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Liisa-Maria Voipio-Pulkki

Publications and source records attributed to Liisa-Maria Voipio-Pulkki.

At least 19 recordsLinked to original sources

Cardiomyocyte apoptosis is related to left ventricular dysfunction and remodelling in dilated cardiomyopathy, but is not affected by growth hormone treatment.

BACKGROUND AND AIMS: Cardiomyocyte apoptosis (CA) is a common feature of end-stage heart failure. We examined whether CA is associated with cardiac dysfunction and remodelling in heart failure due to dilated cardiomyopathy and studied the effect of human growth hormone (hGH) on CA. METHODS AND RESULTS: We studied 38 patients, included in a phase III multi-center, randomised, double-blind and placebo-controlled trial of biosynthetic hGH treatment in dilated cardiomyopathy, at baseline and after 14 weeks treatment. Twenty-six patients received hGH and 12 received placebo. CA was quantified in endomyocardial biopsies using the TUNEL assay. CA correlated with left ventricular size (r=0.43, p=0.007). Compared to patients with CA below the median of 0.53%, patients with CA above the median had significantly larger left ventricular volumes and lower ejection fractions (EF) by echocardiography (median (interquartile range)) 200 ml (84) vs. 257 ml (134) and 27% (11) vs. 23% (9). Expression of the Fas receptor was associated with a high rate of CA. hGH treatment significantly increased serum IGF-1 levels, but it had no effect on CA or cardiac structure and function. CONCLUSION: CA is related to left ventricular enlargement and dysfunction in dilated cardiomyopathy. CA is not affected by short-term treatment with hGH.

Apoptosis↗

Pregnancy-associated plasma protein A: a biomarker in acute ST-elevation myocardial infarction (STEMI).

BACKGROUND: Elevated circulating levels of pregnancy-associated plasma protein A (PAPP-A), a novel marker of atherosclerotic plaque instability, are associated with increased risk of future cardiac events in patients with acute coronary syndromes (ACS). However, little is known of the kinetics or clinical significance of circulating PAPP-A after plaque rupture in acute ST-elevation myocardial infarction (STEMI). AIM: To evaluate the 48-hour release of pregnancy-associated plasma protein A (PAPP-A) and its association with 12-month outcome in patients with acute ST-elevation myocardial infarction (STEMI). METHODS: Sixty-two consecutive STEMI patients were included (40 men and 22 women, median age 67.5 years (range 34-84)), of whom 54 (87.1%) received reperfusion therapy. PAPP-A was measured at admission and 6-12, 24 and 48 hours thereafter. In 14 patients, samples were obtained also at 1, 2 and 4 hours. RESULTS: There was an early peak of circulating PAPP-A during the first 12 hours from symptom onset, followed by rapid normalization. A second, late PAPP-A elevation was noticed in 20/62 patients (32.3%). Admission PAPP-A >10.0 mIU/L (highest tertile) was associated (P = 0.049) with increased 12-month risk of cardiovascular death or non-fatal myocardial infarction. Moreover, the combination of failed early reperfusion together with late PAPP-A elevation was strongly (7/13 versus 10/49 patients, P = 0.016) associated with adverse outcome. Admission PAPP-A did not correlate with admission C-reactive protein or cardiac troponin I. CONCLUSIONS: PAPP-A is elevated early in STEMI and then declines rapidly, a pattern consistent with release from the ruptured plaque. The variability of PAPP-A kinetics at 48 hours reflects the success of reperfusion. This study also shows that PAPP-A may have prognostic value in STEMI.

Adult↗

Quality of emergency room care for atrial fibrillation.

OBJECTIVES: Atrial fibrillation (AF) is the most common arrhythmia in emergency rooms (ER). We surveyed the clinical characteristics and quality of care of AF patients in three emergency rooms in Helsinki, Finland. DESIGN: Observational data of the treatment of 179 consecutive symptomatic AF patients were prospectively collected. The quality of care was analysed according to a predestined set of criteria. RESULTS: Mean age of the patients was 63 years and 61% were men. The leading symptom was palpitation (86%). Sinus rhythm was achieved in 70%. New anticoagulation was initiated in 20% and cardiovascular medication modified in 42% of patients. Considering the overall quality of care, including documentation in the patient chart, it was classified as good in 53% of all patients, whereas the quality of therapeutic decisions and planning for follow-up was good in 77%. CONCLUSIONS: The ER visit results in extensive treatment modifications in two of three patients. Although inadequate care is rare, maintaining good quality requires adherence to clinical guidelines, careful documentation and plans for follow-up.

