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Objective: To investigate differences in clinical presentation, anticoagulation pattern and outcomes in patients with dementia and atrial fibrillation (AF).Methods: A total of 1217 hospitalized patients with non-valvular AF from two institutions were retrospectively evaluated. Diagnosis of dementia was established by a psychiatrist or a neurologist prior to or during hospitalization. Adequacy of warfarin anticoagulation was assessed during follow-up using at least 10 standardized international ratio values. In addition to unmatched comparison, nested case-control study was performed to further evaluate differences in clinical outcomes between patients with and without dementia.Results: A total of 162/1217 (13.3%) patients were diagnosed with dementia. Among other associations, patients with dementia were significantly older with higher number of comorbidities, had lower estimated glomerular filtration rate (eGFR) and lower left ventricular ejection fraction (LVEF), (P < 0.05 for all analyses). Patients with dementia were significantly less likely to receive direct oral anticoagulants (DOACs ; 27.2% vs 40.3% ; P = 0.001) and were significantly more likely to be inadequately anticoagulated with warfarin (38.9% vs 28.6% ; P = 0.008) than patients without dementia. After matching based on age, eGFR, LVEF, and CHA2DS2-VASC patients with dementia were significantly more likely to experience inferior overall survival (HR = 1.8 ; P = 0.001) and shorter time to thrombosis (HR = 2.3 ; P = 0.019).Conclusion: Our findings speak in support of increased thrombotic and mortality risks in patients with dementia, possibly due to inadequate anticoagulation and higher number of comorbidities.

Objective: Our objective was to investigate the predictors of falls requiring a visit to the emergency department in patients with nonvalvular atrial fibrillation (AF) receiving different types of anticoagulants and to investigate the clinical consequences of falling in the same population. ----- Methods: A total of 1217 patients with nonvalvular AF from two institutions were retrospectively evaluated. Each patient underwent a physical examination, and clinical histories and medication profiles were taken from each patient at baseline. ----- Results: The median age of our cohort was 71 years; 52.3% were males, and 86.1% of patients were receiving anticoagulation at study baseline. The 5-year freedom-from-falling rate was 81.6%. The use and type of anticoagulation was not significantly associated with the risk of falling (P = 0.222), whereas higher Morse Fall Scale (MFS), CHA2DS2-VASC (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke or transient ischemic attack, vascular disease, age 65-74 years, sex category), and HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile international normalized ratio, elderly [> 65 years], drugs/alcohol concomitantly) scores were significantly associated with a higher hazard of the first fall in univariate analyses. In the multivariate Cox regression model, MFS, older age, osteoporosis, higher levels of high-density lipoprotein cholesterol, higher diastolic blood pressure, and use of amiodarone, diuretics, or short- and medium-acting benzodiazepines were mutually independent predictors of the first fall. Of 163 patients, 93 (57%) had a bone fracture during the fall. Type of anticoagulation significantly affected survival after the first fall (P < 0.001): patients inadequately anticoagulated with warfarin had worse survival rates, and patients receiving apixaban and dabigatran had the best survival rates after the first fall. ----- Conclusion: Older patients who had comorbidities and were taking amiodarone, diuretics, or short- or medium-acting benzodiazepines had the highest risk of falls. The type and quality of anticoagulation did not seem to affect the risk of falling but did significantly affect survival after the first fall.

Aim : To investigate changes of anticoagulation therapy in patients with atrial fibrillation (AF) and high thrombotic risk.Methods : We retrospectively analyzed 1061 patients with non- valvular AF and indication for anticoagulation therapy referred in a period from 2013 to 2018 and followed-up for a median time of 38 months.Results : Therapy change occurred in 206 (19.5%) patients (195 switches and 11 permanent discontinuations). Only 37% of patients on warfarin had optimal dosing and their duration of therapy was significantly shorter compared to direct oral anticoagulants (DOACs ; (adjusted HR 1.21, 95% CI 1.09-1.37). Therapy change occurred in only 33% of patients with poorly controlled warfarin, and in only 24% of patients that experienced a thrombotic event while taking warfarin. Optimal dosing was an independent factor for any therapy change during follow-up, irrespective of type of anticoagulant drug at baseline. DOAC swapping occurred in 39% of all DOAC to DOAC switches, with one bleeding event and no thrombotic events documented after a DOAC swap.Conclusion : High risk patients with AF rarely discontinue anticoagulation therapy. The need for therapy change should be emphasized in patients with non-optimal dosing, and in patients that experience thrombotic events while taking warfarin.

