Minimal Myocardial Damage Research Articles

A study to observe the association of left ventricular ejection fraction and wall motion score index with duration of early systolic lengthening in patients with non-ST-elevation acute coronary syndrome

Background: Management of non-ST elevation myocardial infarction acute coronary syndrome (NSTEMI ACS) patients is not well defined as that of ST elevation myocardial infarction. The accuracy of results of conventional echocardiography is significantly compromised when imaging is suboptimal, myocardial damage is in small areas, and compensatory hyperkinesias of healthy segment. Aims and Objectives: Duration of early systolic lengthening (DESL) may be employed to identify early myocardial ischemia and thus, may help to prepare treatment strategies for NSTEMI patients. Materials and Methods: A total of 57 patients with NSTEMI ACS attending the cardiology department were included in the study group. Results: More than 80% of patients of NSTEMI have normal or near normal ejection fraction and wall motion score index. In our study, the DESL is prolonged in a significant number of non-ST-elevation acute coronary syndrome patients. Conclusion: As DESL is afterload independent, it is superior to global longitudinal strain in assessing myocardial damage. Several studies including ourselves show that DESL of <50 ms may be the cutoff value to reveal minimal myocardial damage.

Difference between endocardial and epicardial application of pulsed fields for targeting Epicardial Ganglia: An in-silico modelling study

BackgroundPulsed Field Ablation (PFA) has recently been proposed as a non-thermal energy to treat atrial fibrillation by selective ablation of ganglionated plexi (GP) embedded in epicardial fat. While some of PFA-technologies use an endocardial approach, others use epicardial access with promising pre-clinical results. However, as each technology uses a different and sometimes proprietary pulse application protocol, the comparation between endocardial vs. epicardial approach is almost impossible in experimental terms. For this reason, our study, based on a computational model, allows a direct comparison of electric field distribution and thermal-side effects of both approaches under equal conditions in terms of electrode design, pulse protocol and anatomical characteristics of the tissues involved. Methods2D computational models with axial symmetry were built for endocardial and epicardial approaches. Atrial (1.5−2.5 mm) and fat (1−5 mm) thicknesses were varied to simulate a representative sample of what happens during PFA ablation for different applied voltage values (1000, 1500 and 2000 V) and number of pulses (30 and 50). ResultsThe epicardial approach was superior for capturing greater volumes of fat when the applied voltage was increased: 231 mm3/kV with the epicardial approach vs. 182 mm3/kV with the endocardial approach. In relation to collateral damage to the myocardium, the epicardial approach considerably spares the myocardium, unlike what happens with the endocardial approach. Although the epicardial approach caused much more thermal damage in the fat, there is not a significant difference between the approaches in terms of size of thermal damage in the myocardium. ConclusionsOur results suggest that epicardial PFA ablation of GPs is more effective than an endocardial approach. The proximity and directionality of the electric field deposited using an epicardial approach are key to ensuring that higher electric field strengths and increased temperatures are obtained within the epicardial fat, thus contributing to selective ablation of the GPs with minimal myocardial damage.

Computational Model for Therapy Optimization of Wearable Cardioverter Defibrillator: Shockable Rhythm Detection and Optimal Electrotherapy.

Wearable cardioverter defibrillator (WCD) is a life saving, wearable, noninvasive therapeutic device that prevents fatal ventricular arrhythmic propagation that leads to sudden cardiac death (SCD). WCD are frequently prescribed to patients deemed to be at high arrhythmic risk but the underlying pathology is potentially reversible or to those who are awaiting an implantable cardioverter-defibrillator. WCD is programmed to detect appropriate arrhythmic events and generate high energy shock capable of depolarizing the myocardium and thus re-initiating the sinus rhythm. WCD guidelines dictate very high reliability and accuracy to deliver timely and optimal therapy. Computational model-based process validation can verify device performance and benchmark the device setting to suit personalized requirements. In this article, we present a computational pipeline for WCD validation, both in terms of shock classification and shock optimization. For classification, we propose a convolutional neural network-“Long Short Term Memory network (LSTM) full form” (Convolutional neural network- Long short term memory network (CNN-LSTM)) based deep neural architecture for classifying shockable rhythms like Ventricular Fibrillation (VF), Ventricular Tachycardia (VT) vs. other kinds of non-shockable rhythms. The proposed architecture has been evaluated on two open access ECG databases and the classification accuracy achieved is in adherence to American Heart Association standards for WCD. The computational model developed to study optimal electrotherapy response is an in-silico cardiac model integrating cardiac hemodynamics functionality and a 3D volume conductor model encompassing biophysical simulation to compute the effect of shock voltage on myocardial potential distribution. Defibrillation efficacy is simulated for different shocking electrode configurations to assess the best defibrillator outcome with minimal myocardial damage. While the biophysical simulation provides the field distribution through Finite Element Modeling during defibrillation, the hemodynamic module captures the changes in left ventricle functionality during an arrhythmic event. The developed computational model, apart from acting as a device validation test-bed, can also be used for the design and development of personalized WCD vests depending on subject-specific anatomy and pathology.

