Subtle Myocardial Injury Research Articles

Changes in Mitochondrial Function and Cell Death Patterns in Peripheral Blood Mononuclear Cells during Trastuzumab Treatment Following Doxorubicin Chemotherapy.

Trastuzumab, a monoclonal antibody which works against human epidermal growth factor receptor 2 (HER2), possibly causes cardiotoxicity through mitochondrial dysfunction. The usefulness of isolated peripheral blood mononuclear cells (PBMCs) in the assessment of trastuzumab-induced cardiotoxicity remains uncertain. This study aimed to determine the temporal changes in mitochondrial function, oxidative stress, and cell death in the isolated PBMCs of HER2-positive breast cancer patients during breast cancer treatment and to compare the changes with HER2-negative breast cancer patients who did not receive trastuzumab therapy. Eighteen newly diagnosed HER2-positive breast cancer women who received sequential doxorubicin and trastuzumab were consecutively recruited. Age- and gender-matched controls with HER2-negative breast cancer were selected. Echocardiography was carried out, and blood samples for the study of cardiac biomarkers and PBMCs were collected periodically during treatment. Only one patient in our cohort developed asymptomatic left ventricular dysfunction during trastuzumab treatment. However, trastuzumab following doxorubicin aggravated subclinical cardiac injury, determined by cardiac troponin and echocardiography. Cellular and mitochondrial oxidative stress in isolated PBMCs remained unchanged throughout breast cancer treatment. Regarding mitochondrial respiration, the maximal respiration and spare respiration capacity was significantly increased in controls after doxorubicin treatment but not in patients who received trastuzumab therapy. Moreover, the percentage of apoptosis and necroptosis in isolated PBMCs was dramatically decreased in the control, compared to patients with trastuzumab treatment. In conclusion, trastuzumab caused subtle myocardial injury and impaired mitochondrial respiration and cell viability in isolated PBMCs.

214 THE IMPACT OF ARRHYTHMIA ON PROGNOSIS IN HOSPITALIZED COVID-19 PATIENTS. A CARDIAC TELEMETRIC MONITORING STUDY

Abstract Background Cardiovascular abnormalities have been largely reported in patients with COVID-19. Among these, myocardial injury and rhythm disorders represent one of the most important complications in patients affected by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. Moreover, a poorer prognosis has been documented in COVID-19 patients when complicated by arrhythmias, independently by age and sex. Objectives The aims of the present study were to identify some of non-cardiac and cardiac comorbidities and some myocardial electrical features (including QT dispersion) associated with arrhythmia in hospitalized COVID-19 patients. Moreover, another objective was to contribute in analyzing the impact of arrhythmias on outcome in this setting of patients. Methods At admission, each patient underwent cardiac telemetry monitoring through entire hospitalization period. In all the subjects, laboratory analyses, standard 12-lead electrocardiogram (both at admission and on discharge), and lung imaging examination (by means of both ultrasound scans and computed tomography) were performed. Patients exhibiting arrhythmia during in-hospital period were divided into three groups: i, with brady-arrhythmias; ii, with tachy-arrhythmias; and, iii, with tachy- and brady-arrhythmias. Results Two-hundred patients completed the study (males, 123; mean age, 70.1 years); of these, 80 patients (40%) exhibited rhythm disorders on cardiac telemetry. Patients with arrhythmia resulted to be older (p<0.0001) than patients without arrhythmia. Moreover, patients with arrhythmia showed: i, greater number of comorbidities (p<0.0001); ii, higher values of creatinine (p=0.007), B-type natriuretic peptide (p<0.0001), troponin (p<0.0001), c-reactive protein (p=0.01), ferritin (p=0.001), d-dimer (p<0.0001), and procalcitonin (p=0.0008); iii, QT interval (p=0.002), QTc interval (p=0.04), and QTc dispersion (p=0.01); and, iiii, lower values of sodium (p=0.03), magnesium (p=0.04), glomerular filtration rate (p<0.0001), and hemoglobin (p=0.008) as compared to patients without arrhythmia. By comparing the three subgroups of patients, no significant differences were found. Multivariate analysis showed that age (OR=1.14 [95% CI: 1.07-1.22]; p=0.0004), coronary artery disease (OR=12.7 [95% CI: 2.38-68.01]; p=0.005), and circulating troponin (OR=1.05 [95% CI: 1.003-1.10]; p=0.04) represented risk factors independently associated with arrhythmia. By analyzing all-cause in-hospital mortality, it resulted a ∼forty-fold higher among patients with arrhythmia (OR=39.66 [95% CI: 5.20-302.51]; p=0.0004) when compared to patients without rhythm disorders. Conclusion In the present study, arrhythmias have been to be associated with ageing, coronary artery disease, subtle myocardial injury, hyperinflammatory status, coagulative unbalance, and abnormalities in myocardial electrical impulse propagation in patients affected by SARS-CoV-2 infection. In alignment with previous reports, the presence of arrhythmia seems to be associated with a worse in-hospital prognosis. Given its usefulness, routinary use of cardiac telemetric monitoring should be encouraged in COVID wards.