OBJECTIVE: Stratifying patients with paroxysmal or short- term persistent atrial fibrillation (AF) who are at greater risk of developing permanent AF is challenging. Aim of our prospective study was to evaluate association of laboratory parameters (biochemistry and complete blood count (CBC)) together with standard demographic, clinical and echocardiography parameters, with AF progression. METHODS: We prospectively recruited 579 patients with AF and divided them into two groups at index hospitalization: paroxysmal or persistent (non- permanent AF), and long-term persistent or permanent AF patients (permanent AF). Clinical, echocardiographic, and relevant CBC parameters were collected. Non-permanent AF patients were selected for follow-up, with a median follow-up time of 21 months. Endpoint was progression to permanent AF. RESULTS: Out of 409 patients with non-permanent AF, 109 (26.6%) progressed within follow-up. In a multivariate Cox regression model only increased left atrium (LA) diameter (HR 2.16, 95% CI 1.20- 3.87, p = 0.010), and increased red cell distribution width (RDW ; HR 1.19, 95% CI 1.03- 1.39, p = 0.022) showed significant independent association with progression. There were 221/409 patients with both LA ≤45 mm and RDW level ≤14.5% who progressed at a rate of only 17.6%, and showed relative risk of AF progression of 0.47 (95% CI 0.34-0.67 ; p < 0, 001). CONCLUSION: Together with LA size, RDW was independently associated with AF progression. Patients with both LA size ≤45 mm and RDW level ≤14.5% are most probably the best candidates for rhythm control strategies.

Purpose To validate red cell distribution width (RDW) as an improvement in 30-day mortality risk stratification based on the Pulmonary Embolism Severity Index (PESI) in acute pulmonary embolism (PE). Patients and Methods Prospective observational analysis of consecutive adult acute PE patients. Results Among 731 patients, 30-day mortality was 11.9%. With adjustment for the PESI score and number of covariates, higher RDW was associated with higher mortality (RDW continuous: OR 1.21, 95% CI 1.06– 1.38 ; Bayesian OR 1.22, 1.07–1.40 ; RDW ‘high’ [>14.5% in men >16.1% in women] vs normal: OR 3.83, 1.98–7.46 ; Bayesian OR 3.98, 2.04–7.68]. Crude mortality was 3.6% if PESI 86–105 (intermediate risk), but 1.2% if RDW normal and 7.1% if RDW high ; 11.8% if PESI 106–125 (high risk), but 3.6% if RDW normal and 18.8% if RDW high. Adjusted probabilities showed higher mortality (ORs between 3.5–5.8) if RDW was high in any PESI risk subgroup. Crude mortality rates in two random-split subsets (n=365 and n=366) again showed the same patterns. Conclusions On-admission RDW above the normal range improves 30-day mortality risk stratification based on PESI score in acute PE. Particularly, it corrects PESI- based intermediate-risk or high-risk allocation by reclassification into very low-risk (11.0%).

Cardiologists are familiar with valvular heart diseases but often they do not perceive heart valves as source of ventricular arrhythmias (VA). In patients with structural heart disease (SHD) VAs originate from a substrate in diseased myocardium, while in patients without SHD most common origins are outflow tracts (OT)1 . Premature ventricular complexes (PVC) from OT are either from subvalvular, valvular or supravalvular myocardium as there are myocardial extensions above the semilunar valves, these VAs are created predominantly by mechanism of triggered activity or enhanced automaticity1, 2. Papillary muscles, mitral and tricuspid anulus, aortomitral continuity and other sites in a structurally normal heart can also be the origin VAs. There are general and specific ECG characteristics that can localize the origin of VAs: bundle branch block type, axis, QRS polarity in lead V6, QRS duration, precordial transition, maximal deflection index, and so forth, therefore mapping of the PVC starts in the region that is presumed by ECG characteristic3. While different anti-arrhythmic drugs (AAD) aim at different mechanisms ; calcium channel blocker can suppress triggered activity and beta-clocker can suppress automaticity, in general ablation is more effective in clinically meaningful reduction of PVCs compared to AAD (up to 95% vs. up to 25%)4. Ablations are generally safe but complication rates of catheter ablation in aortic root are not negligible and include myocardial rupture and tamponade, stroke, valvular damage, and coronary artery occlusion ; these complications can be lowered by usage of intracardiac ultrasound (ICE)1, 4. When mapping arrhythmias from the valves, we should stop perceiving the heart structures or valves as isolated parts and acknowledge that regional anatomy of these structures is among the most complex of those encountered by cardiac electrophysiologists, e.g., aortic valve is directly related with both atria, the interatrial septum, the right ventricular outflow tract and pulmonary valve, and the aortomitral continuity. Ablation is highly effective in suppression of PVCs, it has low numbers of complications, but ablation in aortic region brings serious complications to the table, therefore shared decision making with the patient and usage of ICE is of upmost importance.

