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L Ljungdahl

Publications and source records attributed to L Ljungdahl.

At least 19 recordsLinked to original sources
PubMed2002

Cardiovascular prevention before admission reduces mortality following acute myocardial infarction in patients with diabetes.

OBJECTIVES: Previous studies have shown that patients with diabetes mellitus have an increased mortality after suffering from acute myocardial infarction (AMI). Patients with diabetes have several risk factors for cardiovascular disease. Our objective was to quantify the prevalence of pharmacological cardiovascular prevention at admission and relate such treatment to short and long-term mortality following AMI in patients with and without diabetes. DESIGN AND SUBJECTS: All patients discharged from the Department of Internal Medicine at Helsingborg Hospital in 1996 and 1997 with a principal diagnosis of AMI were included in the study. Patients were divided into two groups according to the presence or absence of diabetes. Cardiovascular risk factors, on-going medication, type of ward following admission, peak creatine kinase MB mass (CKMB) and immediate treatment were registered. Information about death was obtained from the national register. Kaplan-Meier analysis was performed for life-expectancy. RESULTS: A total of 673 patients with AMI were registered, of which 117 (17.4%) had diabetes. No differences in 30 days (17.1% vs. 15.3%) or 1-year (24.8% vs. 27.4%) mortality were seen between the diabetes and control groups, whereas the 2-year mortality was significantly higher in the diabetes group (40.2% vs. 29.1%). Cardiovascular risk factors occurred more often in the diabetes group and the use of aspirin, ACE-inhibitors, statins and diuretics was significantly more frequent. In patients treated with aspirin, in combination with either statin or angiotensin converting enzyme (ACE)-inhibitor, or both, no differences were seen in 30 days, 1 or 2-year mortality between groups. CONCLUSION: In contrast to earlier studies we did not find an increased 30 days and 1-year mortality in patients with diabetes suffering from AMI. This discrepancy was linked to a higher frequency of pharmacological cardiovascular prevention, a finding supporting the hypothesis that survival of a diabetes patient after AMI could be affected by factors operating before the infarction.

Aged↗
PubMed1999

Can troponin T replace CK MBmass as "gold standard" for acute myocardial infarction ("AMI")?

Diagnosis of definite "Acute Myocardial Infarction" by the old WHO criteria depends on the diagnostic sensitivity and specificity of the biochemical marker used. Troponins have higher diagnostic sensitivity and specificity than the current "gold standard" for AMI, CK MBmass. Troponin T (TnT) provides both diagnostic and prognostic information on Minor Myocardial Damage (MMD) even in patients without increases of CK MBmass. Consequently, we evaluated the possibility of replacing CK MBmass with TnT. We first re-evaluated a previous, well-documented material of 502 time series from AMI-suspected cases, 50% of which were primarily classified as AMI by CK MBmass > or = 10 micrograms/L. We found that a TnT discriminator limit of 0.40 microgram/L gave the same AMI prevalence. We then identified from our laboratory data base 1995-1998 acute patient episodes with > or = 3 pairs of CK MBmass and TnT. This resulted in 754 episodes with max CK MBmass > or = 10 micrograms/L (AMI), 93 episodes with maximal CK MBmass < 10 micrograms/L and TnT > or = 0.10 microgram/L (MMD), and 730 episodes with max concentrations below the discriminators of both markers (NOT-MMD). TnT > or = 0.40 microgram/L detected 91% of all AMI giving a posterior probability of "AMI" > 99%. The criterion: "maximal TnT within the interval 0.10-0.40 microgram/L" detected 94% of all MMD and 9% of all AMI giving posterior probabilities about half MMD and half "small AMI", the latter characterized by less than 3-fold increased maximal CK MBmass. Thus, this TnT interval confirmed the gradual transition between MMD and small AMI. We suggest gradation of myocardial damage by TnT.

Biomarkers↗
PubMed1998

Troponin T: a sensitive and specific diagnostic and prognostic marker of myocardial damage.

Cardiac troponin T (cTnT) in serum is a highly sensitive and specific marker for myocardial damage. Quantitative immunoassays take 9 min. A rapid test (TropT, CardiacT) using plasma detects cTnT concentrations above 0.10 microg/l within 15 min. Both assays are specific for the cardiac isoform. In a study using the maximal values from serial sampling in 502 infarction-suspected patients, we found a diagnostic sensitivity for non-Q- and Q-wave infarctions of 100%, with a specificity of 99%. cTnT has been shown to be a powerful prognostic marker for risk stratification in acute coronary syndromes. In 30-40% of patients with unstable angina, cTnT > or = 0.10 microg/l detects minor myocardial damage (MMD) with poor prognosis. False positives may be found in certain skeletal muscle diseases, such as polymyositis and Duchenne's muscular dystrophy. Constantly increased values in renal failure may be due to uremic cardiomyositis. Even in uremia, a rapid increase of cTnT will indicate acute myocardial damage. We propose a diagnostic strategy based on timed, parallel determinations of myoglobin + cTnT.