Adult↗

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Journal Article↗

Comparative accuracy of manual versus computerized electrocardiographic measurement of J-, ST- and T-wave deviations in patients with acute coronary syndrome.

Accurate and rapid electrocardiographic interpretation is of crucial importance in acute coronary syndrome (ACS). Computerized electrocardiographic algorithms are often used in out-of-hospital settings. Their accuracy should be carefully validated in ACS, particularly in ST-elevation myocardial infarction. This study evaluated the comparative accuracy of lead-specific computer-based versus manual measurements of the J-point, ST-segment, and T-wave deviations in standard 12-lead electrocardiograms (ECGs) (excluding lead aVR). Sixty-nine consecutive patients with suspected ACS were included. The interobserver reliability in the determination of ST-segment deviation>or=0.2 mV in leads V2 and V3 was very good (kappa=0.94 and 0.93, respectively). Agreement between a cardiologist and the computer regarding ST elevation>or=0.2 mV in lead V2 was moderate (kappa=0.72) and in V3 was very good (kappa=0.85). For ST depression or elevation>or=0.05 mV in lead LIII, agreement was good and moderate (kappa=0.79 and 0.51, respectively). Bland-Altman analysis demonstrated clinically acceptable limits of agreement comparing measurements of the J point and the T wave, but clinically inadequate limits of agreement with respect to ST-segment deviation, between the electrocardiographer and the computer. The optimal cut-off points were 0.115 mV (sensitivity 89%, specificity 98%) for the computer program to detect ST elevation>or=0.2 mV and 0.045 mV (sensitivity 74%, specificity 99%) for revealing ST elevation>or=0.1 mV. It was found that automatically measured ST-segment deviations were smaller than those manually measured. In conclusion, a correction should be performed to obtain optimal results in the automated analysis of ECGs, because the results have important implications for clinical decision making.

Acute Disease↗

Hemodynamic variables related to outcome in septic shock.

OBJECTIVE: To assess the impact of hemodynamic variables on the outcome of critically ill patients in septic shock and to identify the optimal threshold values related to outcome with special reference to continuously monitored mean arterial pressure (MAP) and mixed venous oxygen saturation (SvO2). DESIGN AND SETTING: Retrospective cohort study in a university hospital intensive care unit (ICU). PATIENTS: All consecutive 111 patients with septic shock treated in our ICU between 1 Jan. 1999 and 30 Jan. 2002. MEASUREMENTS AND RESULTS: The data on the hemodynamic and respiratory monitoring and circulation-related laboratory tests over the first 48 h of treatment in the ICU were collected from the clinical data management system. Data from 6 h and 48 h were analyzed separately. The 30-day mortality rate was 33% (36 of 111). Univariate analysis and forward stepwise logistic regression analysis were performed using the 30-day mortality as the primary endpoint. Mean MAP and lactate on arrival during 6 h, while mean MAP, the area of SvO2 under 70%, and mean CVP during 48 h were independently associated with mortality. MAP level of 65 mmHg and SvO2 of 70% had the highest areas under receiver characteristics curves. CONCLUSIONS: MAP, SvO2, CVP, and initial lactate were independently associated with mortality in septic shock, with threshold values supporting those published in recent guidelines.

APACHE↗

Measurement and reproducibility of magnetocardiographic filtered atrial signal in patients with paroxysmal lone atrial fibrillation and in healthy subjects.

Magnetocardiography (MCG) is a method complementary to electrocardiography (ECG). We examined recording and reproducibility of atrial depolarization signal by MCG. Multichannel MCG over anterior chest and orthogonal 3-lead ECG were recorded in 9 patients who had paroxysmal lone atrial fibrillation and in 10 healthy subjects in duplicate at least 1 week apart. Data were averaged using atrial wave template and high-pass filtered at 25, 40, and 60 Hz. Atrial signal duration with automatic detection of onset and offset and root mean square amplitudes of the last portion of atrial signal were determined. Coefficient of variation of atrial signal duration by MCG at 40 Hz was 3.3% and difference between the measurements was 3.5 milliseconds on average. The corresponding figures obtained by signal-averaged ECG (SAECG) were 6.1% and 6.9 milliseconds. Coefficient of variation for root mean square of the last 40 milliseconds of atrial signal were 16% in MCG and 17% in SAECG. Reproducibility was best at 40-Hz filter and similar in patients and healthy subjects. In conclusion, the reproducibility of atrial signal variables in MCG is adequate and somewhat better than in SAECG and equal in patients with lone atrial fibrillation and healthy subjects. Magnetocardiography seems to be a potentially valuable method to evaluate features of atrial depolarization in patient studies.

