Non-ischemic Myocardial Injury Research Articles

Causes of Death in Patients With Acute and Chronic Myocardial Injury

BackgroundInformation about causes of death in patients with myocardial injury is limited. The purpose of this study was to explore causes of death in patients with myocardial injury. MethodsIn a cohort of 22,589 patients, 3853 patients with myocardial injury were identified and categorized into: type 1 myocardial infarction, type 2 myocardial infarction, and nonischemic acute and chronic myocardial injury. We included all 1466/3853 (38%) patients who died during follow-up (3.9 ± 2 years). We estimated rates and adjusted odds ratio (OR) with 95% confidence interval (CI) for causes of death in the 4 categories of myocardial injury using patients without myocardial injury 819/17,932 (4.6%) who died as reference. ResultsThe study cohort included 2285 patients. The proportion of cardiovascular deaths was higher in patients with type 1 myocardial infarction (48%), acute (43%), and chronic (45%) myocardial injury and type 2 myocardial infarction (39%) compared with patients without myocardial injury (25%). Adjusted rates for cardiovascular death were similar in patients with myocardial injury. Type 1 myocardial infarction, acute, and chronic myocardial injury was associated with a 77% (OR: 1.77, 95% CI 1.29-2.41), 40% (OR: 1.40, 95% CI: 1.07-1.84), and 36% (OR: 1.36, 95% CI: 1.05-1.76) higher risk of cardiovascular death. ConclusionsPatients with type 1 myocardial infarction and acute or chronic myocardial injury have similar proportions and high risks for cardiovascular death. We believe that these findings stress the need for investigating patients without known heart diseases who present with nonischemic myocardial injury, or type 2 myocardial infarction.

P852Frequency and prognosis of type 2 myocardial infarction vs non ischemic myocardial injury: large observational study from an emergency department

Abstract Background Type 2 Myocardial Infarction (T2MI), due to myocardial oxygen supply-demand mismatch in the absence of atherothrombosis and non-ischemic myocardial injury (NIMI), corresponding to troponin elevation without overt ischemia, are emerging concepts which are suspected to be common in patients hospitalized. However, their respective frequencies, risk profiles and short term prognosis in current routine clinical practice of emergency unit remains to be investigated. Methods Among the medical records of all the patients admitted from January 2014 to December 2016 in a university hospital emergency unit (n=82 543), patients with elevated troponin Ic (≥0.10μg/L) (n=4568) were systematically adjudicated as T2MI in the presence of symptoms or signs of myocardial ischemia (typical chest pain and/or ECG changes), or as NIMI without such signs. Patients with missing biological data on admission (n=112) or T1MI diagnosis (n=2467) were excluded. Results Among the 1989 patients included, 539 (27%) were classified as T2MI and 1450 (73%) as NIMI. When compared with patients with NIMI, T2MI had higher troponin levels (0.27 (0.14–0.71) vs 0.22 (0.13–0.54) μg/L, p=0.008, respectively). NIMI and T2MI had similar risk factors (age (84 (74–90) vs 84 (75–91) y, p=0.3), male sex (43 vs 48%, p=0.07), hypertension (67 vs 71%, p=0.133), diabetes (25 vs 25%, p=0.9), prior CAD (24 vs 26%, p=0.342), systemic inflammatory response syndrome (SIRS, 47 vs 49%, p=0.3), and systolic blood pressure (SBP) (130 (111–153) vs 132 (112–153) mmHg, p=0.545). Biological data on admission were also similar (hyperglycemia (glucose ≥11 mmol/L), 14 vs 13%, p=0.37, creatinine (96 (72–148) vs 94 (72–141) μmole/L, p=0.598), anemia (Hemoglobin rate ≤10g/dL, 13 vs 14%, p=0.5), C-reactive protein elevation (CRP ≥3 mg/L, 88 vs 89%, p=0.7)). Moreover, in-hospital mortality was high and similar for both groups (15 vs 18%, p=0.2). In multivariate analysis, age, troponin rate, SIRS, anemia, SBP, hyperglycemia, creatinine and CRP elevation were independent factors associated with hospital mortality, but not T2MI (vs NIMI) (OR: 0.88 (0.66–1.17)). Older age and hyperglycemia were specific covariates associated with increased risk of mortality in T2MI, but not in NIMI. Conclusions This large real-life study of non-T1MI inpatients with elevated troponins from emergency department shows that myocardial injury without necrosis and T2MI share the same risk factors, characterized by a high rate of infections and anemia and a high risk of hospital mortality. Acknowledgement/Funding University Hospital Center Dijon Bourgogne, France