Background: Pulmonary embolism (PE) severity index (PESI) well predicts 30-day mortality in acute PE patients, yet improvements have been advocated. ----- Objectives: To evaluate predictivity of the red cell distribution width (RDW) through a comparison with PESI and to explore their interaction as a potential improvement in this respect. ----- Methods: Retrospective analysis of consecutive adult PE patients. ----- Results: Of the 299 patients, 19 severely unstable died within 48 h. Among the stabilized patients, 30-day mortality was 12.1% (34/280). With PESI ≤125, mortality was 4.9% (9/185), but it was 0.7% (1/140) if RDW ≤15.0% and 17.8% (8/45) if RDW >15.0%; with PESI >125, mortality was 26.3% (25/95), but it was 15.9% (7/44) if RDW ≤15.0% and 35.3% (18/51) if RDW >15.0%. Adjusted relative risk with PESI >125 vs. ≤125 was 17.5 (95%CI 2.37-129) at RDW ≤15.0% and 1.60 (0.76-3.36) at RDW >15.0%. ----- Conclusions: Thirty-day mortality predictions based on the PESI score may be improved by accounting for RDW.

Previous studies have demonstrated cardiovascular causes to be among the leading causes of death after liver (LT) and kidney transplantation (KT). Although both recipient populations have unique pre-transplant cardiovascular burdens, they share similarities in post-transplant exposure to cardiovascular risk factors. The aim of this study was to compare cardiovascular mortality after LT and KT. We analyzed causes of death in 370 consecutive LT and 207 KT recipients from in-hospital records at a single tertiary transplant center. Cardiovascular causes of death were defined as cardiac arrest, heart failure, pulmonary embolism, or myocardial infarction. After a median follow-up of 36.5 months, infection was the most common cause of death in both cohorts, followed by cardiovascular causes in KT recipients and graft-related causes in LT recipients in whom cardiovascular causes were the third most common. Cumulative incidence curves for cardiovascular mortality computed with death from other causes as the competing risk were not significantly different (P = .36). While 1-year cumulative cardiovascular mortality was similar (1.6% after LT and 1.5% after KT), the estimated 4-year probability was higher post-KT (3.8% vs. 1.6%). Significant pre-transplant risk factors for overall mortality after KT in multivariable analysis were age at transplantation, left ventricular ejection fraction

Atrial fibrillation is the most common cardiac arrhythmia. It increases the risk of death and thromboembolic events. Vitamin K antagonists reduce these risks. Disadvantages of vitamin K antagonist therapy are narrow therapeutic range and interactions with drugs and food. In a single center prospective study, we enrolled 249 patients with atrial fibrillation over a 12-month period. The aim of our study was to evaluate vitamin K antagonist use regarding the indication and adequate dose. Data on 249 consecutive patients with atrial fibrillation were collected before general availability of novel oral anticoagulants. Out of 249 patients, 160 (64.2%) had indication for oral anticoagulant therapy. Only 81 (50.6%) patients had vitamin K antagonist in therapy, 12 (14.8%) of them in adequate dose. We also analyzed 129 patients aged over 75, of which 109 (84.4%) had absolute indication for oral anticoagulant therapy. Only 34 (31.2%) patients aged over 75 had been receiving vitamin K antagonist therapy and 6 (17.6%) had the International Normalized Ratio values within the proposed therapeutic interval. We found a significantly higher rate of anticoagulant therapy introduction in patients under 75 years (p=0.03), but there were no significant differences in the adequacy of anticoagulant therapy (p=0.89) between these two populations. Our results showed clear inadequacies of vitamin K antagonist treatment with a growing need for a wider use of novel oral anticoagulants., Atrijska fibrilacija je najučestalija aritmija koja povećava rizik smrti i tromboembolijskih incidenata. Antagonisti vitamina K smanjuju taj rizik. Problem terapije s antagonistima vitamina K je uska terapijska širina i brojne interakcije s lijekovima i hranom. Cilj ovoga istraživanja bio je utvrditi dostatnost primjene antagonista vitamina K s obzirom na indikaciju i dozu. Prikupljeni su podaci 249 bolesnika s atrijskom fibrilacijom hospitaliziranih u Kliničkoj bolnici “Merkur” u razdoblju od 12 mjeseci i to prije šire dostupnosti novijih oralnih antiokoagulansa. Od svih bolesnika, 160 (64,2%) ih je imalo indikaciju za primjenu oralne antikoagulantne terapije, a tek je njih 81 (50,6%) imalo antagonist vitamina K u terapiji. Samo 12 (14,8%) bolesnika je uzimalo antagonist vitamina K u dostatnoj dozi, a 129 (51,8%) ih je bilo iznad 75 godina starosti. Njih 109 (84,4%) je imalo indikaciju za oralnu antikoagulantnu terapiju, a samo 34 (31,2%) ih je uzimalo antagonist vitamina K, od kojih je 6 (17,6%) imalo INR u terapijskim vrijednostima. Statistička analiza podataka pokazala je da su bolesnici mlađi od 75 godina češće uzimali indiciranu oralnu antikoagulantnu terapiju u odnosu na bolesnike starije od 75 godina (p=0,03), dok nije bilo statistički značajne razlike u dostatnoj primjeni antikoagulantne terapije između ovih dviju populacija (p=0,89). Naši rezultati jasno pokazuju nedostatnosti primjene antagonista vitamina K kao i potrebu bržeg prijelaza prema terapiji novijim oralnim antikoagulansima.

