Exercise training comprising of single 20-s cycle sprints does not provide a sufficient stimulus for improving maximal aerobic capacity in sedentary individuals.

PURPOSE: Sprint interval training (SIT) provides a potent stimulus for improving maximal aerobic capacity ([Formula: see text]), which is among the strongest markers for future cardiovascular health and premature mortality. Cycling-based SIT protocols involving six or more 'all-out' 30-s Wingate sprints per training session improve [Formula: see text], but we have recently demonstrated that similar improvements in [Formula: see text] can be achieved with as few as two 20-s sprints. This suggests that the volume of sprint exercise has limited influence on subsequent training adaptations. Therefore, the aim of the present study was to examine whether a single 20-s cycle sprint per training session can provide a sufficient stimulus for improving [Formula: see text]. METHODS: Thirty sedentary or recreationally active participants (10 men/20 women; mean ± SD age: 24 ± 6 years, BMI: 22.6 ± 4.0 kg m(-2), [Formula: see text]: 33 ± 7 mL kg(-1) min(-1)) were randomised to a training group or a no-intervention control group. Training involved three exercise sessions per week for 4 weeks, consisting of a single 20-s Wingate sprint (no warm-up or cool-down). [Formula: see text] was determined prior to training and 3 days following the final training session. RESULTS: Mean [Formula: see text] did not significantly change in the training group (2.15 ± 0.62 vs. 2.22 ± 0.64 L min(-1)) or the control group (2.07 ± 0.69 vs. 2.08 ± 0.68 L min(-1); effect of time: P = 0.17; group × time interaction effect: P = 0.26). CONCLUSION: Although we have previously demonstrated that regularly performing two repeated 20-s 'all-out' cycle sprints provides a sufficient training stimulus for a robust increase in [Formula: see text], our present study suggests that this is not the case when training sessions are limited to a single sprint.

Acute pontine infarction after percutaneous coronary intervention: a very rare but devastating complication.

A 64-year-old man suffering from an acute posterior wall myocardial infarction underwent primary percutaneous coronary intervention. After several aspiration attempts, tirofiban infusion and pre- and post-dilatation, a bare-metal stent was successfully implanted in the culprit right coronary artery. While the patient did not show any neurological symptoms before or during the procedure, he exhibited hemiplegia and loss of spontaneous speech. Additional magnetic resonance imaging showed an extensive brain stem infarction. This is the first report of a brain stem infarction as a complication of percutaneous coronary intervention.

[Adults with congenital heart disease presenting to the emergency department : Potential pitfalls]. / Erwachsene mit angeborenen Herzfehlern im Notaufnahmedienst : Was ist zu beachten?

The number of adults with congenital heart disease (ACHD) already exceeds the number of children with congenital heart disease in the industrialized world. ACHD patients often show complex pathophysiology and anatomy even after reparative cardiac surgery. In case of complications patients may rapidly deteriorate and become unstable, even when they were asymptomatic or had only mild symptoms before the onset of the complication. Compared to all patients seen by emergency physicians, emergencies in ACHD patients are still rare. This review is aimed to guide management in ACHD emergency situations. Approximately two-thirds of all emergency admissions are caused by arrhythmias or acute heart failure. Sustained arrhythmias may rapidly lead to acute cardiac decompensation in ACHD patients. If medical treatment fails or patients present in hemodynamically unstable conditions, prompt electrical cardioversion is mandatory. Symptomatic bradycardia may require urgent pacemaker implantation. Depending on the underlying heart defect, placement of temporary transvenous pacemaker leads may be impossible. Acute heart failure in ACHD patients is often caused by acute right heart failure. Other more frequent emergencies are infections, syncope, thromboembolic events, and aortic dissection. It is highly recommended to contact the tertiary care center that follows the patient regularly early in case of patient presentation to the emergency room.

Diagnosing ventilator-associated pneumonia (VAP) in UK NHS ICUs: the perceived value and role of a novel optical technology.

