Myocardial injury with biomarker elevation in diabetic ketoacidosis

doi:10.1016/j.jdiacomp.2005.04.003

Journal of Diabetes and its Complications

Volume 19, Issue 6, November–December 2005, Pages 361-363

https://doi.org/10.1016/j.jdiacomp.2005.04.003 Get rights and content

Abstract

We report of two patients with severe ketoacidosis, minute elevations of myocardial biomarkers (troponin T and CK-MB) and initial ECG changes compatible with myocardial infarction (MI). All successive investigations, including coronary arteriography, were normal, and the patients recovered fully without further evidence of ischemic heart disease. We suggest that acidosis and very high levels of free fatty acids could cause membrane instability and biomarker leakage. Regardless of the pathogenesis, these two case stories suggest that nonspecific myocardial injury may occur in severe diabetic ketoacidosis and that the presence of minute biomarker elevation and ECG changes does not necessarily signify MI.

Introduction

Diabetic ketoacidosis and myocardial infarction (MI) are both major medical emergencies, which often occur together, and MI is the leading coexisting cause of death in ketoacidosis (Basu et al., 1993). The clinical picture may be complex and obscured because many MIs are “silent”; that is, they occur without chest pain (perhaps due to neuropathy) and because the level of consciousness of the patient may be compromised. In addition, it is well recognised that ketoacidosis per se is associated with abnormal electrocardiograms, often suggestive of MI (Moulik et al., 2002, Wang, 2004). These changes may relate to hyperkaliemia and are often normalised in the course of treatment without any further clinical evidence of MI; the term “pseudo-MI” has been proposed in such cases (Moulik et al., 2002, Wang, 2004). One case story of one patient has reported massive (100-fold) troponin elevation in a patient with ketoacidosis, chest pain and ECG changes compatible with MI, in whom subsequent coronary arteriography was normal (Tretjak, Verovnik, Vujkovac, Slemenik-Pusnik, & Noc, 2003). We present cases of two patients admitted in 2002 and 2004 with severe ketoacidosis, initial electrocardiographic changes suggestive of MI and minute elevations of circulating cardiac troponin T and CK-MB concentrations, in whom all subsequent investigations, including coronary arteriography and electrocardiograms, were normal.

Section snippets

Methods and case stories

Two patients with Type 1 diabetes for 33 and 30 years were admitted with general discomfort for 1–2 days. There were no complaints of chest pain. Patient 1 had diabetic nephropathy with stable microalbuminuria, hypertension, proliferative retinopathy and peripheral neuropathy. He was not obese nor smoking, had no family history of ischemic heart disease and was physically active. Patient 2 had proliferative retinopathy, no signs of neuropathy or nephropathy, she was not obese nor smoking, she

Discussion

Our patients posed a diagnostic and therapeutic dilemma. According to the Joint Committee of the European Society and American College of Cardiology, MI is defined by the presence of typical changes in biomarkers (troponin and CK-MB) with at least one of the following: (i) ischemic symptoms, (ii) Q waves or ST-segment changes indicative of MI or (iii) coronary artery intervention (e.g., angioplasty)/findings of MI at pathological examination (Tretjak et al., 2003). Hence, on one side, the