COVID-19 and arrhythmia: The factors associated and the role of myocardial electrical impulse propagation. An observational study based on cardiac telemetric monitoring.

BackgroundThe heart is commonly involved in COVID-19, and rhythm disorders have been largely reported.ObjectiveTo evaluate the association of some non-cardiac and cardiac comorbidities and QT dispersion with arrhythmias and their impact on outcomes in hospitalized patients with COVID-19.MethodsEach patient underwent cardiac telemetry monitoring through the entire hospitalization period, laboratory analyses, 12-lead ECG, and lung imaging examination. Patients with arrhythmia were divided into three groups (bradyarrhythmias, tachyarrhythmias, and tachy- and bradyarrhythmias).ResultsTwo-hundred patients completed the study (males, 123; mean age, 70.1 years); of these, 80 patients (40%) exhibited rhythm disorders on telemetry. Patients with arrhythmia were older (p < 0.0001), had a greater number of comorbidities (p < 0.0001), higher values of creatinine (p = 0.007), B-type natriuretic peptide (p < 0.0001), troponin (p < 0.0001), C-reactive protein (p = 0.01), ferritin (p = 0.001), D-dimer (p < 0.0001), procalcitonin (p = 0.0008), QT interval (p = 0.002), QTc interval (p = 0.04), and QTc dispersion (p = 0.01), and lower values of sodium (p = 0.03), magnesium (p = 0.04), glomerular filtration rate (p < 0.0001), and hemoglobin (p = 0.008) as compared to patients without arrhythmia. By comparing the three subgroups of patients, no significant differences were found. At multivariate analysis, age [odds ratio (OR) = 1.14 (95% CI: 1.07–1.22); p = 0.0004], coronary artery disease [OR = 12.7 (95% CI: 2.38–68.01); p = 0.005], and circulating troponin [OR = 1.05 (95% CI: 1.003–1.10); p = 0.04] represented risk factors independently associated with arrhythmia. All-cause in-hospital mortality was ∼40-fold higher among patients with arrhythmia [OR = 39.66 (95% CI: 5.20–302.51); p = 0.0004].ConclusionArrhythmias are associated with aging, coronary artery disease, subtle myocardial injury, hyperinflammatory status, coagulative unbalance, and prolonged QTc dispersion in patients with COVID-19, and confer a worse in-hospital prognosis. Given its usefulness, routinary use of cardiac telemetry should be encouraged in COVID wards.

P3719Myocardial injury during TAVI with self-expanding prosthesis is not associated with patient-prosthesis features, hemodynamics or clinical outcome

