Like father like son.
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Biomedical subjects
Publications and source records attributed to K Lipscomb.
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To test the hypothesis that single-photon emission computed tomography (SPECT) could actually determine left ventricular LV mass in humans, SPECT measurements of LV mass were compared with LV mass determined by cineangiography in 12 patients with normal coronary arteries and LV function. Repeat SPECT determinations of LV mass were carried out in 5 patients. Projection images of the left ventricle were acquired after intravenous injection of thallium-201 (TI-201) using a rotating gamma camera. Transverse sections were reconstructed by filtered backprojection. The boundary of LV uptake of TI-201 in each transverse section was defined using a 3-dimensional threshold detector. Scintigraphic LV mass (total number of voxels demonstrating LV TI-201 uptake X voxel volume X specific gravity of myocardium) was compared with angiographic LV mass. There was good correlation between LV mass determined by SPECT and that determined by cineangiography. Mean angiographic LV mass was 208 +/- 45 g (+/- standard deviation). Mean SPECT LV mass was 204 +/- 42 g. Linear regression analysis revealed the following relation: SPECT LV mass = 0.76 X angiographic LV mass + 46.1 (r = 0.82, root-mean-square deviation from regression = 24.7). The SPECT values of LV mass varied an average of 10.4 +/- 4.6% (+/- standard deviation) in the 5 patients in whom 2 determinations were made. Thus, SPECT of TI-201 can accurately measure LV mass in humans.
This study describes the postpartum course of asymptomatic parturient women who had greater than or equal to 10(2) cfu of high-virulence (HV) bacteria per milliliter of amniotic fluid. Of 60 asymptomatic parturient women with greater than or equal to 10(2) cfu of HV bacteria per milliliter of amniotic fluid, 27 (48%) remained asymptomatic in the puerperium, 16 (27%) developed fever only, and 17 (28%) developed endometritis. In asymptomatic versus symptomatic women, there were no statistically significant differences in number or type of isolates or in length of membrane rupture or labor-to-collection interval. However, there were significant differences in the intervals from collection to delivery and in the rate of cesarean section delivery. For comparison, 40 of these patients were matched with women in whom only low-virulence organisms were detected in the amniotic fluid. In the HV group, 16 women (40%) remained asymptomatic, 15 (37.5%) developed fever only, and nine (22.5%) had endometritis. In the low-virulence group, 27 women (67.5%) remained asymptomatic, 10 (25%) developed fever only, one (2.5%) developed endometritis 10 days post partum, and two (5%) had other infections (p less than 0.01). Clinically evident uterine infection depends upon type and numbers of bacteria in utero, duration of bacteria in utero, and route of delivery.
The effect of antianginal therapy on the incidence of an early positive exercise response as a screening tool for 3-vessel and left main (LM) coronary artery disease (CAD) was examined. Fifty-seven men with stable angina pectoris underwent bicycle ergometry before and after long-acting nitrate or calcium antagonist therapy was instituted. An early positive response was defined as signs of myocardial ischemia at low levels of myocardial and total body workload (corresponding to a workload of less than 300 kpm/min). Thirty-nine patients (68%) had an early positive response before therapy, compared with 14 (24%) after therapy. Of 24 patients undergoing coronary angiography, 12 had 3-vessel CAD (including 2 with LM), 5 had 2-vessel CAD, 6 had 1-vessel CAD and 1 patient had no CAD. The sensitivity and specificity of an early positive response in predicting 3-vessel/LM CAD changed from 92% and 58% before to 42% and 75% after therapy. The positive and negative predictive values changed from 69% and 88% before to 63% and 63% after therapy. It is concluded that antianginal therapy reduces the value of an exercise test as a screening tool for 3-vessel/LM CAD.
