Bivalirudin in Patients with HIT or Clinically Suspected HIT.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 918-918 ◽  
Author(s):  
Luz M. Ramirez ◽  
Teresa L. Carman ◽  
Susan M. Begelman ◽  
Amjad AlMahameed ◽  
Douglas Joseph ◽  
...  
Keyword(s):  
Platelet Count ◽  
Renal Dysfunction ◽  
The United States ◽  
Heparin Therapy ◽  
Left Ventricular ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Suitable Alternative ◽  
Coronary Syndrome ◽  
History Of

Abstract Background: Heparin-induced thrombocytopenia (HIT) is a serious complication of heparin and low molecular weight heparin therapy. All patients with HIT need treatment with a non-heparin anticoagulant. In the United States, two direct thrombin inhibitors are FDA-approved for patients with HIT: lepirudin and argatroban. Lepirudin is eliminated by the kidneys and is not ideal in patients with renal dysfunction. Argatroban is metabolized in the liver and should be used with caution in patients with hepatic insufficiency. Bivalirudin is approved for use in percutaneous coronary intervention and is under study for use in patients with HIT undergoing cardiopulmonary bypass. Bivalirudin has a short half-life (25 min) and is 20% metabolized via the kidneys and 80% by proteolytic cleavage. Methods: We are reporting our experience from a retrospective review of 42 patients with clinically suspected, laboratory-confirmed, or previously diagnosed HIT treated with bivalirudin. Results: Thirteen patients had a history of HIT; 9 were admitted for an interventional procedure or surgery. In 29 (69%) patients, HIT was suspected because of a fall in platelet count and/or thrombosis in the setting of current or recent heparin therapy. HIT was confirmed in 15/29 (51.7%) (Table). Bivalirudin was initiated by continuous intravenous infusion (range 0.03–0.2 mg/kg/h) and adjusted to an aPTT of 1.5–2.5 times patient baseline. The mean infusion rate was 0.1 mg/kg/h. The average duration of therapy was 7.8 (range 1–24) days. 7/42 (16.7%) of patients had overt bleeding and received ≥ 2 units of packed red blood cells during their hospitalization. There were three new thrombotic events: ischemic stroke (subtherapeutic aPTT), cephalic vein thrombosis, and left ventricular thrombus. There were no amputations and 5 patients died: 2 withdrawal of care, 1 MSOF, 1 respiratory failure, 1 disseminated intravascular coagulation. Conclusions: Our experience indicates that bivalirudin is a suitable alternative anticoagulant for patients with HIT or suspected HIT. The bleeding and thrombotic complications were deemed acceptable in our largely critically ill and postoperative patients. Class of patients No. of pts Indication for initial use of anticoagulation Mean platelet count (K/μL) at the time of bivalirudin initiation (Range) Renal dysfunction (RD) OR Liver dysfunction (LD) OR Both (RD&LD) ICU stay OR Required mechanical ventilation (MV) Multi-system organ failure (MSOF) OR Sepsis VTE = Venous Thromboembolism, Mech Valve = Mechanical Valve, ACS = Acute Coronary Syndrome, Afib = Atrial Fibrillation History of HIT 13 VTE 3, Intervention or Surgery 9, Other 1 172 (30–374) RD 23.1%, LD 0%, RD&LD 0% ICU 61.5%, MV 0% MSOF 7.7% Sepsis 0% Clinically suspected HIT 14 VTE 8, Mech Valve 1, ACS 4, Other 1 57.9 (7–115) RD 21.4%, LD 7.1%, RD&LD 7.1% ICU 85.7%, MV 42.9% MSOF 14.3% Sepsis 28.6% Confirmed HIT 15 VTE 3, Afib 2, ACS 4, Other 6 44.6 (10–107) RD 26.7%, LD 6.7%, RD&LD 13.3% ICU 86.7%, MV 53.3% MSOF 20% Sepsis 20%

