scholarly journals Characteristics of clinical signs, laboratory and instrumental examinations in various mechanisms of development of type 2 myocardial infarction

2021 ◽  
Vol 12 (3) ◽  
pp. 132-138
Author(s):  
Dmitrii V. Oblavatckii ◽  
Svetlana A. Boldueva
Keyword(s):  
Myocardial Infarction ◽  
Hypertensive Crisis ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Oxygen Demand ◽  
Microvascular Dysfunction ◽  
Myocardial Oxygen Demand ◽  
Pathogenic Variants ◽  
Severe Pathology

Aim. To identify different pathogenetic variants of myocardial infarction type 2 (MI-2). Material and methods. Reviewed 4168 cases of MI admitted in multidisciplinary hospital for 10 years. 353 patients met the criteria for MI-2 without signs of coronary atherothrombosis (CA). In the study group, the features of clinical and laboratory-instrumental manifestations were evaluated. Results. Cases of IM-2 were subdivided into 4 clinical-pathogenic variants (CPV): 1-CPV developed due an increasing in myocardial oxygen demand; 2-CPV, arising from a decrease in the supply of oxygen; 3-CPV associated with local coronary circulation disorder; 4-CPV developed due to the combined oxygen-energy imbalance. In 72 (20.4%) cases, 1-CPV was detected, caused by a hypertensive crisis and/or tachyarrhythmias; 2-CPV observed in 73 (20.68%) patients with hypotension, anemia, microvascular dysfunction, respiratory failure; 3-CPV caused by spasm and embolism of CA was detected in 47 (13.31%) cases; in 161 (45.61%) patients, IM-2 is associated with increased myocardial oxygen demand with reduced oxygen delivery. The gender and risk factors in groups are comparable. The average age of 1-CPV- and 3-CPV-patients was less and amounted to 65.7 and 56.5 versus 70.2 and 73.8 years in the 2-CPV and 4-CPV. Typical clinical and laboratory-instrumental signs of MI were common for patients with 1-CPV and 3-CPV, while 2-CPV and 4-CPV more often had chronic severe pathology, multivessel coronary disorder, and the clinical presentation and ischemic signs were less common. Conclusion. Clinical manifestations and results of examination of patients with MI-2 depend on the mechanism of its development.

scholarly journals Pathophysiological aspects of development myocardial infarction type 2 in subclinical hypothyroidism

2021 ◽  
pp. 34-41
Author(s):  
A. A. Ivannikov ◽  
A. A. Kanibolotsky ◽  
Kh. G. Alidzhanova ◽  
I. V. Bratischev
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Subclinical Hypothyroidism ◽  
Hormone Replacement ◽  
Myocardial Revascularization ◽  
Oxygen Demand ◽  
Cardiomyocyte Hypertrophy ◽  
Myocardial Oxygen Demand ◽  
Atherosclerotic Stenosis

The main purpose of the following article is to highlight one of the most pressing and poorly studied issues both for cardiology and endocrinology – treatment and prognosis for patients with severe coronary pathology and subclinical hypothyroidism (SH). Pathophysiological mechanisms of type 2 myocardial infarction (MI) development with SH as a background and hormone replacement therapy issues are considered. SH is a modifiable risk factor (RF) for cardiovascular diseases (CVD) and mortality that does not depend on traditional cardiovascular RF. SH is associated with high risk of developing coronary artery disease, MI, heart failure, and CVD mortality. SH incidence of morbidity increases with age, usually the course is oligo- or asymptomatic. SH leads to a number of pathological conditions that cause an imbalance between the myocardial oxygen demand and delivery with a possible development of type 2 MI. Clinical case of type 2 MI development in a patient with severe coronary atherosclerosis and SH is presented. The key point of type 2 MI development mechanism is insufficient oxygen (O2) supply to cardiomyocytes due to multivessel coronary artery atherosclerotic stenosis and sharp increase in O2 demand as a result of cardiomyocyte hypertrophy. Older patients with severe cardiac pathology and SH should refrain from treatment with levothyroxine or start treatment after myocardial revascularization, selecting the dose of the drug individually.