Electroporation of epicardial autonomic ganglia: Safety and efficacy in medium-term canine models.

Endocardial radiofrequency ablation of epicardial ganglionic plexus (GP) for atrial fibrillation (AF) is complicated by myocardial damage. We hypothesized that an epicardial approach with a novel nitinol catheter system capable of causing irreversible electroporation (IRE) with direct current (DC) could selectively and permanently destroy GP without collateral myocardial injury. Acute studies and medium-term terminal studies (mean survival, 1137 days) were performed with seven dogs. In the acute studies, DC was used to target epicardial GP within the transverse sinus, oblique sinus, vein of Marshall, and right periaortic space. Successful electroporation was defined as the presence of ablative lesions in the GP without collateral myocardial damage. A four-point integer system was used to classify histologic changes in tissue harvested from the ablation sites. Atrial effective refractory period (AERP) was measured during the acute and medium-term studies. For six dogs in the medium-term studies, the postablation period was uneventful without complications. Lesions were successfully created at 20 of 21 sites (95.2%) with more than minimal myocardial damage in one dog. An increase in AERP occurred in both atria during the acute studies but was maintained only in the right atrium at medium-term follow-up (5032 milliseconds). No dog had damage to the esophagus, adjacent great arteries, or pulmonary veins. This proof-of-concept study suggests that safe, effective, and selective epicardial ablation of GP can be performed with DC by IRE with minimal collateral myocardial damage.

Pacemaker Implantation Associated Myocardial Micro-Damage: A Randomised Comparison between Active and Passive Fixation Leads

Fixation of the pacemaker leads during pacemaker implantation leads to an increase of cardiac Troponin T (cTnT) that can be interpreted as a sign of minimal myocardial damage. This trial evaluates whether the mechanism type of lead fixation influences the magnitude of cTnT release. Patients having a de-novo cardiac pacemaker implantation or a lead revision were centrally randomized to receive either a ventricular lead with an active (screw) or passive (tine) fixation mechanism. High-sensitive Troponin T (hsTnT) was determined on the day of the procedure beforehand and on the following day. 326 Patients (median age (IQR) 75.0 (69.0–80.0) years, 64% male) from six international centers were randomized to receive ventricular leads with an active (n = 166) or passive (n = 160) fixation mechanism. Median (IQR) hsTnT levels increased by 0.009 (0.004–0.021) ng/ml in the group receiving screw-in ventricular leads and by 0.008 (0.003–0.030) ng/ml in the group receiving tined ventricular leads (n.s.). In conclusion pacemaker implantations are followed by a release of hsTnT. The choice between active or passive fixation ventricular leads does not have a significant influence on the extent of myocardial injury and the magnitude of hsTnT release.

Troponin T elevation after permanent pacemaker implantation.

