Biomedical subjects
Publications and source records attributed to R S Gibson.
The information presented in this review illustrates the different and potentially important clinical data that are obtainable from currently or soon-to-be-available radionuclide imaging procedures. Each modality has unavoidable intrinsic limitations. Nevertheless, in concert they have been useful in the clinical assessment of patients in the acute or convalescent phase of myocardial infarction.
A considerable amount of data now exists that indicates that exercise ECG--due to its suboptimal sensitivity and specificity--has limited diagnostic and prognostic value in asymptomatic subjects, patients with chest pain of unclear etiology or those with chronic stable angina pectoris, and in patients recovering from acute myocardial infarction. Because of this and the well-recognized advantages of thallium-201 scintigraphy, there appears to be a strong rationale for recommending exercise perfusion imaging, rather than exercise ECG alone, as the preferred method for detecting CAD and staging its severity. This recommendation seems justified given the fact that (1) thallium-201 scintigraphy is far more sensitive and specific in detecting myocardial ischemia than exercise testing; (2) unlike stress ECG, thallium-201 scintigraphy can localize ischemia to a specific area of areas subtended by a specific coronary artery; and (3) thallium-201 scintigraphy has been shown to be more reliable to risk stratification of individual patients than exercise testing alone. The more optimal prognostic efficiency of thallium-201 scintigraphy is due, in part, to the fact that the error rate in falsely classifying patients as low-risk is substantially and significantly smaller with thallium-201 scintigraphy than with stress ECG.
Trace elements occur in the body in very small or 'trace' amounts. Deficiencies of essential trace elements produce multiple and diverse clinical signs and symptoms. These may arise from inadequate dietary intake, decreased bioavailability, iatrogenic factors, certain disease states in which decreased absorption, excessive excretion and/or utilization occurs, and physiological states in which trace element requirements are increased and/or body stores are reduced. This review discusses both the static and functional laboratory tests used for the assessment of chromium, copper, selenium, and zinc status in humans, with emphasis on those tests suitable for community use. Static tests measure the total quantity of the trace elements in various accessible tissues and body fluids such as hair, nails, blood or some of its components, and urine; functional tests measure the activity of trace-element-dependent enzymes, or a physiological or behavioural function dependent on a specific trace element. The advantages and limitations of each test are discussed, together with the effects of non-nutritional factors that may confound the interpretation of the results. Interpretive criteria are also given, where possible.
Left ventricular (LV) hypertrophy is known to be an independent risk factor for cardiac death, but its significance in non-Q-wave acute myocardial infarction (AMI) has not been assessed previously. In a randomized diltiazem-placebo-controlled therapeutic trial of non-Q-wave AMI confirmed by creatine kinase-MB (CK-MB), 126 of 544 patients (23%) exhibited LV hypertrophy using standard voltage criteria. Compared to patients without LV hypertrophy, patients with LV hypertrophy were significantly older (65 vs 60 years, p less than 0.0001) and had smaller peak adjusted CK levels (490 +/- 376 vs 666 +/- 726 IU/liter, p less than 0.001) than patients without LV hypertrophy. Patients with and without LV hypertrophy did not differ significantly in acute mortality during hospitalization, progression to Q waves, reinfarction by CK-MB criteria or angina associated with transient electrocardiographic changes. Compared with patients without LV hypertrophy, those patients with non-Q-wave AMI and LV hypertrophy had a 2-fold higher incidence of reinfarction (24 vs 12%, p less than 0.005) and death (19 vs 9%, p = 0.044) during the first year of follow-up. Multivariate regression analysis revealed that the relative risk of death and reinfarction during the initial year after AMI was increased by a factor of 1.7 and 2.1 among patients with LV hypertrophy, respectively. It was therefore concluded that, although patients with LV hypertrophy and non-Q-wave AMI have smaller enzymatic infarcts and the same short-term prognosis as do patients without LV hypertrophy, their reinfarction and mortality rates are significantly increased during the first year of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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A 2-part prospective study was performed to evaluate the clinical outcome of patients with hemodynamically confirmed asymptomatic valvular aortic stenosis (AS). During phase 1, linear regression analysis showed continuous wave Doppler to be highly accurate in predicting