite essentially identical baseline and exercise hemodynamics, postoperative coarctation subjects demonstrated enhanced ventricular contraction, as determined by the peak ejection rate at rest (-3.79 versus -3.20 stroke volume/s, p less than 0.01) and exercise (-3.00 versus -2.90 stroke volume/s, p = NS), and overall ejection fraction at rest (56.4 versus 48.0%, p less than 0.01) and exercise (70.8 versus 59.3%, p less than 0.01). An intrinsic activation-contraction delay was observed, as illustrated by a prolonged time to peak ejection rate at rest (27.7 versus 21.5% of the RR interval, p less than 0.01) and exercise (28.4 versus 21.2% of the RR interval, p less than 0.01), and total systolic time at rest (50.2 versus 43.4% of the RR interval, p less than 0.01) and exercise (56.8 versus 50.4% of the RR interval, p less than 0.01). Although left ventricular meridinal wall stress was statistically indistinguishable (62 versus 74 mm Hg/mm2, p = NS), intrinsic myocardial contractility, as assessed by the peak systolic pressure/volume ratio, was increased in the postoperative coarctation group (1.88 versus 2.87 mm Hg/ml, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological

Abnormal thallium kinetics in postoperative coarctation of the aorta: evidence for diffuse hypertension-induced vascular pathology.

After operative correction of congenital coarctation of the aorta, patients continue to have excess cardiovascular mortality, including manifestations of ischemic heart disease. Previous morphologic studies support the concept of direct hypertensive vascular injury in these patients. To determine whether abnormalities of myocardial perfusion were present in an asymptomatic group of patients with coarctation repair, 18 men and 9 women with a mean age of 26 years (range 19 to 41) were studied between 2 and 25 years after operative correction. Stress electrocardiography and quantitative thallium imaging by a circumferential profile technique were used. These patients were compared with a normal group, statistically defined as having a less than 1% prevalence of significant obstructive coronary artery disease. The postoperative coarctation group demonstrated a reduction in global thallium redistribution in each view analyzed. As compared with findings in the control subjects, thallium washout in the anterior view (41.9 versus 48.6%, p = 0.02) and left anterior oblique projection (40.5 versus 48.2%, p = 0.007) was significantly diminished. Although the postoperative coarctation group had a lower thallium redistribution rate in the lateral view (41.4 versus 46.3%, p = 0.09) this difference did not reach statistical significance because of the intrinsic variability of this projection. Plots of the median percent thallium washout revealed independence from circumferential profile angle, indicating global abnormalities in perfusion. No correlation between clinical variables and thallium kinetics could be established, suggesting marked individual variability in the development of this vascular lesion. The observation of abnormal thallium kinetics in patients with coarctation repair may have consequences for long-term follow-up and therapy.

Adult