BACKGROUND: Diagnosing ventilator-associated pneumonia (VAP) in an intensive care unit (ICU) is a complex process. Our aim was to collect, evaluate and represent the information relating to current clinical practice for the diagnosis of VAP in UK NHS ICUs, and to explore the potential value and role of a novel diagnostic for VAP, which uses optical molecular alveoscopy to visualise the alveolar space. METHODS: Qualitative study performing semi-structured interviews with clinical experts. Interviews were recorded, transcribed, and thematically analysed. A flow diagram of the VAP patient pathway was elicited and validated with the expert interviewees. Fourteen clinicians were interviewed from a range of UK NHS hospitals: 12 ICU consultants, 1 professor of respiratory medicine and 1 professor of critical care. RESULTS: Five themes were identified, relating to [1] current practice for the diagnosis of VAP, [2] current clinical need in VAP diagnostics, [3] the potential value and role of the technology, [4] the barriers to adoption and [5] the evidence requirements for the technology, to help facilitate a successful adoption. These themes indicated that diagnosis of VAP is extremely difficult, as is the decision to stop antibiotic treatment. The analysis revealed that there is a clinical need for a diagnostic that provides an accurate and timely diagnosis of the causative pathogen, without the long delays associated with return of culture results, and which is not dangerous to the patient. It was determined that the technology would satisfy important aspects of this clinical need for diagnosing VAP (and pneumonia, more generally), but would require further evidence on safety and efficacy in the patient population to facilitate adoption. CONCLUSIONS: Care pathway analysis performed in this study was deemed accurate and representative of current practice for diagnosing VAP in a UK ICU as determined by relevant clinical experts, and explored the value and role of a novel diagnostic, which uses optical technology, and could streamline the diagnostic pathway for VAP and other pneumonias.

Large intestinal mast cell count and proteinase expression is associated with larval burden in cyathostomin-infected horses.

REASONS FOR PERFORMING STUDY: Cyathostomins are the principal pathogenic nematode of equidae worldwide. In other species mast cell (MC) proteinases, in particular chymases, appear to have protective roles. Knowledge of the equine intestinal immune response to cyathostomins is limited. OBJECTIVE: To investigate MC numbers and proteinase expression in equine cyathostomin-infected large intestine. HYPOTHESIS: MC populations in the large intestine are positively associated with cyathostomin burden and predominantly express chymase. METHODS: The caecal cyathostomin burden of naturally infected horses (n = 25) was determined by luminal counts and pepsin digest (mural count). MC were identified and enumerated in caecal tissue using toluidine blue (TB). Immunofluorescent labelling with polyclonal rabbit antibodies was used to demonstrate expression of equine tryptase and the chymase equine mast cell proteinase-1 (eqMCP-1) in Carnoy's fixed caecal sections. RESULTS: Significant positive linear relationships were found between TB-stained mucosal and submucosal MC counts and total cyathostomin burden (P<0.001, r² >36%), and both luminal (P<0.010, r² >25%) and mural (P<0.001, r² >36%) larval counts. Similar relationships were found with mucosal and submucosal chymase and tryptase-labelled MC counts (total: P<0.004, r² >29%; luminal: P<0.004, r² >30%; and mural: P<0.030, r² >19%). With all three MC labels, mean MC counts were higher in the submucosa compared to the mucosa (P<0.001). All caecal MC appeared to express chymase, with a small number of MC expressing both tryptase and chymase. CONCLUSIONS AND POTENTIAL RELEVANCE: Large intestinal MC counts are significantly associated with cyathostomin burden, with a predominance of chymase-positive MC. The burden is significantly associated with expression of MC proteinases, supporting their likely involvement in the intestinal immune response to cyathostomin infection. Further work to investigate the kinetics of proteinase expression, the possibility of differential proteinase expression and the role of these MC proteinases is warranted.

Clinical evaluation of 2 flowable composites.

