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Biomedical subjects

R Roberts

Publications and source records attributed to R Roberts.

At least 613 records · Page 34Linked to original sources
PubMed1976

Considerations in the use of biochemical markers of ischemic injury.

Results of estimation of infarct size with a selected biochemical marker in blood, creatine phosphokinase (CPK), have suggested that infarct size is an important determinant of prognosis, impaired ventricular function, early ventricular dysrhythmia, and the severity of clinical manifestations. Estimates based on serial changes in serum CPK activity have correlated with morphological estimates and have been employed to evaluate therapeutic interventions. Improved estimates with any biochemical marker require exclusion of noncardiac sources of the marker and characterization of the influence of physiological alterations on parameters in empirical or physiologically based mathematical models utilized. Use of MB CPK instead of total CPK therefore improves enzymatic estimates when infarction is accompanied by release of noncardiac CPK into the circulation. Preliminary results with physiologically based models of CPK release from the infarct and its disappearance from the circulation suggest that release may be diffusion-limited and that the CPK disappearance rate is relatively uninfluenced by profound hemodynamic derangements or myocardial infarctions per se. The substantial inactivation of CPK in lymph in vitro and in situ underscores the importance of defining factors influencing the proportion of a biochemical marker depleted from necrotic myocardium appearing in blood, since the proportion is one parameter used in models employed to quantitatively estimate irreversible ischemic injury.

Animals↗
PubMed1976

Concordance of electrocardiographic and scintigraphic criteria of myocardial injury after cardiac surgery.

The concordance of transmural electrocardiographic (ECG) changes and myocardial infarct imaging in detecting myocardial injury in the perioperative period was evaluated in 50 patients undergoing coronary artery bypass surgery and in 6 patients without coronary artery disease undergoing valve replacement. Scintigraphy with technetium-99m (Sn) labeled pyrophosphate was performed 3 to 7 days after surgery. Plasma creatine phosphokinase (CPK) levels were determined preoperatively and daily for 7 days postoperatively. Plasma MB-CPK was assayed fluorometrically in samples obtained at 12 hour intervals for 36 hours. Total CPK and MB-CPK concentrations were normal in all patients preoperatively but increased in every patient postoperatively. A total of 8 patients (16%) had evidence of perioperative infarction. Six of these patients (12%) with coronary artery disease exhibited abnormal images after bypass surgery, associated with transmural ECG changes in each case. The other 2 patients (4%) with coronary artery disease who had abnormal images were among 4 patients who developed bundle branch block after the operation. Abnormal images did not occur in any patient undergoing valve replacement despite total CPK and MB-CPK elevations. These results indicate that total CPK and MB-CPK elevations occur consistently after cardiac surgery and cannot be relied upon for detection of transmural infarction. Furthermore, new conduction defects may not necessarily be a sign of perioperative infarction, and infarct imaging may be a useful means of establishing myocardial infarction in this group of patients.

Acute Disease↗
PubMed1975

Specificity of elevated serum MB creatine phosphokinase activity in the diagnosis of acute myocardial infarction.

Creatine phosphokinase (CPK) isoenzyme determinations are useful in the diagnosis of myocardial infarction. However, until suitably sensitive and precise quantitative procedures became available, the diagnostic specificity of serum CPK isoenzyme elevations could not be thoroughly examined. In this study an assay procedure capable of accurately determining activity of individual CPK isoenzymes even in serum samples with normal total CPK activity was employed to obtain two types of information. First, CPK isoenzyme profiles were examined in extracts of a spectrum of human tissues obtained at operation to determine whether the isoenzyme associated with myocardium is presented in other human tissues in quantities sufficient to produce increased activity in serum. In addition, CPK isoenzymes were analyzed quantitatively in serial serum samples from 50 hospitalized control subjects, 100 patients with acute myocardial infarction, 100 patients undergoing non-cardiac surgery and 50 patients undergoing cardiac catheterization to determine whether insult to tissues other than the heart is associated with increased "myocardial" CPK isoenzyme activity in serum. Results from analyses of tissue extracts indicated that myocardium is the only tissue surveyed containing sufficient MB CPK to account for substantial increases in serum MB activity. Results from analyses of serial serum samples indicated that MB CPK activity levels are consistently elevated after myocardial infarction, averaging 0.089 IU/ml. However, after cardiac cathetrization or noncardiac surgery peak serum MB activity remains low, averaging only 0.004 IU/ml despite marked elevations in total serum CPK activity. Thus, elevated serum MB CPK activity is a highly specific as well as sensitive criterion of myocardial injury.

