Peak Total Creatine Kinase Research Articles

Abstract 13969: Iterative Changes in Alcohol Septal Ablation at the Medical University of South Carolina: A Single-Center Experience

Introduction: Alcohol septal ablation (ASA) is an effective procedure to treat medically refractory hypertrophic obstructive cardiomyopathy (HOCM). Several modifications have been made to the procedure since its inception. We seek to assess the changes in the procedure and outcomes over the past 20 years Methods: We retrospectively analyzed 845 ASA procedures performed from January 2000 to February 2022 using an internally maintained database. These procedures were then split into three groups, with procedures occurring from 2000-2004 (Cohort 1), 2005-2011 (Cohort 2), and 2006-2022 (Cohort 3). Patient demographics, echocardiographic measurements, and procedural data were recorded. Results: Average patient age was 53.06 (143:161 M:F, 52.96% female), 59.71 (125:140, 52.83% female), and 63.86 years (99:177, 64.13% female) in Cohorts 1, 2, 3 respectively. The peak resting left ventricular outflow tract (LVOT) gradient was significantly higher in Cohort 2 and 3 (69.893 mmHg, 72.218 mmHg) versus Cohort 1 (57.32 mmHg, p<0.0001). The number of septal arteries injected increased slightly, but the total amount of alcohol injected decreased, thereby implying a reduced amount of alcohol injection per septal artery. The overall infarct size did not show a significant difference between the three Cohorts (peak total creatine kinase, p=0.0871). The average length of hospital stay decreased and pacemaker incidence continued to be <10%. There were no procedural deaths since 2008. See Figure 1. Conclusions: ASA has become increasingly safer over the past twenty years at MUSC with maintained efficacy and zero procedural mortality since 2008. Improved patient selection, transition to a bi-radial approach, contrast echocardiographic imaging, slower alcohol injection rate, reduced alcohol volume per septal artery and increased operator experience are responsible for the improvement.

Rhabdomyolysis in COVID-19 Patients: A Retrospective Observational Study.

BackgroundThe coronavirus disease 2019 (COVID-19) pandemic has caused significant morbidity and mortality worldwide. Knowledge about the pathophysiology of the disease and its effect on multiple systems is growing. Kidney injury has been a topic of focus, and rhabdomyolysis is suspected to be one of the contributing mechanisms. However, information on rhabdomyolysis in patients affected by COVID-19 is limited. We aim to describe the incidence, clinical characteristics, and outcomes of patients hospitalized with COVID-19 who developed rhabdomyolysis.Materials and methodsA retrospective observational cohort consisted of patients who were admitted and had an outcome between March 16 to May 27, 2020, inclusive of those dates at a single center in the Bronx, New York City. All consecutive inpatients with lab-confirmed COVID-19 were identified. Patients with peak total creatine kinase (CK) over 1,000 U/L were reviewed; 140 patients were included in the study. The main outcomes during hospitalization were new-onset renal replacement therapy and in-hospital mortality.ResultsThe median age was 68 years (range: 21-93); 64% were males. The most common comorbidities were hypertension (73%), diabetes mellitus (47%), and chronic kidney disease (24%). Median CK on admission was 1,323 U/L (interquartile range [IQR]: 775 - 2,848). Median CK on discharge among survivors was 852 (IQR: 170 - 1,788). Median creatinine on admission was 1.78 mg/dL (IQR: 1.23 - 3.06). During hospitalization, 49 patients (35%) received invasive mechanical ventilation, 24 patients (17.1%) were treated with renal replacement therapy (RRT), and 66 (47.1%) died.ConclusionsRhabdomyolysis was a common finding among hospitalized patients with COVID-19 in our hospital in the Bronx. The incidence of new-onset renal replacement therapy and in-hospital mortality is higher in patients who develop rhabdomyolysis. McMahon score, rather than isolated creatine kinase levels, was a statistically significant predictor of new-onset RRT. Clinicians should maintain a high level of suspicion for rhabdomyolysis in COVID-19 patients throughout their admission and use validated scores like McMahon score to devise their treatment plan accordingly.

