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Yasmin Rustamova and Dan Dobreanu

Open access

Theodora Benedek and Dan Dobreanu

Abstract

Cardiogenic shock (CS) is a critical condition which often complicates the evolution of an acute myocardial infarction (AMI). At the same time, co-existence of chronic multi-vessel disease can lead to the development of cardiogenic shock in cases with pronounced haemodynamic instability. Different clinical studies have tried to identify the most appropriate treatment for critical cases of CS complicating AMI. This review aims to present the current status of recommended therapeutic strategies for severe cases of CS presenting as a complication of AMI, and try to shed light on the most appropriate therapeutic strategy as outlined in the current literature. The paper will discuss the different current strategies available for use in the treatment of this condition, includig interventional revascularisation, (complete or culprit), the role of new devices for providing mechanical circulatory support, and the potential role of new drug therapies and of hypothermia.

Open access

László Hadadi, Éva Katalin Lakatos, Mariana Țăruși and Dan Dobreanu

Abstract

Introduction: combined myocardial infarction (MI) is defined as the simultaneous ischemic injury of two different myocardial territories, raising the possibility of multiple culprit lesions. The anomalous origin of a coronary artery could represent an important challenge during percutaneous coronary intervention (PCI). Case presentation: A 46 year old, smoker Caucasian male presented to a territorial hospital four hours after the onset of severe angina. Consecutive electrocardiograms showed complete atrioventricular block and inferior ST segment elevation (STE), later PQ prolongation with right bundle branch block plus STE in leads V4-V6. After administration of thrombolytic treatment, the patient was transferred to the regional PCI center. Emergent coronary angiography revealed acute occlusion of the left anterior descending artery (LAD) and a thrombus containing, severe stenosis of the anomalously originated right coronary artery (RCA). Rescue PCI with stent implantation in the LAD and RCA was performed nine hours after pain onset. At the 1 year follow-up visit the patient had no angina or heart failure symptoms. Conclusion: this is the first report of a combined MI caused by acute, sequentially occurring thrombotic occlusion of two coronary arteries, one of them with anomalous origin, in a patient treated by rescue PCI following partially successful thrombolysis.

Open access

Rudzik Roxana, Şuş Ioana, Hadadi László, Şerban Răzvan Constantin and Dobreanu Dan

Abstract

Introduction: Coronary vasospasm is a possible cause of ventricular tachyarrhythmias and is frequently associated with atherosclerotic lesions. The revascularization of mild to moderate coronary artery stenosis which causes symptoms only due to associated vasospasm is still a matter of debate, as the standard treatment of Prinzmetal angina is represented by the long term administration of calcium-channel blockers.

Case presentation: We present the case of a 46 year old woman with an intermediate severity coronary artery stenosis complicated by vasospastic angina and subsequent polymorphic ventricular tachycardia. Although the functional significance of the fixed coronary artery lesion was equivocal at invasive fractional flow reserve measurement, a combined pharmacologic and interventional treatment strategy was chosen with stent implantation and long acting calcium channel blocker administration with a symptom-free, good clinical outcome.

Conclusion: Patients with vasospastic angina and intermediate severity atherosclerotic coronary artery stenoses are at risk of malignant ventricular arrhythmias, therefore myocardial revascularization should be considered in addition to the standard medical treatment.

Open access

Laszlo Hadadi, Ioana Sus, Eva Katalin Lakatos, Razvan Constantin Serban, Alina Scridon, Zoltan Demjen and Dan Dobreanu

Abstract

Coronary chronic total occlusion (CTO) is caused by organized thrombi or atherosclerotic plaque progression. The presence of a CTO is an independent predictor of mortality in patients presenting with ST-segment elevation myocardial infarction (STEMI). Platelets have a crucial role in the pathophysiology of atherosclerosis. The aim of this retrospective study was to investigate platelet indices as predictors of CTO in patients with STEMI treated with primary percutaneous coronary intervention (pPCI). A total number of 334 patients admitted for STEMI between January 2011 and December 2013 were included and divided in two groups based on the presence of CTO (48 patients in CTO+ group, 286 patients in CTO-group). Platelet count, mean platelet volume (MPV), platelet distribution width (PDW), platelet-large cell ratio (P-LCR), lymphocyte and neutrophil count determined on admission were analyzed. MPV was larger in patients with CTO compared with patients without CTO (p=0.02), as were PDW (p=0.03) and P-LCR (p=0.01). Platelet-to-lymphocyte ratio (PLT/LYM) was lower in patients with CTO: 105.2 (75.86-159.1) compared to 137 (97-188.1), p<0.01. Receiver-operator characteristic curve analysis identified an area under the curve of 0.61 (95%CI=0.57-0.67, p< 0.01) for PLT/LYM in predicting the presence of a CTO, with a cut-off value at 97.73. Lower values than this were independent predictors of a CTO in multivariate logistic regression analysis, with an Odds Ratio of 2.2 (95%CI=1.15-4.20, p=0.02). Our results support the use of platelet indices and PLT/LYM as predictors of CTO in patients presenting with STEMI.

Open access

Mihai Mărginean M, Sebastian Trancă, Alina Ardelean-Maghiar (Mărginean), Dan Dîrzu, Adina Huțanu, Oana Platon (Antal) and Dan Dobreanu

Abstract

Background: Sepsis is a systemic host response to an infection which may evolve into severe sepsis and septic shock. It raises many health care related concerns around the world, carrying almost 30% mortality rates and a high financial burden. The disease is characterized by the triggering of some inflammatory pathways that are ultimately proven deleterious to the host organism. Although antibiotics, fluid administration, vasopressor therapy and infectious source control remain the recommended management strategies, emerging scientific data proposes statins as a new line of treatment. These drugs were first introduced in clinical practice for their cholesterol-lowering effect but the inhibition of HMG-CoA reductase and cholesterol biosynthetic pathway exhibits some less studied effects generally referred to as pleiotropic: anti-inflammatory, antithrombotic, immunomodulatory and antioxidant properties. Objective: To asses and compare the anti-inflammatory effect of two statins - Simvastatin and Rosuvastatin - measuring blood levels of IL-1β, IL-6 and TNFα using a previously described murinic model of sepsis. Methods: We compiled four groups (C, n=7; SEP, SV, RV, n=8). Statins were administered in two doses 18 and 3 hours before surgical intervention. Sepsis was induced using the caecal ligation and puncture technique. Blood samples were obtained by venepuncture from each subject in day 1, 4, 7 and 14 (the last samples were obtained by cardiac puncture). Complete blood count, Procalcitonin, IL-1β, IL-6 and TNF-α levels were assessed. Results: White blood cell counts differed across the groups showing a higher count for the septic but untreated group. Procalcitonin reacted in all septic groups but both statin treated groups had lower levels when compared to untreated group. IL-1β levels were higher in the Rosuvastatin treated group. IL-6 levels were more heterogeneously dispersed but higher levels were noticed in the untreated septic group. The Simvastatin treated group had higher levels compared to the Rosuvastatin treated one. TNFα levels were higher in the septic untreated group and in the Rosuvastatin treated one. For the Simvastatin treated subjects, the level of TNFα was similar with the control group. Conclusion: We concluded that both drugs showed anti-inflammatory effects on the murinic CLP-induced sepsis model. Between the two, Simvastatin had greater impact by lowering blood levels of established pro-inflammatory markers.