Browsing by Author "Babić, Rade (16165040200)"

Objective - To assess the relation between ventricular arrhythmias after myocardial infarction and left ventricular remodelling. Design - Prospective study with consecutive patients. Methods - 97 patients with acute myocardial infarction underwent serial echocardiographic examinations (days 1, 2, 3, and 7, and after 3 weeks) to determine end diastolic volume, end systolic volume, and ejection fraction; volumes were normalised for body surface area and expressed as indices. Holter monitoring was performed on the day of the final echocardiogram. Coronary angiography was performed in 88 patients before hospital discharge. Results - Complex ventricular arrhythmias (defined as Lown class 3-5) were found in 16 of 97 patients. In logistic regression models, variables predictive of complex ventricular arrhythmias were end systolic volume index on admission (b = 0.054, P = 0.015) and end diastolic volume index after three weeks (b = 0.034, P = 0.012). Complex arrhythmias were also related to the increase of end diastolic and end systolic volume indices throughout the study (F = 5.62, P = 0.046 and F = 6.42, P = 0.017, respectively by MANOVA). A two stage linear regression model of ventricular volume versus time from infarct showed that both intercept (initial volume) and slope (rate of increase) were higher for patients with complex arrhythmias in both diastole and systole (P < 0.001 for all). Conclusions - Complex ventricular arrhythmias after myocardial infarction are related to the increase of left ventricular volume rather than to depressed ejection fraction. Complex arrhythmias may be an aetiological factor linking left ventricular remodelling with higher mortality, but larger follow up studies of patients with progressive left ventricular dilatation after myocardial infarction are necessary to answer these questions.

In this article, the potential value of color Doppler in improving diagnostic accuracy of transesophageal echocardiography (TEE) in patients with incomplete obstruction of large pulmonary vessels is illustrated. We present an unusual case of massive pulmonary embolism that was unequivocally detected by color Doppler TEE both before and after pulmonary angiography, which failed to demonstrate filling defects in the pulmonary artery.

Aims: This study was aimed to compare insulin sensitivity and secretion response, lipoprotein and plasminogen activator inhibitor 1 (PAI-1) levels between the subjects with and without coronary artery endothelial dysfunction (ED). Methods: ED was detected by intracoronary injection of acetylcholine (ACh) in 47 nondiabetes subjects without stenotic coronary arteries, selected from 316 consecutive patients with coronary angiography performed for suspected coronary artery disease. The subjects were divided into two groups: presence of ACh-induced coronary spasm (group ED+, N = 30) and absence of ACh-induced coronary spasm (group ED− N = 17). Insulin sensitivity (Si) was evaluated by frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis and by HOMA-IR, insulin secretion by acute insulin response (AIR) (calculated from the first 8 min of FSIGTT) and by disposition index (DI) (Si × AIR). Lipids and PAI-1 levels were determined enzymatically, and LDL particle size by gradient gel electrophoresis. Results: Si was significantly lower (4.22 ± 0.62 vs 6.98 ± 1.47 min−1/mU/l × 104; p < 0.05) while HOMA-IR was significantly higher in ED + group vs ED− group (2.8 ± 0.3 vs 1.7 ± 0.2; p < 0.05). Simultaneously, AIR and DI was significantly lower in ED + vs ED− groups (p < 0.05 and p < 0.01, respectively). Investigated groups did not differ in fasting lipid levels but ED+ group had significantly smaller LDL particles (p < 0.01) and higher PAI-1 levels (p < 0.05). Regression analysis shown that DI was a strong independent predictor of appearance of ED, together with PAI-1 and LDL particle size. Conclusions: Both insulin resistance and impairment in insulin secretion response strongly correlate with coronary ED in subjects without diabetes. © 2018 Elsevier B.V.

Aims: This study was aimed to compare insulin sensitivity and secretion response, lipoprotein and plasminogen activator inhibitor 1 (PAI-1) levels between the subjects with and without coronary artery endothelial dysfunction (ED). Methods: ED was detected by intracoronary injection of acetylcholine (ACh) in 47 nondiabetes subjects without stenotic coronary arteries, selected from 316 consecutive patients with coronary angiography performed for suspected coronary artery disease. The subjects were divided into two groups: presence of ACh-induced coronary spasm (group ED+, N = 30) and absence of ACh-induced coronary spasm (group ED− N = 17). Insulin sensitivity (Si) was evaluated by frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis and by HOMA-IR, insulin secretion by acute insulin response (AIR) (calculated from the first 8 min of FSIGTT) and by disposition index (DI) (Si × AIR). Lipids and PAI-1 levels were determined enzymatically, and LDL particle size by gradient gel electrophoresis. Results: Si was significantly lower (4.22 ± 0.62 vs 6.98 ± 1.47 min−1/mU/l × 104; p < 0.05) while HOMA-IR was significantly higher in ED + group vs ED− group (2.8 ± 0.3 vs 1.7 ± 0.2; p < 0.05). Simultaneously, AIR and DI was significantly lower in ED + vs ED− groups (p < 0.05 and p < 0.01, respectively). Investigated groups did not differ in fasting lipid levels but ED+ group had significantly smaller LDL particles (p < 0.01) and higher PAI-1 levels (p < 0.05). Regression analysis shown that DI was a strong independent predictor of appearance of ED, together with PAI-1 and LDL particle size. Conclusions: Both insulin resistance and impairment in insulin secretion response strongly correlate with coronary ED in subjects without diabetes. © 2018 Elsevier B.V.