Periprocedural myocardial injury (PMI) and contrast-induced nephropathy (CIN) are frequent complications of percutaneous coronary intervention (PCI) associated with early and late major adverse cardiovascular events. Both conditions are associated with similar risk factors, which could imply their possible association. The aim of our study was to assess the correlation of PMI and early postprocedural creatinine shift (ECS) as a marker of renal injury. A total of 209 hospitalized patients with stable coronary artery disease (CAD) were enrolled, who underwent an elective PCI in a period of 12 months. All patients had their serum high-sensitivity troponin I (hsTnI) measured at baseline and 16 hours after the PCI. PMI was defined according to the elevation of postprocedural hsTnI using criteria provided by both the most recent consensus documents as well as evidence-based data. Renal injury was evaluated using the ECS concept. Serum creatinine (SCr) was also measured at baseline and at 16 hours. ECS was defined as SCr >5% at 16 hours compared to baseline. Although incidence of both PMI (77.5%) and ECS (44.5%) were high, no association of these 2 conditions could be found. Further analyses of our data showed that diabetes is associated with a higher incidence of ECS, while patients on beta-blocker therapy had a lower incidence of ECS. In our study, no association between PMI and ECS was found. Additional studies with a larger number of patients and longer patient observation are needed to assess the correlation between PMI and CIN as well as to validate the attractive, but controversial, concept of ECS as an early marker of CIN.

Introduction: Transthoracic echocardiography (TTE) is recommended as the standard of care in evaluation of cardiovascular (CV) disease in liver (LT) and kidney (KT) transplant candidates.1,2 Guidelines for preoperative CV assessment are oriented at the immediate perioperative period and non-ischemic CV processes that would predict poor outcomes after LT and KT are defined less clearly. Aim: to establish whether ≥moderate mitral (MR), tricuspid regurgitation (TR) or ≥mild aortic stenosis (AS) on pretransplant TTE are associated with mortality, graft survival or major CV adverse events (MACE) in the late postoperative period (>30 days). Patients and Methods: Patients were stratified into cohorts based on the presence of ≥moderate MR, TR and ≥mild AS. Exclusion criteria was loss to follow up, incomplete TTE findings and death within 30 days of transplantation. MACE were defined as stroke, myocardial infarction (MI) or heart failure. Patient survival was defined as time from transplantation to death or last follow-up and graft survival as time from transplantation to last follow-up, death, graft dysfunction or re-transplantation. Outcomes of interest were compared between cohorts via logistic or Cox regression. Results: 306 LT (median age 59, IQR 53-64) and 196 KT patients were included (median age 52, IQR 40- 61). Median follow up was 36 months for LT (range 14.3 – 55.9), 40,5 months for KT (range 18-64.9). MACE occurred in 4.25% LT and 4.59% KT recipients. Upon univariate analysis AS was associated with MACE in KT recipients but crossed the significance level after adjusting for common confounders (age, sex, hypertension, diabetes, smoking). 11.76% LT and 9.69% KT recipients died. The most common cause of death was sepsis. MR was found to be associated with LT patient survival, but the association was lost after adjusting for age. In an age adjusted model MR was found to be associated with KT patient survival (HR 2.97, 95% CI 1.06-8.26, P=0.037). Graft survival was not associated with any potential predictors. Conclusion: Associating TTE findings with adverse outcomes after LT and KT might help distinguish patients who would benefit from closer management in the late postoperative period. Moderate or more severe MR was found to be associated with late mortality in KT recipients, however the significance of this is yet to be determined in larger sample studies.

