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J L Ritchie

Publications and source records attributed to J L Ritchie.

At least 91 records · Page 5Linked to original sources
PubMed1985

Left ventricular volume determination using single-photon emission computed tomography.

A new method for measuring left ventricular (LV) volume based on gated single-photon emission computed tomography (SPECT) is described. Preliminary phantom studies showed an excellent correlation between SPECT and observed volumes (r = 0.99, standard error of the estimate [SEE] = 4.9 ml). SPECT was performed 24 hours after biplane contrast LV angiography in 36 patients. Transaxial blood pool tomograms were reconstructed by filtered back projection and reoriented to views orthogonal to the cardiac axes. Volume was calculated from serial short-axis tomograms by determining the base, apex and lateral borders of the LV blood pool, ascertaining the number of pixels in this volume and multiplying by the known volume of a pixel. Gated SPECT volumes were compared with contrast angiographic volumes. At end-systole, r = 0.96 and SEE = 12 ml; at end-diastole, r = 0.81 and SEE = 27 ml. For ejection fraction, r = 0.85 and SEE = 0.06. To test interobserver variation in processing, count data from 5 patients were processed twice (r = 0.98, SEE = 8.3 ml). There is an excellent correlation between SPECT and contrast angiographic volumes at end-systole; at end-diastole the relation is good. SPECT requires no arbitrary background correction, allows systematic isolation of the left ventricle from other overlapping cardiac chambers and requires no geometric assumptions for volume determination. It has promise as a direct method for measuring LV volume in a minimally invasive manner.

Adult↗
PubMed1985

Out-of-hospital sudden coronary death: rest and exercise radionuclide left ventricular function in survivors.

One hundred fifty-four survivors of out-of-hospital ventricular fibrillation (VF) with coronary artery disease underwent radionuclide ventriculography an average of 4.2 months after VF. All patients were studied at rest, and 91 of these patients were also studied during supine bicycle exercise. Clinical histories and 24-hour ambulatory electrocardiograms were also assessed, and patients were followed for an average of 3.1 years after ventriculography. The mean left ventricular (LV) ejection fraction (EF) at rest was 40 +/- 16%; in 34% of patients, it was 30% or less; in 37%, 31 to 50%; and in 29%, more than 50%. Regional LV wall motion was normal in 18%. The most severe segmental abnormality was hypokinesia in 22%, akinesia in 45% and dyskinesia in 14%. Wall motion abnormalities were usually located at the apex. During exercise, only 3% of patients (3 of 91) had a normal increase in EF of more than 5%, and the mean EF decreased from 42 to 38%. New exercise-induced wall motion abnormalities occurred in 30%. During the follow-up period, 54 patients died (35%): 48 from cardiac causes and 42 from unexpected and sudden causes. Predictors of death included EF at rest, presence of akinesia or dyskinesia on the ventriculogram at rest, the number of abnormal LV segments, history of congestive heart failure, history of acute myocardial infarction, absence of acute myocardial infarction at the time of VF and the presence of ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1985

The effect of sulfinpyrazone on platelet deposition on Dacron vascular grafts in man.

To determine if sulfinpyrazone inhibits platelet deposition on chronically implanted (greater than 9 months) Dacron aortic bifurcation grafts in man, we performed indium-111 platelet imaging over 24 to 96 hours after labeled platelet injection in 10 males with grafts before and during sulfinpyrazone therapy (200 mg four times daily). Platelet accumulation was quantitated by a graft/blood ratio that compared indium-111 platelet image activity in the graft to platelet activity in well-counted whole blood. In addition, independent visual analysis compared platelet accumulation in the graft area to adjacent native arteries. By quantitative evaluation, sulfinpyrazone did not decrease the graft/blood ratio compared to baseline at 24 hours (3.2 +/- 0.4 vs 3.3 +/- 0.5, mean +/- SEM), 48 hours (4.6 +/- 0.6 vs 4.6 +/- 0.9) , 72 hours (6.8 +/- 0.8 vs 6.7 +/- 1.3), or 96 hours (9.7 +/- 1.6 vs 9.7 +/- 1.6) after labeled platelet injection. Visual interpretation also revealed no decrease in deposition in any patient during sulfinpyrazone therapy. We conclude that sulfinpyrazone does not inhibit platelet deposition on chronically implanted Dacron arterial graft surfaces in man. The techniques described provide a useful method of evaluating antithrombotic drug effects in patients with intravascular prosthetic materials.

