Antiphospholipid Syndrome - A Case Report of Pulmonary Thromboembolism, Followed with Acute Myocardial Infarction in Patient with Systemic Sclerosis

AIM: We are presenting an uncommon case of pulmonary embolism, followed with an acute myocardial infarction, in a patient with progressive systemic sclerosis. CASE PRESENTATION: A female 40 years of age was admitted with signs of pulmonary embolism, confirmed with CT scan, which also reviled a thrombus in the right ventricle. The patient had medical history of systemic sclerosis since the age of 16 years. She suffered an ischemic stroke 6 years ago, but she was not taking any anticoagulant or antithrombotic medications ever since. She received a treatment with thrombolytic therapy, and subsequent UFH, but, on the second day after receiving fibrinolysis, she felt chest pain accompanied with ECG changes consistent for ST-segment elevation myocardial infarction (STEMI). Urgent coronary angiography was undertaken, which reviled cloths causing total occlusion in 4 blood vessels, followed with thromboaspiration, but without successful reperfusion. Several hours later the patient developed rapid deterioration with letal ending. During the very short hospital course, blood sampling reviled presence of antiphospholipid antibodies. CONCLUSION: The acquired antiphospholipid syndrome is common condition in patients with systemic autoimmune diseases, but relatively rare in patients with systemic sclerosis. Never the less, we have to be aware of it when treating the patients with systemic sclerosis

Antiphospholipid Syndrome - A Case Report of Pulmonary Thromboembolism, Followed with Acute Myocardial Infarction in Patient with Systemic Sclerosis

AIM: We are presenting an uncommon case of pulmonary embolism, followed with an acute myocardial infarction, in a patient with progressive systemic sclerosis. CASE PRESENTATION: A female 40 years of age was admitted with signs of pulmonary embolism, confirmed with CT scan, which also reviled a thrombus in the right ventricle. The patient had medical history of systemic sclerosis since the age of 16 years. She suffered an ischemic stroke 6 years ago, but she was not taking any anticoagulant or antithrombotic medications ever since. She received a treatment with thrombolytic therapy, and subsequent UFH, but, on the second day after receiving fibrinolysis, she felt chest pain accompanied with ECG changes consistent for ST-segment elevation myocardial infarction (STEMI). Urgent coronary angiography was undertaken, which reviled cloths causing total occlusion in 4 blood vessels, followed with thromboaspiration, but without successful reperfusion. Several hours later the patient developed rapid deterioration with letal ending. During the very short hospital course, blood sampling reviled presence of antiphospholipid antibodies. CONCLUSION: The acquired antiphospholipid syndrome is common condition in patients with systemic autoimmune diseases, but relatively rare in patients with systemic sclerosis. Never the less, we have to be aware of it when treating the patients with systemic sclerosis

Thoracic Aortic Disease - Aortic Dissection

The term Thoracic Aortic Disease (TAD), covers a wide range of degenerative, structural, acquired, genetically based and traumatic diseases, conditions and presentations of the thoracic aorta. In 2010 several professional associations published joint Recommendations for diagnosis and treatment of TAD, and last year ESC published new Guidelines for diagnosis and treatment of Aortic Disease. Interesting enough is the fact that, 2010 Guidelines were the first recommendations accompanied by a campaign designed for the general population, with a purpose to increase awareness of the existence and importance of these conditions. It was explained by the fact that dissection of the thoracic aorta, the most distinguished acute clinical manifestation of TAD, is recognized as one of the twenty most common causes of death. This is a condition that is diagnosed mainly based on data obtained by a detailed history and clinical examination, for the existence of high-risk situations, high-risk features of the chest pain and high risk clinical findings. Unfortunately, yet, there isn’t sensitive and specific biomarker that could help in the diagnosis of this acute condition. The definitive confirmation of the disease is made by imaging of the aorta with one of the imaging modalities such as transoesophageal echocardiography (TOE), computed tomography (CT) or magnetic resonance (MRI). And in terms of rapid diagnosis, this condition is still characterized with high mortality. This paper is an attempt to give an overview of the situation with TAD in our country, through a retrospective analysis of the medical database at the University Clinic of Cardiology of all patients hospitalized during the year 2009 with a working diagnosis of AoD

