Aim. The study addresses the role of left ventricular hypertrophy (LVH) in development of sudden cardiac death (SCD) in patients with myocardial infarction (MI). The incidence of characteristic features of arrhythmogenic substrate in myocardium (late ventricular potentials, left ventricular ejection fraction) and trigger factors of fatal arrhythmias (decreased heart rate variability, ventricular arrhythmias) was higher in patients with MI and LVH. The level of leukocytes, monocytes and eosinophils, CD-95 lymphocytes was significantly higher in patients with LVH. The incidence of general mortality and of SCD was also higher in group with LVH.
The results and pattern of therapy were analyzed in 772 patients with acute myocardial infarction (AMI) who were treated at two Saint Petersburg hospitals in 1998 to 2007. A follow-up indicated that drug treatment quality and therapy adherence improved a year after AMI, resulting in a significant reduction in sudden cardiac death rates. At the same time, inadequate primary myocardial reperfusion and myocardial revascularization failed to significantly reduce mortality from chronic heart failure and incidence of myocardial reinfarction. Key words: acute myocardial infarction, sudden cardiac death, myocardial reinfarction, guidelines for the management of myocardial infarction, drug therapy adherence.
Funding Acknowledgements Type of funding sources: None. Introduction The number of patients with myocardial infarction (MI) and atrial fibrillation (AF) is increasing every year. Purpose to assess the incidence of AF among the patients with MI, the features of the in-hospital prognosis among the patients with MI and AF compared with MI without AF. Methods The patients with type 1 MI and preexisting AF have been selected from all MI patients MI admitted in 2013-18. They have formed the main group (100 patients). The control group (200 patients with type 1 MI without AF), has been created by "pair selection" method. Patients in the groups did not differ in gender, age, MI date and had not severe comorbidities. Results 1660 patients with MI were analyzed. AF occurred in 309 patients (18.6% of patients with MI). Preexisting AF was in 59.2%. Patients with MI and AF were older than MI without AF (mean age 75.2 ± 10.1 versus 64.6 ± 12.8, p <0.0001) with women’s prevalence (52.4% versus 35.5%, p <0.0001). Type 1 MI predominates among all patients. Type 2 MI occurred 5 times more often among main group (p <0.0001). 2 groups were adjusted for sex (58% of women in both groups), age (mean age 75.5 ± 8, 7 in the main versus 75.2 ± 8.5 in the control group, p = 0.775). Diabetes (45% versus 31.5%, p = 0.030), previous MI (40% versus 25.5%, p = 0.012) and stroke (21% versus 11.5%, p = 0.037) were more common in the main than in the control. Patients with MI and AF had lower GFR (56.8 ± 19.4 versus 61.7 ± 17.9 ml/min/1.73 m2, p = 0.031), LDL (2.8 ± 0.9 versus 3.3 ± 1.0 mmol/L, p = 0.0002). Patients with AF had a lower left ventricular ejection fraction (55.2 ± 10.5 versus 59.8 ± 10.0 %, p = 0.0005). Significant mitral regurgitation was more common in the main group (53.9% versus 30.3% in the control group, p = 0.0002). There were no differences in the incidence of acute heart failure (HF) Killip’s 3-4 (20% versus 13%, p = 0.127). Patients did not differ in the number of affected coronary artery (p = 0.7327), the level of stenosis (p = 0.1956), in the frequency of revascularization (p = 0.0686). Patients with MI and AF had worse in-hospital prognosis. Pulmonary embolism (PE) (9% in main versus 1% in control group, p = 0.0011), minor bleeding (21% versus 9.5%, p = 0.0057), combined endpoint (stroke + PE + mortality) (19% versus 10.5%, p = 0.0415) were more common in the main group. At discharge, patients with AF had HF III NYHA in 21.8% cases versus 5.5% in patients without AF, p = 0.0001. There were no significant differences in other in-hospital endpoints (recurrent myocardial infarction, stroke, major bleeding, and mortality) between the groups. In-hospital mortality was 13% in the main versus 9.5% in the control group (p = 0.4276). Conclusion AF occurs in 18.6% of patients with MI. Patients with AF and MI are older with female prevalence. Type 1 MI predominates. Patients with type 1 MI and pre-existing AF is a group of high risk because of more severe HF, PE, minor bleeding and combined endpoint (stroke + PE + mortality)
We present clinical case of portal vein thrombosis at the liver cirrhosis patient with signs of severe decompensation of liver function and portal hypertension. A feature of this case is that after consumption of alcohol condition of the patient was estimated erroneously as alcoholic hepatitis with high Maddrey index (105). However, later diagnosis of portal vein thrombosis was confirmed. The cancellation of antiinflammatory therapy and administration of anticoagulants allowed to stabilizate of critical situation. Thus, the clinical experience has shown that dopplersonography is necessary at the liver cirrhosis, especially in case of decompensation.