Aged↗
PubMed1985

Late effects of intracoronary streptokinase on regional wall motion, ventricular aneurysm and left ventricular thrombus in myocardial infarction: results from the Western Washington Randomized Trial.

To determine whether intracoronary streptokinase improves late regional wall motion or reduces left ventricular aneurysm or thrombus formation in patients with acute myocardial infarction, two-dimensional echocardiography was performed at 8 +/- 3 weeks after infarction in 83 patients randomized to streptokinase (n = 45) or standard therapy (n = 38) in the Western Washington Intracoronary Streptokinase Trial. Among the patients treated with streptokinase, the average time to treatment was 4.7 +/- 2.5 hours after the onset of chest pain, and 67% had successful reperfusion. Regional wall motion was assessed in nine left ventricular segments on a scale of 1 to 4 (normal, hypokinetic, akinetic and dyskinetic). Left ventricular thrombus formation was interpreted as positive, equivocal or negative. All patients received anticoagulant therapy in the hospital and 52 received such therapy after hospital discharge. The mean (+/- SD) global (1.5 +/- 0.4 in both groups) and regional wall motion scores in the streptokinase-treated and control groups were not significantly different. The prevalence of aneurysm was 16% in both groups. Left ventricular thrombus was identified in only five patients (positive identification in four, and equivocal in one), all in the streptokinase-treated group (p = NS). There were also no differences between streptokinase and control treatment in any of the echocardiographic variables in subgroups of patients with anterior infarction, inferior infarction, no prior infarction or reperfusion with streptokinase. It is concluded that intracoronary streptokinase given relatively late in the course of acute myocardial infarction does not result in improved global or regional wall motion or a reduction in left ventricular thrombus or aneurysm formation in survivors studied 2 months after myocardial infarction.

Aged↗
PubMed1985

Hemodynamic effects of epinephrine: concentration-effect study in humans.

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

Adult↗
PubMed1985

Coronary anatomy and left ventricular function in the first 12 hours of acute myocardial infarction: the Western Washington Randomized Intracoronary Streptokinase Trial.

The relationships among clinical variables, coronary anatomy, and left ventricular function during the early hours of acute myocardial infarction (AMI) were evaluated from data acquired in the Western Washington Intracoronary Streptokinase Trial. All patients had symptoms and electrocardiographic changes typical of AMI. All data were obtained before treatment with streptokinase. Mean time to catheterization was 4.1 hr after onset of symptoms. Coronary angiograms (n = 245) were analyzed for location of infarct-related occlusion and collateral flow to the infarct bed. Left ventricular ejection fraction and regional left ventricular function were quantitated in 227. Sixty-two percent of occlusions were in the most proximal segment of the involved coronary artery. Collateral circulation was seen in 42% overall, in 31% with left anterior descending artery (LAD) occlusion, and in 52% with right coronary artery (RCA) occlusion (p less than .005). Left ventricular ejection fraction was lowest and regional function was most abnormal in the group with proximal LAD occlusion. Hyperkinesis was present in 32%; in those with hyperkinesis, hyperkinetic segment length was longest in those with RCA or circumflex occlusion. Multivariate analysis identified proximal LAD occlusion as the factor most closely associated with left ventricular ejection fraction and with measures of left ventricular regional hypofunction. We conclude that (1) AMI is usually caused by occlusion or subtotal occlusion in the most proximal portion of the involved coronary artery, (2) collateral circulation is more frequent with RCA than with LAD occlusion, and (3) location of the infarct-related occlusion is the most important determinant of global and regional left ventricular function in the early hours of AMI.