Glicoregulation in diabetic and no diabetic patients and the impact on early clinical outcome in patients with acute coronary syndrome

Aim of the study: The aim of our study was to analyse the impact of glicoregulation before and during the hospital treatment in patients with acute coronary syndrome on early in-hospital clinical outcome (CE). Methods: We included in the analyse ACS patients (STEMI, NSTEMI, APNS) treated with PCI, in whom we analysed: demographics, risk profile, basic biochemical variables (Hgb, BUN, creatinine, Na, K), lipid profile (Tg, HDL, LDL Hol, lpa), HgbA1C, admitting glucose level and levels of glucose during the hospitalisation, and TIMI flow before and after PCI procedure. We divided patients in diabetics and non-diabetics. Than based on the level of HgbA1C measured at admition we subdivided diabetics in good (6.5%) DM, and patients without previously known diabetes in three groups: no diabetics (6.5) HgbA1C. Based on glycaemic levels we divided pts. in groups: good regulation (5-10mmol/L), bed regulation: >10mmol/L epizodes, and <5mmolL aeizodes. We analized influence of glikoregulation on biochemical variables and lipide profile, PCI results (TIMI flow), and cardiac events (heart failure, shock, dysrhythmias, GIT bleeding, CVI and cardiac death). Statistical analyse: descriptive and comparative statistics with t-test, Chi square test, uni and multivariate analyse. Significance determined at 0.05. Results: 80 pts. Were included in the analyse (33.8% females and 66.2% males), at mean age of 60.2±10.8y. Risk profile: 51% had HTA, 6.3% HLP, 36.3% positive family history, 33.8% were diabetics, 61.4% smokers, 5% previous CAD. Mean Hgb 14.6±1.4mg/dl, BUN 5.9±3.2, creatinine 80.5±30.6 micromol/L, Na 137.5±3.4, K 4.2±0.5. No differences in biochemical and lipide profile was found between groups. Among 53 no diabetic patients prior to ACS, we identified 4 (5%) patients with diabetes (>6,5), and 18 (22.5%) with pre-diabetes (5.6-6.5%). Mean TIMI flow was 0.45±0.79 before, and 2.96±0.19 after PCI, r -.221, p 0.000. The single independent predictor in multivariate analyse (included HgbA1C, admitting glycaemic level, glucoregulation and diabetic group) on TIMI flow was admitting glycaemia (beta -.327, p 0.003). 12/80 pts. had CE, and again we included same variables and identified two independent predictors of CE: admitting glycaemic level (beta .386, p 0.007) and HgbA1C (beta .254, p 0.070). Conclusion: Acute coronary syndrome identified patients with previously no diagnosed diabetes. Stress glycaemia (admition glycaemic level) was found to be significant predictor of PCI results, and together with HgbA1C level of CE in ACS patients treated with PCI

Association of biomarkers of oxidative stress, stress glycaemia and glycated haemoglobin with coronary artery disease

Introduction: Reactive oxygen species (ROS) are responsible for generalized oxidation which results in cell dysfunction, necrosis or apoptosis. Assessment of oxidative stress markers could modify course of treatment of patients with coronary artery disease (CAD). The aim of this study was to evaluate association of markers of oxidative stress, stress glycaemia and glycated hemoglobin (HgbA1c) with CAD. Methods: Crosssectional observational study. Variables: demographics, risk factors and comorbidities, lipoprotein and glycemic profile, oxidative stress biomarkers: malondialdehyde (MDA) and hydro peroxide (HP), and antioxidant enzymes: superoxide dismutase (SOD), CATALASE and glutathione peroxidase (GPS). Comparison was performed between CAD patients and healthy controls, patients with acute coronary syndrome (ACS) versus chronic CAD, and between PCI revascularised and stable post MI patients. Results: 300 patients, (64.7% m/36.3% f), mean age 62±11 y. (p=ns between genders). 187 (62.3%) were ACS and 113 (37.7%) chronic CAD patients. There was no statistical significant difference in the risk profile between the CAD groups. Patients with CAD had significantly higher prooxidative and significantly lower antioxidative levels of biomarkers (Table 1), as compared with healthy volunteers. Statistically significant differences were observed for HP and SOD between ACS and HCAD group. In HCAD group, revascularized patients demonstrated higher oxidative stress as compared to stable post MI patients. In ACS patients statistical significant intergroup difference was registered, but not pointing to the single type of ACS. ACS patients had also higher levels of stress glycaemia and HgbA1c. Significant positive correlation were found for HgbA1c and stress glycaemia with MDA (r=,154**, p=0,008; r=,254**, p=0,024 respectively). Conclusion: CAD patients demonstrated pronounced oxidative stress when compared to healthy controls, ACS patients had higher oxidative stress as compared with chronic CAD patients, PCI subgroup performed worse that stable post MI patients. Higher oxidative stress activity was linked to worse glycemic control as measured threw stress glycaemia and HbA1c

