Biomedical subjects
Publications and source records attributed to A Sjögren.
The past decade has improved our understanding of the pathophysiological mechanisms underlying the congestive heart failure syndrome. The same decade has seen a considerable expansion in modes of therapy for this syndrome. A review of the present forms of treatment is given.
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We made continuous recordings of the X, Y and Z Frank leads in 43 patients with their first myocardial infarction admitted within 4 hours of the onset of pain. Sequential hourly analysis of the ST and QRS vector changes during the first 24 hours was performed. In short-term survivors (n = 38) mean serial changes of ST vectors showed an initial rapid decline until the 8th-10th hour, whereas QRS vector changes lasted longer and were completed within 13.5 +/- 3.6 hours (inferior infarction) and 10.2 +/- 2.4 hours (anterior infarction) respectively. The initial ST vector magnitude was significantly correlated to the subsequent cumulative QRS vector change (r = 0.82). The individual ST vector changes showed a rapid decline in 33 of 38 patients (87%), whereas in 5 patients the ST vector magnitude increased to reach its maximum after 4-6 hours. After the initial decline new increases of the ST vector magnitude was noted in 16 patients on 20 occasions. In 13 instances this was associated with recurrent pain. The spatial change of ST vector direction with reference to the initial direction was significantly greater when recurrent ST rises were accompanied by additional QRS vector changes, compared to those without associated QRS changes (P less than 0.025). The individual QRS vector slopes could be characterized as (1) monophasic (n = 21, 55%), (2) polyphasic (n = 11, 29%) and (3) irregular (n = 6, 16%). We conclude that continuous vectorcardiography is a suitable method for following ST and QRS vector changes that accompany acute myocardial infarction and that ST vector changes can be used to predict subsequent QRS vector changes.
Echocardiographic mapping was performed in 44 patients on arrival in hospital and day 2 following acute myocardial infarction (AMI). To evaluate left ventricular (LV) function the per cent deviation of the mean systolic wall velocity (PD-V) from the normal was measured from 16 LV segments. Adequate data were obtained from 89% of the segments. The number of hypokinetic segments was somewhat higher in anterior than inferior AMI, reaching significance (p less than 0.05) on day 2. Dyskinetic segments were also more common in patients with anterior infarction (p less than 0.001), who also had significantly higher enzyme maxima than patients with inferior AMI (p less than 0.01). Enzyme maxima correlated well with the sum of PD-V from all hypokinetic segments on day 1 (r = 0.79, p less than 0.01). Compensatory hyperkinesia was more common in inferior than anterior AMI (p less than 0.001). Global LV function, estimated by subtracting the number of hyper- from hypokinetic segments (score sigma S:Adj), was significantly related to heart failure (Killip classification) (p less than 0.01) and the respiratory rate (r = 0.71, p less than 0.01) in the acute phase as well as to heart failure during the first post AMI month (New York Heart Association classification).
The antiarrhythmic effects of tocainide, administered as a bolus injection of 750 mg followed by oral therapy, and conventional lidocaine therapy were evaluated in 40 patients admitted for suspected acute myocardial infarction (AMI) and showing high-grade premature ventricular complexes (PVCs). The mean hourly PVC rate before therapy was 928 and its reduction was equally significant in the tocainide group, 73%, and in the lidocaine group, 68%. The number of 5-minute periods with multiform, paired and R/T PVCs or ventricular tachycardia was also significantly reduced, by 78% in the tocainide group and by 71% in the lidocaine group. Ten patients in the tocainide group reported moderate side-effects, compared to 13 in the lidocaine group, where the infusion had to be discontinued in 5 patients and the rate had to be reduced in 4. Tocainide, an amine analogue of lidocaine, is considered just as effective as lidocaine in patients with high-grade PVCs and suspected AMI.
The M-mode and 2-dimensional echocardiographic findings in an 18-year-old man are described. The findings are compatible with the diagnosis of false tendons in the left ventricle.
From each of 24 women undergoing minilaparotomy at various stages of the luteal phase of the cycle, the corpus luteum (CL) was excised in toto, decapsulated, cut into pieces, and incubated for short time periods (5--120 min). Incubations were carried out in the absence and presence of hCG, prostaglandin F2 alpha (PGF2 alpha) and PGE2, both alone and in combination. Dating of the CL was done meticulously using several parameters. After incubation, the tissue levels of cAMP and the media concentrations of progesterone (P) were determined. The basal P production in vitro was highest in CL of the midluteal phase. hCG stimulated cAMP formation in CL of all ages, with the highest levels of cAMP being produced in CL of the midluteal phase. PGE2 was found to increase cAMP formation and potentiate the hCG effect in young CL, but not in CL of the midluteal phase. PGF2 alpha, alone or in combination with hCG, had no effect on cAMP or P formation in either young or old CL, while in CL of the midluteal phase, PGF2 alpha significantly counteracted the stimulatory effect of hCG on both cAMP and P formation. These in vitro data show that PGF2 alpha is capable of inducing functional luteolysis in humans.
