3 research outputs found

    Diastolic disorder inherent to doxorubicin cardiotoxicity

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    Background: The doxorubicin (Dx) cardiotoxicity is manifested by a marked heart failure evolution. The impact of Dx on lusitrop functions of the heart and the inherent diastolic disorders have a theoretical and practical value for the connection cardiology-oncology. Material and methods: Dx cardiotoxicity was reproduced by its administration i/p in white rats in cumulative dose 16 mg/kg (Dx group n=9). Control group (n=9) received only physiological solution. The study was performed in vitro by using models of isolated heart perfusion in either isovolumic or exterior working regimens. The assayed indices of diastole functioning were: left ventricle (LV) end-diastolic pressure (LVEDP), diastolic stiffness, isovolumic relaxation velocity (-dP/dTmax) and protodiastolic pressure of LV (LVPDP). Results: The indices of diastolic disorders induced by Dx were elevation of LVEDP, diastolic stiffness and LVPDP in a range of 97-168% comparing to control as well as diminution of -dP/dTmax in the physiological pattern of hemodynamics. LVEDP increased more in conditions of calcium overloading or endothelin-1 (ET-1) action that are involved in pathogenesis of diastolic rigidity. Dx action led to decrease of myocardium resistance to ischemiareperfusion action resulting in the LVEDP elevation by 53% comparing to control. Conclusions: 1. Diastolic disorders inherent to Dx cardiotoxicity are manifested by the increase of LVEDP and diastolic stiffness. 2. Diastolic disorders compromised the volume-pressure relationship of LV, the adaptation of the heart to effort with volume, being more pronounced during the action of calcium excess and ET-1

    Myocardial remodeling in NSTEMI patients with intermediate and low cardiovascular risk exposed to delayed revascularization

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    Department of Interventional Cardiology, Institute of Cardiology, Chisinau, the Republic of Moldova, Department of Pathophysiology and Clinical Pathophysiology, Nicolae Testemitanu State University of Medicine and Pharmacy, Chisinau, the Republic of MoldovaAbstract Background: Nowadays, the impact of the delayed myocardial revascularization (DMR) (>72h) in patients with myocardium infarction without STsegment elevation (NSTEMI) having either intermediate or low cardiovascular risk (ILCR) on quality of post-infarction myocardial remodeling is not well established. Aim of the study: The comparative evaluation of cardiac functional recovery of NSTEMI patients undergoing either revascularization <72h or DMR (72h–30 days) in a follow-up of 6 months. Material and methods: The study was realized in 2 homogenic series of NSTEMI patients with ILCR exposed to revascularization: <72h (control) or to DMR (72h–30 days). The echocardiographic and physical test indices were registered at the 2nd day since revascularization and after 6 months. Results: The increasing ratio of ejection fraction was significantly higher in patients with DMR compared to control (5.24% vs 1.73%). Likewise, the contractility ability of left ventricle improved better, proven by systolic volume diminution, lower value of akinetic areas, and less patients with class III of heart failure according to New York Heart Association (4 vs 29%). More than that, DMR was associated with higher physical endurance. Conclusions: NSTEMI patients with ILCR exposed to delayed myocardial revascularization (72h–30 days) had a better post-infarction recovery after 6 months according to dynamics of echocardiographic and physical tolerance indices in comparison with patients revascularized <72h

    Features of hemostasis in patients with non-ST-elevation myocardial infarction

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    Background: Coronary thrombosis is the key pathogenic mechanism of acute heart attack, including non-ST segment elevation (NSTEMI). Given that, the detection of reliable markers of hemostasis disorders is important in the process of optimizing the diagnosis of NSTEMI. Material and methods: The study was conducted on 54 patients with NSTEMI (average age 69.7±1.5 years). In 60% of cases, 3-vessel disease was noted; 56% of patients had ejection fraction >50%, and Killip class I of heart failure was revealed in 78% of patients. With the help of the STA-Liatest (France) equipment, the blood tests determined the following hemostasis markers: fibrin monomers (FM), thrombotic complex activity of factors II, VII and X. Additional markers like Procoag, the coagulation indicator dependent on circulating phospholipids or SPA, D-dimers, as well as factors C, S and antithrombin III were appreciated. The values of these markers determined by the same method in 20 healthy persons (control group) were used as normal values. Results: Circulating level of FM on admission was increased twice, while the values of Procoag and SPA were significantly decreased by 35.3% compared to the control. Factors C, S and antithrombin III were 54-80% of the control value range, and D-dimers were within the permissible values. In the acute phase of the heart attack, a deterioration of hemostasis indicators was noted, excepting the D-dimers. The levels of FM determined 24 and 72 hours after revascularization were consistently increased (up to 3.8 times) compared to the control, while Procoag and SPA decreased by 54-57%. Further reduction of factors C, S and antithrombin III accounted for 42-54% of normal indicators. After 5 days, an improvement in hemostasis markers was observed, but a significant difference still remained comparing to the control group. Conclusions: The hemostasis particularities discovered in patients with NSTEMI indicate the features of an activated prothrombotic status, and FM could be an important diagnostic marker of NSTEMI, due to its most significant deviation from the normal value (>100%). It can reliably reflect the thrombin level, which triggers the last enzymatic phase of thrombus formation
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