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Biomedical subjects

S Ahnve

Publications and source records attributed to S Ahnve.

At least 37 records · Page 2Linked to original sources

Smoking status at the time of acute myocardial infarction and subsequent prognosis.

A population of 2955 patients admitted to the hospital with acute myocardial infarction (AMI) was followed for 1 year after AMI or until death. Smokers as compared to nonsmokers were over 10 years younger (p less than 0.001) and had a lower prevalence of hypertension (p less than 0.01), congestive heart failure (p less than 0.0001), angina pectoris (p less than 0.01), and diabetes (p less than 0.0001). They had less severe myocardial infarction evidenced, for example, by lower prevalence of pulmonary congestion on chest x-ray (p less than 0.01). Both early (1 month) and late (6 and 12 months) mortality rates were lower in the smoking population (p less than 0.0001 at 1 month, p less than 0.05 at 6 months, and p less than 0.01 at 1 year). Adjusting for age and other variables reduced but did not reverse the survival differential favoring smokers at 1 month, but adjusting for age alone eliminated the differences in mortality rates at 6 and 12 months. We conclude that while smoking is a risk factor for cardiovascular disease and may contribute to the occurrence of AMI at a younger age, smoking at the time of AMI does not appear to be an independent predictor of death during the first year after AMI.

Age Factors↗

The influence of exercise training on the ventilatory threshold of patients with coronary heart disease.

Out of 156 patients with stable coronary heart disease randomized to either an exercise intervention group or a control group, 41 had complete gas analysis data. Continuous gas exchange data, including the ventilatory threshold, and selected heart rates were determined initially and at 1 year. The mean attendance for the exercise group was 2.2 +/- 0.7 days a week at an intensity of 60 +/- 9% of estimated peak oxygen uptake for 1 year of the study. Statistically significant differences (p less than 0.05) were observed between the exercise group (n = 19) and the control group (n = 22) for peak oxygen uptake (L/min), total treadmill time, and supine rest and submaximal heart rates after 1 year. The most remarkable change was a 16% increase in treadmill time. There was no difference between groups for the ventilatory threshold expressed either as an absolute oxygen uptake or as a percentage of peak oxygen uptake at 1 year. However, there was a significant correlation (r = 0.45; p less than 0.05) between the absolute change in peak oxygen uptake and the absolute change in the ventilatory threshold. These results indicate that a moderate exercise program is inadequate to alter the ventilatory threshold in patients with coronary heart disease and that changes in ventilatory threshold do not explain the increase in treadmill time that usually occurs.

Coronary Disease↗

Spatial R wave amplitude changes during exercise: relation with left ventricular ischemia and function.

Thirty patients who exhibited increased and 65 patients decreased spatial R wave amplitude during exercise testing were compared for left ventricular function and ischemic variables. Spatial R wave amplitude was derived from the three-dimensional Frank X, Y, Z leads using computerized methods. All patients had stable coronary artery disease and they were classified into two groups: one that attained a higher (n = 48) and one a lower (n = 47) median value of maximal heart rate during exercise (161 beats/min). Within these two groups, patients with increasing or decreasing spatial R wave amplitude during exercise were analyzed for differences in oxygen consumption, exercise-induced changes in spatial R wave amplitude, ST segment depression laterally (ST60, lead X), ST displacement spatially, left ventricular ejection fraction at rest, change in left ventricular ejection fraction with exercise and thallium-201 ischemia during exercise. Significant differences were demonstrated only in exercise-induced spatial R wave amplitude changes (p less than 0.0001). There was no significant correlation between exercise-induced change in heart rate and change in spatial R wave amplitude in either the group with increasing or the group with decreasing spatial R wave amplitude. It is concluded that changes in spatial R wave amplitude during exercise are not related to ischemic electrocardiographic or thallium-201 imaging changes or to left ventricular ejection fraction determined at rest or during exercise.

Coronary Disease↗

Errors in the visual determination of corrected QT (QTc) interval during acute myocardial infarction.

