Readmission of older acutely admitted medical patients after short-term admissions in Denmark: a nationwide cohort study.

BACKGROUND: Knowledge of unplanned readmission rates and prognostic factors for readmission among older people after early discharge from emergency departments is sparse. The aims of this study were to examine the unplanned readmission rate among older patients after short-term admission, and to examine risk factors for readmission including demographic factors, comorbidity and admission diagnoses. METHODS: This cohort study included all medical patients aged ≥65 years acutely admitted to Danish hospitals between 1 January 2013 and 30 June 2014 and surviving a hospital stay of ≤24 h. Data on readmission within 30 days, comorbidity, demographic factors, discharge diagnoses and mortality were obtained from the Danish National Registry of Patients and the Danish Civil Registration System. We examined risk factors for readmission using a multivariable Cox regression to estimate adjusted hazard ratios (aHR) with 95% confidence intervals (CI) for readmission. RESULTS: A total of 93,306 patients with a median age of 75 years were acutely admitted and discharged within 24 h, and 18,958 (20.3%; 95% CI 20.1 - 20.6%) were readmitted with a median time to readmission of 8 days (IQR 3 - 16 days). The majority were readmitted with a new diagnosis. Male sex (aHR 1.15; 1.11 - 1.18) and a Charlson Comorbidity Index ≥3 (aHR 2.28; 2.20 - 2.37) were associated with an increased risk of readmission. Discharge diagnoses associated with increased risk of readmission were heart failure (aHR 1.26; 1.12 - 1.41), chronic obstructive pulmonary disease (aHR 1.33; 1.25 - 1.43), dehydration (aHR 1.28; 1.17 - 1.39), constipation (aHR 1.26; 1.14 - 1.39), anemia (aHR 1.45; 1.38 - 1.54), pneumonia (aHR 1.15; 1.06 - 1.25), urinary tract infection (aHR 1.15; 1.07 - 1.24), suspicion of malignancy (aHR 1.51; 1.37 - 1.66), fever (aHR 1.52; 1.33 - 1.73) and abdominal pain (aHR 1.12; 1.05 - 1.19). CONCLUSIONS: One fifth of acutely admitted medical patients aged ≥65 were readmitted within 30 days after early discharge. Male gender, the burden of comorbidity and several primary discharge diagnoses were risk factors for readmission.

Detection of meticillin-resistant Staphylococcus aureus and carbapenemase-producing Enterobacteriaceae in Danish emergency departments - evaluation of national screening guidelines.

BACKGROUND: Multi-resistant bacteria (MRB) are an emerging problem. Early identification of patients colonized with MRB is mandatory to avoid in-hospital transmission and to target antibiotic treatment. Since most patients pass through specialized emergency departments (EDs), these departments are crucial in early identification. The Danish National Board of Health (DNBH) has developed exposure-based targeted screening tools to identify and isolate carriers of meticillin-resistant Staphylococcus aureus (MRSA) and carbapenemase-producing Enterobacteriaceae (CPE). AIM: To assess the national screening tools for detection of MRSA and CPE carriage in a cohort of acute patients. The objectives were to investigate: (i) if the colonized patients were detected; and (ii) if the colonized patients were isolated. METHODS: This was a multi-centre cross-sectional survey of adults visiting EDs. The patients answered the DNBH questions, and swabs were taken from the nose, throat and rectum. The collected samples were examined for MRSA and CPE. Screening performances were calculated. FINDINGS: Of the 5117 included patients, 16 were colonized with MRSA and four were colonized with CPE. The MRSA screening tool had sensitivity of 50% [95% confidence interval (CI) 25-75%] for carrier detection and 25% (95% CI 7-52%) for carrier isolation. The CPE screening tool had sensitivity of 25% (95% CI 1-81%) and none of the CPE carriers were isolated. CONCLUSION: The national screening tools were of limited use as the majority of MRSA and CPE carriers passed unidentified through the EDs, and many patients were isolated unnecessarily.

Relation between job strain and myocardial infarction: a case-control study.