Funding Acknowledgements Type of funding sources: None. Introduction In the acute period of myocardial infarction (MI) inflammatory disorders of blood are registered, but data of prognostic significance of these disorders is multiple-valued. Purpose Research of manifestation of the inflammatory response in patients who suffered MI, and estimation of its prognostic significance. Materials and methods 772 patients with myocardial infarction were examined. Prospective follow-up from 1 to 7 years was performed. Results The death rate during all years of follow-up was 14,2 % of all included in the study. 61% of patients died suddenly, but 26% of them died as a consequence of the progression of chronic cardiac insufficiency. In patients died suddenly lower level of lymphocytes in the first 24 hours: 1,30 ± 0,47 * 109/l vs 1,80 ± 0,73*109/l, (p = 0,03) was registered. In patients who died due to heart failure progression, authentically registered higher leukocytosis in the first 24 hours, in comparison to survived ones, reached 13,83 ± 6,00*109/l (vs 11,9 ± 3,12*109/l; p = 0,005), but to 5th day in the compared groups leukocytes levels had practically the same values (7,36 ± 1,89*109/l vs 7,47 ± 1,99*109/l; accordingly p = 0,8). In the compared groups the number of lymphocytes, expressing CD 95 did not differ authentically, but in died abruptly patients this index was rather lower. There were not authentic differences detected among groups of dead and survived patients, in terms of interleukins 1β,2, and 6, whereas TNF-α was almost twice as high in patients who died due to CHF progression. Studying inflammatory markers were not included in the number of independent indexes, connected with the risk of death when conducting multivariate regressive Cox-analysis. Conclusion In our opinion, inflammatory factors were displaced from the prognostic model for assessing the risk of death, both sudden and due to heart progression, by more powerful structural-functional predictors.
Funding Acknowledgements Type of funding sources: None. Introduction Structural postinfarction abnormalities is connected with inflammation. For better understanding of pathogenesis of postinfarction remodeling, it was studied the intensity of inflammatory disorders in early postinfarction period. Purpose Research of the intensity of inflammatory response in early postinfarction remodeling. Materials and methods 772 of patients with myocardial infarction (MI) were examined. Clinical blood analysis was performed at admission and on the 5th day of MI, as well as immunological examination, Echocardiography. Results In patients with end-diastolic diameter (EDD) of left ventricle (LV) ≥ 55 mm, 5 day MI white blood cells (WBC) level (8,0 ±2,1*109/l vs 7,3 ± 1,9*109/l, p = 0,0001), absolute number of neutrophils (5,0 ± 1,7* 109/l vs 4,5 ± 1,4*109/l, p = 0,0006) and monocytes (0,64 ± 0,30*109/l vs 0,57 ± 0,30*109/l, p = 0,005) were higher compared patients with EDD ≤ 55 mm. The inflammatory alterations in patients with increased end-diastolic volume (EDV) and end-systolic volume (ESV) of left ventricle was similar. The LV EDD was correlated with WBC level (r = 0,3; p = 0,00002), also with absolute number of neutrophils (r = 0,3; p = 0,0002) and monocytes (r = 0,3; p = 0,007). The positive connection of EDV LF with level of WBC (r = 0,3; P = 0,007) and absolute number of neutrophils (r = 0,3; p = 0,0002) was revealed. The positive connection of ESV LV with absolute number of neutrophils (r = 0,3, р=0,04; accordingly). It should be noted that increase of ESD LV more 37mm was not accompanied by authentic increase of inflammatory factors, but the connection of ESV LV with Il-6 was noted (ρ=0,3; р=0,03). As far as contractive function of myocardium declined, it was registered the increase of neutrophils (neutrophils on the 5 day in EF 55% and more - 4,5 ± 1,4*109/l, EF 55-40% - 4,8 ± 1,5*109/l, EF less 40% - 5,1 ± 2,1*109/l, p = 0,002), also in formation of areas of akinesia (neutrophils on the 1 days - 9,2 ± 3,3*109/l vs 8,3 ± 3,1*109/l, р=0,05) and aneurysm of LV (5,08 ± 1,71*109/l vs 4,52 ± 1,48*109/l, р=0,0006). It should be noticed that functional activity of monocytes in patients with aneurism of LV was lower than in patients without aneurism (CD14 0,035 ± 0,02*109/l vs 0,049 ± 0,02*109/l, р=0,05). It appears important obtained data that with hypertrophy LV and diastolic disfunction was noticed authentic increase of lymphocytes, expressing the marker of apoptosis CD95 (0,458 ± 0,276*109/l vs 0,335 ± 0,155*109/l, р=0,05; 0,441 ± 0,26*109/l vs 0,342 ± 0,21*109/л, р=0,01, accordingly). Conclusion The increased activity of inflammatory markers, decline of functional activity of monocytes, the elevation of apoptosis marker, associated with bigger intensity of postinfarction remodeling processes. The acute phase of inflammation is necessary stage of healing, but with long-term clinical case, excessive activation or alteration of functional activity of leukocytes can lead to growth of structural and electrical remodeling.
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