Outcomes of Cardiovascular Surgery Utilizing Heparin versus Direct Thrombin Inhibitors in Cardiopulmonary Bypass in Patients with Previously Diagnosed HIT

2019 ◽  
Vol 120 (02) ◽  
pp. 300-305
Author(s):  
Daniel S. Carlson ◽  
John R. Bartholomew ◽  
Marcelo P. Gomes ◽  
Keith R. McCrae ◽  
Shruti Chaturvedi
Keyword(s):  
Cardiopulmonary Bypass ◽  
Heparin Therapy ◽  
Serotonin Release ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Severe Bleeding ◽  
Heparin Group ◽  
Severe Hemorrhage ◽  
Life Threatening ◽  
History Of

AbstractHeparin-induced thrombocytopenia (HIT) is a life-threatening complication of heparin therapy. Heparin is generally avoided in patients with a history of HIT; however, it remains the anticoagulant of choice for cardiac surgery requiring cardiopulmonary bypass (CPB) because of limited experience with alternative anticoagulants such as direct thrombin inhibitors (DTIs) during CPB. We report outcomes of surgery requiring CPB (30-day mortality, rate of thrombosis, and hemorrhage) in patients with prior HIT who received either heparin or a DTI intraoperatively. Seventy-two patients with a prior diagnosis of HIT confirmed by a positive serotonin release assay underwent CBP with a positive HIT antibody at the time of surgery. Thirty-day mortality was 0 and 8.5% in the DTI and heparin cohorts (p = 0.277). Thrombotic events occurred in 1 (7.7%) of the patients treated with DTI and 15 (25.4%) receiving heparin (p = 0.164). In the DTI cohort, 7 (53.8%) had minimal bleeding, 5 (38.5%) had mild bleeding, 1 (7.8%) had moderate bleeding, and none had severe bleeding. In the heparin group, 16 (27.1%) had minimal bleeding, 14 (23.7%) had mild bleeding, 25 (42.4%) had moderate bleeding, and 4 (6.8%) had severe bleeding (p = 0.053). DTI was associated with a lower rate of moderate to severe hemorrhage than heparin (odds ratio 0.097 [95% confidence interval 0.011–0.824], p = 0.033) in a logistic regression model adjusted for thrombocytopenia and length on bypass. DTI appears to be safe in selected patients undergoing CPB after a diagnosis of HIT, and was not associated with higher rates of 30-day mortality, thrombosis, or hemorrhage.

The uncalibrated prothrombinase-induced clotting time test

2010 ◽  
Vol 30 (04) ◽  
pp. 212-216 ◽  
Author(s):  
R. Jovic ◽  
M. Hollenstein ◽  
P. Degiacomi ◽  
M. Gautschi ◽  
A. Ferrández ◽  
...  
Keyword(s):  
Factor Xa ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Coagulation Cascade ◽  
Diagnostic Tools ◽  
Direct Thrombin Inhibitors ◽  
Functional Assay ◽  
Clotting Time ◽  
Coagulation Time ◽  
Time Test

SummaryThe activated partial thromboplastin time test (aPTT) represents one of the most commonly used diagnostic tools in order to monitor patients undergoing heparin therapy. Expression of aPTT coagulation time in seconds represents common practice in order to evaluate the integrity of the coagulation cascade. The prolongation of the aPTT thus can indicate whether or not the heparin level is likely to be within therapeutic range. Unfortunately aPTT results are highly variable depending on patient properties, manufacturer, different reagents and instruments among others but most importantly aPTT’s dose response curve to heparin often lacks linearity. Furthermore, aPTT assays are insensitive to drugs such as, for example, low molecular weight heparin (LMWH) and direct factor Xa (FXa) inhibitors among others. On the other hand, the protrombinase-induced clotting time assay (PiCT®) has been show to be a reliable functional assay sensitive to all heparinoids as well as direct thrombin inhibitors (DTIs). So far, the commercially available PiCT assay (Pefakit®-PiCT®, DSM Nutritional Products Ltd. Branch Pentapharm, Basel, Switzerland) is designed to express results in terms of units with the help of specific calibrators, while aPTT results are most commonly expressed as coagulation time in seconds. In this report, we describe the results of a pilot study indicating that the Pefakit PiCT UC assay is superior to the aPTT for the efficient monitoring of patients undergoing UFH therapy; it is also suitable to determine and quantitate the effect of LMWH therapy. This indicates a distinct benefit when using this new approach over the use of aPPT for heparin monitoring.