Biomarkers↗
PubMed1997

Detection of myocardial damage by serial measurements of cardiac troponin T, CK MBmass, and TROPT rapid test.

Detection of cardiac damage is greatly facilitated by serial blood measurements of myocardial cell markers. In many hospitals creatine kinase MBmass concentration (CK MBmass) constitutes the biochemical criterion (WHO) for acute myocardial infarction (AMI). Cardiac troponin T (TnT) is an even more sensitive and specific marker for myocardial damage. With discriminator levels of 10.0 and 0.10 micrograms/l, respectively, serial measurements of both markers provide a useful diagnostic strategy for ischemic heart disease. This survey reviews representative cumulated time curves in individual patients covering the spectrum of myocardial damage, including unstable angina pectoris (UAP), non-Q-wave and Q-wave infarctions with and without early reperfusion, re-infarction, and subacute infarction. Increased TnT detects minor myocardial damage (MMD) in over 30% of patients with UAP, although CK MBmass remains below its discriminator. Subacute infarction is detected by the wide diagnostic time window of the serum TnT at a time when CK MBmass has already returned to normal. In a substudy of 502 suspected cases of AMI, the distributions of maximum serum TnT concentrations within each patient series demonstrated that TnT had a diagnostic sensitivity of 100% and a specificity of 99%. Median, 5th and 95th percentiles of maximum TnT values within the diagnostic subgroups showed that serum TnT was increased five-fold more than CK MBmass. Median values of Q-wave AMI were higher than in non-Q-wave AMI. A diagnostic strategy using TROPT, a rapid test specific for the cardiac isoform of TnT with a detection limit 0.10 microgram/l, is presented.

Aged↗
PubMed1997

An improved rapid troponin T test with a decreased detection limit: a multicentre study of the analytical and clinical performance in suspected myocardial damage.

In a multicentre study, we evaluated the analytical and diagnostic performance of the second version of the TROPT rapid test (TROPT 2, CARDIACT in the US). We tested TROPT 2 on 796 blood samples from 487 patients admitted on suspicion of myocardial infarction between 1 and 72 h after onset of symptoms and determined cTnT ELISA and CK MB mass in the corresponding serum samples. Frequency distributions of the results with TROPT 2 showed a detection limit of 0.18 microgram/l (for 50% positive results) as determined by the quantitative cTnT ELISA method. In a total of 796 samples the sensitivities in the detection of myocardial infarction (WHO criteria) 8-12 h after onset of symptoms were highest for cTnT ELISA (98%), followed by the rapid assay and CK MB mass (92%). A subgroup of 87 patients was primarily classified by the WHO criteria for definite infarction. Based on the maximum values within each patient time-series, diagnostic sensitivities for infarction were 100% for TROPT2, cTnT ELISA and CK MB mass. The corresponding specificities were 90%, 82% and 100%, respectively. After reclassification summarizing all cases of myocardial damage (acute and subacute myocardial infarctions and minor myocardial damage) the sensitivities were 87% (TROPT2), 100% (cTnT ELISA) and 71% (CK MB mass). The specificities of all three markers were 100%. Over 50% of all cases of minor myocardial damage were detected by TROPT 2. The clinical evaluation showed that the diagnostic performance of TROPT 2 is only slightly lower than that of cTnT ELISA.

Angina, Unstable↗
PubMed1994

[Troponin T in acute myocardial infarction. Diagnosis and prognosis in patients admitted for suspected acute myocardial infarction].

Cardiac troponin T (TnT) is a new serological marker for use as a diagnostic tool for myocardial damage. A blinded prospective multicentre study representing 298 patients who on admission were suspected of acute myocardial infarction (AMI) to the coronary care units of six Scandinavian hospitals was undertaken to assess the diagnostic performance and prognostic efficacy of a new cardiospecific TnT immunoassay. We used a discriminator value of TnT of 0.20 micrograms/l. One hundred and fifty-five patients (52%) had definite AMI, based on WHO criteria (all had peak S-TnT values > or = 0.20 micrograms/l); 127 patients (43%) had ischaemic heart disease (IHD) without AMI; and 16 patients (5%) had non-IHD (all had peak S-TnT values < 0.20 micrograms/l). The 127 IHD-patients without definite AMI could be subdivided into a group of 44 patients with S-TnT peak values > or = 0.20 micrograms/l, and a group of 83 patients with TnT below this level. A follow-up study was able to define the clinical significance of these findings. The cumulative six months probability of suffering cardiac death or AMI was significantly higher in the subgroup with increased TnT values (14% (6/44)) as compared to the other subgroup (4% (3/83)) (Log-rank test, p = 0.025). The probability of cardiac events was 15% for the patients with definite AMI. We conclude that increased troponin T in serum can detect a subgroup of IHD-patients in whom AMI has been ruled out, but who still have a prognosis as serious as that of patients with definite AMI.