Background: It has been shown that successful reperfusion of the infarct- related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were detected from several days to several months after infarction. To date, however, no study has shown that these effects can be demonstrated within hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patency on ventricular volume and function. The aim of this study was to assess separate effects of thrombolysis and patency of the infarct-related artery on left ventricular size and function by serial two-dimensional echocardiographic examinations. Methods and Results: We evaluated 131 consecutive patients with first acute myocardial infarction by two-dimensional echocardiography in the following sequence: days 1, 2, 3, 7, and after 3 and 6 weeks. Intravenous streptokinase was administered in 81 patients, and 50 patients were treated without thrombolysis. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were determined from apical two- and four-chamber views using the Simpson biplane formula and normalized to body surface area. Coronary angiography was performed in 107 patients after a mean of 26.0±20.2 (mean±SD) days after infarction. Patency of the infarct-related artery was assessed using TIMI criteria, with 54 considered patent (TIMI 3) and 53 with TIMI grade <3. On day 1, end-systolic volume was significantly higher in patients not receiving thrombolysis (37.7±15.3 versus 33.0±10.6 mL/m2, P=0.45). End-systolic volume (ESVi) was significantly higher in patients treated without thrombolysis throughout the study, whereas significant differences in end-diastolic volume (EDVi) were detected from day 3 (P=.041) onward and in ejection fraction (EF) from day 2 (P=.025) onward, all differences becoming progressively more significant with time (6-week values: EDVi, 78.8±25.4 versus 65.9±15.7 mL/m2, P=.001; ESVi, 45.4±22.6 versus 33.9±15.1 mL/m2, P=.002; EF, 45.1±11.6% versus 50.2±10.1%, P=.018). Patients with an occluded infarct-related artery (TIMI <3) demonstrated highly significant differences at 6 weeks compared with patients with patent vessels (EDVi, 76.8±24.7 versus 65.2±15.6 mL/m2, P=.006; ESVi, 44.6±23.3 versus 31.9±12.2 mL/m2, P=.001; EF, 45.0±11.6% versus 52.1±9.0%, P<.001), but these differences developed more slowly than that seen among the thrombolytic subgroups. Indeed, multivariate analysis demonstrated that thrombolysis was the major determinant of initial volumes (P=.08, .02, and .08 for EDVi, ESVi, and EF, respectively), while vessel patency was the overwhelming determinant of subsequent changes (P=.0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejection fractions lower in patients with anterior versus inferior infarction, but even adjusting for these differences as well as those associated with age, sex, and initial ventricular volume, the additive and independent impact of thrombolysis and infarct vessel patency persisted. Conclusions: These data indicate that the beneficial effect of thrombolysis on left ventricular size and function can be demonstrated in the earliest phases of acute myocardial infarction and that subsequent changes are mediated primarily through patency of the infarct-related artery. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myocardial infarction.

Introduction. Coronary artery anomalies are infrequent but anticipated findings during percutaneous coronary interventions (PCI). Compared to consistent reporting in angiographic series, they seem to be underreported in interventional studies, and particularly in the setting of primary PCI, where their prompt recognition is of the utmost importance. Case report. We present a 50 years old male with inferior ST-elevation of myocardial infarction (STEMI) and right ventricular involvement with solitary ostium for all three coronary arteries in the right aortic sinus of Valsalva. The patient had an extremely rare variant of coronary artery origination belonging to the type A4b2c2 of Angelini's classification. Correspondingly, it belongs to the left Anomalous origination of a Coronary Artery from the Opposite Sinus of Valsalva (ACAOS) class with the intraseptal course of left anterior descending artery. We managed successfully to implant a drug eluting stent in the proximal right coronary artery in a lengthy and stormy procedure, with the need for guiding catheter exchange, temporary pacing and dealing with no-reflow phenomenon. Conclusion. We summarize diagnostic hints for angiographic recognition of dominant variants of the left ACAOS and practical aspects of performing PCI in such patients. Also, we debate on the functional significance of coronary anomalies and its further implications from the prognostic and therapeutic aspects. We propose adoption of the novel classification of coronary anomalies of Angelini's group in the routine clinical practice. Finally, we call for the inclusion of specific training in coronary artery anomalies into the interventional cardiology fellowship curriculum. © 2020 Inst. Sci. inf., Univ. Defence in Belgrade. All rights reserved.