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Biomedical subjects

J D Rutherford

Publications and source records attributed to J D Rutherford.

At least 55 records · Page 3Linked to original sources
PubMed1987

Prognosis after cardiac arrest due to ventricular tachycardia or ventricular fibrillation associated with acute myocardial infarction (the MILIS Study). Multicenter Investigation of the Limitation of Infarct Size.

Previous studies have reached conflicting conclusions about whether cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation (VF) in acute myocardial infarction (AMI) is of long-term prognostic significance. The mortality rate in 849 patients with confirmed AMI was analyzed. The mortality rate during the initial hospitalization was higher for patients in whom VT/VF occurred (27% vs 7%, p less than 0.001). The in-hospital mortality rate for patients with primary VT/VF, that is, VT/VF occurring in the absence of hypotension or heart failure, was similar to that of patients who did not have VT/VF (8% vs 7%, difference not significant), whereas the rate for patients with secondary VT/VF was significantly greater than that for patients with no VT/VF (51% vs 7%, p less than 0.001). The timing of occurrence of VT/VF also influenced mortality: Patients in whom VT/VF occurred more than 72 hours after admission had a higher in-hospital mortality rate than did patients in whom it occurred within 72 hours (57% vs 20%, p less than 0.05). All cases of primary VT/VF occurred within the first 72 hours of admission. The long-term mortality rate for hospital survivors was not significantly different for patients who had had VT/VF during acute infarction compared with those who had not (19% vs 21%) (mean follow-up 32 months). Thus, cardiac arrest due to ventricular tachyarrhythmia was associated with a higher in-hospital mortality rate but was not a prognostic factor among hospital survivors. Patients resuscitated from primary VT/VF, which characteristically occurs early after AMI, do not have an adverse prognosis.

Aged↗
PubMed1987

Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death.

We have previously reported that the frequencies of myocardial infarction and of sudden cardiac death are highest during the period from 6 a.m. to noon. Since platelet aggregation may have a role in triggering these disorders, we measured platelet activity at 3-hour intervals for 24 hours in 15 healthy men. In vitro platelet responsiveness to either adenosine diphosphate (ADP) or epinephrine was lower at 6 a.m. (before the subjects arose) than at 9 a.m. (60 minutes after they arose). The lowest concentration of these agents required to produce biphasic platelet aggregation decreased (i.e., aggregability increased) from a mean +/- SEM of 4.7 +/- 0.6 to 3.7 +/- 0.6 microM (P less than 0.01) for ADP and from 3.7 +/- 0.8 to 1.8 +/- 0.5 microM (P less than 0.01) for epinephrine. The period from 6 to 9 a.m. was the only interval in the 24-hour period during which platelet aggregability increased significantly. We subsequently studied 10 subjects on alternate mornings after they arose at the normal time and after delayed arising. The morning increase in platelet aggregability was not observed when the subjects remained supine and inactive. Thus, there is a temporal association between increased platelet aggregability in the morning and an increased frequency of myocardial infarction and of sudden cardiac death. Demonstration of this association does not establish a cause--effect relation, but together with other evidence linking platelets to these disorders, it may provide insight into the mechanisms precipitating myocardial infarction and sudden cardiac death and aid in the design of more effective preventive measures.

Adenosine Diphosphate↗
PubMed1987

High-risk subgroups of patients with non-Q wave myocardial infarction based on direction and severity of ST segment deviation.

To determine the significance of the direction of ST segment deviation on admission of patients who evolved non-Q wave myocardial infarction (MI), 97 patients with initial ST segment depression were compared to 207 patients with initial ST segment elevation. Patients with ST segment depression developed smaller infarcts than those with ST segment elevation (creatine kinase MB isoenzyme 8.2 vs 13.3 gmEq/m2, p less than 0.002), but had a lower left ventricular ejection fraction on admission (44% vs 51%, p less than 0.001), more in-hospital complications, and a higher cumulative 1-year mortality (29% vs 11%, p less than 0.001) that could be accounted for by an excess of adverse baseline characteristics. Although a severity index (combining magnitude and extent of the initial ST segment deviation) was not useful for discriminating prognosis of patients with non-Q wave MI who presented with ST segment depression, it was useful in identifying a subgroup of patients with ST segment elevation with an adverse prognosis. The poor outcome of patients with non-Q wave MI presenting with either ST segment depression or severe ST segment elevation on admission suggests that patients in these subgroups should receive close surveillance and should possibly be considered for aggressive therapy.

Electrocardiography↗
PubMed1987

Prognostic implications of an early peak in plasma MB creatine kinase in patients with acute myocardial infarction.