Adult↗
PubMed1993

Troponin-T and CK MB (mass) in early diagnosis of ischemic myocardial injury. The Helsingborg Study, 1992.

We evaluated cardiac troponin T (S-troponin T) versus CK MB in serum (S-CK MB) sampled 4, 10, 16, and 22 h after onset of acute symptoms in 207 consecutive cases admitted to our coronary care unit in Helsingborg, Sweden, May-October 1992. These were primarily classified into 106 acute myocardial infarctions (AMI) and 101 NOT-AMI cases by conventional cardiological criteria plus S-CK MB (mass). Time curves of S-troponin T and S-CK MB data were plotted for each individual case. Twelve of the 101 cases in the NOT-AMI group showed increased S-troponin T indicating ischemic myocardial injuries. The same cases also showed changes of S-CK MB (mass), though below its discriminator. Seven of these cases were reclassified as minor myocardial damage, constituting 25% of our 28 cases of unstable angina. The remaining five cases showed a combination of constantly increased S-troponin T and decreasing or low S-CK MB mass values as seen after a recent infarction. Consequently, the patient material was reclassified into 118 cases of ischemic myocardial injury (106 conventional AMI + 7 minor myocardial damage + 5 postinfarctions) and 89 cases of NOT-ischemic myocardial injury. The frequency distributions of the maximal S-troponin T and S-CK MB (mass) values of each case were plotted in double test evaluation histograms. For troponin T, discriminator 0.20 micrograms/L, clinical sensitivity for ischemic myocardial injury was 97% and specificity 99%. With a lower discriminator of 0.10 micrograms/L, sensitivity increased to 99% and specificity decreased to 89%. For S-CK MB (mass), discriminator 10 micrograms/L, sensitivity was 91%, specificity 98%. With a lower discriminator of 5 micrograms/L sensitivity increased to 96% and specificity decreased to 78%. We conclude that as a single routine test, S-troponin T is the marker of choice for early diagnosis of ischemic myocardial damage. The combination S-troponin T and S-CK MB (mass) provides additional, detailed information in reinfarction and postinfarction unstable angina pectoris.

Aged↗
PubMed1993

Rational diagnostic strategy in diagnosis of ischemic myocardial injury. S-troponin T and S-CK MB (mass) time series using individual baseline values.

The new and sensitive serum markers S-troponin T and S-CK MB (mass) can detect minor myocardial damage (MMD) in patients after an episode of acute myocardial ischemia even when accepted criteria for a myocardial infarction are not fulfilled. High-risk MMD patients constitute about one-third of unstable angina pectoris cases. Since 1989 we have compared S-troponin T and S-CK MB (mass concentration) with catalytic S-CK and S-CK MB determinations in several studies comprising more than 600 patients. We conclude that the combination of the two most cardiospecific and sensitive markers, S-troponin T + S-CK MB (mass), is highly informative in studies and evaluations. If only one marker can be routinely used, S-troponin T may replace current tests. Rational utilization of S-troponin T and S-CK MB (mass) requires an adequate number of determinations within the respective diagnostic time windows using a sampling time schedule relating to time of onset pain in each patient. Individual reference values of each marker may easily be obtained by taking baseline samples in a stable phase, e.g. during convalescence. The data are best understood when they are presented as time series in graphic laboratory reports. The relative increases of the myocardial markers are three to five-fold higher when they are plotted relative to the individual baseline value of each patient than when they are plotted against the respective, general discriminator values for infarction.

Angina Pectoris↗
PubMed1993

Diagnostic performance and prognostic value of serum troponin T in suspected acute myocardial infarction.