Aged↗
PubMed1984

The effects of antithrombotic drugs in patients with left ventricular thrombi: assessment with indium-111 platelet imaging and two-dimensional echocardiography.

Patients with left ventricular thrombi not caused by recent myocardial infarction were prospectively studied by indium-111 platelet imaging and two-dimensional echocardiography to determine the reproducibility of these techniques and the short-term effects of sulfinpyrazone (200 mg four times daily), aspirin (325 mg three times daily) plus dipyridamole (75 mg three times daily), and full-dose warfarin. At baseline, all patients underwent indium-111 platelet imaging and echocardiography, and the results were positive for thrombus. In six patients on no antithrombotic drug therapy, repeat platelet scans and echocardiographic studies at 6.0 +/- 3.3 weeks remained positive and were unchanged. In seven patients studied on sulfinpyrazone, three platelet scans became negative, two became equivocal, and two were unchanged; the presence and size of thrombus was constant by echocardiography in all seven patients. Of the six patients studied on aspirin plus dipyridamole, one platelet scan became negative, those of three became equivocal, and two were unchanged; all echocardiographic findings remained positive, but one patient had decreased thrombus size. Among four warfarin-treated patients, three had resolution of platelet deposition and one was unchanged; by echocardiography, thrombus resolved in one patient, was decreased in size in one, and was unchanged in two. We conclude that, in the absence of antithrombotic drug therapy, platelet imaging and echocardiographic findings are stable in patients with left ventricular thrombi not caused by recent myocardial infarction. Sulfinpyrazone, aspirin plus dipyridamole, and warfarin all interrupt platelet deposition in some patients with chronic left ventricular thrombi.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Failure of ticlopidine to inhibit deposition of indium-111-labeled platelets on Dacron prosthetic surfaces in humans.

In a randomized double-blind trial we sought to determine whether short-term therapy with ticlopidine (250 mg bid for 14 days) inhibited platelet deposition on Dacron aortic bifurcation grafts that had been in place a year or longer. A total of 10 men, 42 to 69 years old, underwent indium-111 platelet imaging during both placebo and drug phases of the trial at 24, 48, and 72 hr after the injection of labeled platelets. Platelet accumulation was quantitated by a graft/blood ratio that compared background-corrected activity of indium-111-labeled platelets in the graft with whole-blood activity of indium-111-labeled platelets. Additionally, blinded qualitative visual analysis of the unprocessed images was used to compare graft area activity with activity in adjacent native arteries. Ticlopidine significantly prolonged the template bleeding time from 5.3 +/- 0.5 to 17.1 +/- 3.1 min (+/- SEM) (p = .003). However, by quantitative analysis there was no significant reduction in platelet deposition in the graft during ticlopidine therapy compared with placebo at 24 hr (graft/blood ratio 2.3 +/- 0.4 vs 2.6 +/- 0.3), 48 hr (3.1 +/- 0.5 vs 3.2 +/- 0.4), or 72 hr (3.9 +/- 0.7 vs 4.0 +/- 0.6) after injection of labeled platelets. By visual analysis, nine patients had positive results for abnormal platelet deposition when on placebo that were unchanged when on ticlopidine. The tenth patient had an equivocal result for abnormal platelet deposition when on placebo and a negative result for abnormal platelet deposition when on ticlopidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Global and regional left ventricular function and tomographic radionuclide perfusion: the Western Washington Intracoronary Streptokinase In Myocardial Infarction Trial.

