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Diana Opincariu, András Mester, Mihaela Raţiu, Nora Rat, Lehel Bordi, Roxana Hodas, Mirabela Morariu, Beáta Jakó, Camelia Tănăsuc and Zsuzsanna Suciu


Introduction: Pulmonary embolism (PE) is the most common cause of vascular death after myocardial infarction and stroke, being associated with high mortality and morbidity rates. The aim of this study was to assess the factors related to 1-year mortality in patients with acute pulmonary embolism who survived the acute event.

Material and methods: In total, 104 patients who had survived the acute episode of pulmonary embolism and underwent a one-month follow-up after the acute event were included in the study. The patients were divided into two groups: Group 1 – patients who had survived at one year after being diagnosed with acute PE (80.76%, n = 84), and Group 2 – patients who had died after one year (19.23%, n = 20).

Results: There were no differences between the 2 groups in relation to gender (p = 0.3), or cardiovascular risk factors (diabetes: p = 0.5, smoking: p = 0.3, hypertension: p = 1, hypercholesterolemia: p = 0.5, hypertriglyceridemia: p = 0.4). Patients who had deceased were significantly older (73.35 ± 9.37 years vs. 66.36 ± 11.17 years, p = 0.005) and had a higher weight compared to the survivors (85.8 ± 21.09 kg vs. 75.89 ± 22.69 kg, p = 0.03). Left ventricular ejection fraction, measured by cardiac ultrasound, was significantly lower in the deceased group compared to survivors (45.63 ± 8.9% vs. 52.86 ± 6.8%, p = 0.03). Multivariate analysis identified the hemodynamic instability (OR = 3.17, p = 0.007), the presence of left QRS axis deviation (OR = 4.81, p = 0.001), associated pulmonary pathologies (OR = 3.2, p = 0.02) as well as the presence of chronic kidney disease (OR = 5, p = 0.04) as the most powerful predictors of death at 1 year in patients with acute PE surviving the acute event.

Conclusions: Factors associated with a higher mortality rate at 1 year in patients who had survived at 1 month following an acute pulmonary embolism episode included: older age, higher body weight, presence of associated pulmonary pathologies, chronic kidney disease, left axis deviation, low left ventricular ejection fraction, hemodynamic instability requiring inotropic support, cardiogenic shock at presentation or cardiac arrest during the acute phase.

Open access

Adrian Corneliu Iancu, Mihaela Ioana Dregoesc, Aurelia Solomoneanu and Theodora Benedek

Balloon Support for Myocardial Infarction with Cardiogenic Shock. N Engl J Med. 2012;367:1287-1296. doi: 10.1056/NEJMoa1208410. 33. Ouweneel DM, Schotborgh JV, Limpens J, et al. Extracorporeal life support during cardiac arrest and cardiogenic shock: a systematic review and meta-analysis. Intensive Care Med 2016;42:1922-1934. doi: 10.1007/s00134-016-4536-8. 34. Flaherty MP, Khan AR, O'Neill WW. Early Initiation of Impella in Acute Myocardial Infarction Complicated by Cardiogenic Shock Improves Survival: A Meta-Analysis. JACC Cardiovasc

Open access

Monica Marton-Popovici and Aura-Gabriela Casu

.07.006. 6. Bækgaard JS, Viereck S, Palsgaard Møller T, Kjær Ersbøll A, Lippert F, Folke F. The Effects of Public Access Defibrillation on Survival After Out-of-Hospital Cardiac Arrest – A Systematic Review of Observational Studies. Circulation. 2017;136:954-965. . 7. Ringh M, Fredman D, Nordberg P, Stark T, Hollenberg J. Mobile phone technology identifies and recruits trained citizens to perform CPR on out-of-hospital cardiac arrest victims prior to ambulance arrival. Resuscitation. 2011;82:1514-1518. doi: 10.1016/j

Open access

Arnon Nagler

-German cohort study. Br J Haematol. 2014;167:385-393. doi: 10.1111/bjh.13039. 6. Zhu T, Pan K, Wang Y. Successful resuscitation with thrombolysis of pulmonary embolism due to thrombotic thrombocytopenic purpura during cardiac arrest. Am J Emerg Med. 2015;33:132.e3-4. doi: 10.1016/j.ajem.2014.06.025. 7. Berntorp E. Thrombosis in patients with hemorrhagic disorders. Minerva Med. 2013;104:169-173. 8. Riva N, Donadini MP, Ageno W. Epidemiology and pathophysiology of venous thromboembolism: similarities with atherothrombosis and the role of inflammation. Thromb

Open access

Victoria Rus, Diana Opincariu, Roxana Hodas, Tiberiu Nyulas, Marian Hintea and Theodora Benedek


Background: The impact of nutritional status on the early outcome of subjects with acute myocardial infarction (AMI) is still not completely elucidated. This study aimed to assess the correlation between nutritional status, as expressed by the CONUT and PIN scores, and (1) clinical and laboratory characteristics, (2) complication rates, and (3) length of hospitalization, in patients with AMI.

Materials and methods: We included 56 consecutive patients with AMI who underwent primary percutaneous intervention and stenting. Evaluation of the nutritional status was comprised in the calculation of the CONUT and PNI scores. The study population was divided into 2 groups according to the calculated CONUT score, as follows: group 1 – CONUT score <3 points (normal to mildly impaired nutritional status) and group 2 – CONUT score ≥3 points (moderate to severe malnutrition). The primary end-point of the study was the rate of in-hospital complications (left ventricular free wall rupture, hemodynamic instability requiring inotropic medication, high-degree atrioventricular block, the need for temporary cardiostimulation, supraventricular and ventricular arrhythmias and in-hospital cardiac arrest). The secondary end-points included the duration of hospitalization and the length of stay in the intensive cardiac care unit.

