Thalidomide-induced symptomatic third-degree atrioventricular block.
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Aged↗
Biomedical subjects
S Kääb
Publications and source records attributed to S Kääb.
[Genetics of atrial fibrillation: rare mutations, common variants and clinical relevance?].
Atrial fibrillation (AF) is considered the, by far, the most common arrhythmia of man, affecting millions of patients worldwide. The high socio-economic relevance is due to several severe complications and therefore requires profound scientific research in the field of etiology and treatment options. Atrial fibrillation typically occurs in the older patient who often suffers from a number of underlying diseases that act as predisposing factors. That genetics contribute strongly to this rhythm disorder is therefore not evident at a first glance. However, there are a number of investigations that prove familial accumulation for lone AF. Furthermore it is remarkable that many older patients suddenly develop atrial fibrillation without underlying disease, while others remain in sinus rhythm although suffering from a series of risk factors. Considering all this, genetic interference becomes most probable. Therefore in the recent past remarkable endeavours have been ventured to clarify the genetic basis of both lone AF and AF in the context of underlying diseases. For the former, until now four different genetic loci and three disease genes have been identified as causative. Concerning AF in the general population, mainly studies turning the spotlight on single-nucleotide polymorphisms (SNPs) have been applied. It is assumed that SNPs in disease-causing genes are distributed differentially among healthy and diseased individuals. These differences in frequency have been investigated with case-control studies. Up to now six different genes have been found to be associated with AF, including the genes for angiotensin-converting enzyme, angiotensinogen and several cardiac ion channels. Promising new technologies, especially high-throughput SNP genotyping and the genome wide scan for new candidate genes using chip arrays capable of genotyping up to 500 000 SNPs at a time, will multiply the speed to achieve new results. With that the possibility, approaches to optimize existing therapies and to open up new pathways to treat AF.
Atrial Fibrillation↗
Long QT syndrome. Why does sex matter?
There is increased awareness of the extent to which cardiac function is influenced by gender. One of the most dramatic and potentially lethal differences is that seen in cardiac repolarization reflected in the QT interval of the surface ECG. Gender differences in QT and QTc intervals have been observed to change during the lifetime in the general population. These differences can be explained to a large extent by sex hormone driven differences in gene expression of myocardial ion channels. Numerous studies have shown that women's risk to suffer arrhythmias in the context of QT prolonging drugs is doubled compared to men. For familial long QT syndrome there is no conclusive evidence for gender effects with respect to disease onset or mortality. Only subgroup analysis by genotype demonstrated a higher risk in female patients carrying mutations in the LQT2 locus. Special attention should be given to drug-induced QT prolongation in women.
Adolescent↗
Bioinformatics for medical diagnostics: assessment of microarray data in the context of clinical databases.
MOTIVATION: To identify genes suitable for medical diagnostics microarray data is assessed in the context of clinical databases, which store complex information about the patient phenotype. The wealth of data and lacking standards make it difficult to analyse this kind of data. RESULTS: We present a workflow for exploratory analysis of microarray data together with clinical data consisting of four steps: definition of clinically meaningful research questions in a masterfile, generation of analysis files, selection and characterization of differentially expressed genes, and estimation of classification accuracy. We applied this workflow to large data sets from the field of cardiology and oncology (n~500 patients). Systematic data management of microarray data and clinical data helps to make results more transparent and comparable.
Cardiology↗
Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, I: experimental studies.