OBJECTIVE: This study evaluated the clinical efficacy of 2 flowable resin composites used to restore occlusal carious lesions. Tetric Flow (Vivadent) and Esthet-X Flow (Dentsply/Caulk) are resin composites with decreased filler loading and lower viscosity compared to conventional resin composites. METHOD AND MATERIALS: Sixty occlusal restorations (30 of each material) were placed. After tooth preparation and caries removal, each material was inserted with rubber dam isolation. Prime & Bond NT (Dentsply/Caulk) was used to bond both flowable composites, which were incrementally placed and light-cured for 20 seconds. Each restoration was evaluated at baseline (1 week after restoration placement), 3 months, 6 months, and 1 year for marginal discoloration, secondary caries, anatomic form, retention, polishability, marginal adaptation, and color match. Groups were compared at 1 year and the data analyzed statistically with a .05 level of significance. RESULTS: A marginally significant difference in color match was observed at 1 year (favoring Esthet-X Flow). No other differences were observed between materials. Marginal discoloration significantly worsened for all restorations at 6 months and 1 year, and marginal adaptation significantly worsened at 1 year for all restorations. A positive association between preparation size and sensitivity was detected at 3 months; no association was found at 6 months and 1 year. At 1 year, restoration size was positively associated with marginal adaptation. Despite some changes from baseline, all restorations were clinically acceptable at 1 year. CONCLUSION: Although flowable resin composites are advocated for occlusal restorations, it is recommended that they be limited to small and moderate-sized restorations.

[Technical feasibility of the implantation of a monorail stent system into the renal arteries without pre-dilatation]. / Technische Machbarkeit der Implantation eines Monorail-Stent-Systems in die Nierenarterien ohne vorherige Dilatation.

PURPOSE: To evaluate the technical feasibility of the implantation of the monorail RX Herculink system into the renal arteries without pre-dilatation. MATERIALS AND METHODS: Forty-two patients (mean age 71 years) from four centers with a total of 44 renal artery stenoses underwent implantation of the RX Herculink stent. The mean grade of the stenosis was 83.8 %, the mean length 7.5 mm. The stenoses were ostial in 38 cases and in immediate proximity to the ostium in 6 cases. The mean follow-up-period was 57 weeks (24 - 176 weeks). RESULTS: In 42 cases, the implantation was successful without pre-dilatation. In 2 cases, pre-dilatation was carried out. In none of the cases, detachment of the stent from the balloon was observed. In one stenosis with a length of 17 mm, implantation of two stents was performed. In 9 cases, post-dilatation with a larger balloon or higher balloon pressure was necessary. Residual stenoses exceeding 30 % were not observed. Two patients developed local bleeding at the puncture site. During the follow-up, restenoses were observed in 5 stents after 26 to 126 weeks, which necessitated a second intervention in 3 cases (PTA in 2 cases, re-stenting in 1 case). The primary patency rate after 6 and 12 months was 0.92 +/- 0.056 according to Kaplan-Meier, the secondary patency rate after 6 and 12 months was 1.0 +/- 0.0. CONCLUSION: Implantation of the RX Herculink stent system into the renal arteries without pre-dilatation is technically feasible and safe. Even without pre-dilatation, the stent-system can be advanced through the stenosis without detachment. The complication rate is low. Our clinical results are comparable to previous studies.

Hypoxia induces heat shock protein expression in human coronary artery bypass grafts.