The Western Washington Intracoronary Streptokinase In Myocardial Infarction Trial enrolled 250 patients with acute myocardial infarction. After the coronary angiographic diagnosis of thrombosis, patients were randomly assigned to receive either conventional therapy with heparin or intracoronary streptokinase followed by heparin. Of the 232 patients who survived at least 60 days, 207 (89%) underwent radionuclide ventriculographic determination of global and regional ejection fraction at a single institution at 62 +/- 35 days after infarction. In the first 100 patients, infarct size was also determined by quantitative single-photon emission tomographic imaging with thallium-201 (201Tl) and expressed as a percentage of the left ventricle with a perfusion defect. Overall, global ejection fraction did not differ between patients treated with streptokinase (45.9 +/- 13.9%; n = 115) and control patients (46.1 +/- 14.4%; n = 92, p = NS). Similarly, the regional posterolateral, inferior, and anteroseptal ejection fraction did not differ between the two groups. Infarct size as measured by 201Tl tomography was 19.4 +/- 12.8% (n = 52) of the left ventricle for the streptokinase group and 19.6 +/- 11.8% (n = 48; p = NS) for the control group. When patients were compared within groups by electrocardiographic location of infarction, time to treatment, or the presence or absence of vessel opening, there were no significant differences between streptokinase and control patients. Statistical inclusion of the 18 patients who died early and were unavailable for study also failed to modify the results, except for a possible reduction in inferior infarct size as measured by 201Tl tomography.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Quantitation of size of relative myocardial perfusion defect by single-photon emission computed tomography.

The purpose of this study was to validate a semiautomatic method for quantitating the size of relative myocardial perfusion defects from single-photon emission computed tomographic (SPECT) images. We compared the size of the image defect in vivo, expressed as percent of involved left ventricle, as determined by this method with the anatomic size of the defect in vitro in 19 dogs. To test the method under optimal conditions, we first labeled the left ventricular myocardium in nine dogs by left atrial injection of 99mTc-labeled macroaggregated albumin particles after acute occlusion of one coronary artery. The "defect volume" was defined as the volume of the left ventricular myocardium for which counts fell 2 or more SDs below the distribution of counts in the myocardium supplied by a normal coronary artery in a series of animals. The relative in vivo defect volume by SPECT occupied 26.46 +/- 12.7% of the left ventricular volume (mean +/- SD), compared with a relative defect size in vitro of 33.3 +/- 13.7% (p = NS) of left ventricular volume as determined by well counting of myocardial samples. There was a close correlation between the two measurements (r = .92). However, myocardial relative defect volumes involving less than 5% of myocardium were not identified by SPECT. The defect volume weighted for the relative reduction in flow within the defect zone or the relative "reduced perfusion volume" was also determined. The correlation between the estimates by SPECT and those made in vitro for relative reduced perfusion volume was also high (r = .94).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1983

Western Washington randomized trial of intracoronary streptokinase in acute myocardial infarction.

Two hundred fifty patients were enrolled in a multicenter, community-based study of the efficacy of intracoronary streptokinase thrombolysis in acute myocardial infarction; 134 were randomly assigned to streptokinase therapy and 116 were controls. All patients underwent left ventricular angiography and coronary arteriography before the random assignment. The mean time from the onset of symptoms to hospitalization was 134 +/- 144 minutes (S.D), and the mean time to random assignment was 276 +/- 185 minutes. Coronary reperfusion was achieved in 68 per cent of the streptokinase-treated group. The overall 30-day mortality was 18 (7.2 per cent); there were five deaths in the streptokinase-treated group (3.7 per cent) and 13 in the control group (11.2 per cent, P less than 0.02). Fifteen of the 18 deaths occurred in patients with anterior infarction. Intracoronary streptokinase therapy resulted in a nearly threefold reduction in the 30-day mortality after hospitalization for acute myocardial infarction.

Adult↗
PubMed1983

Natural history of platelet deposition on Dacron aortic bifurcation grafts in the first year after implantation.