Background/Objectives:Cachexia is a state of involuntary weight loss. The latest generic definition states that aside from weight loss, patient needs to fulfill additional criteria to be diagnosed with cachexia. New, condition-specific definitions also take the weight loss as a principal criterion, and additional criteria are not mandatory but are a part of further assessment. The aim of this study was to reveal the influence of additional criteria on the prevalence of cachexia in patients with various diseases linked to cachexia. Owing to this, we used the last generic definition. Possible differences in clinical presentations of patients with documented weight loss, with the respect of fulfillment of additional criteria were sought.Subjects/Methods:Clinical and anthropometric data on 137 consecutive patients with malignant diseases and chronic heart failure from a single institution were collected.Results:Fourty-two (30.6%) patients had >5% weight loss in the last 12 months. Only 30 (21.8%) of them were found to meet additional three out of five criteria proposed by the new definition. This observed difference in the prevalence of cachexia diagnosed with or without using additional criteria was found to be significant (P=0.0006). Comparison of clinical/laboratory data showed significantly higher levels of C-reactive protein and lower levels of albumin, as well as lower measurements of mid-arm circumference, triceps and suprailiac skinfolds in patients that fulfilled additional criteria. Survival analysis did not show reduced survival of patients fulfilling additional criteria.Conclusions:Additional criteria 'reduce' the prevalence of cachexia. They are indicative of differences in laboratory and clinical features of cachectic patients but do not influence their survival.

Aim To compare the overall and disease-specific mortality of Croatian male athletes who won one or more Olympic medals representing Yugoslavia from 1948 to 1988 or Croatia from 1992 to 2016, and the general Croatian male population standardized by age and time period. Methods All 233 Croatian male Olympic medalists were included in the study. Information on life duration and cause of death for the Olympic medalists who died before January 1, 2017, was acquired from their families and acquaintances. We asked the families and acquaintances to present medical documentation for the deceased. Data about the overall and disease-specific mortality of the Croatian male population standardized by age and time period were obtained from the Croatian Bureau of Statistics (CBS). Overall and disease-specific standard mortality ratios (SMR) with 95% confidence intervals (CI) were calculated to compare the mortality rates of athletes and general population. Results Among 233 Olympic medalists, 57 died before the study endpoint. The main causes of death were cardiovascular diseases (33.3%), neoplasms (26.3%), and external causes (17.6%). The overall mortality of the Olympic medalists was significantly lower than that of general population (SMR 0.73, 95% CI 0.56-0.94, P = 0.013). Regarding specific causes of death, athletes’ mortality from cardiovascular diseases was significantly reduced (SMR 0.61, 95% CI 0.38-0.93, P = 0.021). Conclusions Croatian male Olympic medalists benefit from lower overall and cardiovascular mortality rates in comparison to the general Croatian male population.

Coronary artery disease (CAD) is the leading cause of mortality in patients with chronic kidney disease (CKD). Patients with CKD who undergo percutaneous coronary intervention (PCI) may have more ischemic events than patients without CKD. The aim of our study was to determine the incidence of periprocedural myocardial injury (PMI) after elective stent implantation in patients with CKD using the Third Joint ESC/ACCF/AHA/WHF PMI definition.In a single center prospective cohort study, we enrolled 344 consecutive patients who underwent elective PCI in a period of 39 months. Serum troponin I (cTnI) concentrations were measured at baseline and at 8 and 16 hours after PCI. Periprocedural increase of cTnI, according to the most recent PMI definition, was used to define both the presence and intensity of PMI. Patients were further stratified according to the estimated glomerular filtration rate (eGFR) using 4 variable Modification of Diet in Renal Disease (MDRD) equation: control group with eGFR >90 mL/min/1.73 m and the CKD group with eGFR 90 mL/min/1.73 m) and the CKD group (