The objective of the study is to study the incidence, significance, and factors associated with cardiac troponin T (CTNT) elevation after pacemaker implantation. Three hundred seventy-four patients (104 single-chamber pacemakers or ICD, 243 dual-chamber pacemakers, and 27 cardiac resynchronization therapy/cardiac resynchronization therapy defibrillator) who had normal levels of CTNT at baseline and underwent implantation of a permanent pacemaker system were included in this study. Serum levels of CTNT were measured at baseline, 6 and 24h after the implantation procedure. The median of CTNT levels increased from 0.012ng/mL at baseline to 0.032 and 0.019ng/mL at 6 and 24h after the procedure, respectively (all p<0.0001). Elevated CTNT levels were noted in 208 patients (55.6%) at 6h after the implantation, among which 29 patients (7.8%) had CTNT levels exceeding the range of minimal myocardial damage (>0.09ng/mL). After 1-year follow-up, the incidence of complications including dislodgement of the lead, pocket infection, pneumothorax, hemothorax, and vein thrombus and cardiac outcomes including hospitalization of heart failure, coronary artery disease, arrhythmia, and cardiovascular mortality was not significantly different between the normal and elevated CTNT groups at 6h after the procedure. By logistic regression analysis, gender, N-terminal pro-B type natriuretic peptide (NT-pro-BNP) at baseline, left ventricular ejection fractions (LVEF), estimated glomerular filtration rate (eGFR), and fluoroscopy time were independently associated with CTNT elevation after adjusted for age, pacemaker types, right ventricle lead location (RVA or RVOT), heart function, and left ventricular end systolic dimension. Pacemaker implantation was found to be accompanied with CTNT elevation in 55.6% of the patients at 6h after the procedure, and its kinetics were fast, which might not be related to the complications and adverse cardiac outcomes within 1year of follow-up. Moreover, gender, NT-pro-BNP at baseline, LVEF, eGFR, and fluoroscopy time were found to be independent predictors of CTNT elevation.

DEVELOPMENT OF TRANSMYOCARDIAL LASER REVASCULARIZATION IN PATIENTS WITH ISCHEMIC HEART DISEASE

The use of laser radiation in cardiac surgery allows to provide more effective and targeted care for patients with ischemic heart disease. The article summarizes the multistage teamwork of several research centers in Tomsk on determination of the most effective type of laser and techniques of cardiac surgery using lasers. The study had an experimental and a clinical phase. In the experimental phase, effectiveness of various laser types for indirect laser myocardial revascularization was assessed, including carbon dioxide, neodymium, and a semiconductor laser types. During clinical phase, efficacy of clinical use of semiconductor laser in various timepoints after surgery was evaluated. The experimental phase revealed that semiconductor laser provides the best neoangiogenesis efficiency, minimal myocardial damage and ease of use. During clinical phase, its safety for a patient was established and a significant clinical benefit was observed.

Early systolic lengthening may identify minimal myocardial damage in patients with non-ST-elevation acute coronary syndrome

Ischaemic myocardial segments tend to stretch as the intraventricular pressure rises steeply during the isovolemic contraction phase, before they contract during ejection. We hypothesized that the time they remain stretched, called duration of early systolic lengthening (DESL), correlates with final infarct size as defined by contrast enhanced magnetic resonance imaging (CE-MRI). We also assessed whether DESL could identify patients with acute coronary occlusion, and compared it with traditional measures for myocardial function. In this retrospective study, 150 consecutive patients with Non-ST-elevation acute coronary syndrome (NSTE-ACS) referred for coronary angiography were included. Speckle tracking echocardiography was performed prior to angiography to determine DESL. The final infarct size was quantified at follow-up 9 ± 3 months after initial admission in 61 patients and echocardiography performed in 143 patients. DESL showed good correlation with the final infarct size (r = 0.67, P < 0.001). Thirteen patients had no visible sign of infarct on CE-MRI (minimal myocardial damage), and DESL was significantly shorter in these patients than in patients with signs of infarct (27 ± 19 vs. 84 ± 41 ms, P < 0.001). Compared with left ventricular ejection fraction, wall motion score index, and global longitudinal strain, DESL showed the best accuracy in detecting patients with minimal myocardial damage, with an area under the receiver operating characteristic curve of 0.92 (0.82 to 0.99, P < 0.001). DESL was more prolonged in patients with coronary occlusions, compared with those without occlusions (86 ± 45 vs. 63 ± 31 ms, P < 0.01). DESL was significantly shorter at follow-up, compared with baseline (P = 0.04). DESL could identify patients with minimal myocardial damage, differentiate between occlusion and non-occlusion, and may be helpful in the risk stratification of patients with NSTE-ACS.