The relation between arrhythmic sensations and objective findings of ectopic arrhythmic activity was studied in 150 middle-aged men. Objective arrhythmias were studied by 24-hour Holter monitoring and subjective symptoms assessed by a questionnaire and a dairy protocol during the ECG recording. Psychological characteristics were described by means of a personality inventory, the Emotions Profile Index. No direct relationship was found between subjective symptoms and objective findings of cardiac arrhythmias. Those men, however, who complained of arrhythmic sensations but had no clinically important arrhythmias exhibited a few specific characteristics. They had no signs of organic heart disease and appeared less trustful and more aggressive than those with arrhythmias.
Corrected QT (QTc) intervals were measured retrospectively in 160 consecutive survivors of acute myocardial infarction under 66 years of age. Calculations were made the first 2 d in the coronary care unit (CCU), the first post-CCU day, at discharge, and at 1-3, 6, and 12 months after discharge. All patients were in sinus rhythm and without bundle branch block at discharge from the hospital. Sixteen patients died during the first follow-up year. Twenty patients suffered a reinfarction, five of whom died. The highest QTc values were registered in the CCU and the lowest at the 1-year control. Patients with subendocardial infarcts had longer QTc intervals than those with transmural infarcts, especially during the acute phase. Patients with inferior infarcts had shorter QTc intervals during the CCU period. Those who reinfarcted or died a cardiac death (particularly when sudden) during the follow-up year had longer QTc intervals during the post-CCU phase. A multivariate analysis of risk factors revealed that the QTc interval at discharge was of significant independent value for predicting major cardiac events after discharge from the hospital. It is concluded that repeated measurements of QTc may be of value when assessing prognosis after acute myocardial infarction.
The effect of metoprolol on corrected QT interval (QTc) was studied retrospectively in 111 survivors of AMI below 70 years of age. Prior to discharge the patients were stratified by age, infarction size and ventricular arrhythmias and randomized. Metoprolol, 100 mg b.i.d., or placebo were given double-blindly to 59 and 52 patients, respectively. QTc intervals were measured four times prior to randomization and three times during the follow-up year. The highest QTc mean was registered on the second day in the CCU. QTc intervals subsequently decreased significantly in both groups between discharge and the three-month control (p < 0.001). Patients on metoprolol had significantly shorter QTc intervals during the follow-up year than those on placebo (0.394 +/- 0.028 vs. 0.406 +/- 0.034 sec, p < 0.001). The QTc-shortening effect of beta-receptor blockade was most marked in patients with prolonged QTc intervals at discharge. Patients who died suddenly had prolonged QTc intervals prior to discharge. In this group the proposed beneficial effect of beta-receptor blockade on QTc interval cannot be evaluated as most of these patients had died before the first control.
The association between psychological characteristics and ventricular arrhythmias was investigated in 150 men (50 with manifest IHD, 50 with risk indicators of IHD and 50 healthy men). Arrhythmias were recorded with 24-hour Holter monitoring. Psychological characteristics were assessed by the Emotions Profile Index and the Structured Interview for pattern A behaviour. A depressive emotional state was associated with prognostically severe ventricular arrhythmia in healthy men, but not in men with overt IHD or risk indicators of IHD. When clinical characteristics and age were taken into account, depressiveness was-among healthy men-the second most important factor after high age. The results suggest that-in absence of IHD or other cardiovascular disease-a depressive emotional state may participate in the formation of ventricular arrhythmia.
Immature female rats were injected sc with a single dose of PMSG to induce growth and maturation of ovarian follicles. In the morning of prooestrus the rats were given a single ip injection of LH (10 micrograms/rat) or 0.154 M NaCl, 2 h prior to sacrifice. Granulosa cells were isolated fro the pre-ovulatory follicles and incubated in Krebs bicarbonate buffer, for 1 h with or without in vitro addition of various test substances. Following incubation the amounts of cAMP in tissue plus medium were determined. It was found that the isolated granulose cells exposed to LH in vivo responded to the addition of LH in vitro with a production of high amounts of cAMP, i.e. these cells were not refractory to LH stimulation and in fact responded better than granulosa cells isolated from ovaries not exposed to LH in vivo. The addition to the incubation medium of follicular fluid (FFl) obtained from pre-ovulatory follicles decreased the effect of LH in vitro when added at a final concentration of 1% and completely abolished it at a concentration of 3%. Removal of steroids from the FFl did not influence the inhibitory effect and the addition of a phosphodiesterase inhibitor (IBMX) in vitro did not alter the results in principle. These results point to the existence of a factor in the FFl which interacts with the sensitivity of the isolated pre-ovulatory granulosa cells to repeated exposures to LH. Characterization of this factor is subject to further investigations.
