Recurrent myopericarditis in association with Crohn's disease.

Myopericarditis is a rare extraintestinal complication of inflammatory bowel disease (IBD). It has also been described as a side-effect of the treatment of IBD. We report a 37-year-old-woman with Crohn's disease who had several mild episodes of myopericarditis, two of which were associated with a pleural effusion, and two with conduction abnormalities in the atrioventricular node. During the last episode, a nodal rhythm was followed by a third-degree atrioventricular block and a prolonged pause, resulting in loss of consciousness and convulsions. A permanent pacemaker was implanted. Our patient is also human lymphocyte antigen (HLA) B27-positive. HLA B27 is known to be associated with conduction disturbances in the AV node. Recurrent myopericarditis can be a sign of IBD.

Serum and plasma as alternative sample types in analysis of cardiac markers in the clinical routine.

There is an increasing demand for the results of cardiac markers (troponin I or T, creatine kinase MB mass and myoglobin) to be made available promptly after sample-taking. In order to shorten the turnaround time, the possibility of using EDTA- or heparin-plasma instead of serum was investigated. The study population comprised 391 patients with acute chest pain. Four different instruments and systems routinely used in Finland giving quantitative results were studied for the assays of creatine kinase isoenzyme MB mass, myoglobin, and troponin I or troponin T. In addition to serum samples, heparin-plasma seems to be useful for all three assays using the Access and Immulite systems, while EDTA-plasma seems to be useful for all three assays with the Access and Elecsys systems. For the AxSYM assays, serum samples seem to be the best alternative. In conclusion, it is possible to use a single EDTA- or heparin-plasma sample for Access, Elecsys and Immulite analysers, and thereby to shorten the turnaround time. In this way the quantitative analyses from plasma can be performed 30 min after taking the sample.

Differences in the diagnosis of myocardial infarction by troponin T compared with clinical and epidemiologic criteria.

We investigated the difference in the number of myocardial infarction (MI) diagnoses based on troponin T compared with clinical and epidemiologic (modified FINnish Multinational MONItoring of trends and determinants in CArdiovascular diseases) diagnoses, and the prognosis of patients with discordant diagnoses. Five hundred fifty-nine consecutive patients (315 men and 244 women, median age 69 years) were admitted to the hospital with a suspected acute coronary syndrome. Median follow-up time was 17 months. Of the 559 patients, 127 had a clinical and 137 an epidemiologic diagnosis of MI. When a diagnosis of MI was primarily based on troponin T (>0.10 microg/L), the number of MIs was 169, which increased by 33% compared with the number of MIs by clinical diagnosis, and by 23% compared with those by epidemiologic diagnosis. However, troponin T was not elevated in 13% of the 127 patients with the clinical diagnosis and in 14% of the 137 patients with the epidemiologic diagnosis of MI. Among patients in whom clinical diagnosis of MI was not made, the prognosis with regard to coronary death or nonfatal MI was not significantly worse in patients with troponin T >0.10 microg/L than < or =0.10 microg/L (hazard ratio 1.07; 95% confidence interval 0.62 to 1.84). In patients with a suspected acute coronary syndrome, troponin T-based diagnostics leads to an increase in the number of patients diagnosed with MI compared with clinical or epidemiologic diagnosis. The prognostic impact of troponin T in patients without clinical diagnosis of MI based on elevations in conventional enzyme activities needs further study in larger series of patients.

C-reactive protein, fibrinogen, interleukin-6 and tumour necrosis factor-alpha in the prognostic classification of unstable angina pectoris.