Abstract Background Transcatheter aortic valve implantation (TAVI) has been associated with increases in markers of myocardial injury but underlying mechanisms as well as relevance for prosthesis hemodynamics, cardiac function and clinical outcome remain unclear. Purpose To study the trajectory of high-sensitivity troponin T (hs-TnT) during TAVI and elucidate putative associations with demographics, anatomical and procedural features, as well as clinical and echocardiographic outcome. Methods This prospective real-world registry study included all patients (n=275) undergoing transfemoral TAVI using a self-expanding or balloon-mounted system at a large tertiary university hospital over the most recent three-year period. Plasma levels of hs-TnT (reference level 0–14 ng/l) at 24 hours (h) before TAVI and at 9h, 18h, 30h, 42h and 72h after TAVI were analyzed. Patients with ongoing myocardial ischemia and acute coronary syndrome were excluded. We studied the association between hs-TnT values and patient characteristics, echocardiographic and CT findings at baseline as well as procedural features including the use of pre- and postdilatation. Moreover, we studied the association between hs-TnT and and echocardiography and clinical outcome at 1 year after TAVI. Results In this real-world TAVI cohort (median age 83.2±0.2 years; 48.7% women; 5.2±0.2 comorbidities; eGFR 58.0±6.0 ml/min/1.73m2; mean±standard error), 100% of patients exhibited significant elevations of hs-TnT at approximately 9-fold (207.0±11.0) compared to baseline (23±0.2 ng/L, median±SE). Peak hs-TnT values were reached at 9 h post-TAVI (207±11 ng/L) with subsequent gradual decline (figure). Myocardial injury was confirmed by elevated creatin kinase (CK) and CKMB isozyme. No significant association was found between peak hs-TnT, delta hs-TnT (peak minus baseline values) or area under the curve (AUC) of hs-TnT on the one hand, and patient demographics including renal dysfunction, comorbidity, age and gender on the other side. Moreover, no significant association between hs-TnT and anatomical features, prosthesis sizing, or use of pre- and postdilatation was found. No association between hs-TnT during TAVI and NYHA functional class, transvalvular pressure gradient, cardiac function or survival at 1 year was found. In subjects with at least one year of follow-up after TAVI (n=138), NYHA functional class (1.7 vs 2.7) and NT-proBNP plasma levels (1126±316 vs 1581±563 ng/L) were significantly lower compared to pre-TAVI. Conclusions Modest transient elevations of hs-TnT occur in all patients undergoing TAVI and are consistent with subtle myocardial injury. The lack of significant association between the extent of myocardial injury during TAVI and clinical and hemodynamic outcome as well as all-cause mortality is reassuring for current real-world practice.

Early Impairment Left Ventricular Mechanics in Children With Mitral Valve Prolapse

Early impairment of left ventricular (LV) function has been reported in some inherited connective tissue diseases such as Marfan syndrome or rheumatic heart disease in pediatric patients. However, there is no study about cardiac strain in pediatric patients with primary mitral valve prolapse (MVP). The aim of this study was to evaluate the LV functions in pediatric patients with primary MVP, mild or moderate mitral regurgitation (MR), and normal LV ejection fraction. The study group included 72 consecutive patients (40 female, mean age: 13.1 ± 5.2 with primary MVP who had mild or moderate MR, and normal systolic function (LV ejection fraction ≥60%) were compared with 40 healthy children using conventional echocardiography, tissue Doppler imaging, and 2-dimensional speckle tracking echocardiography. Patients were divided into subgroups according to the MR severity: mild (n:34), and moderate (n:38) and leaflet thickness: classical (n: 40), and nonclassical (n: 32). The children with MR had significantly lower values for global early diastolic strain rate ([SRe] patients: 1.40 ± 0.25 vs controls: 1.62 ± 0.54; p = 0.001), and E/SRe (patients: 72.7 ± 5.6 vs controls: 62.1 ± 4.9; p <0.04) when compared with the control group. In subgroup analysis, SRe (mild: 1.49 ± 0.38 vs moderate: 1.32 ± 0.31; p <0.001) was lower in MVP patients with moderate MR compared to mild MR, and E/SRe (mild: 69.4 ± 5.1 vs moderate: 75.1 ± 6.4; p <0.001) value was higher in MVP patients with moderate MR compared to mild MR. Diatolic strain parameters, SRe, and E/SRe are more sensitive markers of early subtle myocardial injury in pediatric patients with primary MVP.

Assessment of atrial conduction times in prediabetic patients with coronary artery disease.

Objective:Prediabetes is a dysglycemic state and is associated with subtle myocardial injury and dysfunction. We evaluated atrial conduction times (ACTs) and atrial electromechanical delays (EMDs) in prediabetic patients with coronary artery disease (CAD).Methods:In the present study, we recruited 128 consecutive patient candidates (40 euglycemic, 48 prediabetic, and 40 diabetic patients) for coro- nary artery bypass grafting. ACTs were measured using tissue Doppler imaging (TDI). The time intervals between the beginning of the P wave in the surface electrocardiogram and the peak of the a¢ wave in TDI (PA) in the septal and lateral mitral annuli and the lateral tricuspid annulus were measured and termed as “septal PA,” “lateral PA,” and “right ventricular (RV) PA,” respectively. The differences between lateral and septal PA, septal and RV PA, and lateral and RV PA were termed as “left intra-atrial EMD,” “right intra-atrial EMD,” and “inter-atrial EMD” respectively.Results:Septal PA, lateral PA, RV PA, left and right intra-atrial EMDs, and inter-atrial EMD were not statistically different between these three groups. Furthermore, multivariable linear regression models, adjusted for potential confounders, showed that glycemic state was not associated with ACTs, left and right intra-atrial EMDs, and inter-atrial EMD.Conclusion:There were no significant differences between the euglycemic, prediabetic, and diabetic patients with CAD regarding ACTs and atrial EMDs.