Introduction: Implantation of implantable cardioverter defibrillator (ICD) as a primary prevention (PP) is indicated in patients with dilated cardiomyopathy (DCM) with a reduced ejection fraction as well as a life expectancy longer than a year. Implantation of ICD as a secondary prevention (SP) is indicated after cardiac arrest and in patients with symptomatic ventricular tachycardia. Results of a Danish register did not show mortality to decrease in patients with non-ischaemic cardiomyopathy (NCM).1, 2 The goal of our research is to analyze results from University Hospital “Merkur”. Results and Conclusion: From 2012 up to 2017 a total of 89 ICDs were implanted due to DCM, 69 for PP and 20 for SP. Data was collected retrospectively and analyzed. The average age of our patients was 62.9 years, 13 out of 89 were women. The average follow up lasted 32 months. 69 patients were treated due to PP, 36 with ischemic cardiomyopathy (ICM) vs 33 with NCM. Death occurred in 9 patients (7 with ICM vs 2 with NCM), 7 died due to heart failure (HF) and 2 due to noncardiovascular cause (in NCM group). Sudden cardiac death (SCD) was prevented in 12 patients (7 ICM vs 5 NCM). There were 30 appropriate ICD therapy deliveries, significantly more in the group of patients with ICM (23 vs 7 ; p < 0.05). In patients younger then 59 (29 patients) ICD therapy was delivered in 3 patients, and in a group of older patients (40 patients) ICD therapy was delivered in 9 patients. 15 patients with ICM and 5 with NCM were treated due to SP. Death occurred in 5 patients (3 ICM vs 2 NCM), all due to HF. In 4 patients SCD was prevented (3 ICM vs 1 NCM). There were 8 appropriate ICD therapy deliveries (7 ICM vs 1 NCM). 16 patients were older then 59, and all patients in which SCD was prevented, were older then 59. In both groups there were 51 patient with ICM and 38 with NCM. Death occurred in 14 patients (5 ICM and 9 NCM). SCD was prevented in 16 patients (10 ICM vs 6 NCM). In total there were 38 appropriate ICD therapy deliveries (30 ICM and 8 NCM, p

Introduction: Lidocaine is an essential drug used as a local anesthetic and as antiarrhythmic medication of the class Ib type. There are multiple reports in literature that lidocaine can cause coronary artery spasm both in vitro and in vivo1, 2. Elevation of the ST-segment is described during dental or neurosurgical procedures using locoregional lidocaine anesthesia2, 3. We present a case in which intra-articular lidocaine instillation caused a vasospastic ST-segment elevation myocardial infarction (STEMI). Case: A 49-year-old male patient presented to the emergency clinic with chest pain that had begun an hour ago. The pain occurred at rest, was independent of exertion and radiated to the left arm. Previously that morning, he was at the surgical outpatient clinic due to a chronic knee condition where he underwent punction and intra-articular instillation of 100mg lidocaine. The chest pain started 30 minutes after the procedure. The patient had never experienced chest pain or intolerance of exertion before. Previous medical history was notable for well-controlled arterial hypertension, without any family history of coronary artery disease. He previously received lidocaine anesthesia without complications and had no known allergies. There was 1mm elevation in leads II, III, aVF and inferior STEMI was diagnosed (Figure 1). The patient was transferred to the catheterization laboratory for primary percutaneous coronary intervention. The coronary arteriography was without any evidence of Bojana Gardijan*, Matija Marković, Darko Počanić, Tomislav Letilović University Hospital Merkur, Zagreb, Croatia KEYWORDS: ST-segment elevation myocardial infarction, lidocaine, vasospasm. CITATION: Cardiol Croat. 2016 ; 11(3-4):97-98. | DOI: http://dx.doi.org/10.15836/ccar2016.97 *ADDRESS FOR CORRESPONDENCE: Bojana Gardijan, Klinička bolnica Merkur, Zajčeva 19, HR-10000 Zagreb, Croatia. / Phone: +385-98-1650-393 / E-mail: bojana.gardijan@gmail.com ORCID: Bojana Gardijan, http://orcid.org/0000- 0002-1768-2277 • Matija Marković, http://orcid.org/0000-0002-2852-3730 Darko Počanić, http://orcid.org/0000-0003-3257- 110X • Tomislav Letilović, http://orcid.org/0000- 0003-1229-7983 A case of ST-segment elevation myocardial infarction due to intra-articular lidocaine instillation Extended Abstract ACUTE CORONARY SYNDROME RECEIVED: February 9, 2016 ACCEPTED: February 20, 2016 FIGURE 1. The 12-lead electrocardiogram recording on admission showing discrete ST-segment elevation in inferior leads. Cardiologia Croatica 2016 ; 11(3-4):98. VII. nacionalni sastanak o kardiovaskularnim intervencijama s međunarodnim sudjelovanjem VI. sastanak intervencijskih kardioloških medicinskih sestara i tehničara stenosis (Figure 2). The patient received protocol STEMI care. Echocardiography showed no abnormalities or regional wall motion abnormalities. The initial high-sensitivity cardiac-specific troponin I was beneath the value of detection, with the peak value on the second day of stay, 4678.3 ng/L (reference value