Transseptal left heart catheterization was performed in 106 instances in 101 patients using right anterior oblique fluoroscopy to define septal boundaries during interatrial septal puncture, and using a preshaped guide wire to catheterize the left ventricle. By using these two modifications of the classic transseptal technique, the left atrium was entered in 105 instances (99%) and the left ventricle was catheterized in all 87 attempts (100%), including attempts in eight patients with mitral stenosis (valve area 1.29 +/- 0.39 cm2 [mean +/- standard deviation] ). No deaths occurred as a direct result of transseptal catheterization; nonfatal complications occurred in 2.8% of patients (hemopericardium in one patient, ventricular fibrillation in one patient and transient vagal reaction in one patient). The use of the right anterior oblique projection to adequately visualize both the interatrial septum and the intended point of puncture, the use of a pigtail catheter positioned in the ascending aorta to define the relation of the puncture site to the aorta in this projection and the utilization of a flexible preshaped guide wire to catheterize the left ventricle are the major factors contributing toward this improved success rate and low incidence of complications.
This study was performed to assess the accuracy of qualitative angiographic grading in persons with aortic regurgitation (AR) or mitral regurgitation (MR) and to determine the factors that may influence the reliability of such grading. In 230 patients (152 men, 78 women, aged 52 +/- 14 years) with AR or MR, forward cardiac index was measured by the Fick and indicator dilution techniques and left ventricular (LV) angiographic index by the area-length method, from which the regurgitant volume index was calculated. In 124 other patients (89 men, 35 women, aged 52 +/- 11 years) without regurgitation, there was good agreement between forward and angiographic cardiac indexes (r = 0.87, p less than 0.001). In the 83 patients with AR, the regurgitant volume indexes in those with 1+ (0.87 +/- 0.57 liters/min/m2) and 2+ (1.72 +/- 1.19 liters/min/m2) angiographic regurgitation were not significantly different from one another, but were significantly different from those with 3+ (3.0 +/- 1.42 liters/min/m2) and 4+ (4.80 +/- 2.25 liters/min/m2) regurgitation; at the same time, the regurgitant volume indexes of patients with 3+ and 4+ AR were not significantly different from one another. In the 147 patients with MR, the regurgitant volume indexes in patients with 1+ regurgitation (0.61 +/- 0.64 liters/min/m2) were significantly lower than other grades, but the regurgitant volume indexes of 2+ (1.14 +/- 0.85 liters/min/m2) vs 3+ (2.14 +/- 1.37 liters/min/m2) and of 3+ vs 4+ (4.60 +/- 2.31 liters/min/m2) were not significantly different. With AR and MR, regurgitant flow within each angiographic grade varied widely, especially in grades 3+ and 4+, and there was considerable overlap of regurgitant volume indexes between grades.(ABSTRACT TRUNCATED AT 250 WORDS)
A method of generating a three-dimensional image of the human left ventricle by computer techniques is described. The volume of each image was estimated by a modification of Simpson's rule. The method was applied to nine suitable patients and estimations of end-diastolic and end-systolic volumes were compared to volumes determined by cineangiography. Significant linear correlation coefficients of 0.95 and 0.94 were obtained for end-diastolic and end-systolic volumes, respectively. The standard errors of estimate were 9 ml for end-diastolic volumes and 7 ml for end-systolic volumes. The value of this methodology lies in the ability to estimate left ventricular volumes with accuracy, using an imaging technique of little inconvenience and no risk to the patient and computer hardware that is readily available at most clinical institutions.
The proper position of a catheter to measure pulmonary wedge pressure is usually confirmed by measuring the oxygen saturation of withdrawn blood. However, this method of confirmation is tedious and frequently unsuccessful. A fluoroscopic method to confirm proper catheter position to measure wedge pressure was tested. Between 2 and 5 ml of contrast medium was injected into the artery distal to the catheter tip. Lack of movement for 15 seconds after injection indicated proper catheter position. As judged by the saturation of withdrawn blood and by comparison of wedge and left atrial or ventricular pressure, the fluoroscopic method of confirmation was correct in 71/75 attempts. Thus the fluoroscopic method of confirmation of proper catheter position is simple, rapid, and reliable.