Results: In total, 56 patients (44.64% with STEMI, 55.35% with NSTEMI) with a mean age of 61.96 ± 13.42 years, 58.92% males were included in the study. Group distribution was: group 1 – 76.78% (n = 43), group 2 – 23.21% (n = 23). There were no differences between the two groups regarding age, gender, cardiovascular risk factors, or comorbidities. PNI index in group 1 was 54.4 ± 10.4 and in group 2 41.1 ± 2.8, p <0.0001. Serum albumin was significantly lower in group 1 – 4.1 ± 0.3 vs. group 2 – 3.6 ± 0.3 (p <0.0001), similarly to total cholesterol levels (group 1 – 194.9 ± 41.5 vs. group 2 – 161.2 ± 58.2, p = 0.02). The complete blood cell count showed that group 2 presented lower levels of hematocrit (p = 0.003), hemoglobin (p = 0.002), and lymphocytes (p <0.0001) compared to group 1, but a significantly higher platelet count (p = 0.001), mean platelet volume (p = 0.03), neutrophil/lymphocyte (p <0.0001) and platelet/lymphocyte (p <0.0001) ratios, indicating enhanced blood thrombogenicity and inflammation. Regarding in-hospital complications, group 2 presented a higher rate of hemodynamic instability (group 1 – 11.6% vs. group 2 – 38.4%, p = 0.02). The overall hospitalization period was 7.7 ± 1.4 days in group 1 vs. 10.2 ± 4.8 days in group 2, p = 0.06; while the duration of stay in the intensive cardiac care unit was 2.6 ± 0.5 days in group 1 vs. 4.0 ± 2.5 days in group 2, p = 0.02.

Conclusions: This study proved that nutritional deficit in acute myocardial patients who undergo revascularization is associated with an increased rate of in-hospital complications and with a longer observation time in a tertiary intensive cardiac care unit.

Open access

Friedo Zölzer, Tamare Mußfeldt and Christian Streffer

. Little JB. Delayed initiation of DNA synthesis in irradiated human diploid cells. Nature 1968; 218: 1064-5. 5. Cuddihy AR, Bristow RG. The p53 protein family and radiation sensitivity: Yes or no? Cancer Met Rev 2004; 23: 237-57. 6. Zölzer F, Streffer C. Quiescence in S-phase and G1 arrest induced by irradiation and/or hyperthermia in six human tumour cell lines of different p53 status. Int J Radiat Biol 2000; 76: 717-25. 7. Terasima T, Tolmach LJ. Variations in several responses of HeLa cells to xirradiation during the

Open access

Alexandru Florin Rogobete, Ovidiu Horea Bedreag, Sonia Elena Popovici, Adriana Mariana Sas, Adrian Tudor Stan, Emil Robert Stoicescu and Dorel Sandesc

REFERENCES 1. Oddo M, Rossetti AO. Predicting neurological outcome after cardiac arrest. Curr Opin Crit Care. 2011;17:254-259. doi: 10.1097/MCC.0b013e328344f2ae. 2. Zakkar M, Ascione R, James AF, Angelini GD, Suleiman MS. Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery. Pharmacol Ther. 2015;154:13-20. doi: 10.1016/j.pharmthera.2015.06.009. 3. Doehner W, Haehling S Von, Pschowski R, Storm C, Schroeder T. Influence of core body temperature on Tryptophan metabolism, kynurenines, and estimated IDO activity in

Open access

Theodora Benedek

J. 2018;39:1065-1074. doi: 10.1093/eurheartj/ehy004. 8. Ouweneel DM, Schotborgh JV, Limpens J, et al. Extracorporeal life support during cardiac arrest and cardiogenic shock: a systematic review and meta-analysis. Intensive Care Med. 2016;42:1922-1934. doi: 10.1007/s00134-016-4536-8. 9. Thiele H, Jobs A, Ouweneel DM, et al. Percutaneous short-term active mechanical support devices in cardiogenic shock: A systematic review and collaborative meta-analysis of randomized trials. Eur Heart J. 2017;38:3523-3531. doi: 10.1093/eurheartj/ehx363.

Open access

Dan Păsăroiu, Zsolt Parajkó, Noémi Mitra and Diana Opincariu

National Heart, Lung, and Blood Institute and Heart Rhythm Society Workshop. Circulation. 2010;122:2335-2348. doi: 10.1161/CIRCULATIONAHA.110.976092. 7. Jollis JG, Granger CB. Improving care of out-of-hospital cardiac arrest: next steps. Circulation. 2016;134:2040-202. . 8. Sesselberg HW, Moss AJ, Mc Nitt S, et al. Ventricular arrhythmia storms in postinfarction patients with implantable defibrillators for primary prevention indications: a MADITII substudy. Heart Rhythm. 2007;4:1395-1402. doi: 10.1016/j

Open access

Igor Piotrowski, Katarzyna Kulcenty, Wiktoria Maria Suchorska, Agnieszka Skrobała, Małgorzata Skórska, Marta Kruszyna-Mochalska, Anna Kowalik, Weronika Jackowiak and Julian Malicki

radiation. Results indicate that ATM plays an important role in early DSB recognition and can be responsible for inefficient DSB repair, which is in line with conclusions reached by Osipov et al . 24 Authors also observed that doses higher than 0.5 Gy of carbon ion radiation caused an early G2/M arrest dependent on ATM. Some authors suggest that occurrence of this arrest might support DNA DSB repair, while a failure to induce early G2 arrest can be one of the factors responsible for low dose hyper-radiosensitivity (HRS). 28 Low-dose hyper radiosensitivity (HRS