To estimate variations in intra- and interindividual measurements of the corrected QT (QTc) interval, duplicates of 50 twelve lead electrocardiograms (100 photocopies, paper speed 50 mm/s) were given to each of nine investigators in random order. The electrocardiograms were recorded from patients with acute myocardial infarction consecutively admitted to a coronary care unit. Patients receiving drug therapy and those manifesting various arrhythmias were included. Two-way analysis of variance was used to evaluate the results from all 900 QTc measurements. Significant differences in these measurements were registered among investigators and were of major importance (p less than 0.001). This finding illustrates the difficulty in comparing mean values from different studies and emphasizes the difficulties in applying limits for a normal QTc interval to data obtained by different observers. Of less but still significant importance was the interaction between the investigator and electrocardiogram (p less than 0.001). Finally, the random error was calculated and proven to be of no importance (less than 0.5 mm) when more than 11 measurements were performed.

Analysis of Variance↗

Survival after hospital discharge in matched populations with inferior or anterior myocardial infarction.

Prognostic differences between patients with anterior or inferior myocardial infarction are often related to such variables as previous infarction or the size of the myocardial infarct. We examined the determinants of mortality in 997 hospital survivors of acute Q wave infarction (anterior in 449, inferior in 548) who, although not preselected, were well matched with respect to age, sex and prior infarction or congestive heart failure. Additionally, there was no significant difference in peak serum creatine kinase (CK) between the groups with anterior and inferior infarction (1,459 +/- 1,004 versus 1,357 +/- 1,036). Among the patients with anterior infarction who died during the 1 year follow-up period, 56% died in the first 60 days after hospital discharge compared with 18% of those without inferior infarction (p less than 0.01). Survival curves then became nearly identical at 3 months, and remained so until 1 year when the total mortality rate was 10% for the anterior and 7% for the inferior infarction group (p = NS). Variables associated with heart failure during the hospital phase were more prevalent in anterior infarction, but rales above the scapulae during the hospital stay (p less than 0.0001) and ventricular gallop at the time of discharge (p less than 0.0001) were the top two predictors of 1 year mortality by both univariate and multivariate analysis in inferior infarction. Age (p less than 0.0001) and peripheral edema (p less than 0.0001) were the strongest predictors of mortality in anterior infarction. Previous infarction, although just as common in the group with anterior infarction, was present at 1 year in 48% of nonsurvivors of the group with inferior infarction compared with only 19% of survivors (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

QT interval prolongation in acute myocardial infarction.

The relationship between corrected QT (QTc) interval and clinical factors in acute myocardial infarction (AMI) was studied, as well as long-term prognostic implications of QTc after AMI. QTc was measured on admission to the coronary care unit (CCU). Patients with AMI who showed ventricular fibrillation or severe ventricular tachycardia (n = 27) had prolonged QTc in comparison to AMI patients without ventricular arrhythmias (VA) and noninfarction patients. QTc was measured at discharge from hospital in 463 survivors of AMI. Patients with anterior infarcts had longer QTc than those with inferior infarcts. Patients with VA in the CCU had longer QTc. Patients who died (3-6 years) had shorter QTc; explained by digitalis therapy. Among patients (less than 66 years) without bundle branch block digitalis and quinidine, those who died within six months tended to have longer QTc than the survivors. QTc intervals were measured on the first two days in the CCU, the first post-CCU day, at discharge, and at 1-3, 6 and 12 months after discharge, in 160 AMI patients (less than 66 years). The highest QTc values were registered in the CCU, the lowest at the 1-year control. During the acute phase, patients with anterior infarcts had longer QTc than those with inferior infarcts. Those with subendocardial infarcts had longer QTc intervals. Patients who reinfarcted or died (particularly when sudden) after discharge had longer QTc during the post-CCU period; QTc at discharge was of significant independent value for predicting major cardiac events. QTc intervals were measured as in study III. Metoprolol (n = 59) or placebo (n = 52) were given prior to discharge to AMI patients (less than 70 years). QTc decreased in both groups between discharge and the 3-month control; most marked in those on beta-receptor blockade with prolonged QTc. Patients on metoprolol had shorter QTc during the follow-up. Patients who died suddenly had longer QTc prior to discharge than those without major cardiac events. In a prospective collaborative study, QTc intervals were measured at discharge from hospital in 865 patients. All patients who died after discharge within 30 days after admission were on medication or pacemaker therapy which would influence QTc. When this was taken into consideration, QTc was significantly longer in patients who died within 180 days and 1 year.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

Prognosis after extension of myocardial infarct: the role of Q wave or non-Q wave infarction.