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Human corpora lutea of defined ages were excised at operation, cut into pieces and incubated in the presence of HCG, PGF2 alpha and PGE2 alone or in combination. Following incubation cAMP formation in tissue and medium was determined. HCG-stimulated tissue cAMP content was most pronounced at a corpus luteum age of 7-10 days after ovulation. This stimulation was antagonized by PGF2 alpha in corpora lutea older than 6 days. PGE2 stimulated cAMP formation per se and this effect was more pronounced when HCG and PGE2 were combined. A possible role for PGF2 alpha as a luteolytic substance in the human is suggested.
Consecutive patients (n=184) surviving 48 hours in a coronary care unit were divided into one rapidly (RM) (n=55, 30%) and one conventionally mobilized (CM) group (n=129, 70%). The selection of RM patients was based on the absence of five early risk indicators (RI), reflecting electrical and mechanical heart dysfunction. During after-care, five late RIs were evaluated, including a submaximal bicycle exercise test to 50 W, which excluded nine (16%) additional patients from the RM group. After excluding four patients for non-cardiac reasons, the remaining 42 RM patients were rapidly mobilized and discharged after a mean of nine days, in contrast to a mean of 19 days in the CM group, comprising 121 patients. No RM patient dies in hospital and only one patient died during a six-month follow-up, compared to 17 (p less than 0.01) and 28 (p less than 0.01) patients respectively, in the CM group. Both reinfarction and mortality increased with the number of positive RIs. The early exercise test excluded four patients from the RM group. Altogether 22 of 45 patients showed some abnormality during exercise. Half of these 22 patients were readmitted due to cardiac complications during the follow-up period. These findings indicate that it is possible to identify a group of patients with AMI suitable for early discharge, and that an early exercise test in selected good risk patients is safe and identifies a group prone to complications during the early follow-up period.
Psychosocial factors, experienced pain and anxiety in relation to patient delay were studied in 100 patients admitted for suspected acute myocardial infarction (AMI). More severe pain was reported by women, by those who had recently consulted a physician, who experienced severe anxiety, who fell ill away from their place of work, or who possessed little medical knowledge. These patients tried to get relief from pain by resting. Patients experiencing more severe anxiety were younger, had not consulted a physician recently, had poor medical knowledge, belonged to lower socio-economic groups or were impatient. These patients also sought relief from pain by resting. Pain, but not anxiety, was related to delay. Long delay was seen more often in patients who did not believe they had suffered an AMI and who were psychologically inactive prior to the onset of pain. Recent physician consultation, failure to call for help and belonging to lower socio-economic groups were also related to long delay. Medical knowledge was unrelated to patient delay. Patients with a low degree of pain rarely reported considerable anxiety, whereas several patients with severe pain had little or no anxiety.
The prognostic weight of ventricular ectopic beats (VEBs) was evaluated in 160 patients discharged after a CCU-treated acute myocardial infarction (AMI) and followed for two years. VEBs were registered prior to discharge by 6 hours of telemetry (3 hours during daytime including exercise and 3 hours at night) and again one year after the AMI. During the first year of follow-up, 11 patients died suddenly and 20 suffered reinfarction. Sixteen (55%) of these had shown severe VEBs, i.e. multiform, paired, R-on-T, or ventricular tachycardia, as compared to 42 (29%) of the remainder. During the second year of follow-up, eight patients suffered reinfarction and five died suddenly. The occurrence of severe VEBs prior to discharge was not of prognostic value for the second year per se but continued to carry prognostic weight for the first plus the second year. One year after the AMI the VEB incidence in 122 survivors without reinfarction increased insignificantly from 71 to 78%. VEB severity increased in 43% and decreased in 27% and the shift towards severe forms is significant. Severe VEBs one year after the AMI carry a prognostic weight for the second follow-up year, as 18% of patients with severe VEBs reinfarcted or died suddenly against 5% of those with nor or uniform VEBs only. Patients who had severe VEBs both prior to discharge and one year later did especially badly.