EARLY SYSTOLIC LENGTHENING MAY IDENTIFY MINIMAL MYOCARDIAL DAMAGE IN PATIENTS WITH NON ST-ELEVATION ACUTE CORONARY SYNDROME

Aims Ischaemic myocardial segments tend to stretch as the intraventricular pressure rises steeply during the isovolemic contraction phase, before they contract during ejection. We hypothesized that the time they remain stretched, called duration of early systolic lengthening (DESL), correlates with final infarct size as defined by contrast enhanced magnetic resonance imaging (CE-MRI). We also assessed whether DESL could identify patients with acute coronary occlusion, and compared it with traditional measures for myocardial function. Methods and results In this retrospective study, 150 consecutive patients with Non-ST-elevation acute coronary syndrome (NSTE-ACS) referred for coronary angiography were included. Speckle tracking echocardiography was performed prior to angiography to determine DESL. The final infarct size was quantified at follow-up 9 ± 3 months after initial admission in 61 patients and echocardiography performed in 143 patients. DESL showed good correlation with the final infarct size ( r = 0.67, P < 0.001). Thirteen patients had no visible sign of infarct on CE-MRI (minimal myocardial damage), and DESL was significantly shorter in these patients than in patients with signs of infarct (27 ± 19 vs. 84 ± 41 ms, P < 0.001). Compared with left ventricular ejection fraction, wall motion score index, and global longitudinal strain, DESL showed the best accuracy in detecting patients with minimal myocardial damage, with an area under the receiver operating characteristic curve of 0.92 (0.82 to 0.99, P < 0.001). DESL was more prolonged in patients with coronary occlusions, compared with those without occlusions (86 ± 45 vs. 63 ± 31 ms, P < 0.01). DESL was significantly shorter at follow-up, compared with baseline ( P = 0.04). Conclusions DESL could identify patients with minimal myocardial damage, differentiate between occlusion and non-occlusion, and may be helpful in the risk stratification of patients with NSTE-ACS.

Usefulness of high-sensitivity troponin T for the evaluation of patients with acute chest pain and no or minimal myocardial damage

Although high-sensitivity troponins allow early diagnosis of acute myocardial infarction, their role for identification of acute coronary syndrome in patients with normal conventional troponin remains unclear. A total of 446 patients presenting to the emergency department with chest pain and normal troponin (common practice assays) in 2 serial samples were included. Both samples were also centrally analyzed for high-sensitivity troponin T (hs-TnT) (Roche Diagnostics, Basel, Switzerland). Detection (>3 ng/L) and 99th percentile (≥ 14 ng/L) cutoffs of the maximum hs-TnT levels (hs-TnTmax) were considered. The end points were acute coronary syndrome diagnosis and the composite of in-hospital revascularization or 30-day cardiac events. Acute coronary syndrome was adjudicated to 84 patients (19%), and 62 (14%) had the composite end point. In univariate setting, hs-TnTmax >3 ng/L exhibited high sensitivity (87% and 92%, respectively) and negative predictive value (93% and 97%) for both end points, whereas hs-TnTmax ≥ 14 ng/L provided high specificity (90% and 89%), although low positive predictive values (40% and 33%). After adjusting for clinical (pain characteristics and risk factors) and electrocardiographic data, there was a stepped increase of risk across hs-TnTmax categories (≤ 3, >3 but <14, and ≥ 14 ng/L) for both end points; however, the discriminative capacity added was marginal (integrated discrimination improvement of 2.6% and 3.5%, respectively). Clinical and electrocardiographic data remain the most important tools for the evaluation of patients with chest pain and with no or minimal myocardial damage. The main contribution of hs-TnT is the high negative predictive value of undetectable levels (≤ 3 ng/L).

Usefulness of Mean Platelet Volume as a Biomarker for Long-Term Outcomes After Percutaneous Coronary Intervention

Larger size platelets have enhanced reactivity. The mean platelet volume (MPV) is a marker of platelet activation and is usually measured as part of blood testing. The aim of the present study was to investigate the utility of the MPV as a biomarker in prognosticating the long-term outcomes after percutaneous coronary intervention (PCI). The baseline MPV values from consecutive patients undergoing PCI were screened. Of the 1,432 patients, the composite primary end point of mortality or myocardial infarction at 1 year occurred in 80 (5.6%). The patients in the highest tertile (MPV >9.1 fL) had an increased frequency of the primary end point compared to those in the mid (8.1 to 9.1 fL) and lowest (<8.1 fL) tertiles (9.0%, 4.5%, and 3.5%, respectively; p <0.01). Logistic regression analysis demonstrated diabetes (odds ratio 2.44, 95% confidence interval 1.48 to 4.00) and highest tertile of MPV (odds ratio 2.42, 95% confidence interval 1.47 to 3.99) as the best predictors of adverse outcomes. In patients with acute coronary syndrome, the preprocedural MPV and troponin levels demonstrated a comparable predictive relation to the primary end point (receiver operator characteristics curve analysis, area under the curve 0.64, p = 0.01; and 0.63, p = 0.01, respectively). In conclusion, an elevated MPV was a strong independent predictor of long-term outcomes after PCI. The preprocedural MPV had prognostic value similar to that of troponin in patients with acute coronary syndrome. These findings could be of importance in the clinical evaluation of patients before PCI and the design of future studies assessing antiplatelet therapies.