scholarly journals Heparin-induced thrombocytopenia: in vitro studies on the interaction of dabigatran, rivaroxaban, and low-sulfated heparin, with platelet factor 4 and anti-PF4/heparin antibodies

Blood ◽  
2012 ◽  
Vol 119 (5) ◽  
pp. 1248-1255 ◽  
Author(s):  
Krystin Krauel ◽  
Christine Hackbarth ◽  
Birgitt Fürll ◽  
Andreas Greinacher
Keyword(s):  
Factor Xa ◽  
Platelet Factor 4 ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Alternative Anticoagulation ◽  
Heparin Complexes ◽  
History Of

Abstract Heparin is a widely used anticoagulant. Because of its negative charge, it forms complexes with positively charged platelet factor 4 (PF4). This can induce anti-PF4/heparin IgG Abs. Resulting immune complexes activate platelets, leading to the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT). HIT requires treatment with alternative anticoagulants. Approved for HIT are 2 direct thrombin inhibitors (DTI; lepirudin, argatroban) and danaparoid. They are niche products with limitations. We assessed the effects of the DTI dabigatran, the direct factor Xa-inhibitor rivaroxaban, and of 2-O, 3-O desulfated heparin (ODSH; a partially desulfated heparin with minimal anticoagulant effects) on PF4/heparin complexes and the interaction of anti-PF4/heparin Abs with platelets. Neither dabigatran nor rivaroxaban had any effect on the interaction of PF4 or anti-PF4/heparin Abs with platelets. In contrast, ODSH inhibited PF4 binding to gel-filtered platelets, displaced PF4 from a PF4-transfected cell line, displaced PF4/heparin complexes from platelet surfaces, and inhibited anti-PF4/heparin Ab binding to PF4/heparin complexes and subsequent platelet activation. Dabigatran and rivaroxaban seem to be options for alternative anticoagulation in patients with a history of HIT. ODSH prevents formation of immunogenic PF4/heparin complexes, and, when given together with heparin, may have the potential to reduce the risk for HIT during treatment with heparin.

Can left ventricular global function index be a novel marker of unfavorable outcome in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
L Minushkina ◽  
V Brazhnik ◽  
N Selezneva ◽  
V Safarjan ◽  
M Alekhin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Coronary Syndrome ◽  
Left Ventricular ◽  
Global Function ◽  
Coronary Syndrome ◽  
History Of ◽  
Coronary Events