P1543Causes of death in patients with myocardial infarction, and non-ischemic myocardial injury

Abstract Background Information about causes of death in patients with non-ischemic acute and chronic myocardial injury is limited. Purpose To explore causes of death, mortality rates and risks of cardiovascular and non-cardiovascular causes of death in patients with type 1 MI (T1MI), type 2 MI (T2MI), and acute and chronic myocardial injury compared with patients without myocardial injury. Methods From a cohort of 39,558 patients who visited the ED at our University Hospital during 2011–2014 and who had high-sensitivity cardiac troponin T (hs-cTnT) levels measured, we identified 3,853 patients with hs-cTnT levels above the 99th percentile value and categorised them into the following groups: i) T1MI, ii) T2MI, iii) acute and iv) chronic myocardial injury. Among these we included all patients who died during follow-up. Causes of death were obtained from the Swedish Cause-of-Death register. All deaths among patients without myocardial injury (n=819) from the same cohort were used for comparison. We calculated incidence rates of cause-specific deaths in the different groups and used logistic regression to estimate odds ratios (OR) with 95% confidence intervals (CIs) adjusted for age and sex for different causes of death, using patients without myocardial injury as referent. Results 2,285 patients died during follow-up at a mean age of 76 (±13) years of whom 46% were female. Patients without myocardial injury died at a younger age (mean 70 years) compared with patients in the groups with myocardial injury (mean 79–82 years). The proportion of cardiovascular (CV) deaths were considerably higher in patients with T1MI (48%), T2MI (39%), acute (43%), and chronic (45%) myocardial injury compared with patients with no myocardial injury (25%). 42% of patients without myocardial injury died from cancer, compared with 18% to 24% among patients with different myocardial injury. Age- and sex-adjusted incidence rates for CV-death were similar for T1MI, T2MI and acute myocardial injury (27 per 100 person-years), slightly lower in patients with chronic myocardial injury (22 per 100 person-years) and almost half in patients with no myocardial injury (14 per 100 person-years). The adjusted ORs with 95% CIs for CV death were highest in patients with T1MI (1.99, 1.48–2.69) and acute myocardial injury (1.72, 1.29–2.11), while only marginally lower in patients with T2MI and chronic myocardial injury (1.43, (0.94–2.16), and 1.65, (1.29–2.11) respectively). Conclusions Patients with T1MI and acute or chronic myocardial injury have similar risks to die from cardiovascular causes. Patients without myocardial injury died younger and the proportions of cancer-related deaths were twice as high as in the groups with myocardial injury. Proportions and risks of CV-death among patients with T2MI were higher than in patients without myocardial injury, but lower than in patients with T1MI and acute or chronic myocardial injury. Acknowledgement/Funding None

Clinical Progress Notes: Updates from the 4th Universal Definition of Myocardial Infarction.

In this clinical practice update, we aim to review the updated definition of Type 2 MI (T2MI) and nonischemic myocardial injury (NIMI), since these are the two predominant diagnoses among patients with elevated troponin in the absence of T1MI. We also provide a clinical framework for clinicians to think through elevated serum cardiac troponin levels and identify opportunities for quality improvement around this critical issue.

Assessment and Treatment of Patients With Type 2 Myocardial Infarction and Acute Nonischemic Myocardial Injury

Although coronary thrombus overlying a disrupted atherosclerotic plaque has long been considered the hallmark and the primary therapeutic target for acute myocardial infarction (MI), multiple other mechanisms are now known to cause or contribute to MI. It is further recognized that an MI is just one of many types of acute myocardial injury. The Fourth Universal Definition of Myocardial Infarction provides a taxonomy for acute myocardial injury, including 5 subtypes of MI and nonischemic myocardial injury. The diagnosis of MI is reserved for patients with myocardial ischemia as the cause of myocardial injury, whether attributable to acute atherothrombosis (type 1 MI) or supply/demand mismatch without acute atherothrombosis (type 2 MI). Myocardial injury in the absence of ischemia is categorized as acute or chronic nonischemic myocardial injury. However, optimal evaluation and treatment strategies for these etiologically distinct diagnoses have yet to be defined. Herein, we review the epidemiology, risk factor associations, and diagnostic tools that may assist in differentiating between nonischemic myocardial injury, type 1 MI, and type 2 MI. We identify limitations, review new research, and propose a framework for the diagnostic and therapeutic approach for patients who have suspected MI or other causes of myocardial injury.

