scholarly journals Postoperative ‘STEMI’ in Intracerebral Hemorrhage due to Arteriovenous Malformation: A Case Report and Review of Literature

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Ravinder Datt Bhanot ◽  
Jasleen Kaur ◽  
Shitiz Sriwastawa ◽  
Kendall Bell ◽  
Kushak Suchdev

Electrocardiogram (ECG) changes suggestive of cardiac ischemia are frequently demonstrated in patients with ischemic stroke and subarachnoid hemorrhage. However, little is known of such changes particularly acute ST segment myocardial infarction (STEMI) in patients with intracerebral hemorrhage (ICH), especially after neurosurgery. We present a patient with intraparenchymal hemorrhage due to cerebral arteriovenous malformation (AVM) who exhibited acute STEMI after neurosurgery. Serial cardiac biomarkers and echocardiograms were performed which did not reveal any evidence of acute myocardial infarction. The patient was managed conservatively from cardiac stand point with no employment of anticoagulants, antiplatelet therapy, fibrinolytic agents, or angioplasty and recovered well with minimal neurological deficit. This case highlights that diffuse cardiac ischemic signs on the ECG can occur in the setting of an ICH after neurosurgery, potentially posing a difficult diagnostic and management conundrum.

2017 ◽  
Vol 2017 ◽  
pp. 1-3 ◽  
Author(s):  
Bashar Alzghoul ◽  
Ayoub Innabi ◽  
Anusha Shanbhag ◽  
Kshitij Chatterjee ◽  
Farah Amer ◽  
...  

Pneumothorax is a well-recognized complication of central venous line insertion (CVL). Rarely, pneumothorax can lead to electrocardiogram (ECG) findings mimicking ST-segment elevation myocardial infarction. We present a 63-year-old man with iatrogenic right-sided pneumothorax who developed ST-segment elevation on a 12-lead ECG suggestive of myocardial infarction. The ECG findings completely resolved after needle decompression and chest tube placement. This case points up this rare electrocardiographic finding with discussion of possible mechanisms and differential diagnosis.


2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Joseph Donovan ◽  
Mark Jackson

Acute coronary syndrome is a common cause of presentation to hospital. ST segment elevation on an electrocardiogram (ECG) is likely to be cardiac in origin, but in low-risk patients other causes must be ruled out. We describe a case of a man with hypercalcaemia, no evidence of cardiac disease, and ECG changes mimicking acute myocardial infarction. These ECG changes resolved after treatment of the hypercalcaemia.


1972 ◽  
Vol 17 (10) ◽  
pp. 319-325 ◽  
Author(s):  
M. Afzal Mir

Out of 284 patients admitted to the Coronary-Care Unit, 60 patients showed an acute monophasic injury pattern (M-Complex) on their initial electrocardiogram (ECG). There were 13 fatalities on the first day of myocardial infarction; 6 from the M-complex group. Three of these 6 patients died with cardiac rupture. The ECG features of these 3 patients were compared with the 3 non-rupture patients. A progressive increase in the elevated R-ST segment of the M-complex with an upward ‘pull’ of the R-ST junction, proved to be an ominous ECG sign of impending cardiac rupture in patients with protracted chest pain and persistent hypertenison. The 3 non-rupture patients remained in a hypotensive state from admission to the time of death. Atrioventricular block and A-V junctional tachycardia were the commonest rhythm disturbances in patients dying with cardiac rupture.


2012 ◽  
Vol 32 (6) ◽  
pp. 35-41
Author(s):  
Stacy H. James

Drugs that work on the hematologic system play an important role in helping to limit the morbidity and mortality that can be associated with an acute coronary syndrome. The pharmacology of the fibrinolytic agents, thrombin inhibitors, and antiplatelet agents is described. A case study of a woman having an ST-segment elevation myocardial infarction is reviewed to highlight the importance of drugs that work on the hematologic system.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Wayne D Rosamond ◽  
Rachel Kloss ◽  
Natalia Petruski-ivleva ◽  
Lisa Wruck ◽  
Erin Michos ◽  
...  