Abstract T3: Type 2 Myocardial Infarction Predicts Outcome In Hypertensive Crisis Patients: Nationwide Analysis

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Ahmed M Maraey ◽  
Ahmed Elzanaty ◽  
Hadeer R Elsharnoby ◽  
Mahmoud Salem ◽  
Mahmoud Khalil ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Hospital Mortality ◽  
Hypertensive Crisis ◽  
Primary Diagnosis ◽  
Hypertensive Emergency ◽  
Secondary Outcome ◽  
Hypertensive Urgency ◽  
Emergency Presentation ◽  
The Impact

Background: Type 2 Myocardial infarction (T2MI) can occur in hypertensive crisis patients. The impact of T2MI in this population is poorly understood due to limited available data. Objective: To assess the impact of T2MI on patients admitted to the hospital with hypertensive crisis. Methods: We queried National Readmission Database (NRD) of year 2018 for adult patients admitted with a primary diagnosis of hypertensive crisis. Patients were excluded if they had type 1 myocardial infarction (T1MI), septic shock, or bleeding in the index admission. Primary outcome was 90-day readmission due to T1MI. Secondary outcome was in-hospital mortality. Subgroup analysis was done according to urgency and emergency presentation. Multivariate regression was done to account for confounders. Results: A total of 101211 patients were included in our cohort of whom 3644 (3.6%) were diagnosed with T2MI and 24471 (24.2%) were readmitted within 90 days of discharge. Of those, 912 (3.7%) were diagnosed with T1MI on readmission. T2MI was independently associated with increased odds of 90-day readmission with T1MI (Adjusted odds ratio (aOR): 2.67, 95% CI [1.91-3.75], P=0.000). T2MI effect was observed in hypertensive urgency, and in hypertensive emergency. T2MI was associated with increased in-hospital mortality in hypertensive urgency population (aOR: 4.21, 95% [1.58-11.25], P=0.004) but not in hypertensive emergency (table 1). Conclusion: In hypertensive crisis patients, T2MI was associated with increased 90-day readmission with T1MI. Aggressive management of cardiovascular risk factors and risk stratification should be considered at the time of diagnosis.

scholarly journals Predictors of mortality in children with lupus nephritis

2014 ◽  
Vol 54 (6) ◽  
pp. 338
Author(s):  
Lukman Oktadianto ◽  
Risky Vitria Prasetyo ◽  
Ninik Asmaningsih Soemyarso ◽  
Mohammad Sjaifullah Noer
Keyword(s):  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Renal Involvement ◽  
Hypertensive Crisis ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Predictors Of Mortality ◽  
Cox Proportional Hazard ◽  
Kaplan Meier ◽  
Mean Time

Background Renal involvement during the clinical course ofsystemic lupus erythematosus (SLE) is generally considered to bethe most important factor influencing disease prognosis in termsof morbidity and mortality. Various factors have been reported toinfluence the prognosis of lupus nephritis (LN).Objective To analyze clinical signs and laboratory parameters thatmight serve as predictors associated with mortality in pediatricLN.Methods Retrospectively, medical records of children with LNat Soetomo Hospital from 1998 to 2011 were studied. Diagnosisof SLE was based on Revised American Rheumatism Associationcritera, while patients with clinical manifestations of hypertension,abnormal urinalysis, and serum creatinin > 1 mg/dL wereconsidered as lupus nephritis. Cox proportional hazard modelingwas used to assess for associations of clinical signs and laboratoryparameters with mortality. Kaplan-Meier survival analysis wasused to assess the cumulative survival from the time of diagnosisto the outcome.Results There were 57 children with LN of whom 43 (75%) weregirls. The female-to-male ratio was 3:1. Subjects’ mean age was 10.6(SD 6.87) years. The mean time of observation was 51 (SD 74.54)months and 23 (40%) children died. Age, gender, hypertension,hematuria, proteinuria, and anemia were not significant aspredictors for mortality. However, hypertensive crisis (HR=2.79;95%CI 1.16 to 6.75; P=0.02) and initial glomerular filtration rate(GFR) of <75 mL/min/1.73m2 (HR=3.01; 95%CI 1.23 to 7.34;P=0.01) were significant predictors of mortality in children with LN.The mean survival time of LN with hypertensive crisis and initialGFR <75 mL/min/1.73m2 was 36.9 (SD 12.17) months.Conclusion Hypertensive crisis and GFR <75 mL/min/1.73m2 aresignificant predictors of mortality in children with LN.

scholarly journals Type 2 Myocardial Infarction in Acute Medical Care

2016 ◽  
Vol 01 (04) ◽  
pp. 021-024
Author(s):  
K. Sateesh ◽  
Stitha Pragna ◽  
Y Raju
Keyword(s):  
Myocardial Infarction ◽  
Medical Care ◽  
Oxygen Demand ◽  
Type Ii ◽  
Men And Women ◽  
Upper Limit ◽  
Significant Difference ◽  
The Mean ◽  
Acute Medical Care

