scholarly journals Clinical cases of myocardial infarction in pregnant women: the role of hereditary thrombophilia

2020 ◽  
Vol 48 (5) ◽  
pp. 341-347
Author(s):  
S. R. Mravyan ◽  
T. S. Kovalenko ◽  
I. O. Shuginin ◽  
T. S. Budykina ◽  
S. I. Fedorova
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Pregnant Women ◽  
Myocardial Injury ◽  
Past History ◽  
False Negative ◽  
Hereditary Thrombophilia ◽  
History Of ◽  
Pai 1 ◽  
Clinical Cases

Acute myocardial infarction during pregnancy is a threatening complication with high maternal and perinatal mortality. According to the literature, hereditary thrombophilia is commonly associated with obstetric disorders and susceptibility to venous thrombosis, whereas arterial part of the vasculature, including coronary, is rarely involved. The article describes two clinical cases of pregnant women with acute myocardial infarction and post-infarction cardiosclerosis, in whom hereditary thrombophilia, associated with the gene PAI-1-675 polymorphism, was diagnosed. Mothers of both patients had suffered myocardial infarction at a young age, while past history of only one pregnant woman was remarkable for multiple perinatal losses. Myocardial infarction may manifest with intense headache mirroring systemic angiospasm.Based on the clinical observations of acute myocardial infarction in pregnancy, one could conclude that measurements of troponin levels that might be false negative should be done repeatedly, while the signs of transmural myocardial injury at ECG can evolve into those of an intramural myocardial infarction. Miscarriage and fetoplacental insufficiency have been found in the patients with combination of hereditary thrombophilia and myocardial injury. Coronary artery damage in pregnant women can be the result of hereditary thrombophilia, most often associated with the PAI-1-675 gene polymorphism, as well as its combination with the heterozygous state of other genes.The absence of past perinatal losses and venous thromboembolism in pregnant women with myocardial infarction does not exclude hereditary thrombophilia, and additional work-up of the patient and the proband family is mandatory to exclude the underlying pathology. The course of myocardial infarction may not require an intracoronary intervention, and treatment may consist of non-fractionated or low molecular weight heparin and calcium antagonists.

Levels of Activated FXII in Survivors of Myocardial Infarction – Association with Circulating Risk Factors and Extent of Coronary Artery Disease

1998 ◽  
Vol 79 (01) ◽  
pp. 14-18 ◽  
Author(s):  
Hans Kohler ◽  
Angela Carter ◽  
Max Stickland ◽  
Peter Grant
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Past History ◽  
Factor Xii ◽  
Factor Xiia ◽  
History Of ◽  
Artery Disease ◽  
Coronary Atheroma ◽  
Pai 1

SummaryLittle data is available regarding the activated form of factor XIIa (FXIIa) in survivors of myocardial infarction. 292 Caucasian patients characterised for extent of coronary atheroma by angiography and for a past history of myocardial infarction and 77 healthy controls were included in the study. To investigate the relationship between coronary artery disease, activated factor XII and other circulating factors, we studied levels of FXIIa, cholesterol, triglycerides, fasting insulin, fibrinogen, FVII:C, t-PA antigen and PAI-1 antigen. Factor XIIa levels were higher in all patients [2.5 (2.3-2.6) ng/ml] and in patients with a history of MI [2.6 (2.4-2.9) ng/ml] than in controls [1.9 (1.7-2.1) ng/ml], p <0.0001. In patients, FXIIa levels positively correlated with FVII:C, BMI, cholesterol, insulin, PAI-1 antigen, t-PA antigen and triglycerides. In controls FXIIa levels only correlated with PAI-1 antigen and triglycerides. FXIIa levels were strongly associated with extent of coronary stenosis: 2.8 (2.6-3.1) ng/ml and 2.6 (2.3-2.9 ng/ml) in those with 2 and 3 vessels stenosed compared to 2.1 (1.9-2.3) ng/ml in those with 0 vessel stenosed (p = 0.0004). Activated FXII relates to both extent of coronary atheroma and to a past history of myocardial infarction and clusters with features of insulin resistance.