OBJECTIVE: Heat shock proteins (HSPs) are molecular chaperones which are essential for cell survival. Heat shock and hypoxia markedly increase the expression of several HSPs in various tissues, i.e. heart. In our in vitro study, we investigated whether HSPs are inducible in human vessels which are used as coronary artery bypass grafts. METHODS: We used remnants of the saphenous vein and the internal mammary artery from 34 patients undergoing coronary artery bypass surgery. Each vessel was divided into segments, one for control conditions at 37 degrees C (5% CO(2)-95% air), the remaining ones for thermal (30 min at 42 degrees C) or hypoxic treatment (6 h oxygen deprivation with nitrogen). The expression of Hsp60, Hsp72 and Hsp73 was investigated by immunohistochemistry and Western-blot analysis. RESULTS: Compared to controls, segments of the saphenous vein undergoing heat treatment showed significantly increased expression of Hsp72 in the intima (P=0.035) and Hsp73 in the media (P=0.003). In the internal mammary artery, Hsp72 and Hsp73 were expressed in the intima at significantly higher levels (P=0.042 each). A 6 h oxygen deprivation with nitrogen resulted in elevated levels of Hsp60 (media: P=0.048), of Hsp72 (intima: P<0.001 and media: P=0.004) and of Hsp73 (intima: P=0.029) in the saphenous vein. In the internal mammary artery, Hsp73 expression was significantly enhanced (intima: P=0.048 and media: P=0.017). The results were confirmed by Western-blot analysis in representative veins. CONCLUSIONS: These findings demonstrate the common cellular defense mechanism of HSP expression in response to stress in coronary artery bypass grafts. Hypoxia and heat treatment strongly induce Hsp72 and Hsp73 expression in human coronary artery bypass grafts.

Mouse model of myocardial remodelling after ischemia: role of intercellular adhesion molecule-1.

OBJECTIVE: We studied the effects of temporary myocardial ischemia and reperfusion on myocyte injury and ventricular remodelling in wildtype and intercellular adhesion molecule-1- (ICAM-1) deficient mice. METHODS: ICAM-1-/- and ICAM-1+/+ mice were subjected to 30 min of myocardial ischemia and subsequent reperfusion for 2 h, 1 week and 3 weeks, respectively. The evaluation of tissue damage and scar size was performed with histological sections stained with hematoxilin and eosin. Serum levels of troponin T, creatine kinase and lactate dehydrogenase isoenzyme 1 were evaluated as an index of cardiac cellular damage. Immunohistological analysis was employed to determine cell compositions in ischemic regions. RESULTS: After myocardial ischemia (30 min) and 2 h reperfusion, elevation in serum troponin T, creatine kinase and lactate dehydrogenase isoenzyme 1 were found in both groups, but significantly reduced in ICAM-1-/- mice compared with wildtype mice (P<0.05). Absence of a functional ICAM-1 gene in ICAM-1-/- mice resulted in a marked reduction of ischemia-reperfusion injury at the early stage. The damage score and size of the infarct area were lower in ICAM-1 -/- mice by 30 min of ischemia and 2 h of reperfusion (1.4+/-0.54 vs. 2.4+/-0.47, P<0.05). The percentage of MAC-1-positive cells in the ischemic region and the border zone was also significantly diminished in groups of ICAM-1-/- mice. Surprisingly, the scar size in ventricles in animals 1 or 3 weeks after ischemia was similar between ICAM-1-/- and ICAM-1+/+ mice, although the number of infiltrated MAC-1 positive cells in the scar in wildtype mice was higher. CONCLUSION: Our results demonstrate that the absence of ICAM-1 expression results in less myocardial damage induced by ischemia-reperfusion at the early stage, but does not influence the size of myocardial infarction and scar formation.

Stenting for Emergency Colorectal Obstruction: An Analysis of 204 Patients in Relation to Predictors of Failure and Complications.

BACKGROUND AND AIMS: Self-expanding metallic stents are increasingly used in the management of malignant and benign colorectal obstructions. We aimed to identify relevant predictive factors for stent failure and stent-related complications. MATERIAL AND METHODS: We conducted a retrospective single-center analysis of 204 consecutive patients who underwent emergency colorectal stenting procedures because of symptomatic bowel obstructions from 1996 to 2011 at the Sisters of Charity Hospital Linz, Austria. RESULTS: A total of 204 patients (median age 74 years) with 36 (17.7%) benign and 168 (82.3%) malignant obstructions were included in the study. Technical success was achieved in 92.5% and clinical success in 86.8% of the cases. Major complications occurred in 2.9% and minor ones in 19.6%. Overall mortality during a median follow-up period of 4.3 years was 73% (149 patients). Relevant predictors of increased risk of complications were extracolonic obstruction (p = 0.001), complete obstruction (p = 0.066), and inflammatory bowel disease (p = 0.05). Stent localization at the splenic flexure, a stenosis of >8 cm in length, and the need for endoscopic guidance were associated with higher rates of technical and/or clinical stenting failure. CONCLUSION: Colorectal stenting is less invasive than other means of emergency treatment for large bowel obstruction; it is generally safe and effective in different types of colorectal obstruction. However, relevant rates of failure and complications were recorded and predictors could be determined.