BACKGROUND: Inflammatory process has been found to play an important role in the pathogenesis of coronary heart disease (CHD) and in the prognosis of CHD patients. AIM. The aim of this study was to investigate the prognostic value of C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and tumour necrosis factor-alpha (TNF-alpha) in patients with unstable angina pectoris (UAP), including factor analysis to assess their joint effects. METHODS: The study comprised 263 consecutive patients (159 men, 104 women; median age 68 years) with UAP. Blood samples for the acute-phase protein and cytokine determinations were drawn on admission. RESULTS: Coronary mortality during the median follow-up time of 17 months was 6-fold higher in the highest tertile for CRP and IL-6 and 3.5-fold higher in the highest tertile for fibrinogen and TNF-alpha than in the respective combined lower tertiles. Factor analysis produced two underlying factors, ie the 'inflammation' factor, including CRP, fibrinogen and IL-6, and the 'injury' factor, including troponin T, creatine kinase MB mass and TNF-alpha. In Cox models, both of these factors were independent predictors of the risk of coronary death and major coronary events (coronary death or nonfatal myocardial infarction). CONCLUSIONS: Elevated levels of acute-phase proteins and cytokines, particularly CRP and IL-6, are strong predictors of the risk of serious coronary events in patients with UAP.

Ruling out myocardial infarction with troponin T and creatine kinase MB mass: diagnostic and prognostic aspects.

OBJECTIVE: To investigate the time window for ruling out myocardial infarction (MI) with troponin T (TnT) and creatine kinase isoenzyme MB mass (CK-MBm) and the prognosis of patients with ruled-out MI diagnosis. DESIGN: The study was based on 397 patients admitted with a suspected acute coronary syndrome but with relief of symptoms within 24 h. RESULTS: MI diagnosis was confirmed with elevated TnT (>0.10 microg/l) in 108 patients. in 91% within 12-24 h from the onset of symptoms, and in 99% within 12 h from admission. In 94 of these patients CK-MBm became elevated (>5.0 microg/l). in 95% within 10-12 h from the onset of symptoms, and in 99% within 6 h from admission. Among patients with ruled-out MI diagnosis, the 1-year incidence of recurrent coronary events was 29% in those with positive history of coronary heart disease (CHD) but only 7% in those without prior CHD (p < 0.001). CONCLUSION: Using TnT or CK-MBm, MI can be ruled out within 12 h from admission in the majority of patients. Among patients with ruled-out MI diagnosis, positive history of CHD is an important determinant of prognosis.

Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group.

CONTEXT: Results from recent studies on the effects of beta1-blockade in patients with heart failure demonstrated a 34% reduction in total mortality. However, the effect of beta1-blockade on the frequency of hospitalizations, symptoms, and quality of life in patients with heart failure has not been fully explored. OBJECTIVE: To examine the effects of the beta1-blocker controlled-release/extended-release metoprolol succinate (metoprolol CR/XL) on mortality, hospitalization, symptoms, and quality of life in patients with heart failure. DESIGN: Randomized, double-blind controlled trial, preceded by a 2-week single-blind placebo run-in period, conducted from February 14, 1997, to October 31, 1998, with a mean follow-up of 1 year. SETTING: Three hundred thirteen sites in 14 countries. PARTICIPANTS: Patients (n = 3991) with chronic heart failure, New York Heart Association (NYHA) functional class II to IV, and ejection fraction of 0.40 or less who were stabilized with optimum standard therapy. INTERVENTIONS: Patients were randomized to metoprolol CR/XL, 25 mg once per day (NYHA class II), or 12.5 mg once per day (NYHA class III or IV), titrated for 6 to 8 weeks up to a target dosage of 200 mg once per day (n = 1990); or matching placebo (n = 2001). MAIN OUTCOME MEASURES: Total mortality or any hospitalization (time to first event), number of hospitalizations for worsening heart failure, and change in NYHA class, by intervention group; quality of life was assessed in a substudy of 741 patients. RESULTS: The incidence of all predefined end points was lower in the metoprolol CR/XL group than in the placebo group, including total mortality or all-cause hospitalizations (the prespecified second primary end point; 641 vs 767 events; risk reduction, 19%; 95% confidence interval [CI], 10%-27%; P<.001); total mortality or hospitalizations due to worsening heart failure (311 vs 439 events; risk reduction, 31%; 95% CI, 20%-40%; P<.001), number of hospitalizations due to worsening heart failure (317 vs 451; P<.001); and number of days in hospital due to worsening heart failure (3401 vs 5303 days; P<.001). NYHA functional class, assessed by physicians, and McMaster Overall Treatment Evaluation score, assessed by patients, both improved in the metoprolol CR/XL group compared with the placebo group (P = .003 and P = .009, respectively). CONCLUSIONS: In this study of patients with symptomatic heartfailure, metoprolol CR/XL improved survival, reduced the need for hospitalizations due to worsening heart failure, improved NYHA functional class, and had beneficial effects on patient well-being.