2015 AHA Late-Breaking Basic Science Abstracts.

### 23060 ### Validation Of Circulating MicroRnas As Biomarkers In Heart Failure In Two Large Independent Cohorts Antoni Bayes-Genis1, David Lanfear2, Maurice de Ronde3, Josep Lupon1, Joost Leenders4, Elisabet Zamora1, L. Keoki Williams2, De Antonio Marta5, Zhen Liu4, Koos Zwinderman3, Sara-Joan Pinto-Sietsma3, Yigal Pinto3; 1Universitat Autonoma de Barcelona, Barcelona, Spain; 2Henry Ford Hospital, Detroit, MI; 3Academic Med Cntr, Univ of Amsterdam, Amsterdam, Netherlands; 4Mirnext BV, Amsterdam, Netherlands; 5Germans Trias i Pujol Hosp, Badalona, Spain Background: Small studies suggested circulating microRNAs (circmiRs) as biomarkers for Heart Failure (HF). However, standardized approaches and quality assessment are not established, and results have been inconsistent, with little replication between studies. We aimed to implement quality standards to enable comparison between cohorts and assess which circmiRs may add prognostic information in HF. Methods: We measured 15 circmiRs in two independent cohorts totaling >2000 subjects. Cohort I (Barcelona) comprised of n=843 chronic HFrEF patients. Cohort II from Detroit comprised n= 1384 chronic HF patients (892 HFrEF, 492 HFpEF). Each sample was measured in duplicate, and normalized to an abundant and stable circmiR (miR-486-5p). Algorithms were installed to define each circmiR measurement as “valid”, “unmeasurable” or “invalid”. This allowed inclusion of valid low-level circmiR measurements while reducing noise from false amplification signals. Results: In general, between 20–40% of measurements were “invalid”, while miR-499a\_5p and -208a were “unmeasurable” in the majority of patients in both cohorts. Higher levels of circmiRs-133b, -1254, -622, -208a and -499a\_5p were significantly associated with risk of death in both cohorts, with hazard ratios ranging from 1.103 to 1.365 per log increase (p-values 0.001 to 0.05). However, adding these circmiRs to established predictors (age, renal function and NTproBNP) did not further augment the c-stat beyond 0.71 (cohort I) or 0.78 (cohort II). …

13 High sensitive troponin t levels following elective external direct current cardioversion for atrial fibrillation and atrial flutter

<h3>Introduction</h3> External transthoracic direct current (DC) cardioversion is a commonly used method of terminating arrhythmias, emergently or electively. It is known that external DC cardioversion can result in a rise in creatine kinase (CK). Previous research has shown that DC cardioversion resulted in subtle myocardial injury as evidenced by CK-MB, troponin I and troponin T increase, even though only minimally. These studies were based on the outdated monophasic defibrillators and older troponin assays. Since early 2010, the new high sensitive troponin T (Hs-trop T) assays have been used to diagnose myocardial injury and have been found to be highly sensitive and specific. This study aimed to assess the effect of external transthoracic DC cardioversion on myocardial injury as measured by the change in Hs-trop T using the more modern biphasic defibrillators in an elective setting. <h3>Methods</h3> Patients who were admitted for a day-case elective DC cardioversion for atrial fibrillation or atrial flutter were asked to participate in the study. DC cardioversion was performed using the Phillips Heartstart XL biphasic defibrillator. For cardioversions that failed at 200 Joules, the Physio-Control Lifepak 20e 360 J biphasic defibrillator was used. Hs-trop T levels were taken pre-cardioversion and at 6 h post-cardioversion (in keeping with the Third Universal Definition of Myocardial Infarction guidelines on biomarker detection of myocardial injury with necrosis). The assay used was the Roche Elecsys Troponin T hs (high sensitive) immunoassay. Quantitative analysis for haemolysis, icterus and lipaemia (which could result in interference with the Hs-trop T assay) were measured in each blood sample that was taken using the Abbott Architect c16000. <h3>Results</h3> A total of 120 cardioversions were done on 101 patients. Analysis of each of the blood sample taken showed no raised haemolytic, icteric or lipaemic indices above the recommendations for the Hs-trop T assay. Median number of shocks was 1, and the maximum number of shocks was 6. Median cumulative energy was 150 Joules (interquartile range = 387.5 Joules) with the minimum being 50 Joules and maximum being 1730 Joules. A total of 49 (40.8%) patients received a cumulative defibrillation energy of 300 Joules or higher. The highest energy delivered per shock was 360 Joules and median peak impedance levels was 80.80 Ohms (interquartile range = 19.05 Ohms). Median Hs-trop T levels pre-cardioversion was 7 ng/L (interquartile range = 7) and post-cardioversion was 7 ng/L (interquartile range = 6). A Wilcoxon signed-rank test showed no significant difference between pre-and-post cardioversion Hs-Trop T levels (Z = -0.940, p = 0.347). <h3>Conclusions</h3> External DC cardioversion did not result in myocardial injury as measured by high sensitive troponin T. The implications of this study is important as patients who are cardioverted and are found to have a significant troponin rise post-cardioversion should be assessed for causes of myocardial injury and not assumed to have myocardial injury due to the cardioversion itself.