First Multiparametric Cardiovascular Magnetic Resonance Study Using Ultrasmall Superparamagnetic Iron Oxide Nanoparticles in a Patient With Acute Myocardial Infarction

A 50-year-old man presented with acute chest pain that had started about 6 hours prior to admission to our emergency department. His resting ECG revealed an ST-elevation myocardial infarction with typical ST-segment elevation in the leads V1 through V4 and reciprocal ST-segment depression. Consequently, immediate coronary angiography was performed and revealed a proximally occluded left anterior descending artery (Figure 1). The left anterior descending artery was recanalized and a bare-metal stent was implanted. Postinterventional blood analysis revealed a peak total creatine kinase level of 2962 U/L (normal, <190 U/L), a peak creatine kinase–muscle-brain type level of 231 U/L (normal, <25 U/L), a peak high-sensitivity troponin T level of 5705 pg/mL (normal, <14 pg/mL), and a slightly elevated N-terminal pro-brain natriuretic peptide level of 882 pg/mL (normal, <450 pg/mL). Figure 1. Coronary angiograms of the left coronary artery (LCA) and right coronary artery (RCA). A total occlusion of the left anterior descending artery ( left , red arrow) was observed and treated with a bare-metal stent ( middle , red arrow). PCI indicates percutaneous coronary intervention. After coronary angiography, the patient was enrolled in an ongoing clinical trial (Non-invasive myocardial inflammation imaging study 2 [NIMINI-2]) that is attempting to evaluate whether myocardial infarct imaging using ultrasmall superparamagnetic iron oxide nanoparticles (USPIO) and multiparametric cardiovascular magnetic resonance (CMR) techniques allow an improved characterization of infarct as well as peri-infarct pathology (compared with conventional gadolinium-based necrosis/fibrosis imaging). Therefore, multiparametric CMR studies were performed before and after intravenous ferumoxytol (Feraheme, a USPIO; 17 mL IV=510 mg Fe) administration. The first CMR (pre-Feraheme) was performed 3 days after presentation with acute ST-elevation myocardial infarction. Serial CMR studies were then performed 6 hours, 24 hours, 48 hours, 96 hours, and 3 months after intravenous Feraheme administration (post-Feraheme). Only the first (pre-Feraheme) and last CMR study (3 months post-Feraheme) …

Reduced creatine kinase release with statin use at the time of myocardial infarction

Background: Statin pre-treatment has been shown to reduce myocardial infarct size in animal models. We evaluated peak creatine kinase levels in humans based on concomitant or very early statin initiation following myocardial infarction. Methods: We identified 66 consecutive patients who received a statin within 24 h of admission to our coronary care unit for myocardial infarction. Each statin patient was matched with three patients who had not received statin therapy ( n=198). Statin patients were subgrouped into those receiving statin therapy at the time of infarction ( n=44) and those initiated on statin therapy within 24 h of infarction ( n=22). Peak total creatine kinase concentrations were compared between groups. A linear regression model was developed to test for differences in peak creatine kinase after adjusting for differences between groups. Results: Patients receiving statin therapy within 24 h of admission had significantly smaller median peak creatine kinase concentrations compared to those not receiving a statin (416 IU/l [258, 992] vs. 699 IU/l [339, 1728]; p=0.020). Subgroup analysis revealed that the lower peak creatine kinase concentrations within the statin group were a result of lower creatine kinase concentrations in those patients on a statin at the time of myocardial infarction (399 IU/l [255, 869] vs. 678 IU/l [276, 1870]; p<0.05). This difference retained statistical significance after adjustment for differences between groups. Conclusion: Statin therapy at the time of myocardial infarction is associated with lower peak creatine kinase concentrations. This suggests that statins may exhibit protective effects in the setting of myocardial ischemia and/or infarction in humans.

Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I

This study compared the diagnostic accuracy of the measurement of serum cardiac troponin I (cTnI) with creatine kinase (CK) MB mass in patients with minor myocardial injury whose measured total CK activity did not exceed twice the upper reference limit (300 U/L for men; 200 U/L for women). Forty-eight consecutive patients presenting with chest pain and with in-hospital documentation of myocardial injury were enrolled. Electrocardiogram, echocardiogram, and serial serum CK-MB mass, cTnI, and total CK were measured over 36 h after admission. Peak total CK activity was within normal limits in 28 patients (58%). The mean (+/- SD) peak CK-MB mass and cTnI concentrations were: 16.4 (11.8) micrograms/L and 132 (13.0) micrograms/L; respectively. The peak biochemical marker index (defined as CK-MB or cTnI divided by its respective upper reference limit) was significantly (P < 0.05) higher for cTnI than for CK-MB from 7 to 36 h. The clinical sensitivity for detection of myocardial injury for cTnI was 100% [95% confidence interval (CI): 87.2% to 100%], compared with 81.8% (CI: 67.3% to 91.8%) for CK-MB. Thus, cTnI was more sensitive than CK-MB mass for detection of myocardial injury in patients with small increases of total CK.