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Biplane cineradiography is a potentially powerful tool for precise measurement of intracardiac dimensions. The most systematic approach to these measurements is the creation of a three-dimensional coordinate system within the x-ray field. Using this system, interpoint distances, such as between radiopaque clips or coronary artery bifurcations, can be calculated by use of the Pythagoras theorem. Alternatively, calibration factors can be calculated in order to determine the absolute dimensions of a structure, such as a ventricle or coronary artery. However, cineradiography has two problems that have precluded widespread use of the system. These problems are pincushion distortion and variable image magnification. In this paper, methodology to quantitate and compensate for these variables is presented. The method uses radiopaque beads permanently mounted in the x-ray field. The position of the bead images on the x-ray film determine the compensation factors. Using this system, measurements are made with a standard deviation of approximately 1% of the true value.
The Carpentier-Edwards bioprosthesis is a glutaraldehyde-fixed porcine xenograft with a fully flexible thin-walled stent. Cardiac catheterization studies were performed in 17 patients to evaluate use of this valve in the aortic position. Hemodynamic studies established a mean peak gradient across the prosthesis of 19 mm Hg (range 5 to 65). The mean effective orifice area was calculated to be 1.6 cm2 (range 0.8 to 3.3). All patients demonstrated an improvement in functional class after operation. Mean left ventricular ejection fraction increased from 51 +/- 16 to 68 +/- 9 percent (P less than 0.004) in eight patients operated on for aortic stenosis, but was not significantly changed in patients operated on for aortic insufficiency. Hemodynamic comparison of the Carpentier-Edwards bioprosthesis with the standard Hancock xenograft showed similar effective orifice areas for the 23 and 25 mm diameter valves. In two patients studied the 21 mm Carpentier valve demonstrated a greater effective orifice area than that previously reported for the standard Hancock xenograft. The Carpentier-Edwards bioprosthesis affords both clinical and hemodynamic improvement when used in the aortic position and may allow improved effective orifice area when used in the smaller aortic root.
The exercise tests of 26 male patients with significant left main disease were compared with those of 51 patients with three-vessel disease and 38 patients with two-vessel disease. Exercise-induced ischaemia (chest pain and/or greater than 1 mm ST segment change) occurred in 100 per cent of left main, 69 per cent of three-vessel, and 45 per cent of two-vessel disease patients. Though the mean peak work load was significantly higher in the two-vessel disease group than in those with three-vessel of left main disease, there was a wide overlap between groups. No intergroup differences were found in mean peak heart rates. In patients taking propranolol, no differences in mean peak work loads and heart rates were seen. The study showed that the absence of an exercise-induced abnormal electrocardiographic response virtually excludes left main disease. As judged by exercise performance, the presence of left main disease did not correlate with the severity of the patient's symptomatology. Propranolol did not influence the frequency of an ischaemic response in patients with left main or three-vessel disease.
The purpose of this investigation was to determine whether long-term oral administration of commonly prescribed doses of quinidine sulfate and procainamide hydrochloride to patients with ischemic heart disease affects myocardial contractility. Segmental contractility, assessed by the systolic shortening fraction, the relative change in interclip distance from diastole to systole, was measured by cineradiography of metal clips that had been sutured to the epicardium at the time of coronary artery bypass surgery. Global contractility was assessed by gated blood-pool scintigraphy. Systolic shortening fraction determinations and scintigraphy were obtained following five to seven days' administration of procainamide (500 mg every four hours), quinidine (200 mg every six hours), or neither drug in a random sequence. Serum drug levels (milligrams per liter) were 1.8 +/- 0.8 (mean +/- 1 SD) for quinidine and 3.7 +/- 1.1 for procainamide, when measured one hour before the next dose. During quinidine administration, mean segment shortening fraction decreased only slightly, but significantly (P less than 0.02), from 12.4 percent to 10.6 percent. The clinical importance of so small a change is questionable. During procainamide administration, there was a very small, insignificant (P greater than 0.9), decrease in segmental shortening. Global left ventricular function was not significantly changed by either drug. It appears that both drugs can be used over long periods in commonly prescribed doses in patients with ischemic heart disease without a major overall deleterious effect on cardiac performance.