Part 13: pediatric basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.

Part 13: pediatric basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.

Bench-to-bedside review: Significance and interpretation of elevated troponin in septic patients

Because no bedside method is currently available to evaluate myocardial contractility independent of loading conditions, a biological marker that could detect myocardial dysfunction in the early stage of severe sepsis would be a helpful tool in the management of septic patients. Clinical and experimental studies have reported that plasma cardiac troponin levels are increased in sepsis and could indicate myocardial dysfunction and poor outcome. The high prevalence of elevated levels of cardiac troponins in sepsis raises the question of what mechanism results in their release into the circulation. Apart from focal ischemia, several factors may contribute to the microinjury and minimal myocardial cell damage in the setting of septic shock. A possible direct cardiac myocytotoxic effect of endotoxins, cytokines or reactive oxygen radicals induced by the infectious process and produced by activated neutrophils, macrophages and endothelial cells has been postulated. The presence of microvascular failure and regional wall motion abnormalities, which are frequently observed in positive-troponin patients, also suggest ventricular wall strain and cardiac cell necrosis. Altogether, the available studies support the contention that cardiac troponin release is a valuable marker of myocardial injury in patients with septic shock.

Elevated serum uric acid levels in outpatients with chronic heart failure: side effect or marker of myocardial damage?

Background: High serum uric acid level is a marker of impaired oxidative metabolism, a possible mechanism of myocardial damage, and it reflects the degree of xantine oxidasa activation in patients with chronic heart failure (CHF). However, hyperuricemia is frequently found in subjects treated with diuretics or with renal impairment. Objectives: We sought to determine clinical variables associated with hyperuricemia (Uric) in outpatients (pt) with chronic heart failure (CHF) as well as the relationship with elevated cardiac troponin-T levels (cTnT) and long-term prognosis. Methods: One hundred and eighty outpatients from Heart Failure Program were prospectively included. Clinical, echocardiographic, 6 minute walk test distance, and laboratory data were obtained. Serum uric acid level >7 mg/dL, in male and >5.7 mg/dL in female was considered abnormal. Baseline, 3-months and 6 months blood samples were assayed for cTnT with a 3rd generation immunoassay. Minimal myocardial damage was defined as cTnT ≥0.02 ng/mL. Results: The mean age was 63±12 years and 68% were male. Hyperuricemia was found in 92 (51%) patients. In Uric and non-Uric patients NYHA Class was 2.3±0.8 vs 2.5±0.8 (p = ns), ejection fraction was 34±16 vs 38±15% (p = ns) and 6-min walked distance was 368±84 vs 383±91 m(p = ns). In multiple regression analysis, the variables significantly associated with Uric were: sinus rhythm (OR = 0.40, p = 0.026), heart rate (OR = 1.05, p<0.001), aspirin user (OR = 2.9, p = 0.01) and serum creatinine level (OR = 3.1, p = 0.034). In patients with or without Uric, baseline, 3 and 6 months high cTnT levels were detected in 31 vs 19%, 37 vs 16%, 19 vs 7% (all p<0.05), respectively. The rate of worsening heart failure was 48 vs. 21% (p<0.001) in patients with or without Uric, and 8-months free-CHF hospitalization survival was 61 vs. 83% (p = 0.047), respectively. Conclusion: Hyperuricemia was detected in a half of patients with CHF and it was associated with aspirin intake, impaired renal function, tachycardia and absence of sinus rhythm. Higher rate of minimal myocardial damage and worse prognosis suggest that high uric acid levels should be considerer a manifestation of myocite toxicity, probably secondary to release of oxygen free radicals, instead of side effect.