Pacing-induced heart failure in the dog recapitulates many of the electrophysiological and hemodynamic abnormalities of the human disease; however, the mechanisms underlying altered Ca2+ handling have not been investigated in this model. We now show that left ventricular midmyocardial myocytes isolated from dogs subjected to 3 to 4 weeks of rapid pacing have prolonged action potentials and Ca2+ transients with reduced peaks, but durations approximately 3-fold longer than controls. To discriminate between action potential effects on Ca2+ kinetics and direct changes in Ca2+ regulatory processes, voltage-clamp steps were used to examine the time constant for cytosolic Ca2+ removal (tauCa). tauCa was prolonged by just 35% in myocytes from failing hearts after fixed voltage steps in physiological solutions (tauCa control, 216+/-25 ms, n=17; tauCa failing, 292+/-23 ms, n=22; P<0.05), but this difference was markedly accentuated when Na+/Ca2+ exchange was eliminated (tauCa control, 282+/-30 ms, n=13; tauCa failing, 576+/-83 ms, n=11; P<0. 005). Impaired sarcoplasmic reticular (SR) Ca2+ uptake and a greater dependence on Na+/Ca2+ exchange for cytosolic Ca2+ removal was confirmed by inhibiting SR Ca2+ ATPase with cyclopiazonic acid, which slowed Ca2+ removal more in control than in failing myocytes. beta-Adrenergic stimulation of SR Ca2+ uptake in cells from failing hearts sufficed only to accelerate tauCa to the range of unstimulated controls. Protein levels of SERCA2a, phospholamban, and Na+/Ca2+ exchanger revealed a pattern of changes qualitatively similar to the functional measurements; SERCA2a and phospholamban were both reduced in failing hearts by 28%, and Na+/Ca2+ exchange protein was increased 104% relative to controls. Thus, SR Ca2+ uptake is markedly downregulated in failing hearts, but this defect is partially compensated by enhanced Na+/Ca2+ exchange. The alterations are similar to those reported in human heart failure, which reinforces the utility of the pacing-induced dog model as a surrogate for the human disease.
Action Potentials↗
Cellular basis of ventricular arrhythmias and abnormal automaticity in heart failure.
The high incidence of sudden death in heart failure may reflect an increased propensity to abnormal repolarization and long Q-T interval-related arrhythmias. If so, cells from failing hearts would logically be expected to exhibit a heightened susceptibility to early afterdepolarizations (EAD). We found that midmyocardial ventricular cells isolated from dogs with pacing-induced heart failure exhibited an increased action potential duration and many more EAD than cells from nonpaced controls; this was the case both under basal conditions (P < 0.01) and after lowering external K(+) concentration ([K(+)](o)) to 2 mM and exposing cells to cesium (3 mM; P < 0.05). An unexpected finding was the occurrence of spontaneous depolarizations (SD, >5 mV) from the resting potential that were not coupled to prior action potentials. These SD were observed in 20% of failing cells (n = 5 of 25) under basal ionic conditions but in none of the normal cells (n = 0 of 27, P < 0.05). The net inward current that underlies SD is not triggered by Ca(2+) oscillations and thus differs fundamentally from the currents that underlie delayed afterdepolarizations. We conclude that cardiomyopathic canine ventricular cells are intrinsically predisposed to EAD and SD. Because EAD have been linked to the pathogenesis of torsade de pointes, our results support the hypothesis that sudden death in heart failure often arises from abnormalities of repolarization. The frequent occurrence of SD points to a novel cellular mechanism for abnormal automaticity in heart failure.
Action Potentials↗
Molecular basis of transient outward potassium current downregulation in human heart failure: a decrease in Kv4.3 mRNA correlates with a reduction in current density.
BACKGROUND: Despite advances in medical therapy, congestive heart failure remains a major cause of death in the developed world. A disproportionate number of the deaths of patients with heart failure are sudden and presumed to be arrhythmic. Heart failure in humans and in animal models is associated with prolongation of the action potential duration (APD), the result of downregulation of K+ currents-prominently, the Ca2+-independent transient outward current (Ito). The mechanism for the reduction of Ito in heart failure is unknown. The K+ channel alpha-subunit Kv4.3, a homolog of the Drosophila Shal family, is most likely to encode all or part of the native cardiac Ito in humans. METHODS AND RESULTS: We used ribonuclease protection assays and whole-cell electrophysiological recording to study changes in the level of Kv4.3 mRNA and Ito in human tissues and isolated ventricular myocytes, respectively. We found that the level of Kv4.3 mRNA decreased by 30% in failing hearts compared with nonfailing controls. Furthermore, this reduction correlated with the reduction in peak Ito density measured in ventricular myocytes isolated from adjacent regions of the heart. There was no significant change in the steady-state level of any other mRNA studied (HERG, Kv1.4, Kir2.1, Kvss1.3, and the alpha1C subunit of the Ca2+ channel). mRNAs encoding Kv1.2, Kv1.5, and Kv2.1 were found in low abundance in human ventricle. CONCLUSIONS: These data provide further support for the hypothesis that Kv4.3 encodes all or part of the native cardiac Ito in humans and that part of the downregulation of this current in heart failure may be transcriptionally regulated.