Early detection of acute myocardial infarction by measurement of mass concentration of creatine kinase-MB.

The diagnostic sensitivity and performance of immunoenzymometric measurements of creatine kinase (CK)-MB mass concentrations in the early diagnosis of acute myocardial infarction (AMI) were examined and compared with the sensitivities and performances of CK and CK-MB activity, in the context of simultaneous measurements of CK, CK-MB activity, and CK-MB mass concentrations in serially drawn blood samples obtained immediately from 36 patients with AMI and 126 patients with chest pain on admission to the emergency room of the department of internal medicine. In the 36 patients with AMI, who were all admitted no later than 4 hours after the onset of chest pain, pathologic increase occurred significantly earlier in CK-MB mass than in both CK and CK-MB activity, with a median difference of 1 hour each. In patients coming to the emergency room (51 with AMI, 51 with angina pectoris and 24 with chest pain not related to coronary artery disease), CK-MB mass was the best diagnostic measurement for AMI of all markers tested (significantly higher efficiency, Youden index and likelihood ratio than both CK and CK-MB activity). Before initiating thrombolytic therapy, the sensitivity of CK-MB mass is significantly higher than CK-MB activity during the 0- to 6-hour period and significantly higher than CK activity during the 2- to 4-hour period after the onset of chest pain. Consequently, it is often possible to diagnose an AMI on the basis of increased CK-MB mass concentrations even at a time when CK and CK-MB activities are still within the reference interval.

Early and rapid diagnosis of perioperative myocardial infarction in aortocoronary bypass surgery by immunoturbidimetric myoglobin measurements.

STUDY OBJECTIVES: To evaluate measurements of myoglobin in the diagnosis of perioperative myocardial tissue damage in aortocoronary bypass surgery. A new immunoturbidimetric myoglobin assay, which yields quantitative concentrations of myoglobin within approximately 1 min, was used. DESIGN: Prospective clinical study. PATIENTS: Thirty-two patients scheduled for elective aortocoronary bypass surgery. MEASUREMENTS AND RESULTS: Myoglobin concentrations in patients without perioperative myocardial infarction (n = 27) increased with aortic unclamping, peaked after 1 h, and decreased to almost baseline values within 4 h. By contrast, myoglobin concentrations in patients with perioperative myocardial infarction (n = 5) further increased after 1 h of aortic unclamping and were significantly higher (p < 0.05) than in patients without myocardial infarction as soon as 3 h after aortic unclamping. In all patients with myocardial infarction, myoglobin concentrations exceeded 400 micrograms/L over a minimum period of 4 h. Ten of 27 patients without perioperative myocardial infarction had episodes of minor perioperative myocardial ischemia (defined as ST-T segment changes in the ECG without a concomitant increase in the activity of creatine kinase isoenzyme MB). Myoglobin concentrations (but not creatine kinase isoenzyme MB activity) were significantly higher in these 10 patients when compared to the 17 completely uneventful cases. CONCLUSIONS: Plasma concentrations of myoglobin are a sensitive marker of perioperative myocardial tissue damage in aortocoronary bypass surgery. Myoglobin measurements with the immunoturbidimetric assay have an important contribution to make to the early and rapid diagnosis of perioperative myocardial infarction.

A decision tree for the early diagnosis of acute myocardial infarction in nontraumatic chest pain patients at hospital admission.