Anemia, renal impairment and in-hospital mortality, in acute worsening chronic heart failure patients

Aim of the study: To analyze the impact of anemia and renal impairment on in-hospital mortality(IHD), in patients with acute worsening chronic heart failure. Methods: 232 randomly selected patients with symptoms of HF were retrospectively analyzed. Analyzed variables: gender, age, risk factors and co-morbidities: HTA, HLP, DM, COPD, CAD, PVD, CVD, anemia(defined as Hgb ≤10mg/dl), renal failure. Measured variables: systolic and diastolic BP, Hgb, sodium, BUN, creatinine, length of hospital stay and IHD. Comparative analysis was performed between patients with in-hospital mortality(IHD) and survivors, as a function of anemia and renal impairment. Statistical analysis: descriptive and comparative analysis, t-test, Chi square, univariate (binary logistic and linear regression and multivariate linear regression(stepwise backward). Results: Mean age 69.6±11.4, 102(44%)females and 130(56%) males, with females being significantly older 72.6±12.5 vs. 67.7±10.2(p=0.002), with significantly higher SBP, DBP and sodium level (p=0.003; 0.002 and 0.028 respectively), and males having HTA more often OR 1.3; p=0.017. Mean hospital stay was 6.8±5.8 days, with significant difference between IHD and non IHD group(7.9±4.5 vs. 3.8±7.9; p=0.000), with the highest mortality during the first (37.3%) and second hospital day (44.1%). 44 pts.(19%) had anemia, 31(13.4%) had known Chronic Renal Failure(CRF), and 59(25.4%) had IHD. Anemia was significantly associated with IHD (Chi square 6,36, sig 0.012, Exp B 2.48, sig 0.010), meaning pts. with anemia had 2,5 times greater risk for IHD. CRF per se, was not associated with IHD. Univariate linear regression identified creatinine(R square .032, beta .180, sig 0.006), and BUN(R square .034, beta .184, sig 0.005), as predictors of IHD. Multivariate stepwise regression model(anemia, HRF, Hgb, BUN, creatinine, sodium) at step 3(mean square .799, sig 0.002), identified two independent predictors Hgb(beta -.148, sig 0.028), and BUN(beta .163, sig 0.055). Multivariate model that included other known predictors of IHD(EF%, SBP, DBP, HRF, CAD, anemia, Hgb, BUN, creatinine, sodium) at step 8(mean square 1.537, sig 0.000), identified four independent predictors: EF%(beta -.204, sig 0.002), SBP(beta -.130, sig 0.052) as markers of systolic dysfunction and again anemia(Exp B 2.2.06, sig 0.041), and BUN(beta .200, sig 0.002). Conclusion: Anemia and renal impairment are well known comorbidities associated with HF that have great impact on course of HF. We confirmed that anemia and BUN, are significantly independent predictors of in hospital mortality in acute worsening CHF

Association of biomarkers of oxidative stress, stress glycaemia and glycated haemoglobin with acute coronary syndrome

The aim of our study was to comparatively evaluate association between biomarkers of oxidative stress, stress glycemia and HbA1c in patients with coronary artery disease

Predictors of in-hospital mortality in patients with acute or acute worsening chronic heart failure