Abstract   Left ventricular (LV) global function index (LVGFI) is a MRI marker of left ventricular remodeling. LVGFI has high predictive significance in young healthy individuals. The aim of the study was to assess prognostic significance in patients with acute coronary syndrome (ACS). We include into this analysis 2169 patients with ACS (1340 (61.8%) men and 829 (38.2%) women), mean age 64.08±12.601 years. All patients were observed in 2 Russian multicenter observational studies: ORACLE I (ObseRvation after Acute Coronary syndrome for deveLopment of trEatment options) (2004–2007 years) and ORACLE II (NCT04068909) (2014–2019 years). 1886 (87.0%) pts had arterial hypertension, 1539 (71.0%) – history of coronary artery disease, 647 (29.8%) – history of myocardial infarction, 444 (20.5%) - diabetes mellitus. Duration of the follow-up was 1 years after the hospital discharge. Cases of death from any cause, coronary deaths, repeated coronary events (fatal and non-fatal) were recorded. An echocardiographic study was conducted 5–7 days from the time of hospitalization. The LVGFI was defined as LV stroke volume/LV global volume × 100, where LV global volume was the sum of the LV mean cavity volume ((LV end-diastolic volume + LV end-systolic volume)/2) and myocardial volume (LV mass/density). During the follow-up, 193 deaths were recorded (8.9%), 122 deaths (5.6%) were coronary. In total, repeated coronary events were recorded in 253 (11.7%) patients. Mean LVGFI was 22.64±8.121%. Patients who died during the follow-up were older (73.03±10.936 years and 63.15±12.429 years, p=0.001), had a higher blood glucose level at the admission to the hospital (8.12±3.887 mmol/L and 7.17±3.355 mmol/L, p=0.041), serum creatinine (110.86±53.954 μmol/L and 99.25±30.273 μmol/L, p=0.007), maximum systolic blood pressure (196.3±25.17 mm Hg and 190.3±27.83 mm Hg, p=0.042). Those who died had a lower LVGFI value (19.75±6.77% and 23.01±8.243%, p<0.001). Myocardial mass index, ejection fraction and other left ventricular parameters did not significantly differ between died and alive patients. Among the patients who died, there were higher rate of women, pts with a history of myocardial infarction, heart failure, diabetes. In a multivariate analysis, diabetes mellitus OR1.67 95% CI [1.12–2.51] p=0.012, history of heart failure (1.78 [1.2.-2.59], p=0.003), a history of myocardial infarction (1.47 [1.05–2.05], p=0024), age (1.06 [1.05–1.08], p=0.001) and LVGFI <22% (1.53 [1.08–2.17], p=0.015) were independent predictors of death from any cause. The LVGFI was also independently associated with the risk of coronary death, but not with the risk of all recurring coronary events. Thus, LVGFI may be useful the marker to assess risk in patients who have experienced an ACS episode. Funding Acknowledgement Type of funding source: None

Relative Inhibition of Thrombin Activatable Fibrinolytic Inhibitor by Newly Developed Thrombin Inhibitors: Impact on Bleeding and Antithrombotic Actions.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4051-4051
Author(s):  
Michelle R. Florian-Kujawski ◽  
Debra Hoppensteadt ◽  
Josephine Cunanan ◽  
Marianne Wilmer ◽  
Jawed Fareed
Keyword(s):  
Rank Order ◽  
Thrombin Inhibitors ◽  
Bleeding Complications ◽  
Chromogenic Substrate ◽  
Amino Acid Residues ◽  
Thrombin Inhibition ◽  
Coronary Syndrome ◽  
Alternative Means ◽  
History Of ◽  
Thrombotic Complications