STUDY OBJECTIVE: To find an accurate algorithm for the diagnosis of acute myocardial infarction in nontraumatic chest pain patients on presentation to the emergency department. DESIGN: In a prospective clinical study, we compared the diagnostic performances of clinical symptoms, presenting ECG, creatinine kinase, creatine kinase MB activity and mass concentration, myoglobin, and cardiac troponin T test results of hospital admission blood samples. By classification and regression trees, a decision tree for the diagnosis of acute myocardial infarction was developed. SETTING: Emergency room of a Department of Internal Medicine (University Hospital). PATIENTS: One hundred fourteen nontraumatic chest pain patients (median delay from onset of chest pain to hospital admission, 3 h; range, 0.33 to 22): 26 Q-wave and 19 non-Q-wave myocardial infarctions, 49 patients with unstable angina pectoris, and 20 patients with chest pain caused by other diseases. MEASUREMENTS AND RESULTS: Of each parameter taken by itself, the ECG was tendentiously most informative (areas under receiver operating characteristic plots: 0.87 +/- 0.04 [ECG], 0.80 +/- 0.08 [myoglobin], 0.80 +/- 0.04 [creatine kinase MB mass], 0.77 +/- 0.04 [creatine kinase activity], 0.69 +/- 0.06 [clinical symptoms] 0.67 +/- 0.06 [creatine kinase MB activity], 0.67 +/- 0.05 [troponin T]). In patients presenting 3 h or less after the onset of chest pain, ECG signs of acute transmural myocardial ischemia were the best discriminator between patients with and without myocardial infarction. In patients presenting more than 3 h, however, creatine kinase MB mass concentrations (discriminator value, 6.7 micrograms/L) were superior to the ECG, clinical symptoms, and all other biochemical markers tested. This algorithm for diagnosing acute myocardial infarction was superior to each parameter by itself and was characterized by 0.91 sensitivity, a 0.90 specificity, a 0.90 positive and negative predictive value, and a 0.90 efficiency. CONCLUSIONS: We found an algorithm that could accurately separate the myocardial infarction patients from the others on admission to the emergency department. Therefore, this classifier could be a valuable diagnostic aid for rapid confirmation of a suspected myocardial infarction.

Effects of exercise on plasma myosin heavy chain fragments and MRI of skeletal muscle.

The effects of a single series of high-force eccentric contractions involving the quadriceps muscle group (single leg) on plasma concentrations of muscle proteins were examined as a function of time, in the context of measurements of torque production and magnetic resonance imaging (MRI) of the involved muscle groups. Plasma concentrations of slow-twitch skeletal (cardiac beta-type) myosin heavy chain (MHC) fragments, myoglobin, creatine kinase (CK), and cardiac troponin T were measured in blood samples of six healthy male volunteers before and 2 h after 70 eccentric contractions of the quadriceps femoris muscle. Screenings were conducted 1, 2, 3, 6, 9, and 13 days later. To visualize muscle injury, MRI of the loaded and unloaded thighs was performed 3, 6, and 9 days after the eccentric exercise bout. Force generation of the knee extensors was monitored on a dynamometer (Cybex II+) parallel to blood sampling. Exercise resulted in a biphasic myoglobin release profile, delayed CK and MHC peaks. Increased MHC fragment concentrations of slow skeletal muscle myosin occurred in late samples of all participants, which indicated a degradation of slow skeletal muscle myosin. Because cardiac troponin T was within the normal range in all samples, which excluded a protein release from the heart (cardiac beta-type MHC), this finding provides evidence for an injury of slow-twitch skeletal muscle fibers in response to eccentric contractions. Muscle action revealed delayed reversible increases in MRI signal intensities on T2-weighted images of the loaded vastus intermedius and deep parts of the vastus lateralis. We attributed MRI signal changes due to edema in part to slow skeletal muscle fiber injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Skeletal troponin I as a marker of exercise-induced muscle damage.