We examined whether or not subsets of patients with extension of myocardial infarct were at high risk for early and late mortality. Some data suggest increased risk in patients with non-Q wave infarcts and we hypothesized that infarct extension in this group might be associated with a poorer prognosis than that for patients with extension of Q wave infarcts. A total of 1253 patients with acute myocardial infarction who were included in our data base were followed prospectively. The patients were classified according to electrocardiographic results into the following groups: those with non-Q wave (n = 277) infarcts and those with Q-anterior (n = 462) and Q-inferior (n = 497) infarcts. Extension was diagnosed by two of the following criteria: (1) recurrent chest pain 24 hr or more after admission to the hospital, (2) new persistent electrocardiographic changes, and (3) elevation or reappearance of creatine kinase. By these criteria 85 (6%) patients had extension (8% of non-Q wave infarcts, 6% of Q-anterior infarcts, and 6% of Q-inferior infarcts). Hospital mortality in patients with extension was 15% in those with Q wave infarcts vs 43% in those with non-Q wave infarcts (p less than .01). Nine hundred and fifty-two patients were followed for 1 year. In 24% of those who did not survive 1 year there was extension of infarct; only 6% of survivors had extension (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Complex ventricular arrhythmias in patients with Q wave versus non-Q wave myocardial infarction.

We examined whether or not subsets of patients with complex ventricular arrhythmias after myocardial infarction are at high risk with respect to 1 year mortality after hospital discharge. Based on previous studies showing increased risk for those with non-Q wave infarcts, we hypothesized that complex PVCs (premature ventricular complexes) in this group might be associated with a poorer prognosis than complex PVCs in patients with Q wave infarcts. Seven hundred seventy-seven patients entering our study with acute infarction were followed prospectively for 1 year after undergoing a predischarge 24 hr ambulatory electrocardiographic examination. Patients were classified by electrocardiographic criteria into the following groups: Non-Q wave (n = 191), Q wave anterior (n = 261), and Q wave inferior infarction (n = 325). The following arrhythmias were classified as complex: multiform PVCs, couplets, and ventricular tachycardia. Sixty-two percent of patients with non-Q wave infarcts who did not survive 1 year had complex PVCs, compared with 32% of survivors (p less than .01). No differences were seen in the Q wave subgroup. The survival for patients with Q wave and non-Q wave infarction without complex PVCs were nearly identical at 1 year (93% and 90%), whereas in patients with complex PVCs survival for those with Q wave and non-Q wave infarction was 92% and 76%, respectively (p less than .001). Of those with non-Q wave infarction, only 4% of nonsurvivors were free of any PVCs, as compared with 28% of nonsurvivors in the Q wave group (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Prediction of late mortality after myocardial infarction from variables measured at different times during hospitalization.

The long-term prognostic importance of sets of variables from different times in the hospital course after acute myocardial infarction was examined in 818 patients discharged from the hospital. Cardiac mortality during the first year after discharge was 11.1%. For the end point death within 1 year after admission, discriminant function analysis identified 5 important factors from the history and the first 24 hours of hospitalization: maximal level of blood urea nitrogen, previous myocardial infarction, age, displaced left ventricular apex (abnormal apex) on physical examination, and sinus bradycardia (negative correlation). When data from the entire hospitalization were included, extension of infarction and maximal heart rate were also selected. When variables obtained at discharge were included, only the presence of S3 gallop and abnormal apex were selected. In subgroups of patients, neither the left ventricular ejection fraction nor the presence of complex ventricular arrhythmias during a 24-hour ambulatory monitoring were independent predictors. Correct prediction was similar for each analysis, with 55 to 60% of the deaths and 79 to 81% of survivors correctly identified. The high-risk group consisted of 25% of the patients with 28 to 30% predictive value for death in the first year. In conclusion, outcome up to 1 year after acute myocardial infarction can be predicted early after admission. Addition of more information later during the hospitalization and at discharge did not improve correct prediction and may be redundant for prognostic evaluation.

