scholarly journals Post-infections and sepsis associated myocardial infarction: casuistic masks

2021 ◽  
Vol 16 (7-8) ◽  
pp. 106-109
Author(s):  
L.O. Malsteva ◽  
W.W. Nikonov ◽  
N.A. Kazimirova ◽  
A.A. Lopata
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Task Force ◽  
Laboratory Data ◽  
Myocardial Damage ◽  
Time Frame ◽  
Diagnostic Value ◽  
Epidemiological Studies ◽  
Definition Of ◽  
Post Infectious

The review aims to present the chronological sequence of developing universal definitions of myocardial infarction, new ideas for improving the screening of post-infectious and sepsis-associated myocardial infarction (MI) (casuistic masks of myocardial infarction). The stages of the development of the common and global definition of myocardial infarction are outlined: 1 — by WHO working groups based on ECG for epidemiological studies; 2 — by the European Society of Cardiology and the American College of Cardio-logy using clinical and biochemical approaches; 3 — the Global Task Force consensus document of universal definition with subsequent classification of MI into five subtypes (spontaneous, dissonance in oxygen delivery and consumption; lethal outcome before the rise of specific markers of myocardial damage; PCI-associated; CABG- associated); 4 — review by the Joint Task Force of the above document based on the inclusion of more sensitive markers — troponins; 5 — the allocation of 17 non-ischemic myocardial damage, accompanied by an increase in the level of troponin; 6 — characteristic of the atrial natriuretic peptide from the standpoint of its synthesis, storage, release, diagnostic value as a biomarker of acute myocardial dama­ge; 7 — a clinical definition of myocardial infarction, presented in materials of the III Consensus on myocardial infarction 2017. The diagnosis of myocardial infarction using the criteria set in this document requires the integration of clinical data, ECG patterns, laboratory data, imaging findings, and, in some cases, pathological results, which are considered in the context of the time frame of the suspec­ted event. K. Thygesen et al. consider the additional use of: 1) cardiovascular magnetic resonance to determine the etiology of myocardial damage; 2) computer coronary angiography with suspected myocardial infarction. Myocardial infarction is a combination of specific cardio markers with at least one of the symptoms listed above. The formation of myocardial infarction can occur during/after acute respiratory infection. Causal relationships between these two states are established. Post-infectious myocardial infarction is strongly recommended to be individualized as a separate diagnostic entity. In sepsis, global myocardial ischemia with ischemic myocardial damage arises as a result of humoral and cellular factors, accompanied by an increase in troponins, a decrease in the ejection fraction of the left ventricle by 45 % and an increase in the final diastolic size of the left ventricle, the development of sepsis-associated multiple organ fai­lure, which is an unfavourable prognosis factor.

scholarly journals Takotsubo Syndrome — Stress-induced Heart Failure Syndrome

2015 ◽  
Vol 10 (2) ◽  
pp. 83 ◽  
Author(s):  
Mary N Sheppard ◽  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricle ◽  
Cardiac Function ◽  
Myocardial Damage ◽  
Apical Ballooning ◽  
Stressful Event ◽  
Takotsubo Syndrome ◽  
Interventional Angiography ◽  
Specific Trigger

Takotsubo syndrome has been established as an entity in the past 30 years, particularly with the introduction of interventional angiography for investigation of chest pain. Typically, it occurs in middle-aged females as a response to a stressful event, such as bad news, death, accident, natural disaster, etc. but there is not always a specific trigger. Takotsubo mimics acute myocardial infarction with electrocardiogram changes and elevated troponins. On interventional angiography the coronary arteries are normal with typical apical ballooning of the left ventricle. This feature led to its descriptive name, given by Japanese cardiologists, as the left ventricle resembles a lobster trap with a narrow neck extending into a round ventricle. This leads to a reduction in cardiac function. Takotsubo is believed to be a response to catecholamine release following a stressful event resulting in temporary myocardial damage. It usually has a benign course with spontaneous return of cardiac function. However it may recur and in a small percentage of patients can result in sudden cardiac death with arrhythmia, acute myocardial infarction and cardiac rupture. It is usually treated symptomatically depending on the severity of presentation.