Adult↗

Comparison of cardiac troponin I immunoassays variably affected by circulating autoantibodies.

BACKGROUND: We recently provided evidence that circulating autoantibodies against cardiac troponin I (cTnI) or the troponin complex cause negative interference in cTnI immunoassays. By comparing three cTnI immunoassays, we further explored the phenomenon of circulating autoantibodies and their consequences in patient samples. METHODS: We developed a cTnI immunoassay with a novel assay design using three antibodies, two of which bind epitopes outside the stable, central part of cTnI. Samples from 541 chest pain patients were measured with the new cTnI assay and with a first-generation cTnI assay (Innotrac Aio cTnI) using a conventional midfragment assay design. Using another sample cohort, we also compared the new assay with a second-generation cTnI assay (Access AccuTnI). RESULTS: The analytical detection limit of the new cTnI assay was 0.012 microg/L, and the lowest concentration giving a total imprecision (CV) of 10% was 0.060 microg/L. The mean difference (95% limits of agreement) between the new cTnI and Aio cTnI assays was larger in admission samples (21.0%; -107.8% to 149.7%) than in samples taken 6-12 h (12.8%; -61.5% to 87.2%) and 24 h after admission (3.0%; -71.3% to 77.4%; P <0.001). With the lowest concentrations giving 10% CV (0.22 microg/L for Aio cTnI) used as cutoffs, 14.3% (n = 76) of admission samples were positive only with the new assay, whereas 13.5% (n = 72) were positive with both assays. Of samples taken at 6-12 and 24 h, 10.2% (n = 31) and 8.3% (n = 29) were positive only with the new assay. ROC curve analysis of admission samples showed a significantly higher area under the curve for the new cTnI assay (0.940) than for the Aio cTnI assay (0.846; P <0.001). The new cTnI assay gave generally lower results than the AccuTnI assay; the mean (95% limits of agreement) differences were -58.9% (-151.8% to 34.0%) in admission samples. In samples with severe interference from autoantibodies, median ratios between the new assay and AccuTnI were higher than in samples with no apparent troponin autoantibodies (0.875 vs 0.481; P<0.001). CONCLUSIONS: The new cTnI assay, which is based on a novel antibody combination different from the conventional midfragment antibody approach, offers improved detection of cTnI in samples containing troponin autoantibodies.

Autoantibodies↗

Cytomegalovirus infection of the heart is common in patients with fatal myocarditis.

BACKGROUND: Although enteroviruses and adenoviruses are considered to be the leading causes of the usually mild clinical myocarditis, little is known about the etiology of severe or fatal myocarditis. METHODS: We collected all available clinical records and myocardial autopsy samples for patients who had myocarditis recorded as the underlying cause of death in Finland during the period of 1970-1998. Findings for all available patients (20 men and 20 women; median age, 49 years) with myocarditis that fulfilled the Dallas criteria and who had sufficient data were included in the study. Twelve subjects who had died accidentally served as control subjects. Polymerase chain reaction (PCR) and in situ hybridization assays were used for detection of viral genomes (adenovirus, cytomegalovirus, enterovirus, human herpesvirus 6, influenza A and B viruses, parvovirus B19, and rhinovirus) in heart samples. RESULTS: Viral nucleic acids were found in the hearts of 17 patients (43%), including cytomegalovirus (15 patients), parvovirus B19 (4 patients), enterovirus (1 patient), and human herpesvirus 6 (1 patient). In 4 patients, cytomegalovirus DNA was found in addition to parvovirus B19 or enterovirus genomes. No adenoviruses, rhinoviruses, or influenza viruses were detected in this study of fatal myocarditis. In 67% of the patients for whom PCR was positive for cytomegalovirus, in situ hybridization revealed viral DNA in cardiomyocytes. Only 1 of these patients was immunocompromised. In the control group, only human herpesvirus 6 (1 subject) and parvovirus B19 (1 subject) DNA were detected. CONCLUSIONS: In this population-based study, cytomegalovirus was found to be the most common specific finding in immunocompetent patients with fatal myocarditis. This may have important clinical implications for the treatment of severe acute myocarditis.