Action Potentials↗
Loss of cardiac magnesium in experimental heart failure prolongs and destabilizes repolarization in dogs.
OBJECTIVES: We sought to determine whether heart failure results in loss of cardiac magnesium sufficient to alter cellular electrophysiology. BACKGROUND: Free magnesium has numerous intracellular roles affecting metabolism, excitability and RNA synthesis. Total cardiac magnesium content is reduced in heart failure, but it is unclear whether magnesium loss is primary or iatrogenic. Furthermore, it is unknown whether free magnesium levels are affected or whether a change in free magnesium would alter cellular electrophysiology. METHODS: Eight mongrel dogs underwent demand ventricular pacing (VVI) at 250 beats/min for 3 weeks to induce heart failure. Sublingual epithelial magnesium was measured before pacing and at death. Left ventricular myocytes were isolated and loaded with Mag-Indo-1 to measure free magnesium ([Mg2+]i); myocytes from eight normal dogs served as controls. To test whether changes in [Mg2+]i in this range could alter cellular repolarization, current-clamped myocytes were dialyzed with 0.5 or 1.0 mmol/liter MgCl2. RESULTS: Mean sublingual epithelial magnesium fell significantly in the paced animals, from 36.9 +/- 0.5 to 33.9 +/- 0.7 mEq/liter (p < 0.01). Mean cardiac [Mg2+]i was significantly lower in the dogs with heart failure--0.49 +/- 0.06 versus 1.06 +/- 0.15 mmol/liter (p < 0.003). Time to 90% repolarization was significantly shorter in cells dialyzed with 1.0 mmol/liter compared with 0.5 mmol/liter MgCl2 in myocytes from normal dogs or dogs with heart failure (596 +/- 34 vs. 760 +/- 58 ms in normal dogs and 586 +/- 29 vs. 838 +/- 98 ms in dogs with heart failure; p < 0.05 for each). CONCLUSIONS: Experimental heart failure results in both tissue and cardiac magnesium loss in the absence of drug therapy. Free cardiac magnesium is significantly reduced, possibly contributing to abnormal repolarization in heart failure.
Action Potentials↗
Potassium channel down-regulation in heart failure.
Prolongation of action potential duration is the most consistent electrophysiological abnormality in myocardium and myocytes from hypertrophied and failing hearts. Measurements of currents in myocytes from hypertrophied and failing hearts indicate that, in most cases, this is due to a decrease in outward potassium currents. If present, a calcium-independent transient outward current is usually substantially reduced, but delayed rectifier and inward rectifier currents have also been found to be diminished. There is increasing evidence that potassium current down-regulation contributes significantly to the enhanced lability of the repolarization process in heart failure, predisposing to early after-depolarizations, dispersion of repolarization and ventricular arrhythmias. The reduction of outward potassium currents may also be involved in the enhanced sensitivity of failing myocardium to triggering factors like hypokalemia, ischemia, and antiarrhythmic agents with Class III effects. A thorough understanding of the mechanisms of cardiac excitability and arrhythmogenesis at the cellular and molecular level under normal and pathological conditions will be essential for the development of new pharmacological strategies to prevent sudden cardiac death in heart failure.
Action Potentials↗
Repolarization abnormalities, arrhythmia and sudden death in canine tachycardia-induced cardiomyopathy.
OBJECTIVES: This study sought to determine whether the canine model of tachycardia-induced heart failure (HF) is an effective model for sudden cardiac death (SCD) in HF. BACKGROUND: Such a well established HF model that also exhibits arrhythmias and SCD, along with repolarization abnormalities that could trigger them, may facilitate the study of SCD in HF, which still eludes effective treatment. METHODS: Twenty-five dogs were VVI-paced at 250 beats/min for 3 to 5 weeks. Electrocardiograms were obtained, and left ventricular endocardial monophasic action potentials (MAPs) were recorded at six sites at baseline and after HF. Weekly Holter recordings were made with pacing suspended for 24 h. RESULTS: Six animals (24%) died suddenly, one with Holter-documented polymorphic ventricular tachycardia (VT). Holter recordings revealed an increased incidence of VT as HF progressed. Repolarization was significantly (p < 0.05) prolonged, as indexed by a corrected QT interval (mean [+/-SD] 311 +/- 25 to 338 +/- 25 ms) and MAP duration measured at 90% repolarization (MAPD90) (181 +/- 19 to 209 +/- 28 ms), and spatial MAPD90 dispersion rose by 40%. We further tested whether CsCl inhibition of repolarizing K+ currents, which are reportedly downregulated in HF, might preferentially prolong the MAPD90 in HF. With 1 mEq/kg body weight of CsCl, MAPD90 rose by 86 +/- 100 ms in dogs with HF versus only 28 +/- 16 ms in control animals (p = 0.002). Similar disparities in CsCl sensitivity were observed in myocytes isolated from normal and failing hearts. CONCLUSIONS: Tachycardia-induced HF exhibits malignant arrhythmia and SCD, along with prolonged, heterogeneous repolarization and heightened sensitivity to CsCl at chamber and cellular levels. Thus, it appears to be a useful model for studying mechanisms and therapy of SCD in HF.