MINOCA: a heterogenous group of conditions associated with myocardial damage

Heart ◽  
2021 ◽  
pp. heartjnl-2020-318269
Author(s):  
Trisha Singh ◽  
Andrew R Chapman ◽  
Marc R Dweck ◽  
Nicholas L Mills ◽  
David E Newby
Keyword(s):  
Myocardial Infarction ◽  
Obstructive Coronary Artery Disease ◽  
Myocardial Damage ◽  
Disease Classification ◽  
Heterogenous Group ◽  
Diagnostic Confusion ◽  
Artery Disease ◽  
Universal Definition ◽  
Definition Of

Myocardial infarction with non-obstructive coronary arteries (MINOCA) was first described over 80 years ago. The term has been widely and inconsistently used in clinical practice, influencing various aspects of disease classification, investigation and management. MINOCA encompasses a heterogenous group of conditions that include both atherosclerotic and non-atherosclerotic disease resulting in myocardial damage that is not due to obstructive coronary artery disease. In many ways, it is a term that describes a moment in the diagnostic pathway of the patient and is arguably not a diagnosis. Central to the definition is also the distinction between myocardial infarction and injury. The universal definition of myocardial infarction distinguishes acute myocardial infarction, including those with MINOCA, from other causes of myocardial injury by the presence of clinical evidence of ischaemia. However, these ischaemic features are often non-specific causing diagnostic confusion, and can create difficulties for patient management and follow-up. The purpose of this review is to summarise our current understanding of MINOCA and highlight important issues relating to the diagnosis, investigation and management of patients with MINOCA.

Butyrylcholinesterase as an additional marker in the diagnostic network of acute myocardial infarction

2016 ◽  
Vol 40 (2) ◽  
Author(s):  
Ramazan Kocabaş ◽  
Ali Kemal Erenler ◽  
Mücahit Yetim ◽  
Tolga Doğan ◽  
Hacı Kemal Erdemli
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Healthy Subjects ◽  
Early Stage ◽  
Characteristic Curve ◽  
Myocardial Damage ◽  
Diagnostic Value ◽  
Coronary Syndrome ◽  
Additional Marker ◽  
Low Sensitivity

AbstractAcute coronary syndrome defines a broad spectrum of complaints from angina to irreversible myocardial damage. There is an ongoing need for a biomarker to predict and diagnose acute myocardial infarction (AMI) in the early stage. In this study, our aim was to reveal early diagnostic value of butyrylcholinesterase (BChE) in discrimination of healthy subjects and patients with AMI.Eighty-five patients admitted to our hospital due to AMI and 45 healthy subjects were involved in the study. Patients and controls were compared according to BChE, lipid profiles and biochemical parameters.The serum BChE activity was significantly lower in patients with AMI than in the controls (p<0.001). After correlation analysis, while a negative correlation was determined between the serum BChE concentrations and AMI presence (r=–0.363, p<0.001); a positive correlation was determined between the serum BChE and cholesterol (r=0.443, p<0.001), HDL (r=0.243, p=0.006) and LDL (r=0.369, p<0.001) levels. The data indicate that BChE is associated with AMI and a subsequent receiver operating characteristic curve (ROC) analysis revealed that BChE, as an independent indicator, may differentiate AMI patients from controls. A cut-off point set at ≤7.15 kIU/L, BChE showed a sensitivity of 51.2% and a specificity of 84.4% (AUC=0.719, p<0.001).Low BChE level was significantly associated with AMI when compared to healthy subjects. Even though it has low sensitivity, plasma levels of BChE might represent an additional marker in the diagnostic network of AMI.

scholarly journals Non-coronarogenic causes of increased cardiac troponins in clinical practice

2020 ◽  
Vol 10 (4) ◽  
pp. 81-93 ◽  
Author(s):  
Aleksey M. Chaulin ◽  
Lilya S. Karslyan ◽  
Dmitry V. Duplyakov
Keyword(s):  
Myocardial Infarction ◽  
Skeletal Muscle ◽  
Pulmonary Embolism ◽  
Renal Failure ◽  
Myocardial Damage ◽  
Diagnostic Value ◽  
Elevated Troponin ◽  
Heterophilic Antibodies ◽  
Highly Sensitive ◽  
Cardiac Troponins

Cardiospecific isoforms of troponins are the most sensitive and specific biomarkers for the diagnosis of myocardial infarction. However, though elevated troponin levels indicate myocardial damage, they do not determine the cause and mechanism of the damage. With the new highly sensitive methods, very minor damages of the heart muscle can be detected. Myocardial damage can occur in many non-coronarogenic diseases. In this review, we discuss the mechanisms of elevation, the diagnostic value of cardiac troponins in the renal failure, tachyarrhythmias, endocarditis, myocarditis, pericarditis, sepsis, neurogenic pathologies (stroke), pulmonary embolism. In addition, we pay attention to the main reasons for a false-positive increase of the concentration of cardiac troponins: heterophilic antibodies, rheumatoid factor, alkaline phosphatase, cross-reactions with skeletal muscle troponins.

scholarly journals Superiority of wall motion score index over left ventricle ejection fraction in predicting cardiovascular events after an acute myocardial infarction