Frequency and prognosis of type 2 myocardial infarction vs non ischemic myocardial injury: Large observational study from an emergency department

Type 2 Myocardial Infarction (T2MI), due to myocardial oxygen supply-demand mismatch in the absence of atherothrombosis and of non-ischemic myocardial injury (NIMI), i.e. troponin elevation without overt ischemia are new emerging physiopathological entities. We aimed to investigate frequencies and characteristics of T2MI and NIMI in current routine clinical practice of emergency unit. Among patients admitted from 2014 to 2016 in a university hospital emergency unit ( N = 82,543), patients with elevated troponin Ic (≥ 0.10μg/L) ( N = 4568) were adjudicated as T2MI if symptoms or signs of myocardial ischemia (typical chest pain and/or ECG changes), or as NIMI without such signs. Patients with missing admission biological data ( N = 112) or T1MI ( N = 2467) were excluded. Among the 1989 patients included, 539 (27%) were diagnosed as T2MI and 1450 (73%) as NIMI. When compared with NIMI, T2MI had higher troponin levels (0.27 (0.14–0.71) vs 0.22 (0.13–0.54) μg/L, P = 0.008, respectively). Risk factors were similar for both groups (age (84(74–90) vs 84(75–91) y, P = 0.3), male sex (43 vs 48%, P = 0.07), hypertension (67 vs 71%, P = 0.133), diabetes (25 vs 25%, P = 0.9), prior CAD (24 vs 26%, P = 0.342), systemic inflammatory response syndrome (SIRS) (47 vs 49%, P = 0.3), and systolic blood pressure (SBP) (130 (111–153) vs 132 (112–153) mmHg, P = 0.545). Biological data on admission were also similar (hyperglycemia (glucose ≥ 11mmol/L), 14 vs 13%, P = 0.37, creatinine (96 (72–148) vs 94 (72–141) μmole/L, P = 0.598), anemia (Hemoglobin ≤ 10g/dL, 13 vs 14%, P = 0.5), C-reactive protein elevation (CRP ≥ 3mg/L, 88 vs 89%, P = 0.7)). Moreover, in-hospital mortality was high and similar for both groups (15 vs 18%, P = 0.2), even when adjusted for confounding. This large real-life study shows that NIMI and T2MI are common and share the same risk factors, characterized by a high rate of infections and anemia and a high risk of hospital mortality.

Frequency and prognosis of type 2 myocardial infarction vs. non-ischemic myocardial injury: Large observational study from an emergency department.

In current routine clinical practice of emergency unit, frequencies and characteristics of Type 2 Myocardial Infarction (T2MI), due to myocardial oxygen supply-demand mismatch in the absence of atherothrombosis and of non-ischemic myocardial injury (NIMI), i.e. troponin elevation without overt ischemia, remains to be investigated. Among medical records of all the patients admitted from January 2014 to December 2016 in a university hospital emergency unit ( n = 82,543), patients with elevated troponin Ic (≥ 0.10 μg/L) ( n = 4568) were adjudicated as T2MI if symptoms or signs of myocardial ischemia (typical chest pain and/or ECG changes), or as NIMI without such signs. Patients with missing admission biological data ( n = 112) or T1MI ( n = 2467) were excluded. Among the 1989 patients included, 539 (27%) were diagnosed as T2MI and 1450 (73%) as NIMI. When compared with NIMI, T2MI had higher troponin levels [0.27 (0.14–0.71) vs. 0.22 (0.13–0.54) μg/L, P = 0.008, respectively]. Risk factors were similar for both groups [age 84(74–90) vs. 84(75–91) y, P = 0.3], male sex (43 vs. 48%, P = 0.07), hypertension (67 vs. 71%, P = 0.133), diabetes (25 vs. 25%, P = 0.9), prior CAD (24 vs. 26%, P = 0.342), systemic inflammatory response syndrome (SIRS) (47 vs. 49%, P = 0.3), and systolic blood pressure (SBP) (130 (111–153) vs. 132 (112-153) mmHg, P = 0.545). Biological data on admission were also similar [hyperglycemia (glucose ≥ 11 mmol/L), 14 vs. 13%, P = 0.37, creatinine [96 (72–148) vs. 94 (72–141) μmole/L, P = 0.598], anemia (Hemoglobin ≤ 10 g/dL, 13 vs. 14%, P = 0.5), C-reactive protein elevation (CRP ≥ 3 mg/L, 88 vs. 89%, P = 0.7)]. Moreover, in-hospital mortality was high and similar for both groups (15 vs. 18%, P = 0.2), even when adjusted for confounding. This large real-life study shows that NIMI and T2MI are common and share the same risk factors, characterized by a high rate of infections and anaemia and a high risk of hospital mortality.