Background: Epidemiology studies of acute myocardial infarction (MI) often rely on hospital discharge codes or claims data to identify events. The fourth digit of ICD-9 code 410 is meant to identify anatomic location of an MI. Although the validity of ICD-9 410 codes to identify the general category of MI has been studied, far less is known about the validity of ICD codes to identify ST segment MI (STEMI) and non-STEMI (NSTEMI) and to identify anatomic location of STEMI infarcts. Methods: From 1987 to 2010 we evaluated random samples of hospitalizations with ICD-9 discharge codes 410-414, 402, 427, 428, or 518.4 among men and women age 35-74 years from hospitals serving the 4 communities of the Atherosclerosis Risk in Communities (ARIC) Study (400,000 base population in 2010). Trained staff abstracted medical records and copied up to three 12-lead electrocardiograms (ECG) that were coded by Minnesota Code. A standardized algorithm was applied to data on chest pain, cardiac biomarkers, and ECG evidence to determine MI diagnosis. Validated MI events with abnormal biomarkers were further classified by ECGs as STEMI or NSTEMI. ICD-9 codes 410.0-410.6 and 410.8 were used to define STEMI while codes 410.7 or 410.9 defined NSTEMI. STEMI infarct location was assessed by ECG and categorized as anterior, inferior, lateral, or multi-location. We determined the validity of code-based definitions using the ARIC algorithm and ECG evidence as referent standards. All analyses were weighted to account for sampling. Results: Between 1987 and 2010, 208,920 (weighted) hospitalizations with discharge codes suggestive of MI occurred in the 4 ARIC communities. Of these, 19% (38,729/208,920) were validated as MI. The positive predictive value (PPV) of an ICD-9 410 code to identify a validated MI was 72% (22218/30652). This PPV declined slightly from 78% (862/1111) in 1987 to 71% (1031/1462) in 2010. Center differences by community were seen (range 63% (197/315) to 78% (173/222) in 2010). Sensitivity of a 410 code to identify validated MIs remained stable from 1987 to 2010 at about 57% (22218/38,729). The PPV of the ICD-9 code-based STEMI definition improved after 2005 but remained moderate at 41% (175/430) in 2010. The PPV of the ICD-9 code based definition of NSTEMI was 63% (599/945) in 2010 and was stable over time. The PPV of codes to identify anterior and inferior infarctions were high (66% (1145/1741) and 78% (1956/2518), respectively). However codes for lateral and multiple site infarctions had lower PPV (53% (327/619) and 21% (153/727), respectively). Conclusions: The PPV of an ICD-9 code 410 to identify MI remained stable over the past 2 decades, but geographic differences persist. ICD-9 codes are better at correctly identifying NSTEMI than STEMI and better at identifying inferior infarcts than other anatomic locations. These data suggest caution in interpreting studies of MI trends based solely on ICD-9 codes.


2013 ◽  
Author(s):  
R Scott Wright ◽  
Joseph G Murphy

Patients with coronary artery disease (CAD) present clinically when their disease enters an unstable phase known as an acute coronary syndrome (ACS), in which the cap of a previously stable atheromatous coronary plaque ruptures or erodes, which in turn activates a thrombotic cascade that may lead to coronary artery occlusion, myocardial infarction (MI), cardiogenic shock, and patient death. There are nearly 2 million episodes of ACS in the United States annually; it is the most common reason for hospitalization with CAD and is the leading cause of death in the developed world. ACS patients include those with unstable angina (UA), non–ST segment elevation myocardial infarction (non-STEMI), and ST segment elevation myocardial infarction (STEMI) and patients who die suddenly of an arrhythmia precipitated by coronary occlusion. The distinction among various ACS subgroups reflects varying characteristics of clinical presentation (presence or absence of elevated cardiac biomarkers) and the type of electrocardiographic (ECG) changes manifested on the initial ECG at the time of hospitalization. This chapter focuses on UA and non-STEMI. A graph outlines mortality risks faced by patients with varying degrees of renal insufficiency. An algorithm describes the suggested management of patients admitted with UA or non-STEMI. Tables describe the risk stratification of the patient with chest pain, categories of Killip class, examination findings of a patient with high-risk ACS, diagnosis of MI, causes of troponin elevation other than ischemic heart disease, initial risk stratification of ACS patients, and long-term medical therapies and goals in ACS patients. This review contains 2 highly rendered figures, 11 tables, and 76 references.