2016 ◽  
Vol 8 (1) ◽  
pp. 78-85 ◽  
Author(s):  
Alfonso Jurado-Román ◽  
Pilar Agudo-Quílez ◽  
Belén Rubio-Alonso ◽  
Javier Molina ◽  
Belén Díaz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Left Ventricle ◽  
Ejection Fraction ◽  
Wall Motion ◽  
Myocardial Damage ◽  
Composite Endpoint ◽  
Left Ventricle Ejection Fraction ◽  
Wall Motion Score Index ◽  
Score Index

Background: There are few data on the prognostic significance of the wall motion score index compared with left ventricle ejection fraction after an acute myocardial infarction. Our objective was to compare them after the hyperacute phase. Methods: Transthoracic echocardiograms were performed in 352 consecutive patients with myocardial infarction, after the first 48 hours of admission and before hospital discharge (median 56.3 hours (48.2–83.1)). We evaluated the ability of the wall motion score index and left ventricular ejection fraction to predict the combined endpoint (mortality and rehospitalization for heart failure) as a primary objective and the independent events of the combined endpoint as a secondary objective. Results: In 80.7% of patients, the wall motion score index was high despite having an ejection fraction >40%. No patient had an ejection fraction <55% with a normal index. After a follow-up of 30.5 months (24.2–49.5), both variables were predictors of the composite endpoint and all-cause mortality ( p<0.0001), although only the wall motion score index was a predictor of readmission for heart failure ( p=0.007). By multivariate analysis, a wall motion score index >1.8 proved to be the most powerful predictor of the composite endpoint (hazard ratio: 8.5; 95% confidence interval 3.7–18.8; p<0.0001). The superiority of the wall motion score index over ejection fraction was especially significant in patients with less myocardial damage (non-ST elevation myocardial infarction, or left ventricle ejection fraction >40%). Conclusions: Both variables provide important prognostic information after a myocardial infarction. Beyond the hyperacute phase, wall motion score index is a more powerful prognostic predictor, especially in subgroups with less myocardial damage.

UNSTABLE ANGINA : DEFINITION

1987 ◽  
Author(s):  
D G Julian
Keyword(s):  
Myocardial Infarction ◽  
Unstable Angina ◽  
Beta Blockers ◽  
Time Frame ◽  
History Of ◽  
Exercise Induced ◽  
The One ◽  
Definition Of ◽  
The Individual

A satisfactory definition of unstable angina continues to be elusive.Like stable angina, it is a clinicalsyndrome, and mustbe defined in those terms. In both cases, it is understood that myocardial ischaemiabut not infarction is responsible for the symptoms. For angina to earn the “unstable” label, theremust have been the recent development or deterioration of symptoms. Traditionally, “recent” has meant within the last month, but it has become increasingly clear thatthe time frame is of critical importance - the patient with a sudden irruption of severe chest pain in the last two days is likely to have a different pathology and prognosis from the individual who first developed exercise-induced pain two weeks ago, which has not worsened during this period. Likewise, the patient who hadhis last attack of pain one week agois very different from one who had his last attack one hour ago; indeed in the HINT study, there was a high incidence of myocardial infarction undetected on admission in the lattergroup (Br Heart J 1986;56:400-13).A problem that has hardly been addressed is “When does unstable angina stop being unstable?”. The answer must be when it either becomes stable (i.e. stops getting worse),or proceeds to myocardial infarctionor death.Most studies have shown that the vast majority of patients stablise quickly, often losing their symptoms completely. There is, however, a group of patients who fail to respond promptly to medical treatment, and it isthese patients who are most likely to go on to angiography, angioscopy, angioplasty, surgery, myocardial infarction or death. Thus, the enormously valuable information we have obtained from, for example, angiography and necropsy studies applies essentially only to this subset of unstableangina patients, albeit they are themost severe. Unfortunately, such studies tell us relatively little aboutthe more dynamic aspects of the disorder, such as the role of coronary vasomotion.It is only relatively recently that clinicians have appreciated that they have quite simple means of suspecting the mechanisms involved. Thus, the history of progressive exercise-induced angina on the one hand or angina only at rest on theother must tell us something of the underlying physiopathology. Likewise,the fact that the symptoms respond to rest, or beta-blockers, or calcium antagonists also provides evidenceas to causation.Thus, while all would agree that angina is “unstable” whenit has recently developed or worsened, it must bediscussed in subsetsdefined by their history and response to treatment.In this way, we may be able to assign a patient to a particular clinicalgroup, which will indicate that it is likely that he has a particular physiopathology, which inturn will suggest the most appropriate management.

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