Animals↗
Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure.
Membrane current abnormalities have been described in human heart failure. To determine whether similar current changes are observed in a large animal model of heart failure, we studied dogs with pacing-induced cardiomyopathy. Myocytes isolated from the midmyocardium of 13 dogs with heart failure induced by 3 to 4 weeks of rapid ventricular pacing and from 16 nonpaced control dogs did not differ in cell surface area or resting membrane potential. Nevertheless, action potential duration (APD) was significantly prolonged in myocytes isolated from failing ventricles (APD at 90% repolarization, 1097 +/- 73 milliseconds [failing hearts, n = 30] versus 842 +/- 56 milliseconds [control hearts, n = 25]; P < .05), and the prominent repolarizing notch in phase 1 was dramatically attenuated. Basal L-type Ca2+ current and whole-cell Na+ current did not differ in cells from failing and from control hearts, but significant differences in K+ currents were observed. The density of the inward rectifier K+ current (IKl) was reduced in cells from failing hearts at test potentials below -90 mV (at -150 mV, -19.1 +/- 2.2 pA/pF [failing hearts, n = 18] versus -32.2 +/- 5.1 pA/pF [control hearts, n = 15]; P < .05). The small outward current component of IKl was also reduced in cells from failing hearts (at -60 mV, 1.7 +/- 0.2 pA/pF [failing hearts] versus 2.5 +/- 0.2 pA/pF [control hearts]; P < .05). The peak of the Ca(2+)-independent transient outward current (Ito) was dramatically reduced in myocytes isolated from failing hearts compared with nonfailing control hearts (at +80 mV, 7.0 +/- 0.9 pA/pF [failing hearts, n = 20] versus 20.4 +/- 3.2 pA/pF [control hearts, n = 15]; P < .001), while the steady state component was unchanged. There were no significant differences in Ito kinetics or single-channel conductance. A reduction in the number of functional Ito channels was demonstrated by nonstationary fluctuation analysis (0.4 +/- 0.03 channels per square micrometer [failing hearts, n = 5] versus 1.2 +/- 0.1 channels per square micrometer [control hearts, n = 3]; P < .001). Pharmacological reduction of Ito by 4-aminopyridine in control myocytes decreased the notch amplitude and prolonged the APD. Current clamp-release experiments in which current was injected for 8 milliseconds to reproduce the notch sufficed to shorten the APD significantly in cells from failing hearts. These data support the hypothesis that downregulation of Ito in pacing-induced heart failure is at least partially responsible for the action potential prolongation. Because the repolarization abnormalities mimic those in cells isolated from failing human ventricular myocardium, canine pacing-induced cardiomyopathy may provide insights into the development of repolarization abnormalities and the mechanisms of sudden death in patients with heart failure.
Action Potentials↗
Reversal of potassium channel deficiency in cells from failing hearts by adenoviral gene transfer: a prototype for gene therapy for disorders of cardiac excitability and contractility.