To determine the prognostic implications of an early peak in plasma MB creatine kinase (MB CK) in patients with acute myocardial infarction who were not treated with an acute intervention, 342 patients with myocardial infarction confirmed by MB CK were retrospectively studied. The patients were classified into those with an early peak MB CK (less than or equal to 15 hours after the onset of symptoms, n = 84) and those with a late peak MB CK (greater than 15 hours after the onset of symptoms, n = 258). Patients with an early peak MB CK were slightly older, were more frequently female and had a higher incidence of prior myocardial infarction, congestive heart failure and arrhythmias compared with patients with a late peak MB CK. Patients with an early peak MB CK more frequently presented with ST segment depression (23 versus 11%, p less than 0.01), with anterior location of ischemia or infarction (71 versus 52%, p less than 0.01) and with a lower mean left ventricular ejection fraction (41.4 versus 47.4%, p less than 0.01). Despite more extensive left ventricular dysfunction at initial presentation, patients with an early peak MB CK had a smaller mean MB CK infarct size index (12.6 versus 18.9 g-Eq/m2, p less than 0.01), with no difference in the incidence of in-hospital complications, including death. The early left ventricular dysfunction improved in the patients with an early peak MB CK, evidenced by a 4.5% increase in ejection fraction from admission to 10 days after infarction, whereas the ejection fraction did not improve in patients with a late peak MB CK. However, the patients with an early peaking MB CK had myocardium in jeopardy as reflected by a higher incidence of ST segment depression and a decrement in the global left ventricular ejection fraction with exercise. The 4 year life table estimate for the rate of recurrent myocardial infarction after hospital discharge was higher in patients with an early peak MB CK (33 versus 22%, p less than 0.05), with an even more striking difference in the 4 year estimate for the rate of fatal recurrent infarction (20 versus 8%, p less than 0.001). The 4 year mortality estimate was markedly higher in hospital survivors with an early peak MB CK than in those with a late peak (47 versus 19%, p less than 0.0001) and, even after adjustment for differences in baseline characteristics, the residual excess mortality in those with an early peak was still significant (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1986

A simplified method to predict occurrence of complete heart block during acute myocardial infarction.

Data were analyzed from 698 patients with proved acute myocardial infarction (AMI) to develop a method to predict the occurrence of complete heart block (CHB). The presence of electrocardiographic abnormalities of atrioventricular or intraventricular conduction during hospitalization was determined for each patient. The electrocardiographic risk factors considered were: first-degree atrioventricular block, Mobitz type I atrioventricular block, Mobitz type II atrioventricular block, left anterior hemiblock, left posterior hemiblock, right bundle branch block and left bundle branch block. A CHB risk score was developed that consisted of the sum of each patient's individual risk factors. CHB risk scores of 0, 1, 2 or 3 or more were associated with incidences of CHB of 1.2, 7.8, 25.0 and 36.4%, respectively. When applied to an independent AMI data base, as well as to the summed results of 6 previously reported series that identified predictors of CHB during AMI, a similar incremental risk of CHB as predicted by the risk score method was demonstrated.

Electrocardiography↗
PubMed1986

Multivariate analysis of the long-term results of coronary artery bypass grafting performed during 1976 and 1977.

The results of 492 consecutive coronary artery bypass grafting operations performed for angina in the 2-year period from 1976 to 1977 were evaluated 77 months after surgery. Follow-up was complete in 99%. In 80% of patients angina severity was New York Heart Association functional classes III or IV. An ejection fraction of less than 50% and left ventricular end-diastolic pressure of more than 15 mm Hg were each present in one-third of patients. Thirteen patients (2.6%) died in hospital and 70 (14%) died later during the follow-up period. Twenty-six reoperations were performed for recurrent angina (5.3%). Angina was initially relieved by operation in 97% of patients, but only 57% were alive and free of angina 6 years after their operation. Despite this, 91% of patients at last follow-up were in functional class I or II and 94% thought their symptoms were better than preoperatively. The mean postoperative time of onset of angina, estimated independently by family physicians and patients, was 33 months. The significant preoperative predictors of late death were a low left ventricular ejection fraction, previous myocardial infarction, prior cardiac surgery, increased cardiothoracic ratio and the number of coronary arteries with significant narrowing.

Adult↗
PubMed1986

Long-term tolerance of amiodarone treatment for cardiac arrhythmias.

For the 5-year period 1979 to 1983, 242 patients were followed up who had received amiodarone treatment, 156 for supraventricular tachycardia (SVT) and 86 for ventricular arrhythmias. Five patients were lost to follow-up overseas; the rest were followed to cessation of therapy, death or recent review for a mean of 24 +/- 15 months. Male/female incidence was 1.8:1 and mean age was 58 years (range 4 to 88). Half the group had impaired left ventricular function. Adverse effects were recorded in 59% of the patients and led to drug withdrawal in 26% of the total group. In contrast, unsuccessful treatment was the cause of drug withdrawal in only 5% of the patients, although an additional 25% stopped taking the drug for various reasons. Actuarial survival for the whole group, and subgroups with SVT and ventricular tachycardia/fibrillation were 66%, 74% and 52%, respectively, at 50 months. For the whole group, the actuarial probability of being alive and continuing with amiodarone therapy was only 19% at 50 months. Thus, although amiodarone was effective, few patients tolerated the drug on a long-term basis. Although amiodarone remains a valuable treatment for patients with ventricular tachycardia, its long-term effectiveness for patients with SVT is less certain.