Frequency of chronic obstructive airways disease and pulmonary hypertension in patients with acute inferior myocardial infarction with or without right ventricular infarction

Objective: Factors influencing the incidence of right ventricular infarction among patients with acute inferior myocardial infarction have not yet been fully established. Chronic obstructive airways disease and right ventricular hypertrophy were suggested as possible predisposing factors but no definite evidence was shown. This study analyses the frequency of chronic obstructive airway disease and of Doppler assessed pulmonary hypertension among patients with acute inferior myocardial infarction with or without right ventricular infarction. Design and patients: Sixty consecutive patients with acute inferior myocardial infarction were prospectively enrolled into the study. Measurements: Standard 12-lead ECG with right precordial leads (V 3–6R) were recorded on admission to the Coronary Care Unit and on days 2 and 3. Doppler echocardiography was performed within 48 h after the onset of myocardial infarction and repeated 6 weeks later together with a pulmonary function test. Routine biochemical and clinical data were collected. Results: Right ventricular infarction occurred in 35% of patients with acute inferior myocardial infarction. No differences in respiratory indices of chronic obstructive airways disease or in Doppler echocardiography parameters of pulmonary hypertension were revealed among patients with and without right ventricular infarction. Peak total creatine kinase level and creatine kinase myocardial isoenzyme levels were higher in patients with right ventricular infarction than in those without (2925 ± 1321 vs. 1682 ± 1216 U l ; P < 0.001 and 207 ± 108 vs. 127 ± 102 U l ; P < 0.05, respectively). Conclusions: In the course of acute inferior myocardial infarction, the frequencies of chronic obstructive airways disease and/or pulmonary hypertension were not higher among patients with right ventricular infarction than among those without right ventricular infarction. Thus, history of chronic obstructive airways disease and/or pulmonary hypertension do not necessitate specific precautions in respect of right ventricular infarction.

Use of creatine kinase isoforms for diagnosis of infarct artery patency after thrombolytic therapy with streptokinase.

We investigated whether the proportion of creatine kinase (CK) MM3 to total MM isoform, measured in a single blood specimen taken at 3 hours after starting intravenous administration of streptokinase to patients with developing myocardial infarction, would give reliable information on patency or occlusion of the infarct-related coronary artery. Fifty-nine patients received streptokinase 1.5 x 10(6) U intravenously within 6 hours of onset of prolonged chest pain and ST-segment elevation. Patency of the infarct-related coronary artery was assessed by arteriography at 2.6 +/- 0.3 (SD) hours after starting streptokinase. Creatine kinase MM isoforms were measured by chromatofocusing in blood taken at 3 hours after streptokinase. A proportion of CKMM3 to total CKMM of greater than 50% was present in 34 of 34 patients (100%) with a patent, infarct-related artery at arteriography and whose peak total CK activity reached twice the upper normal limit for our laboratory (600 U/L). CKMM3/total CKMM was less than 50% in 14 of 18 patients (78%) in whom the infarct-related artery was occluded. In five of six patients with a nondiagnostic total CK rise (peak < 600 U/L), 3-hour CKMM3/total CKMM was less than 50% despite a patent artery. CKMM3 was not measurable in one patient. A proportion of CKMM3/total CKMM of greater than 50% is highly sensitive for prediction of infarct artery patency at 3 hours after administration of streptokinase. However, the test used in this way is not reliable for patients with "prevented" myocardial infarction. Also, positive tests do occur in patients with angiographically occluded arteries, possibly signifying intermittent reperfusion and occlusion.

Early intervention in acute myocardial infarction: Significance for myocardial salvage of immediate intravenous streptokinase therapy followed by coronary angioplasty

Sixteen patients with acute myocardial infarction underwent treatment with streptokinase up to 3 hours after the onset of chest pain. Nine patients (group I) received streptokinase within 1 hour of the onset of pain, and seven patients (group II) received it within 2 to 3 hours. All underwent multigated radionuclide ventriculography after streptokinase therapy and 1 week later. Percutaneous transluminal coronary angioplasty of the infarct artery was performed within 24 hours in all patients. An effort-limited treadmill stress test was performed before discharge. There was no mortality or serious complication. Mean peak total creatine kinase was 521 +/- 289 mU/ml in group I, and 1,614 +/- 709 mU/ml in group II (p less than 0.05). The mean initial left ventricular ejection fraction was 47 +/- 11% in group I and 37 +/- 10% in group II. After early angioplasty (within 24 hours) and at 1 week recovery, left ventricular ejection fraction increased to 53 +/- 9% in group I (p less than 0.05) and to 40 +/- 7% in group II (p = NS). Seven of the nine patients in group I had normal radionuclide ventriculograms at discharge compared with none of the seven patients in group II. Thrombolytic therapy administered less than 1 hour after the onset of symptoms of acute myocardial infarction followed by angioplasty of the infarct artery results in preservation of left ventricular function, whereas therapy given after 2 hours has only a limited effect.