Adolescent↗

Diagnosis and presentation of fatal myocarditis.

The clinical presentation of myocarditis is highly variable, and histopathology is thus considered to be the cornerstone of diagnosis. We studied how accurately myocarditis was diagnosed in a series of routine autopsies and how fatal myocarditis presents clinically. All death certificates with myocarditis recorded as the underlying cause of death in Finland in 1970 to 1998 were collected retrospectively (N = 639). All cases with cardiac autopsy samples and clinical data available (n = 142; median age, 51 years) were included in this study. The cardiac samples were reexamined for the presence of myocarditis by 3 experienced independent pathologists using the Dallas criteria. The clinical data were evaluated for the presenting signs and symptoms of myocarditis. Histopathologic reanalysis showed that only 32% of the 142 subjects met the Dallas criteria for myocarditis (75% of pediatric and 28% of adult patients, P = .001). Clinicians had suspected myocarditis in only one third of the hospitalized Dallas-positive patients. Dallas-positive patients presented more often with features of myocardial infarction (26% versus 9%, P = .026) or heart failure (35% versus 10%, P = .001) than Dallas-negative subjects. The signs and symptoms of infectious disease were also more common in Dallas-positive patients (61% versus 23%, P < .001). In contrast, Dallas-negative subjects died suddenly or were found dead more frequently (68% versus 39%, P = .004). The most evident cause of death in the Dallas-negative subjects was ischemic heart disease (n = 78, 55% of all cases). Our study provides evidence that myocarditis is overdiagnosed on routine autopsies, particularly in patients who have died suddenly or are found dead. Fatal myocarditis appears to present equally often as heart failure, sudden death, or mimicking myocardial infarction.

Adolescent↗

Molecular distinction of circulating pregnancy-associated plasma protein A in myocardial infarction and pregnancy.

BACKGROUND: In the blood of pregnant women, pregnancy-associated plasma protein A (PAPP-A) is present as a covalent complex with the proform of eosinophil major basic protein (proMBP). Recently, increased serum concentrations of PAPP-A have been found in acute coronary syndromes (ACS). The aim of this study was to investigate whether the circulating PAPP-A in ACS is the same as that in pregnancy. METHODS: We developed two time-resolved immunofluorometric assays based on a relative epitope map constructed by the use of 17 monoclonal antibodies. One assay, which measured total PAPP-A, used two PAPP-A subunit-specific antibodies. The other assay, which measured PAPP-A/proMBP complex, used one proMBP subunit-specific antibody and one PAPP-A subunit-specific antibody. Serum samples from four patients with myocardial infarction (MI), three pregnant women in their first trimester, and one in her third trimester were fractionated by gel filtration on a Superose 6 precision column. The two assays were used to analyze fractions obtained by gel filtration as well as serum samples serially collected from four other MI patients. RESULTS: Pregnancy-related PAPP-A was eluted as a single peak with a molecular mass of approximately 700 kDa, whereas ACS-related PAPP-A was also eluted as a single peak but with a molecular mass of approximately 530 kDa. Pregnancy-related PAPP-A was detected equally by the two assays, whereas increased ACS-related PAPP-A was detected only by the assay for total PAPP-A. CONCLUSIONS: Our results provide the first evidence that circulating ACS-related PAPP-A is different from circulating pregnancy-related PAPP-A in that it is not complexed with proMBP. These findings provide a solid foundation for the design of immunoassays to accurately measure atherosclerosis-associated plasma protein A in the circulation.

Adult↗

Apoptotic cardiomyocyte death in fatal myocarditis.

