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Biomedical subjects

R E Patterson

Publications and source records attributed to R E Patterson.

At least 109 records · Page 6Linked to original sources
PubMed1984

Bayesian comparison of cost-effectiveness of different clinical approaches to diagnose coronary artery disease.

The objective of this study was to compare the cost-effectiveness of four clinical policies (policies I to IV) in the diagnosis of the presence or absence of coronary artery disease. A model based on Bayes' theorem and published clinical data was constructed to make these comparisons. Effectiveness was defined as either the number of patients with coronary disease diagnosed or as the number of quality-adjusted life years extended by therapy after the diagnosis of coronary disease. The following conclusions arise strictly from analysis of the model and may not necessarily be applicable to all situations. As prevalence of coronary disease in the population increased, it caused a linear increase in cost per patient tested, but a hyperbolic decrease in cost per effect, that is, increased cost-effectiveness. Thus, cost-effectiveness of all policies (I to IV) was poor in populations with a prevalence of disease below 10%, for example, asymptomatic people with no risk factors. Analysis of the model also indicates that at prevalences less than 80%, exercise thallium scintigraphy alone as a first test (policy II) is a more cost-effective initial test than is exercise electrocardiography alone as a first test (policy I) or exercise electrocardiography first combined with thallium imaging as a second test (policy IV). Exercise electrocardiography before thallium imaging (policy IV) is more cost-effective than exercise electrocardiography alone (policy I) at prevalences less than 80%. 4) Noninvasive exercise testing before angiography (policies I, II and IV) is more cost-effective than using coronary angiography as the first and only test (policy III) at prevalences less than 80%. 5) Above a threshold value of prevalence of 80% (for example patients with typical angina), proceeding to angiography as the first test (policy III) was more cost-effective than initial noninvasive exercise tests (policies I, II and IV). One advantage of this quantitative model is that it estimates a threshold value of prevalence (80%) at which the rank order of policies changes. The model also allows substitution of different values for any variable as a way of accounting for the uncertainty inherent in the data. In conclusion, it is essential to consider the prevalence of disease when selecting the most cost-effective clinical approach to making a diagnosis.

Angiography↗
PubMed1984

Scintigraphic quantification of asynchronous myocardial motion during the left ventricular isovolumic relaxation period: a study in the dog during acute ischemia.

Asynchronous motion of left ventricular myocardium during the period of left ventricular isovolumic relaxation has often been observed in patients with coronary artery disease. Detection and quantitation of this abnormality with noninvasive nuclear tracer methods, however, have not yet been reported. Thus, functional images of regional left ventricular time to minimum counts (or volume), computed from gated blood pool image sequences, were analyzed to detect and quantitate myocardial asynchrony during this interval. The method was tested by comparing regional with global time to minimum counts before and after coronary artery occlusion in the awake dog. After occlusion, minimum counts in the ischemic region occurred later in the cardiac cycle than did global minimum counts (average difference 69 +/- 37 ms, p less than 0.001). Before occlusion, however, minimum counts in the same region occurred at the same moment as global minimum counts (average difference 4 +/- 12 ms, NS). Thus, acute ischemia in dogs produces a pronounced asynchrony in myocardial motion during the earliest moments of diastole. The magnitude of this asynchrony (69 ms) probably corresponds to the length of the global isovolumic relaxation period in these animals after occlusion. This method might be useful in detecting and quantitating isovolumic asynchrony in ischemia and changes in this asynchrony with therapy (verapamil therapy, for example).

Animals↗
PubMed1984

Relation between exercise-induced changes in ejection fraction and systolic loading conditions at rest in aortic regurgitation.

To examine the role of systolic wall stress at rest in determining left ventricular performance during exercise in aortic regurgitation (AR), systolic wall stress (measured by M-mode echocardiography) was related to changes in left ventricular function during maximal exercise (evaluated by radionuclide ventriculography) in 30 patients with chronic aortic regurgitation. Of these 30 patients, 7 had a normal exercise response, defined as an absolute increase in ejection fraction of 5% or greater (Group I) and 23 had abnormal exercise response, defined as no change (less than 5% change) or a decline (less than or equal to 5%) in ejection fraction (Group II). Patients in Group I had a significantly lower radius/wall thickness ratio (2.5 +/- 0.2 versus 3.1 +/- 0.1, p less than 0.01) and lower peak systolic wall stress (123 +/- 11 versus 211 +/- 12 X 10(3) dynes/cm2, p less than 0.01) than patients in Group II. An increase in ejection fraction during exercise was seen in 6 of the 9 patients with normal systolic wall stress at rest (less than 150 X 10(3) dynes/cm2), but in only 1 of 21 patients with elevated systolic wall stress (p less than 0.001). Peak systolic wall stress at rest varied linearly, and inversely with changes in left ventricular ejection fraction during exercise (r = 0.60, p less than 0.001). Groups I and II did not differ in ejection fraction at rest, clinical symptoms or maximal work load achieved.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Transmural pH gradient in canine myocardial ischemia.