catheterization measured peak systolic aortic valve pressure gradients in 101 consecutive patients aged 36 to 83 years (mean 65 +/- 8) with symptomatic AS. During phase 2, 90 additional patients (51 asymptomatic and 39 symptomatic) with Doppler-derived peak systolic aortic valve gradients greater than or equal to 50 mm Hg (range 50 to 132 [mean 68 +/- 19]) were followed for 1 to 45 months. Both groups of patients in phase 2 had similar Doppler gradients and clinical and auscultatory evidence of moderate to severe AS at baseline. Asymptomatic patients were younger (p = 0.01), had higher ejection fractions (p = 0.001) and were less likely to have an electrocardiographic strain pattern (p = 0.01) and left atrial enlargement (p = 0.02). End-diastolic wall thickness, left ventricular cross-sectional myocardial area and estimated left ventricular mass were 18% (p = 0.0001), 20% (p = 0.0008), and 29% (p = 0.002) greater in symptomatic patients. During 17 +/- 9 months of follow-up, 21 asymptomatic patients (41%) became symptomatic. Dyspnea was the most common initial complaint, occurring 2.5 and 4.8 times more often than angina and syncope, respectively. Compared with the 39 symptomatic patients, the 51 asymptomatic patients had a lower cumulative life table incidence of death from any cause (p = 0.002), and from cardiac causes (p = 0.0001) including sudden death (p = 0.013).(ABSTRACT TRUNCATED AT 250 WORDS)
This study compares the serum insulin and lipid profiles of a group of Southern Ontario tannery workers, with elevated serum and urine Cr levels, with those of men not exposed to industrial chromium (III) oxide. Fasting blood samples were obtained from 72 male tannery workers (TW) (mean age +/- SD = 36 +/- 12 y) and from 52 control subjects (CS) (mean age +/- SD = 41 +/- 13 y), matched by age, sex, race, and socioeconomic group. There were no significant differences between the two groups for median serum insulin (TW = 8 microM/mL vs CS = 9 microM/mL), total cholesterol (TC) (TW = 201 mg/dL vs CS 209 mg/dL), triglycerides (TG) (TW = 131 mg/dL vs 114 mg/dL) and high density lipoprotein cholesterol (HDL-C) (TW = 45 mg/dL vs CS = 43 mg/dL), or, in the calculated median values for low density lipoprotein cholesterol (TW = 117 mg/dL vs CS = 134 mg/dL), percent HDL-C (TW = 23% vs CS = 22%), and the cholesterol atherogenic ratio (TC/HDL-C) (TW = 4.3 vs CS = 4.5). Results of this study, therefore, demonstrate that absorption of trivalent Cr compounds, arising from industrial exposure, has no significant effect on serum insulin and lipid profiles.
The long-term outcome and the significance of residual ischemic myocardium, as assessed by predischarge exercise thallium scintigraphy and vessel patency, were studied in 97 patients with single vessel coronary artery disease by angiography 12 +/- 4 days after uncomplicated myocardial infarction. During a mean follow-up period of 39 +/- 17 months, no patients died, 6 (6%) had a recurrent nonfatal infarction and 25 (26%) experienced rapidly progressive angina requiring hospitalization. Although neither exercise-induced angina nor ST segment depression was predictive of a recurrent cardiac event, the mean number of infarct zone scan segments showing thallium redistribution (1.0 +/- 1.0 versus 0.5 +/- 0.8, p = 0.01) and the percent of patients with infarct zone redistribution (61 versus 39%, p = 0.05) were greater in those patients who experienced a late ischemic event. Kaplan-Meier analysis demonstrated a lower event-free survival rate in patients with redistribution (n = 45) than in those without redistribution (n = 52) (p = 0.019). Although no patient received immediate thrombolytic therapy, the infarct-related vessel was angiographically patent in 40 patients (41%). Vessel patency did not influence event-free survival, although a patent vessel, as compared with an occluded vessel, was associated with a greater prevalence of non-Q wave infarction (58 versus 21%, p less than 0.001), fewer persistent infarct zone thallium defects (1.2 +/- 1.1 versus 2.0 +/- 1.2, p = 0.001), more reversible infarct zone thallium defects (1.0 +/- 1.0 versus 0.5 +/- 0.9, p = 0.02) and a trend toward a higher left ventricular ejection fraction (53 +/- 10% versus 49 +/- 12%, p = 0.07). In summary, uncomplicated myocardial infarction in patients with single vessel coronary artery disease is associated with a very low incidence of subsequent death and reinfarction. The presence of infarct zone thallium redistribution, compared with its absence, is predictive of a higher cardiac event rate. These data should be considered when recommending prophylactic percutaneous transluminal angioplasty after uncomplicated myocardial infarction in asymptomatic patients with single vessel coronary disease. On the basis of these results, future randomized trials designed to evaluate the therapeutic efficacy of revascularization in asymptomatic postinfarction patients with single vessel disease should limit enrollment to those patients with residual ischemia located within the infarct zone.
