Subclinical Myocardial Injury Research Articles

Perioperative myocardial injury: individual and population implications

It is generally understood that patients who have cardiovascular disease are at risk of cardiac complications after surgery. In patients undergoing major or vascular surgery, the risk of such complications can be signi®cant. Eagle and colleagues studied patients enrolled on the CASS (Coronary Artery Surgery Study) registry who subsequently underwent non-cardiac surgery. They reported a perioperative myocardial infarction rate of 8.5% in patients with medically managed coronary artery disease who underwent vascular surgery. The authors de®ned high-risk surgery as surgery associated with a risk of perioperative death or myocardial infarction of greater than 4%. Abdominal surgery, thoracic surgery, and head and neck surgery fell into this category. For patients undergoing these types of surgery who had medically treated coronary artery disease, the overall perioperative myocardial infarction rate was 2.7% and the overall death rate 3.3%. This compared with rates of 0.8 and 1% respectively in patients undergoing similar surgery who did not have coronary artery disease. Data such as these are often considered with information on the prevalence of coronary artery disease to obtain some indication of the population burden of disease. For example, in 1990 Mangano stated that 25 million patients undergo major surgery in the USA each year and suggested that perhaps 6±7 million of these people are at risk of perioperative cardiac complications. Such estimates suggest that perioperative cardiac complications are both a major issue in the care of individual surgical patients and a major public health issue. This review will examine in more detail the population impact of perioperative cardiac morbidity and the implications of this for the individual patient.

Subclinical myocardial injury in small-for-gestational-age neonates

Objective: Small-for-gestational-age (SGA) infants are at risk for premature death from cardiovascular disease (myocardial infarction and stroke), hypertension, and diabetes in adult life. Severe intrauterine growth restriction is often associated with subclinical cardiovascular abnormalities detectable during fetal echocardiography. The objective of this study was to determine whether SGA newborns have evidence of myocardial injury at birth. Study design: Cardiac troponin I, a specific marker of myocardial injury widely used for the diagnosis of myocardial infarction in adults, was determined in umbilical cord blood. Umbilical cord venous blood was obtained at the time of birth from 72 SGA newborns (birth weight below the 10th centile for gestational age) and 309 newborns whose birth weights were appropriate for gestational age (AGA). Cardiac troponin I was determined with a commercially available immunoassay (sensitivity 0.2 ng/ml) employed in clinical laboratories (Immulite 2000, Diagnostic Products Corp., Los Angeles, CA). Results: Cardiac troponin I was not detectable in any of the blood samples from AGA infants. In contrast, 4.2% (3/72) of SGA infants had detectable cardiac troponin I in umbilical cord blood (Fisher's exact test, p = 0.007). Conclusion: A subgroup of SGA newborns undergoes myocardial injury before birth. This insult may predispose to the development of adult premature cardiovascular disease and death.

Subclinical myocardial injury in small-for-gestational-age neonates

Objective: Small-for-gestational-age (SGA) infants are at risk for premature death from cardiovascular disease (myocardial infarction and stroke), hypertension, and diabetes in adult life. Severeintrauterine growth restriction is often associated with subclinical cardiovascular abnormalities detectable during fetal echocardiography. The objective of this study was to determine whether SGA newbornshave evidence of myocardial injury at birth.Study design: Cardiac troponin I, a specific marker of myocardial injury widely used for the diagnosis of myocardial infarction in adults, was determinedin umbilical cord blood. Umbilical cord venous blood was obtained at the time of birth from 72 SGA newborns (birth weight below the 10th centile for gestational age) and 309 newborns whose birth weightswere appropriate for gestational age (AGA). Cardiac troponin I was determined with a commercially available immunoassay (sensitivity 0.2 ng/ml) employed in clinical laboratories (Immulite 2000, DiagnosticProducts Corp., Los Angeles, CA).Results: Cardiac troponin I was not detectable in any of the blood samples from AGA infants. In contrast, 4.2% (3/72) of SGA infants had detectable cardiac troponinI in umbilical cord blood (Fisher's exact test, p = 0.007).Conclusion: A subgroup of SGA newborns undergoes myocardial injury before birth. This insult may predispose to the developmentof adult premature cardiovascular disease and death.

Risk stratification using serum concentrations of cardiac troponin T in patients with end-stage renal disease on chronic maintenance dialysis