Aged↗

Can areas of myocardial ischemia be localized by the exercise electrocardiogram? A correlative study with thallium-201 scintigraphy.

In order to determine whether areas of ischemia identified by thallium-201 scintigraphy could be localized by exercise ECG, we studied 54 patients with stable coronary heart disease. All 54 patients had exercise-induced thallium-201 scintigraphic defects. Their exercise ECG test results were compared to their thallium-201 images and also to 14 low-risk normal subjects. Exercise data were analyzed for spatial ST vector shifts, using a computer program in order to most accurately classify ST segment depression and elevation. Thallium-201 ischemic defects detected in our patients included areas in the septum and the inferior, lateral, and anterior walls. Twenty-six of these 54 patients also had coronary angiography for classification and comparison as having either localized or generalized disease. None of the scintigraphic ischemic sites or angiographic diseased areas could be specifically identified by exercise-induced ST vector shifts. Therefore, the surface exercise ECG has limitations in localizing ischemia to specific areas of the myocardium.

Adult↗

Usefulness of the chest x-ray for predicting abnormal left ventricular function after acute myocardial infarction.

We evaluated 229 patients discharged after a definite acute myocardial infarction. Pulmonary venous congestion determined from chest x-ray films during the hospitalization and at discharge and the cardiothoracic ratio at discharge were compared to the left ventricular ejection fraction measured at discharge by a gated radionuclide technique. During hospitalization, pulmonary venous congestion was found on at least one x-ray frame in 94 patients (41%). At discharge 134 patients (59%) had abnormal ejection fraction (less than 0.51) and 35 had pulmonary venous congestion (15%). The sensitivity of the x-ray for detecting an abnormal ejection fraction was 20% when pulmonary venous congestion was observed on the discharge x-ray film (specificity 92% and predictive value 77%), 52% if pulmonary venous congestion was present on any x-ray film during the hospitalization (specificity 74% and predictive value 73%), and 47% if the cardiothoracic ratio was abnormal (greater than or equal to 0.50) on the discharge x-ray film (specificity and predictive value 66%). We conclude that an abnormal x-ray film at discharge or during the hospitalization will identify approximately one-half of the abnormal ejection fractions at the time of hospital discharge. Therefore, to reliably assess left ventricular function, either for prognostic or therapeutic purposes in the individual patient, a more direct measure of left ventricular function such as radionuclide angiography must be obtained.

Adult↗

A randomized trail of the effects of 1 year of exercise training on computer-measured ST segment displacement in patients with coronary artery disease.

As part of a randomized trial of the effects of 1 year of exercise training on patients with stable coronary artery disease, 48 patients who exercised and 59 control patients had computerized exercise electrocardiography performed initially and 1 year later. The patients who had exercise training as an intervention had a 9% increase in measured maximal oxygen consumption and significant decreases in heart rate at rest and during submaximal exercise. ST segment displacement was analyzed 60 ms after the end of the QRS complex in the three-dimensional X, Y and Z leads and utilizing the spatial amplitude derived from them. Statistical analysis by t testing yielded no significant differences between the groups except for less ST segment displacement at a matched work load, but this could be explained by a lowered heart rate. Analysis of variance yielded some minor differences within clinical subgroups, particularly in the spatial analysis. Obvious changes in exercise-induced ST segment depression could not be demonstrated in this heterogeneous group of selected volunteers with coronary artery disease secondary to an exercise program.

Adult↗

Prognostic importance of digitalis after acute myocardial infarction.

Because previous reports have suggested that digitalis administration may lead to increased mortality after hospital discharge for acute myocardial infarction, the independent importance of digitalis therapy in long-term prognosis after acute myocardial infarction was investigated by analyzing 1,599 patients after definite myocardial infarction. After hospital discharge, mortality rate for the entire group at 4 months was 7.7% and after 1 year 14.2%. At discharge, 36.6% of the patients were taking digitalis. Compared with those not taking digitalis, those taking digitalis had more historical risk factors and a higher incidence of important clinical prognostic variables during the hospitalization. Their cardiac mortality rate after 4 months and 1 year (12.5 and 22.4%, respectively) was significantly higher than that of patients not taking digitalis (5.0 and 9.6%, respectively). Mortality was higher for patients taking digitalis whether or not they had congestive heart failure during hospitalization. However, in a multivariate Cox analysis for 1 year outcome, neither digitalis nor any other medication variable displaced the important clinical variables of age, congestive heart failure during the hospitalization, previous myocardial infarction, maximal heart rate during the hospitalization and previous angina. Quinidine and digitalis at discharge were selected sixth and seventh (not significant) by the analysis. It is concluded that digitalis therapy at discharge after myocardial infarction was not an independent predictor of late mortality in these patients.