The subendocardium is more susceptible to ischemia than the subepicardium. Studies during critical coronary stenosis have demonstrated subendocardial hypoperfusion relative to the subepicardium and transmural gradients in certain tissue metabolites. Although ischemia causes acidosis, the existence of a transmural pH gradient has never been demonstrated or quantitated. Thus we reduced coronary blood flow to 20 +/- 5% of normal in eight open chest anesthetized (morphine sulfate and pentobarbital) dogs and to 45 +/- 5% in two dogs. We implanted specially designed miniature fiber-optic pH probes in normal and ischemic subendocardium (depth 5.5-8 mm) and subepicardium (depth 3-4 mm). Separate experiments validated use of the fiber-optic pH probe system to measure tissue pH. Although both probes were located in the ischemic zone, there was a large transmural gradient, i.e., from normal pH values (7.36) in the subepicardium to severely acidotic (pH 6.94) 2 mm deeper in the subendocardium. This marked difference in pH between nearby transmural layers may have important implications regarding arrhythmogenesis in the setting of acute myocardial ischemia.

Animals↗
PubMed1984

Characterization and autoradiographic distribution of the beta-adrenergic receptor in the rat lung.

An unexpected distribution of the beta-adrenergic receptor in the rat lung was revealed by an autoradiographic technique. [3H]-Dihydroalprenolol binding was stereoselective. L-propranolol was 300 times more potent than D-propranolol in competition experiments. Scatchard analysis revealed a Kd of 1.1 nM and Bmax of 14 fmol/mg wet weight. Relative potencies of beta-adrenergic ligands were: propranolol greater than alprenolol greater than timolol greater than pindolol greater than isoproterenol greater than epinephrine greater than soterenol greater than metoprolol greater than terbutaline greater than norepinephrine. The autoradiograms generated revealed a diffuse pattern with binding always associated with tissue structures. We conclude that beta-adrenergic receptors are extensively distributed in the lung, being present in large and small airways and blood vessels.

Animals↗
PubMed1984

Comparative effects of verapamil, diltiazem, and nifedipine on hemodynamics and left ventricular function during acute myocardial ischemia in dogs.

The calcium channel-blocking drugs verapamil, diltiazem, and nifedipine are being used with increasing frequency in patients with angina pectoris due to coronary artery disease. Although each of these agents possesses negative inotropic potential, their relative effects on myocardial function in relation to their vasodilator potencies are unknown. We understood to study this in 20 conscious dogs that had partial occlusions of their circumflex coronary arteries during therapy with placebo, verapamil, nifedipine, or diltiazem. Myocardial blood flow was measured by use of microspheres, and left ventricular function was measured by radionuclide angiography. Drug effects were compared at doses causing equal decreases in mean arterial pressure and coronary vascular resistance of nonischemic myocardium. Global ejection fraction and ejection fraction of the ischemic region were significantly decreased by verapamil (p less than .01) and increased by nifedipine (p less than .001); diltiazem caused no significant changes. Verapamil significantly increased peak diastolic filling rate (p less than .001); nifedipine also increased diastolic filling rate, but only at doses that markedly decreased mean arterial pressure and coronary vascular resistance. The effect of diltiazem on diastolic filling rate was not significantly different than placebo. For doses causing an equal decrease in mean arterial pressure, verapamil decreased heart rate (p less than .001), and diltiazem and nifedipine increased heart rate (p less than .001). We conclude that the relative potencies of these three calcium channel blocking agents on left ventricular systolic and diastolic function during myocardial ischemia are different when compared with their relative vasodilator potencies. These differences may have important clinical implications.

Animals↗
PubMed1983

Can noninvasive exercise test criteria identify patients with left main or 3-vessel coronary disease after a first myocardial infarction?