Abstract Thrombin activatable fibrinolytic inhibitor (TAFI) or carboxypeptidase U plays a key role in the fibrinolytic cascade. It acts as an inhibitor of fibrinolysis by cleaving the arginine and lysine amino acid residues from the carboxy terminus of fibrin. The cleavage then renders the fibrin resistant to digestion by plasmin, forming a clot that cannot be easily digested. This stabilized thrombus can then cause myocardial infarction, stroke or pulmonary embolism. It has been shown that individuals with acute coronary syndrome tend to have elevated TAFI, which may lead to further complications. Heparin and low molecular weight heparins (LMWHs) are the most common agents given to those at risk of thrombotic complications either during surgery, therapeutically or prophylacticly. Thrombin inhibitors are being developed to provide an alternative means of anticoagulation if a patient cannot be given heparin or LMWHs due to heparin induced thrombocytopenia (HIT) or some other condition. This study was done to determine the effect of different thrombin inhibitors on TAFI functionality and determine if there is a correlation to the thrombin inhibitors anti-IIa effects. Argatroban, one of the thrombin inhibitors used in this study, has been approved for use in patients who have a history of HIT. In addition to argatroban, the following thrombin inhibitors were tested: melagatran, angiomax, LU 208791, hirudin and dabigatran. All thrombin inhibitors were supplemented to normal human pooled plasma (NHP) in various concentrations (10 – 0.16 μg/ml). The functional TAFI levels were determined using a chromogenic substrate based method developed by Pentapharm Inc. (Basel, Switzerland), the Pefakit® TAFI. The anti-IIa (thrombin inhibition) was determined using a chromogenic substrate based method by American Diagnostica (Stamford, CN). All of the thrombin inhibitors were capable of inhibiting TAFI functionality; LU 208791 being the strongest inhibitor with an IC50 of 0.09 μg/ml while angiomax was the weakest with an IC50 of 6.6 μg/ml respectively. The other thrombin inhibitors showed IC50s ranging from 0.38 – 1.4 μg/ml. These results for the most part corresponded to the anti-IIa results. LU 208791 had the strongest anti-IIa with an IC50 of 0.39 μg/ml while angiomax had an IC50 >10 μg/ml. However, the IC50s for TAFI inhibition by argatroban and hirudin (1.3 and 1.2 μg/ml) were not significantly different, their IC50s for thrombin inhibition were (>10 and 3.0 μg/ml). This indicates that argatroban may inhibit TAFIa directly. The anti-IIa rank order was as follows: LU 208791 > dabigatran > hirudin > melagatran > angiomax = argatroban. These results indicate that the bleeding complications observed when using thrombin inhibitors may be due to the indiscriminate inhibition of TAFI yielding fibrin that is easily digested. It is vital that the balance between coagulation and fibrinolysis be maintained in patients on anticoagulants. When this balance is disrupted either bleeding or thrombosis can occur. This study indicates that TAFI may be the key to maintaining this balance. Too much TAFI inhibition may lead to bleeding while not enough inhibition may lead to thrombosis. Persistent inhibition of TAFI by thrombin inhibitors may compromise both their safety and efficacy.

An Unusual Form of Immune Thrombocytopenic Purpura Characertized by a Platelet Activating IgG Antibody.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1086-1086
Author(s):  
Soames Boyle ◽  
Tamas Alexy ◽  
Leanne Rhochanda ◽  
Howard A. Liebman
Keyword(s):  
Platelet Count ◽  
Arterial Thrombosis ◽  
Heparin Therapy ◽  
Platelet Membrane ◽  
Laboratory Evaluation ◽  
Severe Thrombocytopenia ◽  
Membrane Glycoproteins ◽  
Igg Antibody ◽  
Potent Inducer ◽  
History Of

Abstract Autoimmune thrombocytopenia (ITP) is classically a disorder of accelerated platelet clearance and ineffective platelet production due to antibodies directed against common platelet membrane glycoproteins. The most common clinical manifestation of severe thrombocytopenia is bleeding. We report an unusual case of ITP in a 49 y.o. female with a 4 year history of thrombocytopenia, venous and arterial thrombosis secondary to a platelet activating IgG antibody. The patient was referred to one of the authors (HAL) for a second opinion with a diagnosis of ITP and a history of venous and arterial thrombosis. On presentation the patient was noted to have a platelet count of 34 × 109/L, a decreased fibrinogen of 128 mg/dL and D-dimers of greater than 4000 ng/ml. A diagnosis of chronic DIC was made and the patient was treated with therapeutic doses of LMW heparin resulting in an increase in her fibrinogen to 260 mg/dL, reduction in her D-dimers to <500 ng/ml and an increase in her platelet count to 118 × 109/L. An extensive clinical and laboratory evaluation, included screening for occult malignancy, cavernous hemangioma, antiphospholipid antibodies, dysfibrinogenemia, inhibitory antibodies against protein C and S, failed to disclose an etiology for her chronic consumptive coagulopathy. After 2 months of LMWH therapy the patient had a progressive drop in her platelet count to <30 × 109/L without evidence of recurrent coagulopathy. The patient’s thrombocytopenia was refractory to corticosteroids, Rituxan, azathioprine, cyclosporine, but responsive to IVIG. When the patients LMW heparin was stopped, the patient had evidence of a recurrence of her DIC as defined by an increase in her D-dimer and decreased fibrinogen. The patient underwent an open splenectomy which was complicated by portal vein and superior mesenteric vein thrombosis requiring catheter directed fibrinolysis and reinstitution of LMW heparin therapy. Repeated ELISA and functional assays for heparin induced thrombocytopenia were negative. However, the patient’s heat inactivated plasma and serum were shown to induce spontaneous aggregation. Patient IgG was subsequently isolated by staph A chromatography and found to be a potent inducer of platelet aggregation. Platelet specific IgG was further isolated from the patient’s IgG by affinity chromatography on a column of solubilized platelet membrane proteins. The affinity isolated antibody was then analyzed by the Western blotting using solubilized platelet membranes. Patient antibody was found to react with a 50 kD platelet membrane protein which has yet to be fully characterized. At the present time the patient remains on LMW heparin, but requires frequent infusions of IVIG to maintain platelet counts above 30 × 109/L. We are aware of only one other reported case of a spontaneous platelet activating antibody and no other case characterized by chronic DIC.