Acute Disease↗
PubMed1975

Sodium restriction and thiazide diuretics in the treatment of hypertension.

In a group of hypertensive patients it has been shown that moderate sodium chloride restriction has a hypotensive effect that is similar to that produced by thiazide diuretics. Blood pressure changed in relation to body weight in individual patients, and appeared to correlate with their sodium balance. The more a patient was depleted of sodium, the lower was the blood pressure. The serum potassium level fell with the use of thiazide diuretics, but in this group of patients there was little change in total body potassium content. The fall in serum potassium level appeared to relate to a shift into the cells due to the accompanying alkalosis. Potassium supplementation appeared to have had little effect and was unnecessary for most patients who were given diuretics for hypertension. Amiloride corrected the alkalosis and restored the serum potassium level to normal.

Amiloride↗
PubMed1975

Changes in plasma renin activity and blood pressure after acute and chronic administration of beta-adrenergic receptor-blocking drugs.

1. Prindolol and propranolol chronically cause a fall in mean blood pressure and mean plasma renin activity, but no correlation was observed between the two variables. 2. The response of blood pressure to prindolol and propranolol was not predicted by the basal plasma renin activity. 3. Propranolol administered acutely caused the plasma renin activity to fall with no acute change in blood pressure, whereas prindolol caused the blood pressure to fall with no change in plasma renin activity. 4. The effects of beta-adrenergic-blocking drugs on plasma renin activity and blood pressure can be dissociated and it is unlikely that their hypotensive action is mediated through the renin-angiotensin system. 5. Basal plasma renin activity does not identify the patients who will respond to beta-adrenergic-blocking drugs.

Adult↗
PubMed1975

Beta-adrenergic receptor blocking drugs, hypertension and plasma renin.

1 Propranolol and pindolol reduced both the blood pressure and plasma renin activity when given chronically to hypertensive patients. 2 There was no correlation between the fall in blood pressure and the fall in plasma renin activity. 3 Neither the basal nor the random plasma renin activity predicted the patients who would respond to beta-adrenergic receptor blocking drugs. 4 Oral propranolol reduced plasma renin activity but did not reduce blood pressure within 4 h of administration; oral pindolol reduced blood pressure but did not reduce plasma renin activity within 4 h of administration. 5 The reduction of blood pressure by propranolol and pindolol does not seem to be mediated by changes in plasma renin in most patients.

Adult↗
PubMed1975

Serum CPK isoenzymes after cardiac catheterization.

Exclusion of acute myocardial infarction preoperatively, particularly in patients undergoing cardiac catheterization, is an important requirement for optimal results following coronary revascularization. Unfortunately, activity of conventionally measured serum enzymes (AST, LDH, total CPK) is frequently raised because of enzyme released from non-cardiac sources during the catheterization procedure. however, serum activity of the MB CPK isoenzyme, an isoenzyme found primarily in heart muscle, appears to be more specific. Accordingly, in the present study, total CPK and MB CPK activities were determined in serum samples from 53 patients undergoing diagnostic catheterization, immediately before study and serially for 24 hours afterwards. A comprehensive range of catheterization procedures included selective coronary arteriography in 39 patients by brachial (17) or femoral (22) artery approaches. Myocardial infarction was excluded by clinical and electrocardiographic criteria in all patients before and after the procedure. MB CPK isoenzyme activity was also measured in serum samples from 50 patients with actue myocardial infarction documented electrocardiographically, and in 20 controls admitted to hospital but without cardiovascular disease. In patients with acute myocardial infarction, both total CPK and MB CPK isoenzyme levels were significantly raised (0.78 +/- 0.087 and 0.086 +/- 0.037 IU/ml, respectively), exceeding the upper limit of normal in all cases. MB CPK activity remained within normal limits (less than 0.004 IU/ml) in all 20 subjects without cardiovascular disease. Peak total serum CPK activity exceeded control levels in all patients undergoing catheterization (0.260 +/- 0.033). However, in each case, MB CPK isoenzyme activity remained within normal limits (less than .004). Thus, in contrast to an increase of activity of conventionally used serum enzymes, increased MB CPK isoenzyme activity is a reliable indicator of myocardial infarction, even in patients undergoing cardiac catheterization.

Adolescent↗
PubMed1975

Relation between infarct size and ventricular arrhythmia.