Angiogenesis is a physiologic process of new blood vessels formation mediated by various cytokines called angiogenic and angiostatic factors. Although its potential pathophysiologic role in solid tumors has been extensively studied for more than 3 decades, enhancement of angiogenesis in chronic lymphocytic leukemia (CLL) and other malignant hematological disorders has been recognized more recently. An increased level of angiogenesis has been documented by various experimental methods both in bone marrow and lymph nodes of patients with CLL. Although the role of angiogenesis in the pathophysiology of this disease remains to be fully elucidated, experimental data suggest that several angiogenic factors play a role in the disease progression. Biologic markers of angiogenesis were also shown to be of prognostic relevance in CLL. The current findings provide the rationale for investigating antiangiogenic agents in CLL. In the current review angiogenesis in CLL is discussed and its potential diagnostic and therapeutic applications.

1Such different mechanisms could, at least in part, be explained by different demographic characteristics of ISR and non-ISR patients. They could also lead to different approaches to percutaneous coronary interventions (PCI) in those two groups. Patients and Methods: We conducted this retrospective analysis, of our interventional data, in order to find such differences. In years 2014 and 2015 there were 657 elective PCI procedures (41 ISR and 616 non ISR interventions) in our institution. Results: We found no significant differences in major demographic characteristics in ISR vs. non-ISR patients (Table 1). Analysis of procedural characteristics (Table 2) showed that we were probably more aggressive with predilatation in ISR (number of balloons used 1.53±0.59 vs. 1.34±0.77; p=0.03). We were less keen to implant a stent in ISR patients (21.9% vs. 82.3%; p

ygomicosis is a fungal disease caused by fungi from the Zygomycota order that are usually airborne spread, with pulmonary and rhinocerebral involvement being the most common. Once in the bloodstream, spores tend to accumulate in vascular tissues leading to thrombosis, infarction, and necrosis of involved tissues. In immunocompromised patients, such as those with hemophagocytic syndrome, zygomicosis is frequently characterized by fulminant disseminated disease, with a 80% mortality rate. We present a 45-year old patient with hemophagocytic syndrome who was treated with steroids, etoposide, and cyclosporine. Two months after the initial treatment, the patient was admitted for a respiratory infection, and was treated with antibiotics and antiviral drugs with a good clinical and laboratory response to the therapy. On the tenth day there was a sudden clinical deterioration with signs of left-sided heart failure, elevated troponin levels, and ECG showing a complete AV block. Right-sided hemiparesis and elevated inflammatory parameters were also present. A temporary pacemaker was placed. A brain MDCT was performed and multiple ischemic and hemorrhagic lesions were found. Emergency echocardiography study showed a semi-mobile, peduncular mass in the left ventricle. It originated from the anterior mitral leaflet, measuring 4x2 cm and protruding to the LV cavity. There were no disorders of myocardial contractility, and ejection fraction was 60% (Figure 1). Echocardiographic features of the mass resembled a myxoma. The patient died three hours later from multiple organ dysfunc- tion syndrome. Autopsy showed disseminated zygomicosis infecting the heart with a mycotic mass in left ventricle. The leptomeninges, brain, and lungs were also infected. Primary heart tumors are rare, accounting for 0.0017-0.19% on unselected biopsies. In immunocompromised patients with a new heart mass, a mycotic mass as a sign of disseminated mycosis should be considered before a primary heart tumor in order to start appropriate treatment. Mortality of patients with disseminated zygomycosis and heart mass is very high and survival is only possible with a combined surgical and antimicrobial approach. The diagnosis of disseminated zygomycosis was considered however due to the patient’s abrupt clinical deterioration, and fulminant course cardiothoracic treatment could not to be arranged.

©© ) are specifically designed to enable stent deliv ery. 1 The purpose of this report is to present our initial experiences with those devices. Methods and Results: Guide extension devices are available in our catheterization laboratory since June 2015. Until January 2016 we used them in 7 percutaneous coronary interventions (2 left anterior descending, 4 right coronary artery and 1 circumflex artery intervention). According to the ACC/ AHA classification 5 (71%) of lesions were designated as type C lesion by the operator. In total 6 (85%) interventions resulted in procedural success. Guide extension related interventions were done with 1.50±1.74 balloons and 1.8±1.09 stents on average. Mean fluoroscopy time was 23.90±5.82 minutes and average mean contrast use was 231.40±57.67 milliliters. No device related complications were noted. Interestingly we also used, as a support device, Guideliner © during one CRT implantation. Conclusion: Our initial experiences with guide extension devices show that they can enhance procedural success rate in complex coronary interventions. We observed no device related complications in our small group of patients. Those devices could also have a certain role in non-coronary interventions as well.