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Patients with single-vessel disease, with normal or mildly abnormal ventricular function (EF greater than 40%), have a good prognosis both for natural survival and long-range symptomatic improvement; therefore medical therapy is strongly recommended. Surgery is considered only if symptoms persist after aggressive medical therapy. It is possible that single-vessel left anterior descending disease is a special variant of this group, and surgery may, with further reports, show an increased survival. However, no adequately designed study has yet suggested this, and it is currently our opinion that patients with single-vessel disease do not have an improved survival following surgery. It is not clear whether surgery improves survival in patients with multivessel disease and normal or mildly abnormal ventricular function (EF greater than 40%). Consequently, cardiologists are divided as to whether to advise surgery in these patients solely for survival. Currently, it is our opinion that these patients should have surgery only for improvement of symptoms after failure of medical therapy. In left main coronary disease the evidence favoring improved survival after surgery has convinced most cardiologists, including ourselves, to recommend surgery. Patients with poor ventricular function (EF less than 30%) secondary to coronary artery disease often have congestive heart failure and not angina as their chief symptom. Surgery is usually not advisable for these patients, because of the increased operative mortality and lack of improvement in ventricular function. Patients with poor ventricular function with angina are not usually significantly improved by surgery. In patients with moderately abnormal ventricular function (EF = 30-40%), relief of angina is frequently obtained, but with some added surgical risk. We recommend surgery in these patients after aggressive medical therapy has failed. Patients with unstable angina are initially medically stabilized, after which they are generally managed as stable angina. Patients with persistence of pain at rest in spite of vigorous medical therapy are usually managed by early catheterization and surgery.
The hemodynamic mechanism of the effect of coronary artery stenosis on coronary flow was studied in the circumflex artery of 10 open-chest dogs by simultaneously measuring coronary flow, aortic pressure, and coronary artery pressure distal to an adjustable constrictor; while the distal coronary bed was intermittently maximally vasodilated by intracoronary injections of angiographic contrast media (Hypaque-M, 75 per cent). For each stenosis, the pressure gradient across the stenosis varied directly with the flow through the stenosis (r equals 0.99), the slope of the regression indicating the severity of the stenosis. An important observation was that this regression line did not intercept the flow axis at zero flow, but at a positive flow, meaning that for a given regression line slope the pressure gradient was much less than expected. At rest, distal bed resistance decreased as progressive stenosis lowered the distal bed pressure, maintaining flow at control level until the distal bed pressure dropped below 60 mm. HG. However, at maximum hyperemia, distal bed resistance was at a fixed minimum value such that flow was directly proportional to distal bed pressure. Hence, progressive stenosis decreased the ratio of hyperemic to resting flow by: (1) causing the vasodilatory reserve to be used to maintain resting flow, decreasing that available for hyperemia, and (2) dropping the distal bed pressure relatively more for smaller increases in flow. This study provides a hemodynamic explanation for the known fact that progressive stenosis initially limits the maximum hyperemic flow, and only after this flow is decreased almost to resting level, does resting flow fall.
The degree and effectiveness of compensatory changes in the distal coronary vascular bed during progressive proximal coronary stenosis have not been described. In this study, coronary vascular bed resistance and pressure gradient-flow relationships were determined for 157 different stenoses in nine opened-chest dogs by measuring coronary flow, aortic pressure, and coronary pressure distal to a coronary constrictor while flow was varied from resting to maximal values by the intracoronary injection of Hypaque-M, 75% (previously shown to cause transient, maximal vasodilatation comparable to ten second occlusion). This approach provided a means of hemodynamically characterizing coronary stenoses in a standary, experimental manner for quantitative analysis of different arteries at different flow rates as found in the intact coronary circulation. The results show that 1) pressure gradient-flow characteristics or hydraulic resistance of stenoses do not become abnormal enough to alter normal resting coronary flow nor to elicit compensatory changes for stenoses up to constriction of approximately 60% of the diameter, 2) compensatory vasodilatation of the distal coronary vascular bed maintains near normal resting flow for lesions between 60% and 85% diameter stenosis but adaptive vasodilatation fails to compensate for the high resistance of lesions greater than 85% diameter stenosis, and 3) there is vasodilator reserve still present when total coronary artery flow is reduced below normal by a stenosis. This vasodilator reserve probably exists in the epicardium since the endocardium is characteristically underperfused due to the low coronary pressure caused by stenosis and is therefore likely to be maximally vasodilated with no remaining vasodilator reserve.
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