Forty consecutive patients with creatine kinase-MB confirmed myocardial infarction due to circumflex artery occlusion (Group 1) were prospectively evaluated and compared with 107 patients with infarction due to right coronary artery occlusion (Group 2) and 94 with left anterior descending artery occlusion (Group 3). All 241 patients underwent exercise thallium-201 scintigraphy, radionuclide ventriculography, 24 h Holter electrocardiographic (ECG) monitoring and coronary arteriography before hospital discharge and were followed up for 39 +/- 18 months. There were no significant differences among the three infarct groups in age, gender, number of risk factors, prevalence and type of prior infarction, Norris index, Killip class and frequency of in-hospital complications. Acute ST segment elevation was present in only 48% of patients in Group 1 versus 71 and 72% in Groups 2 and 3, respectively (p = 0.012), and 38% of patients with a circumflex artery-related infarct had no significant ST changes (that is, elevation or depression) on admission (versus 21 and 20% for patients in Groups 2 and 3, respectively) (p = 0.001). Abnormal R waves in lead V1 were more common in Group 1 than in Group 2 (p less than 0.003) as was ST elevation in leads I, aVL and V4 to V6 (p less than or equal to 0.048). These differences in ECG findings between Group 1 and 2 patients correlated with a significantly higher prevalence of posterior and lateral wall asynergy in the group with a circumflex artery-related infarct. Infarct size based on peak creatine kinase levels and multiple radionuclide variables was intermediate in Group 1 compared with that in Group 2 (smallest) and Group 3 (largest). During long-term follow-up, the probability of recurrent cardiac events was similar in the three infarct groups. When patients with a circumflex artery-related infarct were stratified according to the presence or absence of abnormal R waves in lead V1 or V2, the abnormal R wave group had more admission ST elevation (p = 0.025), a larger infarct (p less than 0.05) and more extensive coronary artery disease (p = 0.027). In fact, all patients with a circumflex artery-related infarct and an abnormal R wave in lead V1 had multivessel disease. An abnormal R wave in lead V1 had a 96% specificity for circumflex versus right coronary artery-related infarction but a sensitivity of only 21%. Discriminate function analysis of all admission historical and ECG variables identified inferior and lateral ST elevation as independent predictors of circumflex artery-related infarction...