Cardiac troponin T (TnT) is a new serological marker for use as a diagnostic tool for myocardial damage. A blinded prospective multicentre study representing 298 patients suspected of having acute myocardial infarction (AMI), and admitted to the coronary care units of six Scandinavian Hospitals was undertaken to assess the diagnostic performance and prognostic efficacy of a new cardiospecific TnT immunoassay. We used a discriminator TnT value of 0.20 microgram l-1. One hundred and fifty five patients (52%) had definite AMI, based on WHO criteria (all had peak S-TnT values of > or = 0.20 micrograms l-1); 127 patients (43%) had ischaemic heart disease (IHD) without AMI; and 16 patients (5%) had non-IHD (all had peak S-TnT values of < 0.20 microgram l-1). The 127 IHD-patients without definite AMI could be subdivided into a group of 44 patients with S-TnT peak values of > or = 0.20 microgram l-1, and a group of 83 patients with TnT below this level. An equal identification of these patients among the centres was seen (mean +/- SD 35 +/- 13%; range 20-55%). A follow-up study was able to define the clinical significance of these findings. The cumulative 6 months probability of suffering cardiac death or AMI was significantly higher in the subgroup with increased TnT values (14% (6/44)) as compared to the other subgroup (4% (3/83)) (Log-rank test, p = 0.025). The probability of cardiac events was 15% for the patients with definite AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The prognostic value of serum troponin T in unstable angina.

BACKGROUND: Cardiac troponin T is a regulatory contractile protein not normally found in blood. Its detection in the circulation has been shown to be a sensitive and specific marker for myocardial cell damage. We used a newly developed enzyme immunoassay for troponin T to determine whether its presence in the serum of patients with unstable angina was a prognostic indicator. METHODS: We screened 109 patients with unstable angina (25 with accelerated or subacute angina and 84 with acute angina at rest) for serum creatine kinase activity, creatine kinase isoenzyme MB activity, and troponin T every eight hours for two days after admission to the hospital. The outcomes of interest during the hospitalization were death and myocardial infarction. RESULTS: Troponin T was detected (range, 0.20 to 3.64 micrograms per liter; mean, 0.78; median, 0.50) in the serum of 33 of the 84 patients (39 percent) with acute angina at rest. Only three of these patients had elevated creatine kinase MB activity (two were positive for troponin T, and one was negative). Of the 33 patients who were positive for troponin T, 10 (30 percent) had myocardial infarction (3 after coronary-artery bypass surgery), and 5 of these died during hospitalization. In contrast, only 1 of the 51 patients with angina at rest who were negative for troponin T had an acute myocardial infarction (P less than 0.001), and this patient died (P = 0.03). Thus, 10 of the 11 patients with myocardial infarctions had detectable levels of troponin T; only 1 had elevated creatine kinase MB activity. Troponin T was not detected in any of the 25 patients with accelerated or subacute angina, and none of these patients died. CONCLUSIONS: Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial-cell injury than serum creatine kinase MB activity, and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina.

Aged↗
PubMed1991

S-troponin T in suspected ischemic myocardial injury compared with mass and catalytic concentrations of S-creatine kinase isoenzyme MB.

In a multicenter study we compared three tests for ischemic myocardial injury (IMI): a new, automated enzyme immunoassay for S-troponin T (S-TNT; Boehringer Mannheim) and two S-creatine kinase (CK) isoenzyme MB assays (mass and catalytic concentrations). For critical evaluation of clinical sensitivity, we studied 243 cases with an IMI prevalence of 43% and an 18% prevalence of cases with unstable angina. Relative peak values of S-TNT and S-CK-MB (mass) after onset of pain were four- to fivefold higher than S-CK-MB (catalytic) results. Increases of S-TNT and S-CK-MB (mass), even though still within their reference ranges, indicated minor myocardial damage in about one-third of the cases primarily classified as unstable angina. The diagnostic window for S-TNT ranged from hours to weeks after the acute episode. The time courses were frequently biphasic, with the initial S-TNT peak closely paralleling that of the mass concentrations of S-CK-MB. With a biological half-life for S-TNT of 2 h, the prolonged increases in S-TNT indicate a continuous release of S-TNT from necrotizing cells. Clinical specificities of S-TNT and S-CK-MB (mass) were greater than that of S-CK-MB (catalytic), even in the presence of 30% to 40% severe skeletal muscle injuries. The combination of S-TNT and S-CK-MB (mass) is excellent for detection of acute IMI, including minor myocardial damage.

Catalysis↗
PubMed1988

Non-invasive recognition of arrhythmogenic right ventricular dysplasia.

Arrhythmogenic right ventricular dysplasia causes ventricular arrhythmias and sometimes heart failure. The condition is easily overlooked, but once suspected, it may be diagnosed non-invasively. This is illustrated by the case reported. The clinical features of this syndrome are discussed, with special emphasis on the non-invasive findings.

Adult↗