Dual antiaggregation (antiplatelet) therapy is mandatory in patients having received a stent during percutaneous coronary intervention. This therapy usually consists of acetylsalicylic acid (100 mg per day) and clopidogrel (75 mg per day) for at least 6 to 12 months (depending on the type of stent). Such therapy has been shown to reduce significantly unwanted clinical events, although slightly increasing the risk of bleeding. Coronary stents must rarely be implanted in patients who have or develop thrombocytopenia. In such patients, the risk of bleeding is increased manifold. On the other hand, the risk of potentially fatal thrombotic events is unknown. In this case report, we present a patient who developed thrombocytopenia shortly (one month) after the stent had been implanted. After thorough clinical workup, we could not find the remediable cause of thrombocytopenia. Because of the potential of acetylsalicylic acid to induce thrombocytopenia, it was excluded from therapy and a double dose of clopidogrel (150 mg per day) was introduced. Then we decided to evaluate platelet function with the ADP aggregation test (which indicates the degree to which the function of platelets is blocked by clopidogrel) and aspirin resistance test (which indicates the degree to which the function of platelets is blocked by acetylsalicylic acid). In the first set of tests, the patient was shown to be hyperreactive to both substances. We then lowered the dose of clopidogrel to the standard dose and evaluated the function of platelets with the same tests two weeks later and the results were the same. Because the patient was without obvious and laboratory signs of bleeding, we decided not to change the prescribed antiplatelet therapy because of fear from potentially fatal thrombotic events. The use of dual antiplatelet therapy in patients with thrombocytopenia is particularly challenging. We believe that in such patients, firstly, the cause of thrombocytopenia should be sought for by thorough clinical investigation. If not found, as in our patient, tailoring of such therapy should be done using currently available aggregation tests. In such a way, patients could be protected from both excessive bleeding and potentially devastating thrombotic events. Unfortunately, this is a sole example and definite conclusions could only be made on larger studies.

Gaucher’s disease (GD) has variable presentations, but cardiac involvement is a generally uncommon clinical manifestation of the disease. In the past 25 years, the underlying genetic disorder in GD has been well characterized, with almost 300 mutations identified in the glucocerebrosidase gene (GBA). Nevertheless, clear genotype-phenotype correlations have been confirmed only for the most frequent mutations. We present a female patient, who was known to have aortic valve pathology from the age of 30. Despite medical follow up, at the age of 60 she presented with heart failure (NYHA III). At that time echocardiography showed severe fibrosed aortic valve stenosis. Valvuloplasty was planned, when thrombocytopenia, previously considered to be autoimmune, became severe. Anemia and leukopenia were also noted. Moderate splenomegaly and severe bone marrow infiltration were found on MRI. Bone marrow aspiration revealed typical Gaucher cells and the enzyme activity assay confirmed the diagnosis. DNA investigation showed that the patient is homozygous for the G377S mutation. To our knowledge, of all mutations identified so far, only homozygosity for the D409H mutation has been associated with cardiovascular valvular disease in patients with a rare type 3c GD. G377S, found in our patient, is a rare mutation, previously reported as a 'mild’ mutation, because of the finding that homoallelic patients were essentialy asymptomatic or had mild disease. Our patient, also homozygous for G377S mutation, had a severe form of type 1 GD, with rare cardiac valve involvement, which is a previously unreported clinical presentation for this mutation. This case further proves that patients with the same genotypes can have different phenotypes, emphasizing the influence of other genetic and/or environmental factors.

The development of new blood vessels (angiogenesis) is necessary to sustain the growth of primary tumor as well as a process of tumor metastasis. Cancer cells activate the quiescent vasculature to produce new blood vessels via an "angiogenic switch". Understanding of molecular mechanisms involved in that process is essential for the development of antiangiogenic drugs. Drugs that inhibit angiogenesis could offer a treatment that is complementary to traditional chemotherapy. Chemotherapy directly targets tumor cells, which are prone to develop acquired drug resistance due to genetic instability. Antiangiogenic therapy is directed against endothelial cells in tumor stroma, which are genetically stabile. First results from animal studies supported the theory that endothelial cells do not develop drug resistance and had excellent results in inducing tumor quiescence. However, recent clinical trials showed that antiangiogenic therapy has limitations but that it can improve conventional therapeutic modalities of disseminated disease.