Background: It has been recently suggested that cardiac troponin T (cTnT) may be more sensitive than troponin I (cTnI) for subclinical myocardial cell injury in patients on chronic dialysis. Methods: We prospectively compared the predictive value of cTnT with cTnI, atrial (ANP) and brain natriuretic peptide (BNP) in 100 consecutive outpatients on chronic dialysis without acute coronary syndromes over a period of 3 months, and assessed whether the combination of cTnT with clinical information including age, duration of dialysis, and medical histories was useful for risk stratification of these patients. During the 2-year follow-up period, 19 patients died, mostly due to cardiac causes (53%). Results: The area under the receiver operator characteristic (ROC) curve for the cTnT as predictor of both overall and cardiac death was significantly greater than the area under the cTnI curve ( p<0.0001 and p=0.01), the BNP curve ( p<0.001 and p<0.01) or the ANP curve ( p<0.0001 and p<0.005). In a stepwise multivariate Cox regression analysis, only cTnT ( p<0.05 and p<0.01) and a history of heart failure requiring hospitalization ( p<0.05 and p<0.005) were independent predictors of both all cause and cardiac mortality. Using parameters of cTnT ≥0.1 μg/l and/or history of heart failure, the overall and cardiac mortality rate for the low risk group ( n=66) were 4.5% and 1.5%, respectively, 40% and 16% for the intermediate risk group ( n=25), and 67% and 56% for the high risk group ( n=9). Conclusion: cTnT concentrations offer a higher prognostic accuracy than cTnI, ANP and BNP in patients on chronic dialysis. The combination of elevated cTnT and a history of heart failure may be a highly effective means of risk stratification of these patients.

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.

Lack of Detection of Myocardial Injury During Competitive Races of 100 Miles Lasting 18 to 30 Hours

Competitors in an ultramarathon performed under extreme conditions did not demonstrate evidence of subclinical myocardial injury, as determined using cardiac troponin T as a marker. This finding refutes previous data and is likely due to utilization of an improved assay for cardiac troponin T that minimizes cross reactivity with skeletal muscle troponin T.

Evidence of Myocardial Injury During Prolonged Strenuous Exercise

These preliminary data suggest that extremely prolonged intense exercise may induce subclinical myocardial injury. Although questions of assay interference exist, the importance of this finding has prompted planning of a larger study using a methodologically more specific assay.

A three dimensional mid sagittal plane for brain asymmetry measurement

Patterns and determinants of temporal change in highly-sensitivity troponin-T (hs-cTNT), a novel measure of subclinical myocardial injury, among asymptomatic persons have not been well characterized.We studied 8571 ARIC Study participants, free of cardiovascular disease, who had hs-cTNT measured at two time-points, 6 years apart (1990–1992 and 1996–1998). We examined the association of baseline 10-year atherosclerotic cardiovascular (ASCVD) risk-group (< 5%, 5–7.4%, ≥ 7.5%) and individual cardiac risk-factors with change across hs-cTNT categories using Poisson and Multinomial Logistic regression and with mean continuous hs-cTNT change using linear regression.Mean age was 57 years and 43% were male. Mean (SD) 6-year hs-cTNT change was higher across increasing ASCVD risk-groups; + 1.2 (6.1) ng/L [< 5%], + 2.1 (5.4) ng/L [5–7.4%], and + 2.8 (8.8) ng/L [≥ 7.5%]. Major baseline determinants of temporal hs-cTNT increases were: age, male gender, hypertension, diabetes, and obesity. In addition, the relative risk (RR) of incident elevated hs-cTNT (≥ 14 ng/L) was 1.46 (95% CI 1.1–2.0) for persons with sustained hypertension compared to those who remained normotensive. Results for sustained obesity (RR 1.65 [1.19–2.29]) and hyperglycemia (RR 1.76 [1.16–2.67]) were similar. These associations were generally stronger after accounting for survival bias. However, smoking, LDL-cholesterol and triglycerides were not associated with hs-cTNT change. HDL-cholesterol was associated with declining hs-cTNT.Persons in higher ASCVD risk-groups were more likely to have increases in hs-cTNT over 6 years of follow-up. The modifiable risk-factors primarily driving this association were diabetes, hypertension, and obesity; particularly when they were persistently elevated over follow-up. Future studies are needed to determine whether modifying these risk factors can prevent progression of subclinical myocardial injury.

Cardiac troponin T and creatine kinase MB mass concentrations in children receiving anthracycline chemotherapy

Anthracyclines (doxorubicin, daunorubicin, and derivatives) are among the most effective antineoplastic drugs for pediatric cancer with dose-limiting acute and long-term cardiotoxicity. The exact mechanism of the development of cardiomyopathy is still not clear. Anthracyclines may induce subclinical acute myocardial injury leading to lysis of a limited number of myocytes. Alternatively, myocytes may experience a transient loss of cytoplasmic membrane integrity. Both conditions may lead to a transient efflux of small amounts of cytoplasmic enzymes and other proteins specific to the heart muscle fibers. To test these hypotheses we assayed plasma creatine kinase (CK) MB mass and cardiac specific troponin T (TnT). CKMB may be released even in case of reversible cell membrane injury, while prolonged elevation of TnT is the most sensitive and specific marker of limited myocardial necrosis. Thirty-five anthracycline-containing chemotherapy courses in 22 children with cancer were analyzed. CKMB mass and TnT concentrations were within the normal range in all children before anthracycline therapy. Within 72 hours from anthracycline therapy no increment of one of these two marker proteins was detected (ANOVA for repeated measures, P = 0.94 [TnT] and 0.25 [CKMB]). We conclude that only minimal if any acute necroses of cardiac myocytes occur after anthracycline therapy. Even membrane integrity appears to be maintained within the first 3 days after anthracycline therapy, in the absence of electrocardiographic or echocardiographic signs of acute cardiotoxicity.