Myoglobin, creatine kinase MB, troponin T, and troponin I - rapid bedside assays in patients with acute chest pain.

Three new rapid, qualitative bedside immunoassays were evaluated in the diagnosis of patients with acute chest pain. The subjects, 122 patients in group 1 (bedside tests for myoglobin, creatine kinase MB) and 233 patients in group 2 (bedside tests for troponin I and sensitive troponin T) were admitted to hospital with acute chest pain for less than 12 h. The bedside tests were performed on admission, and 2, 4, and 6 h later. The correlation between the two parts of the rapid creatine kinase MB/myoglobin test during the first 12 h after the onset of chest pain was moderate in all patients (kappa=0.401, 95% confidence interval 0.321-0.483). The highest correlation was seen with the patients with definite and probable myocardial infarction. The correlations were smaller but significant also in other diagnostic groups (unstable angina pectoris, prolonged chest pain, and non-cardiac chest pain). The correlation between the rapid sensitive test for troponin T and rapid test for troponin I was significant in all groups (kappa=0.776, 95% confidence interval 0.711-0.841). The myoglobin part of the rapid creatine kinase MB/myoglobin test may be too non-specific for clinical diagnostic purposes [in non-infarct patients the myoglobin part was significantly more often positive than creatine kinase MB or troponin tests (P<0.001)].

Troponin T and creatinine kinase isoenzyme MB mass in the diagnosis of myocardial infarction.

The aim of this study was to compare troponin T (TnT) and creatine kinase isoenzyme MB mass (CK-MBm) with conventional enzymes, ie CK, CK-MB activity and lactate dehydrogenase isoenzyme 1, in the diagnosis of myocardial infarction (MI). 624 patients (351 men and 273 women, median age 69 years) were admitted to hospital with suspicion of an acute coronary heart disease event. TnT was elevated (> 0.10 microg/L) in 100%, CK-MBm (> 5.0 microg/L) in 99%, and both markers in 99% of the 89 patients with the diagnosis of a definite MI according to modified FINMONICA criteria. In the 60 patients with the diagnosis of a probable MI, TnT was elevated in 65%, CK-MBm in 67% and both markers in 60%. In the patients with unstable coronary artery disease (unstable angina or prolonged chest pain attack) and conventional enzymes within normal limits, TnT was elevated in 14%, CK-MBm in 17% and both markers in 9%. The use of TnT and CK-MBm did not lead to a major change in the diagnostics of definite MI. However, TnT and CK-MBm did not confirm the diagnosis of probable MI in one-third of the events. These new markers revealed a myocardial injury in about 15% of those patients who had unstable coronary artery disease and conventional enzymes within normal limits.

Delays in thrombolytic therapy for acute myocardial infarction in Finland. Results of a national thrombolytic therapy delay study. Finnish Hospitals' Thrombolysis Survey Group.

OBJECTIVE: To determine lengths and causes of pre- and in-hospital delays in thrombolytic treatment. DESIGN: A prospective national survey covering 48 of the 51 Finnish university, central and general hospitals to obtain basic data before the start of a public campaign to shorten patient-related delay in acute myocardial infarction. SUBJECTS: One thousand and twelve consecutive patients with acute myocardial infarction who received thrombolytic therapy over 3 months in 1995 and who represent 40% of all patients with confirmed acute myocardial infarction. RESULTS: The median interval between onset of infarction symptoms and initiation of thrombolytic therapy was 160 min (30-647). Only 13% of the patients received thrombolysis within 60 min and 38% within 120 min. The median time from the onset of symptoms to the call for help was 60 min (5-491), and no difference was found in patients with or without a history of previous myocardial infarction (60 and 64 min, respectively). Only 52% of the patients called to the dispatch centre. The median delay from calling for help to hospital arrival was 40 min (10-170). The median in-hospital door-to-needle thrombolysis delay was 40 min (12-196). In 13% of hospitals the median delay was more than 60 min. The emergency physician encountered difficulties in decision making in 33% of cases. CONCLUSIONS: Only 38% of the patient received thrombolysis within 2 h of onset of symptoms. Patient-related delay before they sought help accounted for the major portion of the total treatment delay. Thus the findings emphasize the importance of prompt action when people are confronted with an acute heart attack. Reorganizing the emergency medical service and emergency department routines is also a necessary target to shorten thrombolysis delays. The delay attributable to transporting patients could be shortened by initiating thrombolytic treatment in the pre-hospital setting. In Finnish hospitals, door-to-needle delay was acceptable in cases with clear indications for thrombolysis. However, emergency physicians often had diagnostic difficulties, which led to remarkably longer in-hospital delays.