OBJECTIVES: To study the influence of different job related and socioeconomic factors for development of myocardial infarction (MI). METHOD: The study was a case-control study of 76 male wage earners who had been admitted to hospital with MI. As a control group 176 male wage earners not admitted to hospital who were residents of the same county were used. Both groups were interviewed with an extensive questionnaire on job related conditions. Several indices on job related psychosocial factors were established in accordance with Karasek's job strain model as well as the extension of the model, the isostrain model. RESULTS: The most significant findings were consistent with Karasek's job strain model in that mean with a high degree of demand combined with a low degree of control at work had a significantly increased odds ratio (OR) 95% confidence interval (95% CI) of 2.1 (1.2 to 3.8) for MI after adjustment for age compared with men with a low degree of demand and a high degree of control at work. Further adjustment for smoking, socioeconomic status, employment sector, job category, and social network did not affect the OR substantially (OR 2.3 (1.2 to 4.4)). Other factors significantly associated to MI were job category (blue collar workers v white collar workers, OR 2.8 (1.6 to 5.8)), and employment sector (private v public, OR 3.1 (1.8 to 6.1)). CONCLUSIONS: Thus, the study confirmed the job strain model as well as the well known association between socioeconomic status and risk of MI, whereas the finding of an increased risk among employees in the private sector has not previously been described.

[Publication outcome of research funding by the Danish Heart Foundation 1988-1990]. / Publikationsudbyttet af Hjerteforeningens forskningsbevillinger 1988-1990.

The aim of the survey was to analyse the investment by the Danish Heart Foundation in the cardiovascular research field in the period 1988-1990 and the ensuing research results. One hundred and thirty-nine researchers were allocated a total DDK 24.1 million. Eighty percent of the researchers have concluded their research work and published 362 scientific papers in 131 journals. The total journal impact factor obtained among 270 scientific papers with known journal impact factor was 642. The median journal impact factor was 1.580. Thirty-five percent of the papers were published in journals with journal impact factor greater than three. The productivity, defined as total journal impact factor obtained divided by an estimate of the total amount (DKK 200 million) of economic support received by the researcher from all sources, was estimated to 3.2 Journal Impact Factor/DKK million. A panel of international experts reviewed the outcome of funding by the Danish Heart Foundation, and concluded that the number of publications and their impact factor was adequate in relation to the economic input.

Does in-hospital ventricular fibrillation affect prognosis after myocardial infarction?

AIM: The aim of this study was to estimate the prognostic information to be gained from ventricular fibrillation in patients with myocardial infarction. METHODS AND RESULTS: We studied 4259 consecutive patients with myocardial infarction admitted to one centre in 1977-1988. Five hundred and twenty-eight (12.4%) of the patients had ventricular fibrillation in hospital. The following risk factors were included in multivariate models to estimate their importance for 30-day and long-term (median 7 year) prognosis: age, gender, ventricular fibrillation, congestive heart failure, pulmonary oedema, cardiogenic shock, other cardiac arrest and atrial fibrillation. We found that the odds ratio for death on days 6.30 was 6.34 (3.55-11.30, 95% confidence limits, P < 0.001) for patients with primary ventricular fibrillation (without heart failure) and 4.06 (2.68-6.14, P < 0.001) for patients with ventricular fibrillation secondary to heart failure compared to patients without ventricular fibrillation. For patients surviving more than 30 days, relative risk of death in those with ventricular fibrillation was 1.11 (95% confidence interval 0.93-1.34, P = 0.26). Logistic regression analysis of relative risk associated with ventricular fibrillation in time intervals, indicated that the importance of ventricular fibrillation for risk of death was exhausted during the initial 60 days after infarction. CONCLUSION: Ventricular fibrillation is associated with an independent increased risk of death within 0-60 days after infarction. After this period, the prognosis in survivors of ventricular fibrillation does not differ significantly from patients without ventricular fibrillation.

Apolipoprotein(a) phenotypes and lipoprotein(a) concentrations in patients with hyperthyroidism.

Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL) particle in which apolipoprotein B-100 (apoB) is attached to a glycoprotein called apolipoprotein(a) [apo(a)]. Apo(a) has several genetically determined phenotypes differing in molecular weight, to which Lp(a) concentrations in plasma are inversely correlated. High plasma levels of Lp(a) are associated with atherosclerotic diseases. It is therefore of interest to study whether factors other than the apo(a) gene locus are involved in the regulation of Lp(a) concentrations. We measured plasma concentrations of Lp(a) and other lipoproteins and determined apo(a) phenotypes in 31 patients with hyperthyroidism, before and after the patients had become euthyroid by treatment. The mean concentration of LDL cholesterol rose from 2.67 to 3.88 mmol/l (P < 0.01), apoB rose from 0.79 to 1.03 g/l (P < 0.01), and the median Lp(a) concentration increased from 9.74 to 18.97 mg/dl (P < 0.01) on treatment. Lp(a) concentrations were inversely associated to the size of the apo(a) molecule both before (P < 0.01) and after treatment (P < 0.01). The increase in Lp(a) was significant in patients with high molecular weight apo(a) phenotypes (n = 9; P < 0.01) and in patients with low molecular weight apo(a) phenotypes (n = 16; P < 0.01), but not in those with apo(a) "null types" (n = 6; P = 0.5). The low levels LDL cholesterol and apoB in untreated hyperthyroidism may result from increased LDL receptor activity. The increase in Lp(a) levels were not correlated with the increase in LDL cholesterol or apoB.(ABSTRACT TRUNCATED AT 250 WORDS)

Improving long-term survival of patients with acute myocardial infarction from 1977-1988 in a region of Denmark.