scholarly journals HIT the price point with fondaparinux

Blood ◽  
2016 ◽  
Vol 128 (26) ◽  
pp. 3019-3020
Author(s):  
Nathan T. Connell
Keyword(s):  
United States ◽  
Cost Effectiveness ◽  
The United States ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Heparin Induced Thrombocytopenia ◽  
Price Point ◽  
The Cost

In this issue of Blood, Aljabri and colleagues report on their analysis of the cost-effectiveness of fondaparinux for the treatment of heparin-induced thrombocytopenia (HIT) in the United States.1 HIT is a relatively uncommon but serious complication of the use of heparin-containing products.2 Treatment of HIT requires use of an alternate anticoagulant such as the direct thrombin inhibitors argatroban and bivalirudin.3

Heparin-Induced Thrombocytopenia in Neonates

2005 ◽  
Vol 24 (5) ◽  
pp. 33-37 ◽  
Author(s):  
Julie Martchenke ◽  
Lynn Boshkov
Keyword(s):  
Heart Surgery ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Type I ◽  
Type Ii ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Administration ◽  
Immune Mediated ◽  
Limiting Condition

Heparin-induced thrombocytopenia (HIT), an immune-mediated response to heparin administration, has been recognized in adults for some time, but only recently recognized in neonates and children. HIT Type I is a mild, self-limiting condition. HIT type II is a severe immune reaction to heparin that leads to thrombocytopenia and often thromboembolic complications. The incidence of HIT Type II is 2–5 percent in adults on heparin products and may be as high in neonates and children. The mortality rate from HIT in adults is 7–30 percent and is unknown but potentially high in newborns as well. The cardinal sign of HIT is a drop in platelet count by 50 percent or platelet counts below 70,000–100,000/mm3. This drop usually occurs five to ten days after the first exposure to heparin. Treatment is immediate cessation of all heparin therapy and initiation of alternative anticoagulants, especially the direct thrombin inhibitors lepirudin and argatroban. This article reviews the literature on HIT and presents a case of neonatal HIT following heart surgery.

scholarly journals The level of brain-specific protein S 100B in patients with acute coronary syndrome associated with anxiety-depressive disorders

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
T Poponina ◽  
K Gunderina ◽  
Y Poponina
Keyword(s):  
Acute Coronary Syndrome ◽  
Protein Level ◽  
Depressive Disorders ◽  
Protein S ◽  
Specific Protein ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Coronary Syndrome ◽  
History Of