Relationship of Plasminogen Activator Inhibitor-1 Levels following Thrombolytic Therapy with rt-PA as Compared to Streptokinase and Patency of Infarct Related Coronary Artery

1999 ◽  
Vol 82 (07) ◽  
pp. 104-108 ◽  
Author(s):  
Franck Paganelli ◽  
Marie Christine Alessi ◽  
Pierre Morange ◽  
Jean Michel Maixent ◽  
Samuel Lévy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thrombolytic Therapy ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Plasminogen Activator Inhibitor 1 ◽  
Vessel Patency ◽  
Activator Inhibitor ◽  
Pai 1

Summary Background: Type 1 plasminogen activator inhibitor (PAI-1) is considered to be risk factor for acute myocardial infarction (AMI). A rebound of circulating PAI-1 has been reported after rt-PA administration. We investigated the relationships between PAI-1 levels before and after thrombolytic therapy with streptokinase (SK) as compared to rt-PA and the patency of infarct-related arteries. Methods and Results: Fifty five consecutive patients with acute MI were randomized to strep-tokinase or rt-PA. The plasma PAI-1 levels were studied before and serially within 24 h after thrombolytic administration. Vessel patency was assessed by an angiogram at 5 ± 1days. The PAI-1 levels increased significantly with both rt-PA and SK as shown by the levels obtained from a control group of 10 patients treated with coronary angioplasty alone. However, the area under the PAI-1 curve was significantly higher with SK than with rt-PA (p <0.01) and the plasma PAI-1 levels peaked later with SK than with rt-PA (18 h versus 3 h respectively). Conversely to PAI-1 levels on admission, the PAI-1 levels after thrombolysis were related to vessel patency. Plasma PAI-1 levels 6 and 18 h after SK therapy and the area under the PAI-1 curve were significantly higher in patients with occluded arteries (p <0.002, p <0.04 and p <0.05 respectively).The same tendency was observed in the t-PA group without reaching significance. Conclusions: This study showed that the PAI-1 level increase is more pronounced after SK treatment than after t-PA treatment. There is a relationship between increased PAI-1 levels after thrombolytic therapy and poor patency. Therapeutic approaches aimed at quenching PAI-1 activity after thrombolysis might be of interest to improve the efficacy of thrombolytic therapy for acute myocardial infarction.

scholarly journals 180-day readmission risk model for older adults with acute myocardial infarction: the SILVER-AMI study

Open Heart ◽  
2021 ◽  
Vol 8 (1) ◽  
pp. e001442
Author(s):  
John A Dodson ◽  
Alexandra M Hajduk ◽  
Terrence E Murphy ◽  
Mary Geda ◽  
Harlan M Krumholz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Older Adults ◽  
Acute Myocardial Infarction ◽  
Risk Model ◽  
Functional Mobility ◽  
Derivation Cohort ◽  
History Of ◽  
Reported Health ◽  
Self Reported Health Status ◽  
Readmission Risk

ObjectiveTo develop a 180-day readmission risk model for older adults with acute myocardial infarction (AMI) that considered a broad range of clinical, demographic and age-related functional domains.MethodsWe used data from ComprehenSIVe Evaluation of Risk in Older Adults with AMI (SILVER-AMI), a prospective cohort study that enrolled participants aged ≥75 years with AMI from 94 US hospitals. Participants underwent an in-hospital assessment of functional impairments, including cognition, vision, hearing and mobility. Clinical variables previously shown to be associated with readmission risk were also evaluated. The outcome was 180-day readmission. From an initial list of 72 variables, we used backward selection and Bayesian model averaging to derive a risk model (N=2004) that was subsequently internally validated (N=1002).ResultsOf the 3006 SILVER-AMI participants discharged alive, mean age was 81.5 years, 44.4% were women and 10.5% were non-white. Within 180 days, 1222 participants (40.7%) were readmitted. The final risk model included 10 variables: history of chronic obstructive pulmonary disease, history of heart failure, initial heart rate, first diastolic blood pressure, ischaemic ECG changes, initial haemoglobin, ejection fraction, length of stay, self-reported health status and functional mobility. Model discrimination was moderate (0.68 derivation cohort, 0.65 validation cohort), with good calibration. The predicted readmission rate (derivation cohort) was 23.0% in the lowest quintile and 65.4% in the highest quintile.ConclusionsOver 40% of participants in our sample experienced hospital readmission within 180 days of AMI. Our final readmission risk model included a broad range of characteristics, including functional mobility and self-reported health status, neither of which have been previously considered in 180-day risk models.

scholarly journals Diagnostic markers for discriminating between acute aortic dissection and acute myocardial infarction during the pre-hospital phase: analysis of 3,195 cases

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Watanabe ◽  
H Yoshino ◽  
T Takahashi ◽  
M Usui ◽  
K Akutsu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Back Pain ◽  
Chest Pain ◽  
Aortic Dissection ◽  
Acute Aortic Dissection ◽  
Diagnostic Markers ◽  
Network Database ◽  
History Of ◽  
First Contact