The aim of this investigation was to study secular trends in long-term survival following myocardial infarction (MI). Five thousand one hundred and fifty-seven consecutive cases of MI in 3942 patients were recorded in a well-defined region in the study period 1977-1988. The study period ended before thrombolytic therapy was introduced in the hospital. One and 5-year survival (+/- 95% confidence limits) was 61 +/- 2% and 42 +/- 2% in 1977-1980. These figures changed to 61 +/- 2% and 44 +/- 2% in 1981-1984, and to 64 +/- 2 and 46 +/- 2% in 1985-1988. The improvement with time was statistically significant (P < 0.001). In a Cox proportional hazard model, time of infarction was an independent predictor of survival. Patients were subdivided into a high risk group suffering from either congestive heart failure or cardiac arrest during hospitalization, and a low risk group without these complications. Year of infarction was without importance in the high risk group but highly significant in the low risk group. Long-term survival following MI gradually improved prior to the introduction of thrombolytic therapy. The improvement was confined to low risk patients without cardiac arrest or congestive heart failure.

Interobserver variation in interpretation of electrocardiographic signs of atrial infarction.

The electrocardiogram (ECG) is the only means of diagnosing atrial infarction antemortem. Certain ECG changes (PR-segment displacements) have been taken earlier as signs of atrial infarction. The purpose of this study was to assess the interobserver variation on suggested ECG signs of atrial infarction in patients admitted with acute myocardial infarction. The ECGs from 290 patients were evaluated by three physicians with respect to the occurrence of each of the following seven criteria suggestive of atrial infarction: (1) PR-segment elevation > 0.5 mm in lead I; (2) PR-segment depressions > 0.5 mm in leads II and III; (3) PR-segment depressions > 1.2 mm in leads I, II, and III; (4) PR-segment depressions > 0.5 mm in leads V1 and V2; (5) PR-segment elevations > 0.5 mm in leads V5 and V6; (6) PR-segment depressions > 1.5 mm in precordial leads; and (7) abnormal P waves. Kappa values ranged from 0.00-0.86. Of the seven criteria tested only criteria 2, 4, and 7 could be detected in a reasonable number of patients. The interobserver variations of these criteria were considerable, although the strength of agreement could be designated as fair to moderate.

Treatment of hypothyroidism reduces low-density lipoproteins but not lipoprotein(a).

Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL) particle in which apolipoprotein B-100 (apo B) is attached to a large plasminogen-like protein called apolipoprotein(a) [apo(a)]. Apo(a) has several genetically determined phenotypes differing in molecular weight, to which Lp(a) concentrations in plasma are inversely correlated. LDL and apo B levels are often elevated in untreated hypothyroidism and lowered by thyroxine (T4) treatment, probably due to an increase in LDL receptors. We measured plasma concentrations of LDL, apo B, and Lp(a) in 13 patients with symptomatic primary hypothyroidism before and during T4 therapy. The mean concentration of LDL decreased significantly (P = .006) from 6.05 mmol/L to 4.07 mmol/L, and the mean concentration of apo B decreased significantly (P = .005) from 1.42 g/L to 1.12 g/L. Median Lp(a) concentrations remained unchanged (P = .77); they were 17.05 mg/dL before and 16.59 mg/dL during T4 treatment. In both the untreated condition and during substitution therapy, Lp(a) levels were higher in patients than in healthy controls, probably due to a relatively high frequency of the small Lp(a) phenotypes in our patients. Since Lp(a) contains apo B, which is a ligand for the LDL receptor, it is surprising that Lp(a) is not reduced along with LDL and apo B. These findings suggest that the catabolism of LDL and Lp(a) differ in some respect, and that thyroid hormones have little, if any, effect on Lp(a).

Measurement of basal levels of factor VIIa in hemophilia A and B patients.