Abstract Funding Acknowledgements Type of funding sources: None. Background In clinical medicine, there is still a need for a highly sensitive laboratory marker that reflects brain damage. In some cases, myocardial infarction proceeds with aggravation of cerebral ischemia, stroke, psychosomatic disorders. One of the candidates for laboratory diagnosis of brain damage is the S 100B protein. Aim of the study to analyze the level of brain-specific protein S 100B in blood plasma in patients with acute coronary syndrome associated with anxiety-depressive disorders. Methods and Results All patients were diagnosed with clinically severe anxiety of 55.2 [40; 64] points and depression of an average degree of 24.5 [19; 28] points. In the hospital, blood samples were taken for S 100B protein. The intragroup analysis of the S 100B protein level revealed that in 3 patients (5%) the S 100B protein level was below the normal limit 42.56 [32.6; 52.6] ng/L, in 13 patients (24%) the S 100B was within the normal range of 84.1 [75.27; 86.57] ng/L. In 38 patients (70%), the concentration of S100B protein was increased to 129.65 [110; 144] ng/L. The analysis of the group with a high concentration of S 100B protein found that the highest indicators of the S 100B protein level were in patients suffering from carbohydrate metabolism disorders, with a long history of hypertension, high levels of anxiety and depression. When studying the mental status of patients, a positive correlation was found between the concentration of the S100B protein and the level of anxiety (p = 0.00065). In 5 patients (9%), the maximum increase in the level of protein S 100 B 184.6 [166.26; 209.34] ng/L was revealed. These patients aged 60 to 70 years, had stroke in the past, had a long history of ischemic heart disease, type 2 diabetes, the course of AMI proceeded with a decrease in left ventricular ejection fraction to 34-40%. Patients with a protein level of 84.1 [75.27; 86.57] ng/L were younger, age 50-60 years, without a history of diabetes, with preserved left ventricular ejection fraction. Conclusion An increase in the S 100B protein level was observed in polymorbid patients, with a history of possible impairment of the blood-brain barrier permeability, which could have formed due to the toxic effect of the S 100B protein. This group of patients has more pronounced anxiety-depressive symptoms. Thus, the S 100B protein can be considered as a potential therapeutic target.

scholarly journals Delayed presentation of acute coronary syndrome with mechanical complication during COVID-19 pandemic: a case report

2020 ◽  
Author(s):  
Joo Hor Tan ◽  
Jieli Tong ◽  
Hee Hwa Ho
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Tamponade ◽  
Left Ventricular ◽  
World Health ◽  
Mechanical Complication ◽  
Delayed Presentation ◽  
Left Circumflex Artery ◽  
Coronary Syndrome ◽  
History Of ◽  
The Impact

Abstract Background The World Health Organization declared coronavirus disease 2019 (COVID-19) a global pandemic on 11 March 2020. We report a patient with acute myocardial infarction (AMI) who presented late due to fears of contracting COVID-19. Case summary A 65-year-old man with a history of hypertension presented late to the emergency department (ED) with AMI. He gave a 2-month history of exertional angina but avoided seeking medical consult due to fears of contracting COVID-19. On the day of admission, he had 4 h of severe chest pain before presenting to the ED. He was hypotensive and tachycardic on arrival. Electrocardiogram showed inferolateral ST-elevation myocardial infarction. Chest radiograph revealed widened superior mediastinum and bedside echocardiogram revealed inferoseptal and inferolateral hypokinesia with features of cardiac tamponade. An urgent computed tomography aortogram showed possible left ventricular (LV) wall perforation with resulting haemopericardium and cardiac tamponade. Subsequent coronary angiogram showed 100% occlusion of mid left circumflex artery and a contained LV wall rupture was confirmed with LV ventriculogram. He was transferred to a tertiary centre and underwent successful emergency surgical repair. Discussion Our index case demonstrates the impact of the COVID-19 pandemic on health seeking behaviour due to fears of contracting COVID-19 and the ensuing impact of delayed medical intervention. Cardiologists worldwide are seeing an alarming rate of rare complications of AMI in patients who present late. Physicians need to be aware of this phenomenon and have an active role to play in public education.

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