Comparison of sotalol with digoxin-quinidine for conversion of acute atrial fibrillation to sinus rhythm (the Sotalol-Digoxin-Quinidine Trial).

We randomized 61 patients with paroxysmal atrial fibrillation (AF) ( < 48 hours from onset) to either sotalol or quinidine treatment. Conversion of rhythm was recorded by Holter monitoring. The starting 80 mg dose of sotalol was repeated at 2, 6, and 10 hours if AF persisted (heart rate > 80 beats/min), and if systolic blood was > or = 120 mm Hg. In the quinidine group, if heart rate > 100 beats/min, it was decreased with intravenous digoxin, whereafter 200 mg of oral quinidine sulfate was given maximally 3 times, each dose 2 hours apart. Conversion of AF to sinus rhythm occurred in 17 or 33 patients (52%) taking sotalol, and in 24 of 28 patients (86%) taking quinidine (p < 0.0001). Electric cardioversion was necessary in 39% of the former and in 14% of the latter group. The mean delay from first trial drug to sinus rhythm with the trial medication was 10.2 +/- 7.6 hours in the sotalol group and 4.0 +/- 2.9 hours in the quinidine group (p < 0.01). Treatment was discontinued in 16 patients taking sotalol (48%) because of asymptomatic bradycardia or hypotension, and in 20 taking quinidine (71%) because of rhythm conversion. Asymptomatic wide complex tachycardia (QRS > 0.12 second) was found in 13% and 27% of patients taking sotalol and quinidine, respectively. The longest RR intervals were 6.4 and 3.8 seconds in the sotalol and quinidine groups, respectively. Oral sotalol did not appear as effective as quinidine sulfate treatment in conversion of paroxysmal AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Fatal road accidents caused by sudden death of the driver in Finland and Vaud, Switzerland.

We investigated the incidence of fatal traffic accidents caused by sudden incapacity of the driver due to cardiac and other illnesses. The retrospective analysis was gleaned from Finnish traffic accident data files from 1984-1989, and police records of traffic accidents, from Canton de Vaud, Switzerland from 1986-1989. The annual rates of all traffic fatalities per million inhabitants were 125 in Finland and 212 in Vaud. Sudden driver incapacity due to acute illness caused 1.8 and 7.3 automobile driver deaths annually per million inhabitants in Finland and in Vaud, respectively. The corresponding rates for all-cause traffic deaths were 326 and 423, for driver deaths 105 and 167, and for those due to driver incapacity 4.7 and 15.6. Sudden driver incapacity caused 1.5% of all traffic deaths in Finland, and 3.4% in Vaud. Probable cardiac arrest caused 2.1% of all drivers' deaths in Finland and 1.7% in Vaud, respectively. Deaths caused by professional drivers' sudden incapacity were responsible for 0.11% of all traffic deaths in Finland, and for 0% in Vaud. Old age and short mileage were associated with illness-caused accidents. Accidents caused by sudden incapacity of the driver are rare causes of traffic deaths and hard to foresee. While this report relates to all drivers, we suggest there should be individual risk stratification for professional drivers with heart disease. However, non-professional drivers who are elderly and who have symptomatic cardiac disease should limit their driving to short distances and at low speed.