In order to determine whether ventricular arrhythmia is quantitatively related to infarct size estimated enzymatically we studied 31 patients with acute myocardial infarction without cargiogenic shock. Infarct size index was estimated from hourly serum creatine kinase (CK) changes during periods of 48 to 72 hours. Ventricular arrhythmia was quantified by automated analysis of continuous electrocardiographic recordings over a period of 20 hours with the use of the Argus/H computer system. Patients were classified into three groups according to infarct size index. Patients in all groups had similar average heart rate, blood pressure, serum potassium, and arterial pH and PCO2 values during the first 10 hours after admission. The total number of ventricular ectopic beats (VEB), frequency of couplets, and ventricular tachycardia, and peak rate of ventricular ectopic beats during the first 10 hours after admission were all related to infarct size index. For example, patients with small, medium, and large estimated infarct size averaged 26, 104, and 405 ventricular ectopic beats, respectively. These results suggest that the severity of ventricular arrhythmia early after myocardial infarction is related to the extent of myocardial injury as estimated enzymatically. Thus the apparent efficacy and therefore the evaluation of antiarrhythmic agents early after myocardial infarction may be influenced by the magnitude of injury sustained by the heart.

Arrhythmias, Cardiac↗
PubMed1975

An improved basis for enzymatic estimation of infarct size.

Infarct size has been estimated from serial serum creatine phosphokinase (CPK) changes, but the contribution of noncardiac CPK may interfere. Results would also be influenced if CPK disappearance varied with hemodynamic changes. Since MB CPK is a marker more specific to myocardium. infarct size was estimated from serum MB changes in 16 patients. In addition, 21 chronically instrumented conscious dogs subjected to tachycardia, decreased cardiac output or hepatic or renal ischemia were studied to evaluate the dependence of CPK disappearance on hemodynamics. MB CPK in human tissue extracts and serum was quantified with a new, rapid, glass bead-batch adsorption technique, verified with CPK isoenzymes prepared from human myocardium. Among tissues surveyed, only myocardium contained appreciable MB CPK. Infarct size estimated from MB correlated with total serum CPK in patients with uncomplicated myocardial infarction (r=0.97, N=12). In patients with infarction given intramusclar injections, total CPK curves were distorted but MB CPK curves were not apparently affected. Hemodynamic alterations in conscious dogs did not markedly affect the disappearance rate (kd) of intravenously injected, radioactively labeled, canine myocardial CPK, although kd was shown to depend on reticuloendothelial system activity. These findings suggest that estimation of the extent of infarction based on serum MB CPK should be useful despite hemodynamic deterioration associated with infarction or interference of noncardiac CPK.

Animals↗
PubMed1975

Esophageal disease as a cause of severe retrosternal chest pain.

During one six-month period 11 patients were referred with a diagnosis of coronary artery disease, because of recurrent episodes of severe, prolonged retrosternal chest pain necessitating from one to seven hospital admissions per patient for "suspect myocardial infarction". In no instance was this diagnosis proved by electrocardiogram or serum enzyme changes, but 7 of the 11 patients had abnormal resting electrocardiograms. Selective coronary arteriograms were normal in 10 patients and revealed nonobstructive coronary artery disease in the 11th patient. Esophageal studies revealed hiatus hernia in 9 and mild to severe disordered motored activity of the esophagus in all 11. Acid perfusion into the esophagus reproduced the chest pain in nine patients and in the other two, the hiatus hernia was incarcerated. On direct questioning, all patients indicated that the pain was worsened by lying down and bending over, and in eight patients there was a history of pharyngoesophageal or gastroesophageal dysphagia. In this day when the problem of chest pain with normal coronary arteries is very topical, our report emphasizes the need to consider symptomatic esophageal disease in the differential diagnosis of this problem.

Adult↗
PubMed1975

Rapid separation of plasma creatine kinase isoenzymes by batch adsorption on glass beads.

To separate the MM and MB creatine kinase (EC 2.7.3.2) isoenzymes in small plasma samples, we developed a simple, rapid ion-exchange batch-adsorption procedure with "DEAE Glycophase" glass beads (Corning). All separative steps are performed in a single test tube and can be completed within a few minutes. Results of measurements of isoenzymes in plasma samples from patients with acute myocardial infarction were compared to those obtained with an independent quantitative assay method previously reported. Additional measurements were performed on standard plasma samples containing mixtures of MM and MB isoenzyme purified from human myocardium. Results by the two independent assay procedures agreed well, as did measured isoenzyme activities and activities predicted from the amounts of isoenzyme added. Activities in the fractions containing separated isoenzymes were measured by a direct kinetic fluorometric assay. MB activities in normal plasma averaged 1.6 plus and minus 0.28 U/liter (mean plus and minus SD).

Adsorption↗