Heart failure is a common, often lethal disorder in which conventional pharmacologic strategies have achieved limited success. Failing hearts exhibit a delay of electrical repolarization which predisposes to fatal arrhythmias. To explore the feasibility of gene therapy for this condition, we isolated myocytes from normal and failing dog hearts and quantified electrophysiologic and contractile parameters in primary culture. Action potentials were prolonged in failing cells as a result of diminished potassium currents. Exposure to AdShK, an adenovirus that overexpresses potassium channels, reversed the action potential prolongation of failing cells. The precise phenotype varied as a function of the density of expressed channels; modest increases in potassium current sufficed to mimic the non-diseased state most faithfully, while more robust expression of the transgene excessively abbreviated excitation and contraction. Our results demonstrate that viral gene transfer can modify the electrical properties of adult mammalian heart cells in a manner appropriate to reverse a fundamental disorder of excitability. Realistic application of this form of therapy will need to include a sensitive mechanism for control of the level and distribution of transgene expression.
Action Potentials↗
Early sepsis treatment with immunoglobulins after cardiac surgery in score-identified high-risk patients.
In patients at risk for sepsis after cardiac surgery, the efficacy of intravenous immunoglobulin (Ig) treatment was compared with a historical control population, equivalent in patient characteristics and disease severity. Using APACHE II scores, especially in the high-risk group (IgG), we could discriminate between low-risk patients (score < 19; mortality 1 percent) and the small groups at risk (score 19 to 23) and high risk (score > or = 24) with a significantly higher mortality (14 percent and 76 percent, respectively) [corrected]. Subsequently, among 1,341 consecutive patients we prospectively identified and treated (IgG n = 41 IgGMA: n = 25) these at-risk groups. In contrast to controls (risk: n = 21; high-risk; n = 21), we found a marked fall in APACHE II scores, especially in the high-risk group (IgG, n = 26: p < 0.05; IgGMA, n = 13: p = 0.08) [corrected]. In this group, Ig therapy produced higher (p < 0.05) response rates (score decrease 7 within 4 days: IgG: 54 percent, IgGMA: 62 percent; controls: 19 percent) and reduced mortality (IgG: 46 percent, IgGMA: 46 percent; controls: 76 percent), statistically significant (p < 0.05) for Ig treatment overall. Thus, early Ig treatment improves disease severity and may improve prognosis in prospectively score-identified high-risk postcardiac surgical patients.
Aged↗
Pseudomonas sepsis does not cause more severe cardiovascular dysfunction in patients than non-Pseudomonas sepsis.
To evaluate the clinical relevance of the experimental findings of a more severe cardiac depression in Pseudomonas (P.) than in non-P. sepsis, we retrospectively compared the hemodynamic data in 26 patients with P. sepsis (20 cases, single pathogen; six cases, more positive cultures with P. than with non-P. species), and 102 with non-P. sepsis. As in other studies, the left ventricular stroke work index (LVSWI) was used to assess cardiac performance. The two groups (all numbers are means) had a similar disease and sepsis severity profile (P. vs. non-P: septic shock, 81% vs. 87%; APACHE II scores, 29.1 vs. 29.2; Elebute sepsis scores, 18.1 vs. 18.1; mortality, 58% vs. 62%). Preload (pulmonary capillary wedge pressure 15.0 vs. 16.3 mm Hg) and systemic vascular resistance (588 vs 572 dyn.cm-5.sec) were comparable. Cardiac performance displayed no significant difference (LVSWI, 42.8 vs. 38.3 g.m/m2), a result reproduced in the subgroups with culture-proven bacteremia, with or without preexisting cardiovascular disease or septic shock. Thus, our data suggest that there is no difference in the degree of cardiovascular dysfunction in patients with Pseudomonas compared to non-Pseudomonas sepsis of otherwise equivalent disease severity.
Cardiovascular System↗
[Early immunoglobulin therapy in high risk patients for infection after heart surgery].
The efficacy of early supplemental intravenous immunoglobulin G (ivIgG) treatment was investigated in 41 patients at risk for sepsis following cardiac surgery (APACHE II score > or = 19 on the 1st postoperative day). The ivIgG preparation (Psomaglobin N) was chosen because of its reported high antibody titers and effectiveness in animal models against gram-positive microorganisms, preponderant as infective agents after heart surgery. The control group consisted of a historical cohort of 42 cardiac surgical patients of comparable pretreatment disease and sepsis severity. Following ivIgG therapy on the 1st and 2nd days after surgery, we found a marked improvement in disease severity (fall in APACHE II scores) in contrast to the control patients, especially evident in the high-risk group of patients with an APACHE II score > or = 24 on the 1st postoperative day (n = 26). In this group, ivIgG therapy led to higher (p < 0.05) response rates defined as a score decrease > or = 7 within 4 days (ivIgG-treated patients 54%, controls 19%), and a reduction in mortality (ivIgG-treated patients 46%, controls 76%; p = 0.08). Given the good comparability of the study groups, the results of this trial indicate, despite its nonrandomized design, that early supplemental ivIgG treatment seems to decrease disease severity and probably also improve the prognosis in APACHE II score identified high-risk patients after cardiac surgery.