Effect of Microembolization on Left Ventricular Systolic Wall Motion and Dyssynchrony Using Dipyridamole Stress Two-dimensional Speckle Tracking Imaging: An Experimental Study

To investigate whether subtle myocardial injury caused by coronary microembolization (CME) can induce left ventricular contractile dysfunction or dyssynchrony on swine models. CME swine models were constructed by the injection of 150,000 microspheres into the left coronary artery compared with the control group. The peak systolic values of longitudinal strain (LS), radial strain (RS), and circumferential strain (CS) by two-dimensional speckle tracking imaging (2D-STI) were measured under resting stage and dipyridamole stress prior to, 6 hours after, and 1 week after CME. The mean standard deviation of 12 segmental time-to-peak longitudinal strain (Tls-12SD), radial strain (Trs-12SD), and circumferential strain (Tcs-12SD) of the left ventricle were calculated as the dyssynchrony index. Postmortem analysis demonstrated 29.76% of the left ventricular segments manifested myocardial necrosis in MCE group compared with the control group (0%, p < 0.01). Left ventricular ejection fraction had no significant differences throughout the entire study ( p > 0.05). In the CME group, compared with the baseline, LS on the basal anterior wall deteriorated from −9.72 ± 4.96 % to −6.35 ± 3.75 % ( p < 0.05) and Tcs-12SD was prolonged from 85.00 ± 35.74 ms to 151.30 ± 75.14 ms at 1 week ( p < 0.01) under resting stage. After dipyridamole infusing, a further decrease of contractility on all CME-related segments occurred at 6 hours and/or 1 week ( p < 0.05–0.01). The deterioration of Tls-12SD achieved statistical significance at 1 week (157.66 ± 78.25 ms vs. 112.54 ± 62.52 ms, p < 0.05). Furthermore, Tcs-12SD was progressively delayed from 6 hours to 1 week (148.30 ± 45.53 ms and 162.45 ± 51.67 ms vs. 78.00 ± 40.17 ms, all p < 0.01). Subtle cardiac systolic dysfunction as well as dyssynchrony caused by CME can be detected using dipyridamole stress 2D-STI sensitively. Moreover, left ventricular dyssynchrony could be affected even by slight myocardial injury.

Two-Dimensional Speckle Tracking-Derived Strain to Distinguish Acute Coronary Syndrome from a Marked Early Repolarization in a Patient with Chest Pain: A Fancy Gadget or a Useful Tool?

With a potential of detecting subtle myocardial injury, two-dimensional (2D) speckle tracking-derived strain could help to distinguish between ischemic and nonischemic ST-segment elevation. Little is known if limitations of strain imaging could prevent its applicability in acute cardiac care settings. We present a 56-year-old male with persistent ST-segment elevation in the inferolateral leads and suspected hypokinesia of the inferior wall. Semiautomated 2D speckle tracking strain analysis showed normal longitudinal peak systolic strain (LPSS) in all segments of the inferior wall, ruling out wall-motion abnormalities in this region. Stationary reverberations and spuriously low values of LPSS in the posterolateral wall required operator's expertise to distinguish pathological myocardial deformation from artifacts. Additional workup revealed that early repolarization pattern was mistaken for the inferior wall acute myocardial infarction in our patient. Semiautomated quantification of regional left ventricular function by 2D speckle tracking echocardiography could facilitate decision making even in the emergency settings. Due to intrinsic limitations of this novel method, its actual clinical value in acute cardiac care settings may depend on the expertise of the operator and is yet to be determined.