The utility of skeletal troponin I (sTnI) as a plasma marker of skeletal muscle damage after exercise was compared against creatine kinase (CK), myoglobin (Mb), and myosin heavy chain (MHC) fragments. These markers were serially measured in normal physical education teacher trainees after four different exercise regimens: 20 min of level or downhill (16% decline) running (intensity: 70% maximal O2 uptake), high-force eccentric contractions (70 repetitions), or high-force isokinetic concentric contractions of the quadriceps group (40 repetitions). Eccentrically biased exercise (downhill running and eccentric contractions) promoted greater increases in all parameters. The highest plasma concentration were found after downhill running (median peaks: 309 U/l CK concentration (-CK-)), 466 microgram/l Mb concentration (-Mb-), 1,021 microU/l MHC concentration (-MHC-), and 27.3 microgram/l sTnI concentration ([sTnI]). Level running produced a moderate response (median peaks: 178 U/l -CK-, 98 microgram/l -Mb-, 501 microU/l -MHC-, and 6.6 microgram/l [sTnI]), whereas the concentric contraction protocol did not elicit significant changes in any of the markers assayed. sTnI increased and peaked in parallel to CK and stayed elevated (>2.2 microgram/l) for at least 1-2 days after exercise. In contrast to MHC, sTnI is an initial, specific marker of exercise-induced muscle injury, which may be partly explained by their different intracellular compartmentation with essentially no (MHC <0.1%) or a small soluble pool (sTnI: median 3.4%).

Myocardial damage after minimally invasive coronary artery bypass grafting on the beating heart.

BACKGROUND: In conventional coronary artery bypass grafting, the rate of perioperative myocardial infarction is reported in the 2% to 6% range; however, significantly higher rates are observed if sensitive myocardial marker proteins are used to detect perioperative myocardial damage. For minimally invasive direct coronary artery bypass grafting, few data are available concerning myocardial marker protein release. METHODS: Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 +/- 8.5 years) received minimally invasive direct coronary artery bypass grafting procedures via minithoracotomy on the beating heart. Electrocardiography and transesophageal and transthoracic echocardiography as well as determination of creatine kinase-MB mass concentration and cardiac troponin I level were used for ischemic monitoring. RESULTS: One patient had a perioperative myocardial infarction according to standard criteria and died despite mechanical circulatory support. Determination of cardiac troponin I level showed small but definitive ischemic damage in 4 of 9 patients (44%) who presented transient ischemic signs intraoperatively or postoperatively. In 2 of these 4 patients pathologic findings could be detected on angiographic restudies. CONCLUSIONS: Subclinical myocardial injury is a common event in minimally invasive coronary artery bypass grafting on the beating heart. Cardiac troponin I could serve as an adequate diagnostic tool for diagnosis of perioperative myocardial infarction in minimally invasive direct coronary artery bypass grafting.

Natriuretic peptides and cyclic guanosine 3',5'-monophosphate in asymptomatic and symptomatic left ventricular dysfunction.

BACKGROUND: Screening for patients with asymptomatic left ventricular dysfunction is of considerable importance because they may benefit from early treatment with angiotensin converting enzyme inhibitors. It has been suggested that atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and cyclic guanosine 3',5'-monophosphate (cGMP) might be useful markers for screening. OBJECTIVE: To compare directly the power of the three immunoreactive forms of ANP (CT-ANP, beta-ANP, NT-ANP) and BNP and cGMP to detect asymptomatic left ventricular dysfunction. METHODS AND RESULTS: Radionuclide ventriculography was used to study left ventricular ejection fraction in 37 patients with asymptomatic left ventricular dysfunction, 32 patients with mild to moderate congestive heart failure, and 38 controls. CT-ANP, NT-ANP, beta-ANP, BNP, and cGMP were measured at rest and 3 minutes after exercise. Plasma BNP was the most sensitive marker for patients with asymptomatic left ventricular dysfunction but it reached only a sensitivity of 58% and a specificity of 76% at rest and a sensitivity of 65% and a specificity of 84% after exercise. Combined measurements of all natriuretic peptides and cGMP did not improve the power to detect asymptomatic left ventricular function above that of a single BNP measurement. CONCLUSIONS: Although natriuretic peptides and cGMP measured at rest and three minutes after ergometry may be useful for monitoring left ventricular dysfunction they are unlikely to be suitable for more general routine screening for completely asymptomatic left ventricular dysfunction.