Aged↗
[Early detection of patients at risk for infection after heart surgery].
Since sepsis is a major cause of mortality after cardiac surgery, early identification of the patients at risk of developing septic complications is of considerable importance. In the present study on 110 patients after elective heart surgery, we, therefore, examined scoring systems as well as various single parameters with regard to an early prediction of septic complications. In a first step, the Elebute score definition for postoperative sepsis in general surgery patients (score > or = 12) could be confirmed for cardiac surgery patients as well. Septic complications, defined as an Elebute score > or = 12 on > or = 2 days, occurred in 16 patients and were associated with a significantly worse prognosis than in non-septic patients (mortality 69 vs. 1%). Consequently, other more practicable parameters were investigated: five additional scores (APACHE II, Goris, HIS, SAPS, SSS) were comparable and superior to plasma levels of elastase and neopterin, haemodynamic data, and clinical parameters in predicting septic complications as early as by the 1st postoperative day. For reasons of practicability and availability, the APACHE II score (predictive values: positive 86%, negative 96%, Youden index 0.73; diagnostic cut off point: > or = 19 on the 1st postoperative day) seemed to be best suited. Therefore, this was further investigated within a consecutive prospective study (independent group of 106 patients) which confirmed an APACHE II score > or = 19 as discriminating criterion (mortality 36 vs 0%). Thus, the APACHE II score may be useful for prospective screening, with the intention to treat, of patients after cardiac surgery who are at risk of postoperative septic complications.
Coronary Artery Bypass↗
[The rectus abdominis syndrome].
Three athletes (one female, two males), aged 18-21 years, developed acute abdominal pain, two of them immediately after exercise including abdominal muscle training. The female patient had a pulmonary infection of uncertain cause at the time. The second patient obviously suffered from an allergic or parasitic disease (eosinophilia of 26%). The third patient, a swimmer, had the symptoms in the course of a flu-like infection after drinking about 100 g alcohol. Serum creatinine kinase activity was 7,800-17,500 U/l, making acute muscle damage likely, probably rhabdomyolysis. Ultrasound examination revealed echo-dense areas of the rectus abdominis muscle in two of the patients, in one of them associated with marked muscle swelling. In the third patient ultrasound was unremarkable during a symptom-free interval 8 days after the onset of symptoms. These observations indicate that even during banal infections sport exercise involving special strain on the abdominal musculature should not be undertaken because of the risk of rhabdomyolysis.
Abdominal Muscles↗
Early prediction of septic complications after cardiac surgery by APACHE II score.
In 110 patients admitted to the intensive care unit after cardiac surgery, daily monitoring [clinical parameters, cardiac index (CI), left ventricular stroke work index (LVSWI) and APACHE II score] was performed in regard to its usefulness in the early prediction of septic complications, a major cause of postoperative mortality. Septic complications (defined as Elebute sepsis score of > or = 12 on > or = 2 days) occurred in 16 patients and were associated with a significantly worse prognosis (mortality 69% vs 1%, P < 0.0001) than was seen in patients without sepsis. While preoperative APACHE II score values did not differentiate between the patients with an uneventful postoperative course and those with septic complications, patients who ultimately developed septic complications had significantly (P < 0.001) higher scores as early as on the evening of the operation day ("day 0"). In addition, in contrast to patients without sepsis, whose scores dropped markedly (P < 0.001) between day 0 and day 1, patients with septic complications invariably had high scores. Compared to single parameters (fever, leucocyte count, CI, LVSWI), the APACHE II score proved to be superior in differentiating between patients who developed sepsis and those who did not. A score of 19 or more on the 1st postoperative day had a sensitivity of 75%, a specificity of 98%, a Youden index of 0.73, a positive predictive value of 86%, and a negative predictive value of 96% in regard to prediction of septic complications.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Surgical Procedures↗