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Citation Excerpt :
In humans, HFABP, which is released from cardiomyocytes after an ischemic episode, is used as an early sensitive cardiac biomarker [19–21]. Furthermore, metabolic syndromes such as ketoacidosis in diabetes may lead to elevation of HFABP [22,23]. It has been suggested that high levels of fatty acids and ketones in conjunction with acidosis lead to a destabilization of the cardiac membrane with release of biomarkers such as HFABP.
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Lactate dehydrogenase (P = .001), SDMA (P= .001) and ADMA (P= .002) increased significantly after the endurance race in the finisher group. A significant increase in cTNI and α-HBDH concentration after the endurance race compared to the values before the endurance race was detected in the finisher (P= .001, P= .001) and gait related group (P= .002, P= .007). The longer the distance completed, the more these five blood parameters increased. No differences between the groups could be found and none of the measured blood parameters showed significant differences among groups before or after racing.
Is there excessive troponin testing in clinical practice? Evidence from emergency medical admissions
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Citation Excerpt :
We have previously shown that a clinical decision to request high-sensitivity cardiac troponin T (hscTnT) was a prognostic marker and semi-quantitative mortality predictor in unselected emergency medical admissions [1]. Cardiac-specific troponins are useful because they convey prognostic information that can influence therapeutic decisions, [2] not alone for the diagnosis of acute coronary syndromes [3], but also in non-cardiac presentations [4-17]. However, there is concern that troponin testing may be undertaken inappropriately given that elevated troponin levels in non-cardiac patients infrequently reflect myocardial infarction [18, 19] but may result in prolongation of hospitalizations, echocardiography, cardiac catheterizations, and cardiac monitoring [20, 21].
: To investigate whether excessive high-sensitivity cardiac troponin T (hscTnT) testing, in non-cardiac presentations, increases hospital length of stay (LOS) by driving down-stream investigations.
: We report on all hscTnT tests in emergency medical admissions, performed over a 9-year period between 2011-2019. Troponin testing frequency in different risk cohorts was determined and related to 30-day in-hospital mortality with a multivariable logistic regression model adjusted for other outcome predictors. Downstream utilization of procedures/services was related to LOS with zero truncated Poisson regression.
: There were 66,475 admissions in 36,518 patients. hscTnT was tested in 24.4% of admissions, more frequently in the elderly (>70 years 33.4%, >80 years 35.9%), cardiovascular presentations (33.6%) and in those with high comorbidity (42.2%), and reduced in those with neurologic presentations (20%). A hscTnT request predicted increased 30-day in-hospital mortality OR 3.33 (95% CI: 3.06, 3.64). The univariate odds ratio (OR) of hscTnT test result was 1.45 (95% CI: 1.42, 1.49) and was semi-quantative with worsening outcomes as hscTnT increased. It remained predictive in the fully adjusted model OR 1.17 (95% CI: 1.09, 1.26). LOS was linearly related to the number of procedures/services performed. hscTnT testing did not increase LOS or number of procedures/services
: A clinical request for hscTnT testing is prognostic and risk categorises. Subsequent resource utilization, if increased, appears an epiphenomenon related to risk categorisation, rather than being driven by inappropriate hscTnT testing.
Changes in cardiac biomarkers in goats naturally affected by pregnancy toxemia
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Citation Excerpt :
Similar results were found in human patients with the same type of diabetes (Atabek et al., 2004; Eubanks et al., 2012). Moller et al. (2005) showed elevated cardiac markers, such as CK-MB, suggesting that ketoacidemia can contribute to elevation of cardiac enzymes, due to the large amount of NEFA produced by the lipolytic process, generating large numbers of ketone bodies in the blood, especially when the concentrations of insulin levels are correlated with the degree of acidosis. Another possibility is that the high concentrations of NEFA can lead to their incorporation and the formation of micelles in the myocardial plasma membranes, provoking the destabilization and rupture of the membrane (Van der Vusse et al., 1992).
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Cardiac Troponin I Elevation in Hospitalized Patients Without Acute Coronary Syndromes
2008, American Journal of Cardiology
Citation Excerpt :
Other conditions causing troponin release in the absence of ACS include direct damage to cardiomyocytes by inflammation, infection, toxins, chest contusion, infiltration, or electricity.1–12 Some patients had conditions affecting myocardial cell metabolism (carbon monoxide intoxication, hypoxemia, ketoacidosis, hypercarbia, acute bleeding, and cardiopulmonary resuscitation).9,18–20 In the present study, increased troponin was also noted in 3 patients with pancreatitis.
Increase of cardiac troponins occurs in a variety of clinical situations in the absence of an acute coronary syndrome (ACS). Few data exist regarding the incidence, clinical characteristics, and predictive value of various cardiac diagnostic tests and outcome of patients with a non-ACS–related troponin increase. We studied 883 consecutive hospitalized patients with increased cardiac troponin I levels. The discharge diagnosis was reclassified and troponin increase attributed to ACS or another process. Clinical data and results of cardiac diagnostic tests were collected. Patients were followed for a median of 30 months. Three hundred eleven patients were classified as having a non-ACS–related troponin increase (35.2%). An alternative explanation for troponin increase was found in 99% of these patients. Troponin level had poor accuracy in discriminating patients with and without ACS (area under the receiver operating characteristics curve 0.63). Coronary angiography was frequently unhelpful in excluding a non-ACS–related troponin increase because 77% of patients in the non-ACS group had significant flow-limiting coronary artery disease. Patients with non-ACS–related troponin increase had significantly higher in-hospital (hazard ratio 2.8, 95% confidence interval 2.0 to 3.8) and long-term (hazard ratio 2.0, 95% confidence interval 1.6 to 2.5) mortalities compared with patients with ACS. In conclusion, cardiac troponin level is frequently increased in hospitalized patients in the absence of an ACS and portends poor short- and long-term outcomes. Most of these patients have an alternative explanation for cardiac troponin increase. Cardiac diagnostic procedures are frequently unhelpful in excluding a non-ACS–related troponin increase.
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Case reportMyocardial injury with biomarker elevation in diabetic ketoacidosis

Abstract

Introduction

Section snippets

Methods and case stories

Discussion

J Electrocardiol

J Electrocardiol

J Lipid Res

Lancet

Persisting mortality in diabetic ketoacidosis

Diabetic Med

Regulation of in vivo ketogenesis: role of free fatty acids and control by epinephrine, thyroid hormones, insulin and glucagon

Diabetes Metab

Case report
Myocardial injury with biomarker elevation in diabetic ketoacidosis