57-Year-Old Man With Atypical Chest Pain

57-Year-Old Man With Atypical Chest Pain

Short-Term Prognosis of Myocardial Injury, Type 1, and Type 2 Myocardial Infarction in the Emergency Unit

Type 2 myocardial infarction and nonischemic myocardial injury, corresponding to troponin elevation without atherothrombosis, are emerging concepts suspected of being common in emergency departments (ED). However, their respective frequencies, risk profiles, and short-term prognoses remain to be investigated. Among all the patients admitted from January 2014 to December 2016 in a university hospital ED (n = 33,669), those with elevated conventional troponin Ic (≥0.10 µg/L) (n = 4436, 13%) were systematically adjudicated as having type 1 or type 2 myocardial infarction in the presence of symptoms or signs of myocardial ischemia (typical chest pain or electrocardiographic changes) or myocardial injury without such signs. Among the 4436 patients included, 1453 (33%) were classified as having myocardial injury, 947 (21%) as having type 2 and 2036 (46%) as having type 1 myocardial infarction. Compared with type 1 patients, patients with type 2 myocardial infarction and myocardial injury were markedly older (respective median ages: 67, 81, and 84 years; P < .001) with more frequent comorbidities. In multivariate analysis, myocardial injury was associated with a lower risk of cardiovascular death (odds ratio 43; 95% confidence interval, 0.29-0.65; P < .001) but a higher risk of all-cause in-hospital death (odds ratio 1.43; 95% confidence interval, 1.02-2.00; P = .037). Systolic blood pressure <90mm Hg and heart rate >100 beats per minute at admission were strongly associated with all-cause mortality, and the troponin rate was associated with cardiovascular mortality in all groups. In a large study of patients with elevated troponins in an ED, myocardial injury and type 2 myocardial infarction were frequent and associated with a worse in-hospital prognosis than type 1 myocardial infarction resulting from noncardiovascular events.

PP-068 CARDIAC AMYLOIDOSIS DIAGNOSED WITH ALTERED GADOLINIUM KINETICS ON CARDIAC MR

younger twin, increased trabeculations in left ventricular lateral and apical segments with the ratio of non-compacted to compacted layers of 1.6 were observed. CMR also revealed mid-myocardial and subepicardial late linear gadolinium enhancement indicating nonischemic myocardial injury. Conclusion: Genetic predisposition to the development of cardiomyopathy must be evaluated before management. As in our cases, in the absence of hereditary factors, it is believed that a possible viral intervention during fetal life can produce cardiomyopathy in twins. The CMR findings may prove to have value in diagnosis with high sensitivity and specifity.

Naxos disease presenting with ventricular tachycardia and troponin elevation

Naxos disease is a recessively inherited stereotype association of arrhythmogenic cardiomyopathy with a cutaneous phenotype, characterized by peculiar woolly hair and palmoplantar keratoderma. The cardiomyopathy clinically manifests by adolescence and the symptomatic presentation is usually with syncope and/or sustained ventricular tachycardia of left bundle branch block configuration. We report the case of a 43-year-old man without any history of heart disease who was admitted to the hospital because of an episode of sustained ventricular tachycardia and troponin I elevation, in the absence of coronary artery disease. Diagnostic workup, including genetic assessment, revealed Naxos disease as the underlying cause. In this case, acute myocarditis seems to be the most plausible explanation for the nonischemic myocardial injury.