2017 ◽  
Vol 11 (7) ◽  
pp. 195-197
Author(s):  
Aditya Naraian Chada ◽  
Naga Venkata Krishna Chand Pothineni ◽  
Swathi Kovelamudi ◽  
Deepa S. Raghavan

We present a unique case of a patient with a tension pneumothorax that presented with electrocardiogram (ECG) characteristics typical for ST segment elevation myocardial infarction. The clinical diagnosis was clinched by focused physical examination. Treatment of the pneumothorax lead to resolution of the electrocardiographic abnormalities. Our experience from this unique case is useful for cardiologists and critical care physicians who encounter these patients routinely.


Author(s):  
Aldo Clerico ◽  
Martina Zaninotto ◽  
Alberto Aimo ◽  
Ruggero Dittadi ◽  
Domenico Cosseddu ◽  
...  

Abstract Serial measurements of cardiac troponin are recommended by international guidelines to diagnose myocardial infarction (MI) since 2000. However, some relevant differences exist between the three different international guidelines published between 2020 and 2021 for the management of patients with chest pain and no ST-segment elevation. In particular, there is no agreement on the cut-offs or absolute change values to diagnose non-ST-segment elevation MI (NSTEMI). Other controversial issues concern the diagnostic accuracy and cost-effectiveness of cut-off values for the most rapid algorithms (0 h/1 h or 0 h/2 h) to rule-in and rule-out NSTEMI. Finally, another important point is the possible differences between demographic and clinical characteristics of patients enrolled in multicenter trials compared to those routinely admitted to the Emergency Department in Italy. The Study Group of Cardiac Biomarkers, supported by the Italian Scientific Societies Società Italiana di Biochimica Clinica, Italian Society of the European Ligand Assay Society, and Società Italiana di Patolgia Clinica e Medicina di Laboratorio decided to revise the document previously published in 2013 about the management of patients with suspected NSTEMI, and to provide some suggestions for the use of these biomarkers in clinical practice, with a particular focus on the Italian setting.


1988 ◽  
Vol 254 (3) ◽  
pp. H481-H486 ◽  
Author(s):  
M. N. Gillespie ◽  
D. C. Booth ◽  
B. J. Friedman ◽  
M. R. Cunningham ◽  
M. Jay ◽  
...  

Recent pathological studies of coronary arteries from humans with suspected coronary spasm have revealed an augmented intramural burden of inflammatory cells. To test the hypothesis that inappropriate activation of inflammatory cells participates in the evolution of coronary vasospasm, the present experiments employed a newly developed coronary arteriographic technique for use in pentobarbital-anesthetized rabbits to evaluate the coronary vasomotor actions of the nonselective inflammatory cell stimulant, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). In 10 of 10 animals, selective left intracoronary injection of 200 ng fMLP evoked profound left coronary narrowing accompanied in all cases by ST segment deviation and dysrhythmias. Thallium-201 scintigraphy demonstrated hypoperfusion of the left ventricular free wall and septum supplied by the spastic coronary artery. The fMLP-induced epicardial vaso-constriction, ischemic electrocardiogram (ECG) changes, and thallium perfusion defects were reversed by intravenous nitroglycerin. Neither the right coronary artery nor its distribution were influenced by left coronary injection of fMLP. Additional experiments in isolated, salt solution-perfused rabbit hearts demonstrated that fMLP failed to exert direct coronary vasoconstrictor effects. These observations indicate that the non-selective inflammatory cell stimulant, fMLP, provokes arteriographically demonstrable coronary spasm with attendant myocardial hypoperfusion and ischemic ECG changes in anesthetized rabbits. Such a model may be useful in exploring the dynamic role of inflammatory cells in development of coronary spasm.


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