Valor pronóstico de la troponina T en pacientes hospitalizados con angina o infarto sin elevación del segmento ST

Cardiac troponins are highly specific and sensitive for detecting minimal myocardial damage. The aim of our study was to determine the prognostic value of troponin T levels in patients hospitalized for suspected angina or myocardial infarction without ST-segment elevation. We recorded the frequency of death, acute myocardial infarction, heart failure, or need for coronary revascularization in the three months after the onset of symptoms in 346 consecutive patients admitted for suspected acute coronary syndrome, excluding those who developed myocardial infarction with persistent ST-segment elevation. . Serum troponin T levels were > or = 0.1 ng/ml in 133 patients (troponin T positive group) and lower in 213 patients (troponin T negative group). The relative risk (RR) and 95 percent confidence intervals (95% CI) of individual and grouped events for the troponin T positive group were 3.2 (95% CI, 1.4-7.3; p = 0.006) for death; 2.8 (95% CI, 1.43-5.51; p = 0.003) for death or myocardial infarction; and 2.8 (95% CI, 1.6-5.0; p < 0.001) for death, myocardial infarction or heart failure. Diabetes mellitus and troponin T levels > or = 0.1 ng/ml had independent prognostic value after adjusting for age, sex, and electrocardiographic changes; with RR 2.5 (95% CI, 1.01-5.9) for death, myocardial infarction or heart failure. The prognosis of patients hospitalized for chest pain who do not immediately develop transmural necrosis depends on serum troponin T levels at hospital admission. Troponin T levels > or = 0.1 ng/ml almost triple the risk of major events in the three months after the acute episode. The prognostic value of troponin T is independent of age, sex, presence of diabetes mellitus, and electrocardiographic changes.

Evidence of exercise-induced cardiac dysfunction and elevated cTnT in separate cohorts competing in an ultra-endurance mountain marathon race.

Cardiac damage has recently been implicated in the aetiology of "exercise induced cardiac dysfunction". The humoral markers of cardiac damage that have been utilised to date are not sufficiently cardio-specific to investigate this hypothesis. The aim of the present study was to examine cardiac function following prolonged exercise, and investigate the contention of cardiac damage utilising a new highly cardio-specific marker. Thirty-seven competitors in the 2-day Lowe Alpine Mountain Marathon 2000 volunteered for the study. Competitors were sub-divided into 2 groups. Group 1 (n = 11) were examined using echocardiography pre and post the event, examining left ventricular diastolic and systolic function. Group 2 (n = 26) had venous blood samples drawn prior to the event and immediately following day-1 and day-2. Blood samples were analysed for total creatine kinase activity (CK), creatine kinase isoenzyme MB(mass) (CK-MB(mass)), and cardiac troponin T. Echocardiographic results indicated left ventricular diastolic and systolic dysfunction following cessation of exercise. CK and CK-MB(mass) were both elevated following day-1, and immediately following race completion. Cardiac troponin T levels were below the 99th percentile (0.01 microg/L) in all subjects prior to the event, following day-1 cTnT was elevated above 0.01 microg/L in 13 subjects, but returned to below 0.01 microg/L following race completion on day-2. However, no individual data reached clinical cut-off levels for acute myocardial infarction (AMI) (0.1 microg/L). Two days arduous exercise over mountainous terrain resulted in cardiac dysfunction, and significant skeletal muscular degradation. The elevation of cTnT above the 99th percentile in the present study is suggestive of minimal myocardial damage. The clinical significance of and exact mechanism responsible for such damage remains to be elucidated.

Prognosis and risk indicators of death during a period of 10 years for women admitted to the emergency department with a suspected acute coronary syndrome