Acute myocarditis is often a self-limited process with a good outcome. Experimental animal studies have found that cardiomyocyte apoptosis occurs in severe forms of myocarditis. We studied whether cardiomyocyte apoptosis plays a role in the development of fatal acute human myocarditis. Myocardial autopsy samples from subjects who died of acute myocarditis in Finland between 1970 and 1998 were studied. Thirty-three of these cases(16 men and 17 women; 45 +/- 6 years old) were randomly selected for this study. All cases fulfilled the histopathologic Dallas criteria for myocarditis. Eight subjects who had died accidentally served as controls. Apoptotic DNA fragmentation (terminal transferase-mediated DNA nick end labeling) and activation of caspase-3 (immunohistochemistry) were detected. The mode of death was determined retrospectively from all available clinical data. In fatal myocarditis, large amounts of cardiomyocytes showed apoptotic DNA fragmentation or contained active caspase-3 (2.0 +/- 0.3% and 2.8 +/- 0.4%, respectively). In the controls, few apoptotic cardiomyocytes were found (0.008 +/- 0.003% by terminal transferase-mediated DNA nick end labeling and 0.009 +/- 0.003% by detection of active caspase-3, p <0.001 vs myocarditis). The amount of apoptosis did not correlate with the age or gender of the cases, recognized viral etiology, histologic features, or duration of disease. However, more apoptotic cardiomyocytes were detected in the subjects who had myocarditis and had died of heart failure (n = 18) than in those who had myocarditis and died suddenly of cardiac arrest (n = 15; 2.6 +/- 0.4% vs 1.1 +/- 0.2%, p <0.001). In conclusion, cardiomyocyte apoptosis is a common mechanism of myocardial damage in severe acute human myocarditis. Moreover, higher rates of cardiomyocyte apoptosis are associated with the development of fatal heart failure in acute myocarditis.

Analysis of Variance↗

Out-of-hospital hypoglycaemia is safely and cost-effectively treated by paramedics.

OBJECTIVES: The purpose of this study was to investigate the clinical epidemiology of severe out-of-hospital hypoglycaemia, to evaluate the standard treatment protocol used, to investigate the clinical outcome during a 3-month follow-up period and to evaluate financial savings achieved by not transporting all patients to hospital. METHODS: This study was a prospective, observational study based on questionnaires and patient files. Two paramedic units of the Rescue Department filled in a study form on each hypoglycaemia patient they enrolled between 1 February 2001 and 31 December 2001. These patients were contacted by mail after 3 months and asked to fill in a questionnaire regarding their health. RESULTS: Sixty-nine patients were included in the study. The majority of the patients had diabetes mellitus for more than 5 years. The severity of hypoglycaemia was related to the duration of diabetes (P = 0.003) and insulin therapy (P = 0.021). Fifty-eight patients (84.1%) required intravenous glucose treatment. Sixty-two patients (89.9%) were left at the scene after treatment. No immediate relapses occurred. Mean patient satisfaction was 4.6 (SD 0.8) on a scale from 1 to 5. Satisfaction was related to the duration of diabetes (P<0.0001) and to low haemoglobin A1c values (P<0.0001). The direct savings achieved by not transporting the patient to the hospital emergency department were estimated to be 398.5 per patient. CONCLUSION: The emergency medical services guideline for the treatment of hypoglycaemia and the practice of leaving selected patients at the scene after treatment were found to be effective, safe and economical. Patient satisfaction was found to be high, further supporting the practice of not transporting all patients to hospital.

Adolescent↗

Circulating pregnancy-associated plasma protein a predicts outcome in patients with acute coronary syndrome but no troponin I elevation.

BACKGROUND: Risk stratification in troponin (cTn)-negative acute coronary syndrome (ACS) remains a clinical challenge. We investigated the predictive value of circulating pregnancy-associated plasma protein A (PAPP-A), a novel marker of atherosclerotic plaque activity, in these patients. METHODS AND RESULTS: Two hundred consecutive hospitalized ACS patients were included, of whom 136 (69 men and 67 women; mean+/-SD age, 66+/-16 years) remained cTnI-negative for up to 24 hours. PAPP-A was measured at admission, 6 to 12 hours, and 24 hours. During 6-month follow-up, 26 (19.1%) of the cTnI-negative patients reached a primary end point (cardiovascular death, myocardial infarction, or revascularization). At a cutoff level of 2.9 mIU/L, elevated PAPP-A was an independent predictor of adverse outcome (adjusted risk ratio [RR], 4.6; 95% confidence interval, 1.8 to 11.8; P=0.002). Another independent predictor was admission CRP >2.0 mg/L (RR, 2.6; P=0.03). CONCLUSIONS: Measurement of plasma PAPP-A, a zinc-binding matrix metalloproteinase, is a strong independent predictor of ischemic cardiac events and need of revascularization in patients who present with suspected myocardial infarction but remain troponin negative.