AbstractBackground: Type 2 myocardial infarction (MI) is defined as MI secondary to ischemia due to either increased oxygen demand or decreased supply. It is seen in conditions other than coronary artery disease (CAD) contributes to an imbalance between myocardial oxygen supply and/or demand. Little is known about patient characteristics and clinical outcomes.Methods: A retrospective analysis was performed in patients who were admitted in acute medical care with symptoms suggestive of myocardial ischemia and enzymatic elevation from January 2015 to December 2015. Patients with slight elevation (above the upper limit of normal) of CK-MB were included in the study and compared the clinical and laboratory profile between men and women.Results: This survey includes a total of 54 patients, Out of which complete details were available in 41 patients (M:23; F:18). The mean age was 42.61. The common causes of type-II MI were Infectious (M:9 (39.1%), F:10 (55.6%) followed by haematological disorders (M:3 (13%), F:5 (27.7%). The mean CK-MB was 28.00. The mean CPK was 122.5. There was no hypotension, renal failure at the time of admission. One patient had in-hospital mortality out of all patients, whose primary diagnosis was septicaemia with shock who had normal CPK, elevated CK-MB and elevated NT pro BNP levels. Patients with type-II MI were not referred for coronary interventions and managed conservatively.Conclusions: There is no significant difference in the risk for type 2 MI between men and women. Clinical suspicion and diagnosis of type 2 MI is crucial in acute medical care setting, as the mortality can be reduced with adequate management of underlying condition. The threshold of biomarker levels should be low (above the upper limit of normal in symptomatic ischemia) to label type 2 MI contrary to the third universal definition of MI.

scholarly journals Repetitive Myocardial Infarctions Secondary to Delirium Tremens

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
David Schwartzberg ◽  
Adam Shiroff
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Alcohol Withdrawal ◽  
Delirium Tremens ◽  
Oxygen Demand ◽  
Myocardial Infarctions ◽  
Myocardial Oxygen Demand ◽  
Significant Morbidity ◽  
St Segment ◽  
Patients Experience

Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal.

Myocardial infarction (clinic, diagnostic features, complications, treatment)

1997 ◽  
Vol 78 (2) ◽  
pp. 120-128
Author(s):  
I. A. Latfullin
Keyword(s):  
Myocardial Infarction ◽  
Blood Supply ◽  
Coronary Arteries ◽  
Heart Muscle ◽  
Oxygen Demand ◽  
Myocardial Oxygen Demand ◽  
Ischemic Necrosis ◽  
Diagnostic Features

Myocardial infarction (MI) occurs due to an acute mismatch between myocardial oxygen demand and its blood supply through the coronary arteries of the heart, which results in the development of ischemic necrosis of the heart muscle with subsequent topical changes on ECG.

Myocardial ischaemia: definition and causes

ESC CardioMed ◽  
2018 ◽  
pp. 1325-1329
Author(s):  
Filippo Crea ◽  
Gaetano Antonio Lanza
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Coronary Artery Spasm ◽  
Chronic Stable Angina ◽  
Oxygen Demand ◽  
Microvascular Dysfunction ◽  
Myocardial Oxygen Demand ◽  
Coronary Microvascular Dysfunction ◽  
Coronary Artery Dissection ◽  
The Right

Myocardial ischaemia is caused by a mismatch between myocardial oxygen demand and myocardial blood flow supply, which results in reversible myocardial suffering and, when prolonged, in irreversible injury. The main causes of myocardial ischaemia include (1) atherosclerotic flow-limiting stenoses which are responsible for chronic stable angina; (2) coronary thrombus superimposed on an atherosclerotic plaque which is responsible for acute coronary syndromes; (3) coronary artery spasm which is responsible for vasospastic angina; and (4) coronary microvascular dysfunction which is responsible for microvascular angina and can also contribute to myocardial ischaemia in various clinical settings. Functional alterations (thrombus, spasm, and microvascular dysfunction) may act on angiographically normal coronary arteries or arteries presenting stenoses of variable severity. Less frequent coronary causes of myocardial ischaemia include spontaneous coronary artery dissection, myocardial bridge, coronary thromboembolism, an abnormal origin of the right or left coronary artery, and ascending aorta dissection involving coronary ostia. Finally, myocardial ischaemia can occur in the presence of severe left ventricular hypertrophy as observed in aortic stenosis and hypertrophic cardiomyopathy.

scholarly journals From bedside to bench and back again: translational studies of mechanical unloading of the left ventricle to promote recovery after acute myocardial infarction