Abstract   Both acute aortic dissection (AAD) and acute myocardial infarction (AMI) present with chest pain and are life-threatening diseases that require early diagnosis and treatment for better clinical outcome. However, two critical diseases in the very acute phase are sometimes difficult to differentiate, especially prior to arrival at the hospital for urgent diagnosis and selection of specific treatment. The aim of our study was to clarify the diagnostic markers acquired from the information gathered from medical history taking and physical examination for discriminating AAD from AMI by using data from the Tokyo Cardiovascular Care Unit (CCU) Network database. We examined the clinical features and laboratory data of patients with AAD and AMI who were admitted to the hospital in Tokyo between January 2013 and December 2015 by using the Tokyo CCU Network database. The Tokyo CCU Network consists of &gt;60 hospitals that fulfil certain clinical criteria and receive patients from ambulance units coordinated by the Tokyo Fire Department. Of 15,061 patients diagnosed as having AAD and AMI, 3,195 with chest pain within 2 hours after symptom onset (537 AAD and 2,658 AMI) were examined. The patients with out-of-hospital cardiac arrest were excluded. We compared the clinical data of the patients with chest pain who were diagnosed as having AAD and AMI. The following indicators were more frequent or had higher values among those with AAD: female sex (38% vs. 20%, P&lt;0.001), systolic blood pressures (SBPs) at the time of first contact by the emergency crew (142 mmHg vs. 127 mmHg), back pain in addition to chest pain (54% vs. 5%, P&lt;0.001), history of hypertension (73% vs. 58%, P&lt;0.001), SBP ≥150 mmHg (39% vs. 22%, P&lt;0.001), back pain combined with SBP ≥150 mmHg (23% vs. 0.8%, P&lt;0.001), and back pain with SBP &lt;90 mmHg (4.5% vs. 0.1%, P&lt;0.001). The following data were less frequently observed among those with AAD: diabetes mellitus (7% vs. 28%, P&lt;0.001), dyslipidaemia (17% vs. 42%, P&lt;0.001), and history of smoking (48% vs. 61%, P&lt;0.001). The multivariate regression analysis suggested that back pain with SBP ≥150 mmHg (odds ratio [OR] 47; 95% confidence interval [CI] 28–77; P&lt;0.001), back pain with SBP &lt;90 mmHg (OR 68, 95% CI 16–297, P&lt;0.001), and history of smoking (OR 0.49, 95% CI 0.38–0.63, P&lt;0.001) were the independent markers of AAD. The sensitivity and specificity of back pain with SBPs of ≥150 mmHg and back pain with SBPs &lt;90 mmHg for detecting AAD were 23% and 99%, and 4% and 99%, respectively. In patients with chest pain suspicious of AAD and AMI, “back pain accompanied by chest pain with SBP ≥150 mmHg” or “back pain accompanied by chest pain with SBP &lt;90 mmH” is a reliable diagnostic marker of AAD with high specificity, although the sensitivity was low. The two SBP values with back pain are markers that may be useful for the ambulance crew at their first contact with patients with chest pain. Funding Acknowledgement Type of funding source: None

Levels of anxiety, depression and denial in patients with myocardial infarction

1997 ◽  
Vol 12 (3) ◽  
pp. 149-151 ◽  
Author(s):  
D Sarantidis ◽  
A Thomas ◽  
K Iphantis ◽  
N Katsaros ◽  
J Tripodianakis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Intensive Care Unit ◽  
Family History ◽  
Positive Family History ◽  
Anxiety And Depression ◽  
Previous Myocardial Infarction ◽  
History Of ◽  
Seeking Help ◽  
Anxiety Depression

SummaryIn this study we investigated 1) the changes in anxiety, depression and denial from admission to discharge in patients admitted to the intensive care unit following an acute myocardial infarction and 2) the effect of smoking habits, time lapsed from the appearance of symptoms to seeking help behavior, presence of a person that motivated the patient to seek help, previous myocardial infarction (MI) and family history of MI, on these changes. The results indicated that 1) the levels of both anxiety and depression increased from admission to discharge, while denial decreased; 2) positive family history of MI was associated with lower difference of denial between admission and discharge.

C0347 Thrombin binding to platelets of young patients with a history of acute myocardial infarction

2012 ◽  
Vol 130 ◽  
pp. S104
Author(s):  
Grazia Loredana Mendolicchio ◽  
Monica Bacci ◽  
Dennis Zavalloni ◽  
Lidia Rota ◽  
Zaverio Marcello Ruggeri
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Young Patients ◽  
History Of
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