Aged↗

Computer analysis of exercise-induced changes in electrocardiographic variables. Comparison of methods and criteria.

In order to evaluate computerized methods of electrocardiographic signal processing, determination of QRS end, and measurement of criteria for ischemia, we analyzed the data from 42 male patients with coronary heart disease who underwent maximal treadmill testing. Electrocardiographic data were digitized on-line and leads X, V5, Y and Eigen V were later analyzed for noise content, isoelectric baseline, and ST parameters using the UCSD spatial electrocardiographic computer program. Various ST segment criteria for ischemia were calculated and compared. Noise was greater in lead Y and in all leads when the median was used for signal averaging. Two isoelectric baseline algorithms and three ST segment slope algorithms gave similar results. Spatially derived QRS end was highly correlated with the amplitude measured using a fixed time interval after peak R wave. Both ST area and ST midpoint estimates differed widely using two different algorithms for each. Regression equations were derived that make it possible to estimate QRS end or ST60 amplitudes in V5 from values in X or vice versa.

Adult↗

Influence of heart rate and inhibition of autonomic tone on the QT interval.

To evaluate whether heart-rate-induced changes of the QT interval are dependent on autonomic tone, we studied 13 healthy subjects, mean age 67.5 years. The maximal uncorrected QT from leads I, II, V1 and V6 was determined during atrial pacing at 90 beats/min and 130 beats/min before and after i.v. administration of propranolol, 0.1 mg/kg, and atropine, 0.02 mg/kg. Significant reductions (p less than 0.01) of QT were induced by the paced increases in heart rate before drugs (10%), after propranolol (10%) and after the combination of atropine and propranolol (9%). Propranolol caused no significant change in the QT interval when heart rate was held constant by pacing. In contrast, atropine produced rate-independent reductions of QT interval (5%) in subjects with beta-adrenergic blockade (p less than 0.05). Bazett's formula for heart-rate correction of the QT interval (QTc) was not applicable for atrial overdrive pacing, as it gave proportionately longer QTc values at higher heart rates. These results show that heart rate is a major determinant of the duration of the QT interval and that paced changes in heart rate induce QT-interval responses that are essentially uninfluenced by autonomic tone. The rate-dependent effect of the QT interval produced by elimination of cholinergic tone suggests a direct influence of cholinergic activity on the repolarization of ventricular myocardium.

Aged↗

Circadian variations in cardiovascular parameters during sleep deprivation. A noninvasive study of young healthy men.

Twelve subjects were kept awake for 64 h under conditions of isolation from external time cues. Activity was sedentary and kept as constant as possible over time, as was intake of food and drink. Cardiovascular variables--blood pressure, heart rate, contractility (IJ-amplitude from ballistocardiogram), T-wave amplitude, QRS, PQ and QT intervals--were assessed every 3 h. At the same intervals, urine samples for catecholamine analysis were obtained. Data were analyzed by analysis of variance and cosinor techniques. Adrenaline excretion showed a pronounced circadian rhythm. Noradrenaline excretion and IJ amplitude showed much weaker rhythmicity, statistically significant only with the cosinor technique. The remaining variables showed no rhythmicity with either technique. It was concluded that constant conditions (including sleep deprivation) markedly disturb or even obliterate the circadian rhythms of cardiovascular variables and urinary noradrenaline excretion. It was also concluded that most of the amplitude of cardiovascular circadian rhythms measured under habitual sleep/wake conditions must be due to the alternation between sleeping and waking. The present data do not, however, rule out the existence of selfsustained circadian rhythmicity in cardiovascular variables; a design including continuous wakefulness may well have concealed endogenous low-amplitude rhythms.

Adult↗