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1852 ◽  
Author(s):  
Navin K. Kapur ◽  
Shiva Annamalai ◽  
Lara Reyelt ◽  
Samuel J. Karmiy ◽  
Allen A. Razavi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Pilot Trial ◽  
Oxygen Demand ◽  
Myocardial Damage ◽  
Reperfusion Therapy ◽  
Circulatory Support ◽  
Myocardial Oxygen Demand ◽  
St Segment Elevation

Heart failure is a major cause of global morbidity and mortality. Acute myocardial infarction (AMI) is a primary cause of heart failure due in large part to residual myocardial damage despite timely reperfusion therapy. Since the 1970’s, multiple preclinical laboratories have tested whether reducing myocardial oxygen demand with a mechanical support pump can reduce infarct size in AMI. In the past decade, this hypothesis has been studied using contemporary circulatory support pumps. We will review the most recent series of preclinical studies in the field which led to the recently completed Door to Unload ST-segment Elevation Myocardial Infarction (DTU-STEMI) safety and feasibility pilot trial.

scholarly journals Neonatal Oculocutaneous Albinism Type 2 With Prader-Willi Syndrome

2020 ◽  
Author(s):  
Gaohong Wu ◽  
Dongya Yan ◽  
Meijuan Zhou ◽  
Wenmei Li ◽  
Ping Jiang ◽  
...  
Keyword(s):  
Genetic Testing ◽  
Missense Mutation ◽  
High Throughput Sequencing ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Oculocutaneous Albinism ◽  
Prader Willi Syndrome ◽  
White Skin ◽  
Feeding Difficulties

Abstract Background: To investigate the pathogenesis and clinical characteristics of Oculocutaneous albinism type 2 (OCA2), a genetic condition in the etiology of Prader-Willi syndrome (PWS).Case presentation: A retrospective study of one case presented with poor response to stimuli, difficultfeeding, poor crying, with yellow hair and white skin. We performed genetic testing and investigated disease pathogenesis, clinical manifestations, and diagnosis, and discussed the characteristics of the disease through a literature review. HiSeq high-throughput sequencing result suggested a deletion with 105 genes, including UBE3A, SNRPN, OCA2, and other genes up to 5.18 Mb on the long arm of chromosome (15q11-13 region), a critical region, susceptible to the PWS. A paternally derived deletion Del (15q11. 2q13. 1) [GRCh37 / hg19] (23, 378, 392-28, 563, 050) × 1, and a maternal missense mutation were identified in the OCA2 gene (chr15: 28171296 c .2056G> A (p.A686T). During the period of hospitalization, the child still suffered from poor milk intake, and she was discharged from the hospital at the request of her parents. After discharge, the patient was followed up for two months by telephone. However, the patient died of feeding difficulties and pulmonary infection.Conclusions: OCA2 combined with PWS due to OCA2 gene missense mutation combined with large fragment deletion of 15q11-13 region was first reported in this study, of which the clinical signs can be subtle and symptoms can be more severe, therefore, early genetic testing is crucial for those patients to yield an accurate diagnosis and initiate aggressive interventions to optimize the outcomes.

scholarly journals Coronary Microvascular Dysfunction and the Role of Noninvasive Cardiovascular Imaging

Diagnostics ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 679
Author(s):  
Muhammad Talha Ayub ◽  
Dinesh Kalra
Keyword(s):  
Imaging Techniques ◽  
Oxygen Demand ◽  
Microvascular Dysfunction ◽  
Cardiac Imaging Techniques ◽  
Myocardial Oxygen Demand ◽  
Coronary Microvascular Dysfunction ◽  
Non Invasive ◽  
Treatment Prognosis

Patients with coronary microvascular dysfunction (CMD) have significantly higher rates of cardiovascular events, including hospitalization for heart failure, sudden cardiac death, and myocardial infarction (MI). In CMD, several pathophysiological changes lead to functional and structural abnormalities in the coronary microvasculature, which disrupt the ability of the vessels to vasodilate and augment myocardial blood flow in response to increased myocardial oxygen demand, causing ischemia and angina. With the advent of more advanced non-invasive cardiac imaging techniques, the coronary microvasculature has been subjected to more intense study in the past two decades—this has led to further insights into the diagnosis, pathophysiology, treatment, prognosis and follow-up of CMD. This review will highlight and compare the salient features of the currently available non-invasive imaging modalities used in these patients, and discuss the clinical utility of these techniques in the workup and management of these patients.

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