Acute Disease↗

Effect of vasopeptidase inhibitor omapatrilat on cardiomyocyte apoptosis and ventricular remodeling in rat myocardial infarction.

We have shown earlier that cardiomyocyte apoptosis continues at a high level late after myocardial infarction and contributes to adverse cardiac remodeling. Here we studied whether this process can be inhibited by the vasopeptidase inhibitor omapatrilat, a drug which causes simultaneous inhibition of both angiotensin converting enzyme and neutral endopeptidase. Our hypothesis was that omapatrilat-treated rats would have less cardiomyocyte apoptosis, and less adverse cardiac remodeling compared to rats treated with selective inhibitors of angiotensin converting enzyme, neutral endopeptidase or placebo. Myocardial infarction was produced by ligation of the left anterior descending coronary artery. Rats were randomized to receive omapatrilat, captopril, neutral endopeptidase inhibitor SQ-28603 or vehicle. Rats treated with omapatrilat and captopril had reduced cardiac BNP mRNA levels and less myocardial fibrosis by comparison with the vehicle-treated rats. However, omapatrilat was more effective than captopril in attenuating hypertrophy as measured by relative cardiac weight (3.0+/-0.2 vs. 3.8+/-0.2 mg/g, P<0.01) or by echocardiographically determined left ventricular mass (0.61+/-0.05 vs. 0.83+/-0.06 g, P<0.01). Myocardial apoptosis was elevated both in the infarction border zone (0.129+/-0.017%) and in the remote area (0.035+/-0.005%) still 4 weeks after myocardial infarction. Angiotensin converting enzyme inhibition proved to be important in the prevention of apoptosis since both omapatrilat and captopril reduced the number of apoptotic myocytes whereas selective neutral endopeptidase inhibitor SQ-28603 had no effect. In conclusion, myocardial apoptosis, remaining increased 4 weeks after myocardial infarction, was reduced by angiotensin converting enzyme inhibition. Vasopeptidase inhibition was more effective than selective angiotensin converting enzyme inhibition in preventing adverse cardiac remodeling after myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗

Neurophysiologic parameters and symptoms in chronic renal failure.

We studied: (1) the sensitivity of various neurophysiologic parameters in the diagnosis of uremic polyneuropathy, (2) the relationship between subjective symptoms and neurophysiologic parameters, and (3) the effect of a single hemodialysis on the neurophysiologic parameters in 21 patients undergoing hemodialysis. The following parameters were studied: sensory and motor nerve conduction, including F-wave parameters; vibration detection thresholds; and thermal thresholds. The clinical findings and subjective symptoms were studied using a standardized questionnaire. The most sensitive parameters in the diagnosis of uremic neuropathy were F-wave parameters from lower limbs, vibration detection thresholds from the feet, and the sural nerve sensory action potential amplitude. The nerves from the upper extremities on the side of the fistula should not be used in the diagnosis of uremic polyneuropathy due to numerous mild local nerve lesions. The positive neuropathic symptoms correlated with quantitative vibratory detection thresholds and sensory nerve conduction studies, especially the amplitude of the sensory nerve action potential in the sural nerve. We found no significant change in any of the neurophysiologic parameters following a single hemodialysis session.

Chronic Disease↗

Soluble tumor necrosis factor receptor levels identify a subgroup of heart failure patients with increased cardiomyocyte apoptosis.

BACKGROUND: We studied whether the presence of cardiomyocyte apoptosis (CA) in explanted failing hearts is related to previous exposure to the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha). METHODS: Serum levels of TNF-alpha and its soluble type two receptors (sTNFRII) were measured with ELISAs in 15 cardiac transplant recipients. CA was quantified with TUNEL assay in the explanted failing hearts and autopsy samples from six normal hearts. RESULTS: The number of CA was significantly higher in explanted failing hearts than in normal hearts (0.041% vs. 0.007%, p<0.01). In heart failure patients, serum TNF-alpha was highly variable and did not correlate with CA. In contrast, serum sTNFRII showed a significant correlation (Pearson's r=0.74, p=0.002) with the amount of CA in explanted hearts. sTNFRII level >4500 pg/ml identified seven patients with 2.7 times higher percentage of CA than the other heart failure patients. CONCLUSION: Increased levels of sTNFRII identify a heart failure patient subgroup with high CA activity.

Apoptosis↗