Ischemické a neischemické postižení myokardu: diferenciální diagnostika pomocí postkontrastních odložených scanů magnetické rezonance

Ischemické a neischemické postižení myokardu: diferenciální diagnostika pomocí postkontrastních odložených scanů magnetické rezonance

The Diagnostic Usefulness of Cardiovscular Magnetic Resonance Imaging for Non-Ischemic Myocardial Injury : The Value of the Endocardial Sparing Pattern on Delayed Enhancement

Background and Objectives:Cardiovascuar MR using contrast enhancement has recently been reported to be useful for diagnosing myocarditis. It is also well known that irreversible myocardial injury by epicardial coronary artery flow obstruction spreads from the endocardium to the epicardium in a wave-front pattern with a time-dependent manner. We investigated characteristics of the patterns of contrast-enhanced MR imaging according to the underlying myocardial injury mechanism. Subjects and Methods:Of all 275 patients who underwent coronary angiogram at our hospital due to cheat pain and elevated cardiac enzymes between October, 2002 and August, 2003, 48 patients who underwent cardiac MR were enrolled in this study. We retrospectively analyzed the pattern of delayed hyperenhancement according to presence or absence of a documented infarct related artery. Endomyocardial biopsies were done in selected patients. Results:Contrast MR images of all patients showed delayed hyperenhancement. The study group was divided into 2 groups according to whether the areas of hyper-enhancement were involved in the sub-endocardial portion (endocardial sparing pattern, ESP) or not. In 8 patients (Group A, 17%) who showed the endocardial sparing pattern on contrast MR, the findings of coronary angiogram were all normal. In 40 patients (Group B, 83%), who did not show the endocardial sparing pattern on contrast MR, 39 patients (97.5 %) had an infarct related artery on coronary angiogram (p=0.001). Endomyocardial biopsies were performed in 3 patients of group A. The findings of the 3 biopsies were 2 cases of definite myocarditis and 1 case of myocardial degeneration. Conclusion:The endocardial sparing pattern of myocardial injury demonstrated by delayed enhancement MR imaging was very useful to predict the presence of an infarct related artery in patients with myocardial necrosis that has been determined by elevated cardiac enzymes. This result can be a useful clue to determine the nature of the underlying injury mechanism such as ischemic or non-ischemic. (Korean Circulation J 2004;34(12):1174-1181)

Biochemical markers of ischemic and non-ischemic myocardial damage

Biochemical markers have been an integrative part of non-invasive diagnostic strategies in cardiology for nearly 50 years, experiencing a renascence by the recently acknowledged prognostic potential of cardiac troponins in acute coronary syndromes. According to the guidelines of the National Academy of Clinical Biochemistry and the International Federation of Clinical Chemistry cardiac troponin T and cardiac troponin I should be considered as the new "gold markers" of ischemic myocardial injury. One characteristic feature of these new markers is the improved diagnostic potential, reflected by the choice of two cut-off values to distinguish minor myocardial injury from acute myocardial infarction. In addition, cardiac troponins allow risk stratification in the clinical setting of acute coronary syndromes: approximately threefold higher mortality rate for patients with rest angina or ST segment elevation and cardiac troponin elevation on admission. Other indications for cardiac marker analysis are monitoring of therapeutic success in case of invasive and non-invasive reperfusion strategies and non-invasive diagnosis of non-ischemic myocardial injury (myocarditis, cardiac contusion and chemotherapy). Biochemical cardiac markers are a useful tool in the diagnosis of both ischemic and non-ischemic myocardial injury. Among these, cardiac troponins seem to become the gold markers for the new millennium.

Ischemic and non-ischemic myocyte damage and antimyosin monoclonal imaging.

Antimyosin monoclonal antibody is a specific marker of impaired sarcolemmal integrity resulting not only from ischemia but also from non-ischemic myocardial injury, such as infection, inflammatory, or immunologic reactions, and alcohol or drug intoxication. In addition, antimyosin accumulation has been demonstrated in some forms of cardiomyopathy with unknown as well as known etiologies. Antimyosin positivity appears to indicate precisely the extent of myocardial necrosis and to reflect cardiac dysfunction in an acute stage of active myocardial damage caused by ischemia and inflammation. However, the correlation is not necessarily good in the chronic stages of the disease or in idiopathic cardiomyopathic hearts; in other words, cardiac antimyosin uptake can be detected even in myocardial tissue with a normal histologic appearance independent of the presence of inflammatory responses, myocyte necrosis, or functional or morphologic deterioration. Thus, antimyosin is useful not only for detecting and quantifying acute myocardial necrosis but also for specifically identifying ongoing or latently progressing myocardial degeneration and sarcolemmal disruption, which will certainly lead to myocardial necrosis. These characteristics may contribute to the early detection of myocardial damage and lead to the investigation of pathophysiologic mechanisms. Further progress in immunologic and radiolabeling techniques is necessary for better specificity and less antigenicity against humans in antimyosin monoclonal antibody imaging.