The goal of this study was to determine the prognostic utility of the exercise thallium-201 stress test in ambulatory patients with chest pain who were also referred for cardiac catheterization. Accordingly, 4 to 8 year (mean +/- 1SD, 4.6 +/- 2.6 years) follow-up data were obtained for all but one of 383 patients who underwent both exercise thallium-201 stress testing and cardiac catheterization from 1978 to 1981. Eighty-three patients had a revascularization procedure performed within 3 months of testing and were excluded from analysis. Of the remaining 299 patients, 210 had no events and 89 had events (41 deaths, nine nonfatal myocardial infarctions, and 39 revascularization procedures greater than or equal to 3 months after testing). When all clinical, exercise, thallium-201, and catheterization variables were analyzed by Cox regression analysis, the number of diseased vessels (when defined as greater than or equal to 50% luminal diameter narrowing) was the single most important predictor of future cardiac events (chi 2 = 38.1) followed by the number of segments demonstrating redistribution on delayed thallium-201 images (chi 2 = 16.3), except in the case of nonfatal myocardial infarction, for which redistribution was the most important predictor of future events. When coronary artery disease was defined as 70% or greater luminal diameter narrowing, the number of diseased vessels significantly (p less than .01) lost its power to predict events (chi 2 = 14.5). Other variables found to independently predict future events included change in heart rate from rest to exercise (chi 2 = 13.0), ST segment depression on exercise (chi 2 = 13.0), occurrence of ventricular arrhythmias on exercise (chi 2 = 5.9), and beta-blocker therapy (chi 2 = 4.3). The exclusion of myocardial revascularization procedures as an event did not change the results significantly. Although the number of diseased vessels was the single most important determinant of future events, the exercise thallium-201 stress test when considered as a whole (which included the number of segments demonstrating redistribution on delayed thallium-201 images, change in heart rate from rest to exercise, ST segment depression on the electrocardiogram, and ventricular premature beats on exercise) was equally powerful (chi 2 = 41.6). Combination of both catheterization and exercise thallium-201 data was superior to either alone (chi 2 = 57.5) for determining future events. Exercise stress test alone (without thallium-201 data) was inferior to the exercise thallium-201 stress test or cardiac catheterization for predicting future events (chi 2 = 30.6).(ABSTRACT TRUNCATED AT 400 WORDS)
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We prospectively studied changes in serum lactate dehydrogenase isoenzyme-1 (LD-1, EC 1.1.1.27) in 99 consecutive patients after either coronary artery bypass grafting (CABG, n = 61), isolated cardiac-valve replacement (n = 24), or the two procedures combined (n = 14); 86 of these had no clinical evidence of peri-operative myocardial infarction (MI). Blood was sampled immediately after surgery and at 6-h intervals for up to 42 h thereafter. LD-1 was isolated by using the LD M-subunit antiserum. Samples from the non-MI patients were used to establish the reference intervals for LD-1. By 24 h after surgery, mean serum LD-1 values were higher (P less than 0.001) in non-MI patients who underwent isolated valve replacement (222 +/- 74 U/L) or combined CABG and valve replacement (266 +/- 58 U/L) than in 50 non-MI patients who underwent CABG alone (134 +/- 42 U/L). Separate reference intervals were determined for CABG and other patients at each sampling time. By 24 h after operation, LD-1 exceeded these reference intervals in the 10 CABG and two combined-procedure patients in whom other evidence of MI was present. Measurement of LD-1 24 to 42 h after cardiac surgery appears to be a useful test for the diagnosis of perioperative MI.
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Of 576 patients with non-Q-wave acute myocardial infarction enrolled in the Diltiazem Reinfarction Study, 246 (43%) had 1 or more episodes of angina at rest or with minimal effort during 10.5 days of treatment with either diltiazem (90 mg every 6 hours) or placebo. Reinfarction (12.2% vs 3.6%, p less than 0.0001) or death (6.1% vs 1.5%, p = 0.003) was more likely to occur within 2 weeks of randomization in patients with postinfarction angina than in those without angina. Based on serial electrocardiographic data, 115 of the 246 patients with angina had transient ST-T changes and 131 did not. Comparison of the 14-day event rates in these 2 groups showed that the 115 patients with electrocardiographic evidence of ischemia had a higher frequency of reinfarction (20% vs 5.3%, p less than 0.001), more extensive damage as assessed by peak MB-creatine kinase levels (91 +/- 76 vs 37 +/- 19 IU/liter, p = 0.059 [Wilcoxon rank sum]) and a higher mortality rate (11.3% vs 1.5%, p = 0.001). Angina associated with transient ST-T changes occurred in 70 of the 289 patients in the placebo group but in only 45 of the 287 patients in the diltiazem group--a 28% reduction in cumulative life-table incidence (p = 0.0103 [2-tail, log rank]; 95% confidence interval, 9.3 to 53.8%). It is concluded that patients with early postinfarction angina are at increased risk of reinfarction and death, and angina associated with transient electrocardiographic changes identified a very high risk subset. This subset appeared to have a larger area of viable but jeopardized myocardium and benefited from prophylactic therapy with diltiazem.