GW24-e1764 Speckle Tracking Imaging Combined with High Sensitive Cardiac Troponin T in Early Detection and Prediction of Cardiotoxicity during Anthracycline-based Chemotherapy

ObjectivesTo detect the early subclinical myocardial injury during and shortly after epirubicin exposure in asymptomatic patients with large B-cell non-Hodgkin lymphoma by two-dimensional speckle tracking imaging and high sensitive cardiac...

Binge Drinking–Induced Subtle Myocardial Injury

Most of the clinical, histopathological, and biochemical studies consider the effect of chronic alcohol intoxication on myocardial injury. Much less attention has been paid to acute alcohol (binge drinking)-induced cardiotoxicity, even though alcohol binging is much more common than alcohol dependence. We briefly present some of the binge drinking-induced "holiday heart" effects. The literature was searched to find effects of alcohol on heart. In binge drinking, the literature has demonstrated transient myocardial subtle changes in cardiac magnetic resonance, increased serological markers of myocardial injury and inflammation, abnormal cardiac rhythm, changes in other biochemical and ultrastructural indices of myocardial dysfunction, as well as changes in metabolism, blood pressure, heart rate, thrombosis/fibrinolysis processes, and coronary vasoconstriction. Although acute low alcohol exposure has widely proven positive effect on myocardial function, heavy acute drinking frequent events are related to adverse cardiovascular effects.

Circulation: Cardiovascular Imaging Editors’ Picks

<i>Circulation: Cardiovascular Imaging</i> Editors’ Picks

B-type natriuretic peptide as a marker of subclinical heart injury during mitoxantrone therapy in MS patients—Preliminary study

The aim of this study was to evaluate the plasma level changes of B-type natriuretic peptide (BNP), biochemical marker of heart failure, and echocardiographic parameters during mitoxantrone treatment in 22 multiple sclerosis (MS) patients (8 males, 14 females, mean age 37.1 ± 6.6). Mitoxantrone (after mean cumulative dose of 58.0 ± 7.0 mg/m 2) did not alter left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), posterior wall thickness (PWT) and left ventricular end-diastolic volume (LVEDV). However, mean plasma level of BNP raised from 14.53 ± 3.29 pg/ml at the baseline to 16.79 ± 3.05 pg/ml and 18.83 ± 4.90 pg/ml ( P < 0.01) after mean mitoxantrone dose of 30.7 ± 5.9 mg/m 2 and 58.0 ± 7.0 mg/m 2, respectively. These results strongly suggest subclinical myocardial dysfunction in mitoxantrone-treated group. We assume, that low-cost, repeated BNP measurements may be a good alternative for detection of early subtle myocardial injury in MS patients during routine mitoxantrone therapy.

Cardiac Troponin I Levels Are Normal or Minimally Elevated After Transthoracic Cardioversion

Objectives. The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury.Background. Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB).Methods. We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated.Results. Patients received a mean (±SD) of 2.1 ± 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal ≤0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal <6.7) in only one patient after cardioversion.Conclusions. Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.

Paucity of subtle myocardial injury after angioplasty delineated with MB CK

To determine the extent to which PTCA elicits subtle myocardial ischemic injury, 28 patients were studied prospectively. The presence of myocardial injury was assessed by analysis of frequent (q4 hours) serial samples of MB CK, a sensitive and specific marker of myocardial injury. Immediately prior to angioplasty, baseline 12-lead ECGs and blood samples for evaluation of total CK and MB CK were obtained. Additional ECGs were obtained immediately after the procedure and on the following morning, and serial samples for total and MB CK were obtained at 4-hour intervals for 24 hours. Patients requiring cardiac surgery within 24 hours after PTCA were excluded. Samples (n = 203) were assayed by the glass bead method. Total CK rose by more than 20 IU/L in only five patients, four of whom had received intramuscular premedication. Mean MB CK was 3.4 +/- 6.1 IU/L at 12 hours and 4.1 +/- 4.7 IU/L at 24 hours compared to 3.1 +/- 1.7 IU/L prior to angioplasty. Only one patient with obvious infarction had a value for MB CK above the normal range. Thus, uncomplicated PTCA is not accompanied by objectively detectable subtle myocardial injury.