Aim of the study: to identify predictors of in-hospital mortality in acute HF patients. Patients and methods: 355 randomly selected patients admitted to ICCU with symptoms of HF were analyzed for: risk factors and co-morbidities (COPD, CAD, PVD, anemia, renal failure), heart rate, systolic and diastolic BP, Hgb, sodium, BUN, creatinine, ejection fraction (based on which patients were divided in PEF-HF and REF-HF); length of stay and GWTG-HF score (Get with the Guidelines-HF risk score), calculated from the seven clinical variables in that score. Comparative analyze was performed between patients with in-hospital mortality (IHM) and survivors. Statistical analyze: univariate and multivariate binary and linear logistic regression, ROC Curve for testing of discriminate function of GWTG-HF score. Results: 355 patients at mean age 70.1±10.9, 150 (42%) females and 205 (58%) males were included. Females were older 72.9±11.4 vs. 67.9±10.0 (p=0.000), had higher DBP (p 0.007) and EF (%): 43.6±11.6 vs 41.1±9.5 (p 0.029), and sodium level (p 0.018), more often had HTA (OR 1.4; p=0.001), while males had PAD (OR 1.7; p 0.020), and prior MI (OR 2.2; p 0.001). No significant differences in death rate, length of hospital stay and GWTG-HF score was observed. 82 (23.1%) events were registered (IHD group). The highest mortality rate was observed during the first 48 hours (40.4%). Mean hospital stay was 6.3±5.3 days, with no differences between the groups (5.6±3.9 vs. 6.7±5.9; p=0.056). We identified several univariate predictors: prior MI (beta -.490; p 0.041), PVD (beta -1.01; p 0.007); anemia (OR 1,89; p 0.044); REF-HF (OR 2.43; CI 1.7-3.6; p 0,000); EF (beta -.258; p=0.000); SBP (beta -.299; p=0.000), DBP (beta .315; p=0.000); Hgb (beta -.142; p=0.007), sodium (beta -.107; p 0.045); creatinine (beta .184; p=0.000), BUN (beta .199; p=0.000), and GWTG-HF score (beta .279; p 0.000). Multivariate logistic regression identified SBP (beta -.014; p 0.020) and anemia (ExpB 3.668; p 0.019); as positive, while prior MI (ExpB -2.753; p 0.050); PVD (ExpB -1.348; p 0.005) and DBP (beta .034; p 0.003) as negative predictors for in-hospital death. Mean GWTG-HF score was 38.9 ±10.1 (37.3 ±9.3; 44.0 ±11.0; p 0.000, non-IHD vs IHD pts). It had excellent discriminate function (ROC Curve: Area under the Curve .694, p< 0.000 (CI .627-.778), in predicting IHD. Conclusion: Low sodium, high BUN and creatinine are predictors of IHD, but only anemia, reduced EF and low systolic BP were identified as independent predictors of IHD. GWTG-HF score is a powerful tool for prediction of IHD in acute or acute worsening CHF patients

C-reactive protein is associated with ventricular repolarization dispersion among patients with metabolic syndrome

Background: An increasing body of evidence indicates that inflammatory activation profoundly impacts the electrophysiological properties of cardiomyocytes. A marker of systemic inflammation such as C-reactive protein(CRP), is associated with all parameters of the Mtabolic syndrome(MetS) and that may result in adverse cardiac events via multiple effects, ultimately resulting in a prolongation of Action Potential duration (APD), and thereby of the QTC (QT corrected) interval on ECG. Objective: We sought to investigate the influence of CRP levels on the prevalence of prolonged QT-dispersion and prolonged Tpeak-Tend &ndash;dispersion in the patients with MetS. Methods: We conducted a multicenter observational cross-sectional study. The study population consisted of 200 patients with MetS, stratified in two groups:103 participants (50 females and 53 males) with level of CRP&gt;3mg/l, and 97 participants (47 females and 50 males) with level of CRP&lt;3mg/l), who attended outpatient visits at general cardiology Health Care Clinics during 1 calendar year. For the analysis of the ECG, we performed a manual measurement of the values using a digital caliper with measuring range of 0-150 mm, 0.01 mm resolution, and 0-100 &plusmn; 0.02 mm accuracy. QT interval dispersion was obtained by the difference between the maximum and the minimum QT intervals found in the 12-lead electrocardiogram. The Tpeak-Tend interval was obtained from the difference between QT interval and QTpeak interval. Results: Prolonged QTC. dispersion, was found in 51.4% of participants with level of CRP&gt;3mg/l and in 32.9% of with level of CRP&lt;3mg/l, the differences were statistically significant. (p=0.004). The results showed that 51.4% participants with level of CRP&gt;3mg/l had a prolonged Tpeak-Tend interval, and 32.9% of participants with level of CRP&lt;3mg/l had prolonged Tpeak-Tend interval. Difference were statistically significant.( p=0.04). There were significant association of increased levels of CRP and QTC-dispersion (OR = 2.486, 95% CI 1.389-4.446).There were significant association of increased levels of CRP with Tpeak-Tend Dispersion (OR=2.239,95%CI 1.262-3.976). Prolonged QTC max. Interval OR=2.236,%CI 1.246-4.014),Prolonged Tp-Te-interval. (OR=2.367, 95%CI 1.327-4.222), also there were significant association of increased levels of CRP with BMI. (OR=1.154, 95%CI 1.095-1.227) and significant association of increased levels of CRP with presence of uncontrolled glicemia.(OR=1.779, 95%CI 1.014-3.12). Conclusion: We think we proved the hypothesis that patients with MetS and high level of CRP have higher prevalence of QT- dispersion and Tpeak-Tend dispersion than patients with MetS and lower level of CRP. These findings have both epidemiological and clinical relevance, also these findings might lend further insight into potential mechanisms by which MetS is associated with adverse cardiac events