Adolescent↗
PubMed1986

Prognostic significance of the treadmill exercise test performance 6 months after myocardial infarction.

A submaximal treadmill exercise test performed before hospital discharge after an uncomplicated myocardial infarction is often utilized to estimate prognosis and guide management, but there is little experience with a maximal exercise test performed 6 months after infarction to identify prognosis later in the convalescent period. The performance characteristics during an exercise test 6 months after myocardial infarction were related to the development of death, recurrent nonfatal myocardial infarction and coronary artery bypass surgery in the subsequent 12 months (that is, 6 to 18 months after infarction) in 473 patients. Mortality was significantly greater in patients who exhibited any of the following: inability to perform the exercise test because of cardiac limitations, the development of ST segment elevation of 1 mm or greater during the exercise test, an inadequate blood pressure response during exercise, the development of any ventricular premature depolarizations during exercise or the recovery period and inability to exercise beyond stage I of the modified Bruce protocol. By utilizing a combination of four high risk prognostic features from the exercise test, it was possible to stratify patients in terms of risk of mortality, from 1% if none of these features were present to 17% if three or four were present. Recurrent nonfatal myocardial infarction was predicted by an inability to perform the exercise test because of cardiac limitations, but not by any characteristics of exercise test performance. Coronary artery bypass surgery was associated with the development of ST segment depression of 1 mm or greater during the exercise test. Although clinical evidence of angina and heart failure 6 months after infarction was predictive of subsequent mortality among all survivors, among the low risk group without severely limiting cardiac disease, the exercise test provided unique prognostic information not available from clinical assessment alone. Therefore, a maximal exercise test performed 6 months after myocardial infarction is a valuable, noninvasive tool to evaluate prognosis. It provides information that is independent of and additive to clinical evaluation performed at the same time.

Adrenergic beta-Antagonists↗
PubMed1985

Circadian variation in the frequency of onset of acute myocardial infarction.

To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P less than 0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB-estimated timing confirmed the existence of a circadian rhythm, with a three-fold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis. If the rhythmic processes that drive the circadian rhythm of myocardial-infarction onset can be identified, their modification may delay or prevent the occurrence of infarction.

Adrenergic beta-Antagonists↗
PubMed1985

Prosthetic repair of coarctation of the aorta with particular reference to Dacron onlay patch grafts and late aneurysm formation.

Prosthetic material was used in the repair of coarctation of the aorta in 72 patients followed for 8 months to 24 years after operation. False aneurysms occurred late postoperatively in 1 of 17 instances when a tube graft was used to replace the resected aorta and in 1 of 2 patients when the graft bypassed the obstructed area. A Dacron onlay patch graft (DOPG) was used in 52 patients as the primary method of repair, to revise a previous repair or as an adjunct to another procedure at the time of initial operation. True or false late aneurysm occurred between 6 and 18 years postoperatively in 5 of the 38 patients in whom a DOPG was used for primary repair of the coarctation or to revise an earlier repair, an actuarial incidence of 38% at 14 years. Diagnosis of aneurysm formation late postoperatively depends on awareness of this complication and careful assessment of lateral as well as posteroanterior chest radiographs. DOPG should be avoided whenever possible.

Actuarial Analysis↗
PubMed1985

Electrocardiographic, enzymatic and scintigraphic criteria of acute myocardial infarction as determined from study of 726 patients (A MILIS Study).

Methods for detecting acute myocardial infarction (AMI) were compared in a prospective study of 726 patients with pain presumed to be caused by ischemia that lasted 30 minutes or longer and was associated with electrocardiographic changes (ST-segment deviation greater than or equal to 0.1 mV and/or new Q waves or left bundle branch block). Using MB-CK values of more than 12 IU/liter as the standard criterion for detection of AMI, 639 patients (88%) were judged to have AMI. Total plasma CK values, technetium-99m stannous pyrophosphate images 48 to 72 hours after admission, and serial 12-lead electrocardiograms over 10 days were analyzed by investigators blinded to other clinical and laboratory data. For detection of AMI, total CK, electrocardiograms (ECGs) and pyrophosphate imaging were all highly accurate and sensitive (total CK accuracy 97%, ECG 92%, pyrophosphate 88%; total CK sensitivity 98%, ECG 96% and pyrophosphate 91%). However, both pyrophosphate and ECG were less specific than total CK (p less than 0.01) (total CK specificity 89%, pyrophosphate 64% and ECG 59%). The sensitivity (p less than 0.05) and accuracy (p less than 0.01) of total CK and pyrophosphate for those patients with Q-wave development were slightly greater than for those in whom Q waves did not evolve. The ECG was less accurate (p less than 0.02) and pyrophosphate was less specific (p less than 0.04) in patients with prior MI compared with those with initial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