Aim: To describe the 10-year prognosis and risk indicators of death in women admitted to the emergency department with acute chest pain or other symptoms raising a suspicion of acute myocardial infarction (AMI). Particular interest was paid to women of ≤75 years of age surviving 1 month after admission, who were judged to have suffered a possible or confirmed acute ischemic event with signs of either minor or no myocardial damage. Patients: All women admitted to the emergency department at Sahlgrenska University Hospital, Göteborg, during a period of 21 months, due to acute chest pain or other symptoms raising a suspicion of AMI. Methods: All the women were followed prospectively for 10 years. The subset described previously underwent a bicycle exercise tolerance test and metabolic screening 3 and 4 weeks, respectively, after admission to the emergency department. Results: In all, 5362 patients were admitted to the emergency department on 7157 occasions during the time of the survey and 2387 (45%) of them were women. Of these women, 61% were hospitalised and 39% were sent home directly. The overall 10-year mortality for women was 42.5% (55.5% among those hospitalised and 21.8% among those not hospitalised). Of the variables recorded at the emergency department, the following were independently associated with 10-year mortality: age, history of angina pectoris, history of hypertension, history of diabetes, history of congestive heart failure, pathological ECG on admission, degree of initial suspicion of AMI on admission, symptoms of congestive heart failure on admission and other non-specific symptoms on admission. The majority of these risk factors were more markedly associated with prognosis in women discharged directly from the emergency department than in those hospitalised. In the subset aged ≤75 years defined above ( n=241), the following were independent predictors of death: a history of AMI and working capacity in a bicycle exercise tolerance test. Conclusion: Among women admitted to hospital due to chest pain or other symptoms raising a suspicion of AMI, 42.5% had died after 10 years. Major risk indicators of death were age, history of cardiovascular disease, pathological ECG on admission and symptoms of congestive heart failure on admission. Women presenting with an acute coronary syndrome but minimal myocardial damage, work capacity and a history of AMI predicted a poor outcome.

Effects of Implantable Cardioverter Defibrillator Implantation and Shock Application on Biochemical Markers of Myocardial Damage

Implantable cardioverter defibrillator (ICD) implantation is a common approach in patients at high risk of sudden cardiac death. To check for normal function, it is necessary to test the ICD. For this purpose, repetitive induction and termination of ventricular fibrillation by direct current shocks is required. This may lead to minor myocardial damage. Cardiac troponin T (cTnT) and I (cTnI) are specific markers for the detection of myocardial injury. Because these proteins usually are undetectable in healthy individuals, they are excellent markers for detecting minimal myocardial damage. The objective of this study was to evaluate the effect of defibrillation of induced ventricular fibrillation on markers of myocardial damage. This study included 14 patients who underwent ICD implantation and intraoperative testing. We measured cTnT, cTnI, creatine kinase MB (CK-MB) mass, CK activity, and myoglobin before and at definite times after intraoperative shock application. Depending on the effectiveness of shocks and the energy applied, the cardiac-specific markers cTnT and cTnI, as well as CK-MB mass, showed a significant increase compared with the baseline value before testing and peaked for the most part 4 h after shock application. In contrast, the increases in CK activity and myoglobin were predominantly detectable in patients who received additional external shocks. ICD implantation and testing leads to a short release of cardiac markers into the circulation. This release seems to be of cytoplasmic origin and depends on the number and effectiveness of the shocks applied.

Measurement of cardiac troponin I levels in the emergency department: predictive value for cardiac and all-cause mortality.

To assess the predictive value of cardiac troponin I levels in cardiac and all-cause mortality in patients presenting to an emergency department. A prospective cohort study. The emergency department of a major tertiary teaching hospital in metropolitan Melbourne over a six-week period in 1998. All patients with requests for cardiac enzyme level measurement. Cardiac and all-cause mortality within 30 days of presentation. 424 patients (232 men, 192 women; age range, 16-93 years) were reviewed. The 30-day mortality rate was 7.3% (31/424); in patients with raised levels of both creatine kinase (CK)-MB isoenzyme and troponin I this rate was 27% (7/26; 95% CI, 13%-44%); and in those with troponin I levels above 2 microg/L, but normal CK-MB values, it was 24% (5/21; 95% CI, 5%-43%). The mortality rate in the group with normal results of cardiac markers was 4.3% (14/328; 95% CI, 2.1%-6.5%). Patients with minor increases in troponin I levels (minimal myocardial damage) showed an intermediate 30-day mortality rate (13%, 5/39; 95% CI, 2%-24%). Other predictors of 30-day mortality included age, presentation with shortness of breath, and electrocardiography (ECG) changes diagnostic of acute myocardial infarction or consistent with ischaemia. Cardiovascular causes were responsible for most of the deaths in patients with raised troponin I levels. Multivariate logistic regression analysis showed that raised levels of troponin (> 2.0 microg/L), but not of CK-MB, predict 30-day mortality rate. Compared with CK-MB, cardiac troponin I more accurately predicts 30-day mortality rates in patients presenting to the emergency department. Moreover, troponin I levels identify additional groups of patients at increased risk of death not so identified by measuring CK-MB values.

Part 7: The Era of Reperfusion

Part 7: The Era of Reperfusion