This study defined the dynamics of platelet deposition on Dacron arterial grafts up to 1 year after implantation in human subjects. Indium-111 platelet imaging was performed on 8 men 1 to 2 weeks after graft implantation and on 5 of these patients at a mean of 31 weeks (range 28 to 34) and again at 55 weeks (range 50 to 62). Serial imaging was performed at 24 to 96 hours after platelet labeling and injection in each study. Quantitative analysis was performed using a graft/blood ratio that compared background-corrected indium-111 platelet activity in the graft region to whole-blood indium-111 platelet activity. Additionally, blinded qualitative visual analysis of the images compared graft activity with the activity in adjacent native arteries. The mean of all graft/blood ratios (24, 48, 72, and 96 hours) progressively decreased from 4.4 +/- 2.1 (+/- 1 standard deviation) at 1 to 2 weeks to 3.0 +/- 1.8 at 31 weeks (p = 0.002). There was no further decrease at 55 weeks (2.8 +/- 2.0). For comparison, 12 normal subjects without grafts had a mean ratio of 1.8 +/- 0.7. Visual analysis detected platelet deposition in 7 of 8 grafts at 1 to 2 weeks, 4 of 5 at 31 weeks, and 4 of 5 at 55 weeks. Deposition decreased qualitatively in 2 of 5 patients at late study. It is concluded that there is consistent, early platelet deposition on Dacron grafts in man. Although deposition decreases over 31 weeks, it remains readily detectable in most patients at 1 year. These findings suggest absent or incomplete endothelialization of the graft flow surface in humans in the first year after implantation.

Aged↗
PubMed1983

The acute effects of low flow oxygen and isosorbide dinitrate on left and right ventricular ejection fractions in chronic obstructive pulmonary disease.

The objectives of this study were to determine the effects of low flow oxygen and isosorbide dinitrate on rest and exercise biventricular ejection fractions in patients with chronic obstructive pulmonary disease and to relate these ejection fraction responses to changes in pressure and flow. Nine patients with stable, moderate to severe chronic obstructive pulmonary disease who had no prior history of heart failure performed supine exercise with simultaneous hemodynamic and radionuclide ventriculographic monitoring. Eight patients performed a second exercise during low flow oxygen breathing and five performed a third exercise after ingesting 10 mg oral isosorbide. Oxygen led to a decrease in exercise pulmonary artery pressure in all subjects and a decline in total pulmonary resistance in five of the seven in whom it was measured. Right ventricular ejection fraction increased 0.05 or more only in subjects who had a decrease in total pulmonary resistance. Isosorbide fed to an increase in rest and exercise right and left ventricular ejection fractions with simultaneous decreases in pulmonary artery pressure, total pulmonary resistance, blood pressure and arterial oxygen tension. These results suggest that in patients with chronic obstructive pulmonary disease but without a history of right heart failure, the right ventricular systolic functional response to low flow oxygen and isosorbide at rest and exercise is, in part, determined by changes in total pulmonary resistance. The chronic relation between right ventricular ejection fraction and pulmonary hemodynamics in patients with chronic obstructive pulmonary disease remains to be evaluated.

Blood Pressure↗
PubMed1983

Comparative plasma catecholamine and hemodynamic responses to handgrip, cold pressor and supine bicycle exercise testing in normal subjects.

Serial hemodynamic and plasma catecholamine responses were compared among 10 healthy men (27 +/- 3 years) (+/- 1 standard deviation) during symptom-limited handgrip (33% maximal voluntary contraction for 4.4 +/- 1.8 minutes), cold pressor testing (6 minutes) and symptom-limited supine bicycle exercise (22 +/- 5 minutes). Plasma catecholamine concentrations were measured by radioenzymatic assays: ejection fraction and changes in cardiac volumes were assessed by equilibrium radionuclide angiography. During maximal supine exercise, plasma norepinephrine and epinephrine concentrations increased three to six times more than during either symptom-limited handgrip or cold pressor testing. Additionally, increases in heart rate, systolic blood pressure, rate-pressure product, stroke volume, ejection fraction and cardiac output were significantly greater during bicycle exercise than during the other two tests. A decrease in ejection fraction of 0.05 units or more was common in young normal subjects during the first 2 minutes of cold pressor testing (6 of 10 subjects) or at symptom-limited handgrip (3 of 10), but never occurred during maximal supine bicycle exercise. The magnitude of hemodynamic changes with maximal supine bicycle exercise was greater, more consistent and associated with much higher sympathetic nervous system activation, making this a potentially more useful diagnostic stress than either handgrip exercise or cold pressor testing.