Precordial ST-segment depression is typically observed in anterior non-Q-wave acute myocardial infarction (AMI), and is generally not regarded as an indication for acute thrombolytic therapy. Of 544 patients with creatine kinase (CK)-MB-confirmed non-Q-wave AMI randomized to the prospective multicenter Diltiazem Reinfarction Study, 50 patients (9.2%) had isolated precordial ST-segment depression of 1 mm or more in 2 or more contiguous precordial electrocardiographic leads (V1-V4). Serial electrocardiograms recorded at study entry (mean 50.5 hours after onset of chest pain), on study day 2, study day 3 and at predischarge showed that in 23 of 50 patients (40%) electrocardiographic evidence of posterior AMI evolved, defined as an R wave of 0.04 second or more in lead V1 and an R:S greater than or equal to 1 in lead V2. In 18 of these 23 patients (78%), posterior AMI had evolved by study day 3, and none had an abnormal reelevation of CK-MB (every 12-hour sampling) for up to 14 days of hospitalization. Compared with the remaining 27 patients who had electrocardiographic features of anterior non-Q-wave AMI only, the 23 with initial precordial ST segment depression in whom posterior AMI developed had significantly higher mean peak CK values (1,051 +/- 172 vs 663 +/- 89 IU, p less than 0.009) and greater mean precordial ST-segment depression in lead V1 (0.28 vs + 0.19 mm, p = 0.01), in lead V2 (1.3 vs 0.26 mm, p = 0.003) and in lead V3 (2.0 vs 0.93 mm, p = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)
The prevalence of exercise-induced ischemia was determined by thallium-201 (TI-201) scintigraphic criteria in patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) inducible by programmed electrical stimulation. Thirty-eight patients (age 57 +/- 19 years), of whom 87% had angiographic coronary artery disease, underwent quantitative TI-201 exercise scintigraphy within 14 days of invasive electrophysiologic testing. The mean rest ejection fraction was 38 +/- 9%. Eighty percent of patients had 1 or more regions with akinetic or dyskinetic wall motion. Thallium-201 scan segments were scored as normal or containing redistribution defects or mild or severe persistent defects. Only 4 patients (10%) had only redistribution defects and 9 (24%) had both redistribution defects and persistent defects; 32 of 38 patients (84%) had 1 or more persistent defects, of which 26 had at least 1 severe, persistent defect (more than 50% reduction in TI-201 activity). Patients with and without exercise-induced VT had a similar prevalence of redistribution. Redistribution defect prevalence was similar in patients with polymorphic VT (3 of 13) and monomorphic VT (10 of 25) during programmed electrical stimulation (difference not significant). Thus, patients with VT or VF induced by programmed ventricular stimulation have extensive TI-201 scintigraphic abnormalities on exercise scintigrams, predominantly those suggesting scar, with associated severe regional wall motion abnormalities at rest. The scintigraphic prevalence of exercise-induced ischemia is low and TI-201 redistribution and exercise ST depression are observed with equal frequency in patients with and those without VT induced during exercise.
Liquefaction necrosis of mitral annular calcification occurs in 3% of autopsied cases. The liquified material can spread intramurally in various directions creating suspicious appearing mass lesions on chest x-ray or echocardiography. An incidential finding of an echogenic left atrial calcified mass in a 57-year-old woman was suspected to be an intracardiac tumor for which she underwent exploratory cardiotomy. Instead, culture-negative liquified pasty material was removed from the posterior left atrial wall adjacent to the calcified mitral annulus. This case illustrates that liquefaction necrosis of mitral annular calcification may spread to contiguous structures and masquerade as an intracardiac tumor. This relatively unknown aspect of mitral annular calcification should be considered in the differential diagnosis of echogenic left atrial mass lesions.
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