This study attempts to determine whether exercise treadmill testing with clinical, electrocardiographic, and thallium-201 myocardial perfusion imaging data can identify which patients have left main or 3-vessel (anatomically high-risk) coronary artery disease (CAD) after their first transmural myocardial infarct (MI). Twelve exercise test criteria for high-risk disease were compared in 40 patients referred for cardiac catheterization; 34 had a history of chest pain and 17 had angiographically defined high-risk CAD. A thallium image defect outside the vascular distribution of the MI was the most reliable criterion to distinguish patients with high-risk CAD (p = 0.00052 for Fisher's exact test of discrimination). Thallium imaging was somewhat more sensitive (92 versus 65%, p = 0.108) when patients with negative thallium imaging criteria who failed to achieve 85% of the age-predicted maximal heart rate were excluded. Failure to achieve 85% of predicted heart rate was by itself a useful criterion for detecting high-risk CAD (p = 0.017), especially in patients not taking propranolol (p = 0.004). Development of positive S-T segment depression at less than 70% predicted heart rate also discriminated left main or 3-vessel disease from less extensive CAD (p = 0.016). Other criteria failed to discriminate significantly between high-risk and less extensive CAD in patients after their first MI (p greater than 0.05). S-T segment depression (p = 0.199) or chest pain (p = 0.577) during exercise testing were particularly unreliable. Further, none of the criteria for high-risk CAD were influenced by irreversible left ventricular dysfunction. It is concluded that patients with thallium imaging defects outside the region of the infarct, decreasing blood pressure during exercise, failure to achieve 85% of predicted heart rate, or S-T depression at less than 70% of predicted heart rate have a high probability of having left main or 3-vessel disease. Patients without these criteria have a very low probability of having high-risk CAD and probably do not need coronary angiography for the purpose of excluding these high-risk coronary lesions after a first MI.

Adult↗
PubMed1983

Analysis of coronary collateral structure, function, and ischemic border zones in pigs.

The purpose of this study was to compare coronary collateral structure and function in pigs with those in dogs and to analyze the distribution of collateral blood flow across the lateral and transmural border zones in the pig. After acute occlusion of the left anterior descending coronary artery (LAD) in 26 anesthetized open-chest pigs, minimal collateral blood flow was indicated by retrograde flow (0.2 +/- 0.1 ml/min) and microsphere-myocardial blood flow (0.005 +/- 0.001 ml X min-1g-1). Postmortem injection of the distal LAD followed by clearance of the heart demonstrated few tiny collateral structures and negligible collateral filling of other arteries. In contrast to dogs, pigs showed no measurable gradient of collateral blood flow across the transmural border zone, and pigs showed no change in collateral blood flow or its transmural distribution during retrograde drainage of collateral blood flow or elevated left ventricular filling pressures. Pigs showed higher myocardial blood flow in the lateral border than in the center of the ischemic zone. As in the dog, however, this gradient of blood flow across the lateral border zone was accounted for by overlap between occluded LAD branches and unoccluded coronary arterial branches rather than by preferential collateral perfusion of the lateral border of the ischemic zone. We conclude that the pig has a homogeneous distribution of collateral blood flow across the transmural and lateral border zones after acute coronary occlusion but that the minimal collateral circulation limits the usefulness of the pig as a model of ischemic heart disease.

Animals↗
PubMed1983

The effects of reperfusion and retrograde coronary flow bleeding after coronary occlusion on induced electrical instability in the dog.

Reperfusion achieved by streptokinase infusion early after myocardial infarction (MI) is now being performed in patients, but the effect on electrical instability of increasing or decreasing perfusion in the region at risk for MI is unknown. Accordingly, 34 dogs were randomized to control (13 dogs), reperfusion (11 dogs) and retrograde bleeding (10 dogs) groups. All dogs underwent coronary artery occlusion (23 of the left anterior descending and 11 of the circumflex artery). In the control dogs, occlusion was permanent. In the reperfused dogs, the occlusion was released at 2 hours. In the retrograde bleeding dogs, retrograde flow bleeding distal to the occlusive tie was continued for 2 hours after coronary occlusion. Four days later, all dogs underwent a standard right ventricular pacing protocol. Induced arrhythmias were scored; ventricular fibrillation was assigned the highest score, followed by sustained ventricular tachycardia, nonsustained ventricular tachycardia and repetitive ventricular response. Arrhythmias provocable later in diastole were assigned higher scores than those provocable early in diastole. Infarct size was not different in the three groups (35%, 28% and 39% of the area at risk in control, reperfusion and retrograde bleeding groups, respectively). However, the electrical instability index was lower in the reperfusion group than in the other two groups (e.g., electrical instability index A at 200 beats/min: p less than 0.005 for reperfusion vs control; p less than 0.01 for reperfusion vs retrograde bleeding). Retrograde bleeding did not alter the electrical instability index from the control state. These results suggest that despite no significant reduction in infarct size, reperfusion after infarction may reduce electrical instability.

Animals↗
PubMed1983

Natural history of potassium-deficiency myopathy in the dog: role of adrenocorticosteroid in rhabdomyolysis.