Previous results, presented in abstract form, indicate that replacement of thromboplastin with a mixture of phospholipid and truncated soluble tissue factor apoprotein results in a coagulation assay that can directly measure plasma factor VIIa levels without interference from zymogen factor VII (Atherosclerosis Thromb 11:1544a, 1991 [abstr]). We have exploited the specificity and sensitivity of such a factor VIIa specific coagulation assay to directly assess the in vivo relationship of factor VIII and factor IX on the production of factor VIIa levels under nonthrombotic and nonstimulatory conditions. Normal individuals (n = 20) were found to possess an average circulating factor VIIa level corresponding to 4.34 +/- 1.57 ng/mL, or approximately 1% of their total factor VII antigen. Severe factor VIII deficient patients (n = 13) possessed a slightly lower but statistically significant (P less than .01) decrease in their basal factor VIIa levels (2.69 +/- 1.52 ng/mL), corresponding to approximately 60% of that observed in normal individuals. On the other hand, severe factor IX deficient patients (n = 7) were found to possess even lower levels of factor VIIa corresponding to 0.33 +/- 0.15 ng/mL, or less than 10% of that observed in normal individuals. Measurement of total factor VII antigen levels shows that the variation in basal factor VIIa levels stems from differences in the degree of factor VII activation as opposed to differences in factor VII antigen levels. Our present data are consistent with the hypothesis that factor IXa is the principal in vivo activator of factor VII under basal conditions.

The value of exercise tests after acute myocardial infarction.

The aim of the present study was to relate the clinical course in patients after a first acute myocardial infarction with the response to exercise-tests performed one month after discharge. 90 consecutive patients who suffered an acute myocardial infarction for the first time were followed-up after 12 months in general practice. Six patients had died, and nine patients had suffered another MI. 23 patients were being treated for heart failure, 51 for angina pectoris, and 8 for arrhythmias. 14 patients received treatment for both heart failure and angina pectoris. Of the patients at work, 17.6% did not return to work because of the heart disease. 80 patients were in function groups I-II and 10 in function groups III-IV (New York Heart Association's Classification). Occurrence of ST-segment displacements was without prognostic value. Left ventricular function index (dRPP) and working capacity (W) were predictive with respect to mortality, heart failure, and angina pectoris requiring drug treatment. Exercise tests following acute myocardial infarction could not predict the chances of returning to work.

The relationship between ECG signs of atrial infarction and the development of supraventricular arrhythmias in patients with acute myocardial infarction.

ECGs obtained on arrival at the hospital from 277 patients with acute myocardial infarction were analyzed retrospectively for PR displacements, which were classified as major or minor criteria for atrial infarction and related to the later occurrence of supraventricular arrhythmia in the hospital. Major criteria were (1) PR segment elevation greater than 0.5 mm in leads V5 and V6 with reciprocal PR segment depression in leads V1 and V2, (2) PR segment elevation greater than 0.5 mm in lead I with reciprocal PR segment depression in leads II and III, and (3) PR segment depression greater than 1.5 mm in precordial leads and greater than 1.2 mm in leads I, II, and III. Abnormal P waves were classified as minor criteria. Major and minor criteria were found in 15 (5.4%) and 19 (6.9%) patients, respectively. Eight (53.3%) patients with major and six (31.6%) with minor criteria had supraventricular arrhythmias, giving odds ratios of 9.9 and 3.7, respectively. Enzyme-estimated infarct size, the occurrence of heart failure, and mortality rates did not differ in patients with or without major criteria for atrial infarction. We conclude that the occurrence of PR segment displacements on the admission ECG may predict the risk of developing supraventricular arrhythmias during hospitalization for myocardial infarction.

[Streptokinase as routine treatment in acute myocardial infarction. The effect on pain, arrhythmias and mortality assessed by a historical cohort study]. / Streptokinase som rutinebehandling ved akut myokardieinfarkt. Effekten på smerter, arytmier og letalitet vurderet ud fra en historisk kohorteundersøgelse.