Skeletal muscle injury induced by eccentric muscle action: muscle proteins as markers of muscle fiber injury.

Muscular overuse after high force eccentric muscle action is associated with structural damage of the contractile apparatus that can be observed as Z-line steaming and myofibrillar disruption. Mechanical stress is the major contributing factor for inducing muscle injury, which initiates a cascade of processes resulting in skeletal muscle damage. Disturbances in Ca2+ homeostasis with elevated intracellular [Ca2+] activates the nonlysomal cysteine protease, calpain. Calpain is assumed to play an important role in triggering the response of skeletal muscle protein breakdown, of inflammatory changes, and of regeneration processes in response to eccentric muscle action. The inflammatory response is attributed to changes in hormone and cytokine levels in blood and skeletal muscle. To assess the amount of skeletal muscle damage, plasma CK activity and plasma myoglobin levels have been widely used as markers for muscle injury. As the cytosolic proteins do not necessarily reflect the amount of structural damage, structurally bound proteins such as myosin heavy chains and troponin have been investigated. This paper briefly reviews the cascade of events causing muscle cell injury after unaccustomed eccentric muscle action and the potential of muscle proteins as markers of skeletal muscle damage.

Cardiac troponin I and troponin T: are enzymes still relevant as cardiac markers?

Creatine kinase (CK) MB and lactate dehydrogenase (LDH) isoenzyme 1 are not heart-specific. By contrast, the regulatory proteins troponin I and troponin T are expressed in three different isoforms, one for slow-twitch skeletal muscle fibers, one for fast-twitch skeletal muscle fibers, and one for cardiac muscle (cTnI, cTnT). cTnI and cTnT are usually not detectable in patients without myocardial damage, which is a prerequisite for high diagnostic performance. After acute myocardial infarction (AMI) cTnI, cTnT, and CKMB mass have a comparable early sensitivity. cTnI and cTnT usually peak in parallel except for patients without reperfusion in whom cTnI peaks about 1 day and cTnT approximately 3-4 days after onset of AMI. Both stay increased for at least 4-5 days. cTnT tends to stay increased longer than cTnI. Because the sensitivities of cTnI and cTnT for myocardial injury are comparable, their specificities are the main topic of current debate. Recent reports on mismatches of cTnI and cTnT in patients with renal failure and myopathy without other evidence for myocardial injury suggest that cTnT could be reexpressed similar to CKMB and LDH-1 in chronically damaged human skeletal muscle. In contrast to cTnT, CKMB, and LDH-1, cTnI is not expressed in skeletal muscle during fetal development. So far, an increase in cTnI has been reported only after myocardial damage. Because of currently higher costs, troponin measurement should be restricted at present to clinical settings that really require their high specificity. Based on its distinct functional association with the metabolism of acute ischemic myocardium and according to initial clinical results, glycogen phosphorylase isoenzyme BB is a promising enzyme for the early detection of ischemic myocardial damage.

Glycogen phosphorylase isoenzyme BB to diagnose ischaemic myocardial damage.

Glycogen phosphorylase isoenzyme BB (GPBB) is a key enzyme of glycogenolysis. Its degree of association with the sarcoplasmatic reticulum glycogenolysis complex depends essentially on the metabolic state of the myocardium. With the onset of tissue hypoxia, when glycogen is broken down, GPBB is converted from a structurally bound into a cytoplasmatic form. Considerable amounts of GPBB are only found in human heart and brain. In the first clinical studies GPBB was the most sensitive marker for the diagnosis of acute myocardial infarction within 4 h of chest pain onset. GPBB also increases early in patients with unstable angina and reversible ST-T alterations in the resting electrocardiogram at hospital admission, which could be useful for risk stratification. GPBB is sensitive for the detection of perioperative ischaemic myocardial damage and infarction in patients undergoing coronary artery bypass grafting. The diagnostic specificity of GPBB in non-traumatic chest pain patients was comparable to creatine kinase MB. These results indicate that GPBB is a sensitive marker for ischaemic myocardial damage.