Potassium deficiency occurs in several conditions and is reported to cause muscle weakness and rhabdomyolysis. The mechanisms by which potassium deficiency cause muscle disease remain unknown, but the primary purpose of the present study was to determine whether abnormal muscle glycogen metabolism causes muscle weakness, as suggested by previous work. We monitored the natural history of potassium deficiency in two groups of dogs, one of which also received deoxycorticosterone acetate (DOCA), an agent commonly used in other studies to accelerate potassium loss. Group I dogs on potassium-free diet alone showed a 41% decrease in muscle potassium, no change in serum CO2, creatine kinase (CK), or muscle phosphorylase activity and only mild histopathologic abnormalities before death, after 198 +/- 42 days on the diet (mean +/- S.D.). In contrast, group II dogs on the same diet plus DOCA developed clinically similar severe weakness and died more rapidly than group I, 37 +/- 7 days (p less than 0.03). DOCA dogs showed a more rapid decrease in muscle potassium to the same level as group I, a 37% increase in serum CO2, an increase in serum CK to 1060 to 2775 IU/ml, a 23% decrease in muscle phosphorylase activity, and severe muscle histopathology, including rhabdomyolysis. Neither group showed any change in body weight, electromyogram (EMG), muscle glycogen concentration, glycogen synthetase activity, serum or muscle magnesium or phosphorus, or serum T3 or T4. In conclusion, dietary potassium deficiency in dogs causes severe weakness and death without causing rhabdomyolysis or abnormal muscle glycogen metabolism. Adding DOCA to the potassium-free diet creates a different model characterized by rapid clinical deterioration and rhabdomyolysis.

Animals↗
PubMed1982

Spatial distribution of [14C]-lidocaine and blood flow in transmural and lateral border zones of ischemic canine myocardium.

The purpose of this study was to determine the spatial distribution of lidocaine relative to blood flow in ischemic, normal and border zone canine myocardium. Ischemic zone tissue was distinguished from normal zone tissue by a special microsphere technique in adjacent sections 4 to 5 mm wide from the center to the lateral border of the ischemic region in 14 open chest dogs. Gamma-labeled microspheres were separated by a special technique from carbon-14 ([14C])-lidocaine in the same tissue sample. Blood flow (mean value +/- 1 standard deviation) was reduced to 46 +/- 25 percent of normal in the ischemic subepicardium and 17 +/- 18 percent of normal in the subendocardium. [14C]-lidocaine was 0.56 +/- 0.12 microgram/g in normal myocardium 10 minutes after bolus injection of [14C]-lidocaine; it was reduced to 91 +/- 15 percent of normal in ischemic subepicardium and 58 +/- 12 percent of normal in the subendocardium. Blood flow and lidocaine concentration were uniformly lowest in gross samples from the central and intermediate ischemic zones, and highest in the gross samples from the border normal zone (p less than 0.05). The values for flow and lidocaine in samples from the border ischemic zone were intermediate, that is, higher than values from central ischemic (p less than 0.05) and lower than values from border normal zone samples (p less than 0.05). However, the labeling technique for normal zone tissue revealed that the values of blood flow and lidocaine in the gross samples from the lateral border of the ischemic zone were intermediate between those of adjacent ischemic and normal samples because of the mixture of overlapping normal and ischemic tissues components--not because of a unique mildly ischemic region. Both blood flow and lidocaine concentration were lower in the subendocardial third than in the subepicardial third of the ischemic zone (p less than 0.05) even after the contribution of normal zone tissue was subtracted, suggesting a gradient of ischemia across the transmural border zone. In conclusion, lidocaine is distributed uniformly in ischemic components from the center to the lateral border of the ischemic zone, but there is an endocardial to epicardial gradient. Both lateral and transmural border zone distributions must be considered to understand the mechanisms of drug effects in myocardial ischemia.

Animals↗
PubMed1982

Physiological influences on perfusion imaging in transient myocardial ischaemia: importance of early distribution of thallium-201.

We tested the hypothesis that visualisation of defects on thallium-201 (201Tl) myocardial perfusion images (MPI) depends on the duration of the ischaemic state between 201Tl injection and the time of reperfusion of an occluded coronary artery. Praecordial imaging with a gamma camera was performed in 24 anaesthetised, open-chest dogs with transient coronary occlusion. Results indicated that if the duration of the ischaemic state after 201Tl injection was less than 3 min before reperfusion, then the MPI 5 to 15 min after 201Tl injection was falsely negative (201Tl activity in zone (IZ)/normal zone (NZ)greater than 0.85). Dogs which were ischaemic more than 5 min always had MPI defects 5 to 15 min after 201Tl injection (IZ/NZ201Tl ratio less than 0.85). MPI results (201Tl IZ/NZ) 15 min after 201Tl injection were determined by the duration of the ischaemic state after 201Tl injection (r = -0.86) because prolonged ischaemia allowed 201Tl to distribute from blood to myocardium before reperfusion: 201Tl (IZ/NZ( = 0.356 +/- 1.00 (fraction of total 201Tl remaining in blood at the end of the ischaemic state), r = 0.94.

Animals↗