Control of arterial hypertension and risk of new-onset of atrial fibrillation in patients with metabolic syndrome

Background: An association between Atrial Fibrillation (AF) and Metabolic Syndrome (MS) a constellation of abnormalities (high blood pressure, hyperglycemia, dyslipidemia, and abdominal obesity), has been demonstrated. There have been many studies that have shown that elevated blood pressure (BP), was significantly associated with an increased risk of AF. It is uncertain whether maintaining the optimal BP levels can prevent AF in the patients with MS categorized as &lsquo;high-risk&rsquo; patients.Objective: The aim of this study was to evaluate the influence of control of BP on the occurrence of new-onset atrial fibrillation in patients with Metabolic Syndrome.Methods: Into this observational study, was enrolled 435 consecutive patients (210 males and 225 females) aged 45-79 years who fulfilled criteria for MS. Participants were selected among primary and secondary care patients, who were receiving ongoing care for arterial hypertension in the period from November 2018 till November 2021. The study was conducted at outpatients in 5 Health Care Clinics (3 Secondary Health Care Clinics and 2 Primary Health Clinics). Patient were categorized according to their BP levels as Group 1-patients with controlled BP, {(patients aged &lt; 65 years Systolic Blood Pressure (SBP) of 120 - 130 mmHg, patients aged &ge; 65 years SBP of 130 - 139 mmHg)} and Diastolic Blood Pressure (DBP), {(patients aged &lt; 65 years of &lt; 80 mmHg. but not &lt; 70 mmHg; patients aged &ge; 65 years of 85 - 89 mmHg)}, or Group 2-patients with uncontrolled BP(&gt; 130/80 mmHg),and in patients aged &ge; 65 years BP (&ge; 140/90 mmHg ).&nbsp;Results: New-onset of AF, was more frequent in participants with uncontrolled BP, respectively (34.7% vs. 19.5%, p = 0.009).Patients with uncontrolled BP have more frequent persistent AF (15.2% vs. 0.04%) and permanent AF (0.08% vs. 0.02%), whereas there was not significant changes between groups in relation to frequency of paroxysmal AF, respectively (12.8% vs. 10.9%, p = 0.29). There was observed significant association of uncontrolled BP with: increased frequency of AF (OR = 2.193; 95% CI 1.390 - 3.439), persistent AF (OR = 3.931; 95% CI 1.771 - 8.084), permanent AF (OR = 4.138; 95% CI 1.383-12.381), LA. Dimension &ge; 2.2 cm/m2 (OR = 2.089, 95% CI 1.330 - 3.252), BMI (OR = 5.226, 95% CI 3.155 - 8.659) and 5-risk factors for MS, respectively (OR = 2.998, 95% CI 1.833 - 4.901).Conclusion: Optimal BP levels, can reduce the frequency of new-onset AF in patients with MS categorized as &lsquo;high-risk&rsquo; patients. Uncontrolled BP was associated with an increased risk of both subtypes of AF (persistent and permanent) in the patients with MS categorized as &lsquo;high-risk&rsquo; patients