It has been demonstrated that treatment with streptokinase (SK) in acute myocardial infarction (AMI) has an effect in reducing the mortality. The object of this study was, by means of a historical cohort study in a Danish Cardiological Department, to illustrate the effect of streptokinase on the course of pain, occurrence of arrhythmia and the lethality. Seventy-six patients with their first AMI treated with SK and low-dosage acetylsalicylic acid were compared with 76 patients with their first AMI who were not treated with SK. The median value of the employment of intravenous analgesics was significantly lower in the SK group (20 mg nicomorphine compared with 41 mg nicomorphine) as compared with the control group. Similarly, the duration of pain was briefer in the SK group (3.5 hours compared with 24 hours). Significantly more patients in the control group developed atrial fibrillation (12 patients compared with two). No differences were observed in the occurrence of arrhythmias endangering life in the two groups. Four patients in the SK group died during hospitalization whereas 14 died in the control group (p = 0.02). It is concluded that administration of SK intravenously combined with low-dosage acetylsalicylic acid in the acute phase of myocardial infarction has the effect of reducing 1) the duration of pain and thus the consumption of analgesics, 2) the number of cases of atrial fibrillation and 3) the lethality during the period of hospitalization.

Reduced occurrence of atrial fibrillation in acute myocardial infarction treated with streptokinase.

In a historical follow-up study of 152 hospital patients with acute myocardial infarction, the frequency of life-threatening arrhythmias (ventricular fibrillation, sustained ventricular tachycardia, 3rd degree AV-block, 2nd degree AV-block (Mobitz type II), and asystole) and atrial fibrillation in 76 patients treated with streptokinase was compared with their frequency in 76 patients who did not receive a thrombolytic therapy. Among those treated with streptokinase two patients (3%) developed atrial fibrillation, compared with 12 (16%) in the control group (P = 0.009). Life-threatening arrhythmias occurred with equal frequency in the two groups. Further studies should confirm and clarify the mechanism of the reduced frequency of atrial fibrillation in the streptokinase-treated patients.

Silent ischemia and severity of pain in acute myocardial infarction.

An overall low tendency to complain of pain, due to a low perception of pain, has been suggested in the pathogenesis of silent ischemia, independent of the extent of the diseased coronaries and a history of previous acute myocardial infarction. This hypothesis has been tested indirectly in this retrospective study by comparison of the use of analgesics during admission for a first acute myocardial infarction with the occurrence of silent ischemia at exertion tests four weeks after discharge from hospital. The study did not show a lower use of analgesics in patients with silent ischemia, but this may be due to methodologic problems. Suggestions are given for another study design to overcome these problems.

[Cardiovascular manifestations of hypothyroidism]. / Kardiovaskulaere manifestationer af hypotyreoidisme.

On the basis of a case history, the clinical and paraclinical manifestations of hypothyroidism are reviewed. Exertion dyspnoea without signs of cardiac insufficiency occurs frequently. The minute and stroke volume and heart rate are reduced. The blood pressure may rise (reversible) and hypertension may occur. The function of the left ventricle is reversibly reduced. A tendency to formation of exudates has been observed. X-ray of the thorax may revial massive relatively asymptomatic pleural exudates and cardiomegaly. Pericardial exudate occurs frequently and is demonstrated best by echocardiography. Inter- and intracellular deposits, infiltrations and fibroses have been demonstrated in the myocardium and these probably contribute to some of the non-specific, reversible ECG changes (low voltage, flattening/inversion of T waves, sinus bradycardia). The plasma concentrations of several different enzymes (including creatine kinase (CK), CK-MB and LDH) may be raised in myxoedema. The reason for this is perhaps compromized membrane function in the skeletal muscle cells. The diagnosis of myocardial infarction in myoedema requires that CK-MB constitutes at least 6% of the total CK and that the increase is transient. In patients with coronary sclerosis, substitution treatment should be initiated carefully because the risk of ischaemic symptoms is otherwise considerably increased. It is not elucidated whether the hypothyroidism per se can increase atheroma formation.

[Postcardiac injury syndrome]. / Post cardiac injury syndrome.

The post-pericardiotomy syndrome is a symptom complex which is similar in many respects to the post-myocardial infarction syndrome and these are summarized under the diagnosis of the Post Cardiac Injury Syndrome (PCIS). This condition, which is observed most frequently after open heart surgery, is characterized by pyrexia, pericarditis and increased inflammation parametres. These symptoms develop 2-12 weeks after the trauma. The etiology is unknown but autoimmunity probably plays a part, possibly precipitated by virus infection. PCIS is a diagnosis by exclusion. No definite test is available to identify patients with or without PCIS but demonstration of antimyocardial antibodies may be valuable in the differential diagnostic deliberations. As a rule, the course of the condition is benign and self-limiting but there is a tendency to recurrence. In rare cases, the inflammatory process may encroach on the coronary vessels, with cardiac tamponade and chronic pericardial exudate. In the lighter cases, PCIS may be treated with NSAID and, in the more severe cases, with systemic glucocorticoid which has a prompt effect.