Significance of early two-dimensional echocardiography after acute myocardial infarction

We performed serial two-dimensional echocardiography (2D echo) in 35 pateints with a first transmural myocardial infarction, to correlate initial left ventricular wall motion abnormalities with subsequent in-hospital cardiac complications, peak total creatine kinase level, and haemodynamic alterations, and to observe serial changes in the left ventricular wall motion. A wall motion score was derived by analysing endocardial motion in 15 left ventricular segments. Left ventricular wall motion could be analysed in 30 patients, 14 without (Group 1) and 16 with complications (Group 2). The initial wall motion score in Group 1 patients was 5.2 ± 0.7 (±SEM) compared to 14.2 ± 1.2 in Group 2 patients ( P < 0.001). A wall motion score of ⩾ 10 correlated with the occurrence of complications in 15 of 16 patients (sensitivity 93%, specificity 92%). Initial wall motion score did not correlate significantly with peak total serum creatine kinase and did not change significantly during the first 72 hr in both the groups. In 12 patients who underwent right heart catheterization together with 2D echo, the average wall motion score was 16.4 ± 2.0 and cardiac index 2.4 ± 0.3. Wall motion score correlated inversely with the cardiac index in these patients ( r = −0.78; P < 0.01). Thus, 2D echo performed in first transmural myocardial infarction patients soon after admission can identify those likely to have in-hospital complications. 2D echo wall motion score correlated significantly with the cardiac output in this study.

Immediate detection of early high-risk patients with acute myocardial infarction using two-dimensional echocardiographic evaluation of left ventricular regional wall motion abnormalities

Forty-three patients with acute myocardial infarction (AMI) were studied with serial two-dimensional echocardiography (2DE) to define a high-risk subset for in-hospital cardiovascular complications including pump failure, life-threatening arrhythmias, or death. A 2DE segment score was developed representing the extent of left ventricular (LV) regional wall motion abnormality (WMA) which was correlated with peak total creatine kinase (CK) release. Patients with transmural AMI had a segment score of 7.2 ± 3.8, whereas those with nontransmural AMI had a segment score of 4.7 ± 3.4 ( p < 0.025). Peak total serum CK enzyme level correlated statistically with segment score but with a low correlation coefficient. Thirteen (30%) of the 43 patients had an in-hospital complication and their segment score was 10.0 ± 3.4 compared to 4.6 ± 2.7 in those patients without a complication ( p < 0.005). A segment score ≥ 8 was found in 11 of 13 (85%) of those who suffered a cardiac complication and in only five (16%) of the 30 patients without complication ( p < 0.05; sensitivity 85%, specificity 83%). Patient's initial clinical Killip classification was specific but very insensitive in predicting an early complicated course. Thus, 2DE study of LV regional wall motion can predict in the immediate post-AMI stage the in-hospital likelihood of such patients developing a cardiovascular complication during acute myocardial infarction.

Serum Enzymes with Special Reference to CK-MB Following Coronary Bypass Surgery

In a consecutive series of 25 coronary bypass operations, the postoperative serum activity levels of total creatine kinase (CK) and its more heart-specific isoenzyme CK-MB were examined and related to the levels of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and thermostable lactate dehydrogenase (LD-T), to electrocardiographic (ECG) findings and to surgical characteristics. Detectable CK-MB activity was found in all patients, usually appearing while the operation was still in progress. Peak CK-MB occurred earlier than peak total CK. There was no ECG evidence of myocardial infarction in any patient. The degree of postoperative CK-MB elevation, however, correlated to the duration of extracorporeal circulation (ECC) and aortic cross-clamping (AC). After 120 min of ECC and 70 min of AC, release of CK-MB, as well as of the other enzymes studied, increased considerably. There was a significant correlation between high CK-MB activity and high early postoperative activities of total CK, ASAT and LD-T. When CK-MB determinations are not available, ASAT is preferable to total CK or LD-T in the early evaluation of operative myocardial injury. From the fourth postoperative day, only LD-T is informative in this respect; a second rise of ASAT and ALAT is probably of hepatic origin.

Serum CK-KB Kinetics in Acute Myocardial Infarction and After Coronary Bypass Operations

Serum creatine kinase (CK) isoenzyme MB and total CK activity concentrations in 11 patients with acute myocardial infarction (AMI) were compared with the corresponding enzyme activities in 25 patients after coronary bypass surgery, not complicated clinically by AMI. Peak CK-MB occurred 2 +/- 0 (mean +/- SEM) hours after the end of surgery (mean duration of operation 6 hours), but 17 +/- 1 hours from the onset of symptoms in AMI. The plasma half"life for CK-MB was 11 +/- 1 hours under both conditions. Peak total CK was found after about 20 hours in both series of patients. Total CK half-life was 17 +/- 2 hours in AMI, but 30 +/- 3 hours following surgery. CK kinetics were thus different in these two situations, indicating different mechanisms for the elevations of serum CK-MB activity. In conclusion, the time course for the transient CK-MB elevation following bypass surgery should be considered in the diagnosis of peri operative infarction.