Adult↗
PubMed1983

Tricyclic antidepressants and supine, standing, and exercise plasma norepinephrine levels.

Fourteen depressed patients were treated for 1 to 8 wk (4.1 +/- 0.6, mean +/- SEM) with imipramine, doxepin, or amitriptyline to study the effects of tricyclic antidepressants (TCAs) on sympathetic nervous system (SNS) function. Eight had chronic but medically stable cardiac disease and six were medically healthy. Supine plasma norepinephrine (NE) and epinephrine (EPI) levels, mean arterial blood pressure (MAP), and heart rate were measured at rest, after standing, and during graded, supine maximal bicycle exercise. Eight nondepressed patients with cardiac disease were studied without drug intervention as controls. There were no baseline differences in any of these measures among the medically healthy depressed subjects, the depressed cardiac patients, and the eight nondepressed patients matched for cardiac disease. After TCAs, NE was increased by 51 +/- 6% of basal values and heart rate rose, but EPI and MAP were unchanged. The supine to 10-min standing increment in NE increased from 309 +/- 51 pg/ml at baseline to 406 +/- 55 pg/ml during TCA treatment. These findings are compatible with an increase in SNS outflow after TCAs.

Adult↗
PubMed1982

Cardiovascular effects of tricyclic antidepressants in depressed patients with chronic heart disease.

Twenty-four depressed patients with heart disease were treated for four weeks in a double-blind trial of imipramine, doxepin, or placebo to assess the effects of tricyclic antidepressants on ventricular function and rhythm. The tricyclic antidepressants had no effect on left ventricular ejection fraction at rest or during maximal exercise, as measured by radionuclide ventriculograms obtained before and after treatment. Premature ventricular contractions were reduced by imipramine but were not consistently changed by doxepin or placebo. Treatment with imipramine and doxepin, but not placebo, was associated with significant improvement (P less than 0.001) in standard ratings of depression. Our findings underscore the need for a reappraisal of the cardiovascular risks of tricyclic antidepressants and suggest that in the absence of severe impairment of myocardial performance, depressed patients with preexisting heart disease can be effectively treated with these agents without an adverse effect on ventricular rhythm or hemodynamic function.

Adult↗
PubMed1982

Single photon tomographic imaging of a standard heart phantom with 201T1: a gamma camera based system.

A standard heart phantom (University of Iowa design), including discrete myocardial walls, a central blood pool, and a 24-cc transmural "cold" defect, was studied with both planar and transverse tomographic imaging. The heart phantom was filled with 201T1 and placed within a cylindrical tank containing water and 201T1 to simulate nonmyocardial background activity from the thorax. The tomographic imaging system used was a commercially available, rotating, large field-of-view gamma camera. Image reconstruction from 64 sampling angles was performed in a nuclear medicine minicomputer system. The percentage activity in the region of the defect (actual activity of 0) contrasted to the normal wall was compared between planar and 1.25-cm transaxial tomographic slices. Defect activity fell to between 65% and 85% of that of the opposing normal wall in planar images, whereas it fell to between 26% and 49% of that of the normal wall in the tomographic images. In most cases, tomographic defect activity was half or less than that in the planar image. The geographic extent of the defect was seen in an appropriate number of tomographic slices; i.e., the geographic 3.2-cm defect length was predominantly seen in three 1.25-cm transverse slices. We conclude that camera-based tomographic systems show promise for improved 201T1 myocardial defect detection and quantitation over conventional planar images.

Heart↗