Randomized, placebo-controlled study for immunosuppressive treatment of inflammatory dilated cardiomyopathy: two-year follow-up results.

BACKGROUND: Previous studies have shown disappointing results for immunosuppressive treatment in patients with dilated cardiomyopathy. Therefore, we studied the effectiveness of such therapy in patients with HLA upregulation on biopsy. METHODS AND RESULTS: Of 202 patients with dilated cardiomyopathy, 84 patients with increased HLA expression were randomized to receive either immunosuppression or placebo for 3 months; they were then followed for 2 years. After 2 years, there were no significant differences in the primary end point (a composite of death, heart transplantation, and hospital readmission) between the 2 study groups (22.8% for the immunosuppression group and 20.5% for the placebo). The secondary efficacy end point included changes in ejection fraction, end-diastolic diameter, end-diastolic volume, end-systolic volume and NYHA class; left ventricular ejection fraction increased significantly in the immunosuppression group compared with the placebo group (95% CI, 4.20 to 13.12; P<0.001) after 3 months of follow-up. The early favorable effects of immunosuppressive therapy on left ventricular volume, left ventricular diastolic dimension, and New York Heart Association class were also present. This improvement was maintained in the immunosuppression group at 2 years (ejection fraction: 95% CI, 6.94 to 19.04; P<0.001). In addition, on the basis of the protocol-specified definition of improvement, 71.8% patients in the immunosuppression group versus 20.9% patients in the placebo group met the criteria of improvement after 3 months (P<0.001). At the end of the follow-up period, 71.4% patients from the immunosuppression group versus 30.8% patients from the placebo group were improved (P=0.001). CONCLUSIONS: These data demonstrate a long-term benefit of immunosuppressive therapy in patients with dilated cardiomyopathy and HLA upregulation on biopsy specimens. Thus, restoration of immunosuppressive therapy for such patients should be considered.

[Pharmacological preconditioning as a way of the increasing of myocytes resistance to ischemia]. / Zwiekszanie odpornosci miocytów serca na niedokrwienie przy uzyciu substancji farmakologicznie czynnych, czyli preconditioning farmakologiczny.

This paper is a discussion about pharmacological methods of supporting the cardiomyocytes in a condition of acute ischemia, during interventional cardiology procedures and in cardiosurgery. We present here drugs with potentially protective activity on heart muscle. We provide also some information about cytoprotective effects of trimetazidine, propranolol, phosphocreatine, adenosine and other substances. The results of presented investigations indicate the possibility of using some of these substances in clinical practice.

[Ischemic preconditioning: a new issue in cardiology. Part 2: clinical investigation]. / Hartowanie lub uodpornianie niedokrwienne, czyli preconditioning niedokrwienny--nowe zagadnienie w kardiologii. Czesc 2--Badania kliniczne.

The goal of this paper was to present results of clinical investigations into ischemic preconditioning. Information about conditions necessary for the development of this phenomenon in the heart is also mentioned. We presented the trials of application of protection achieved as a result of this phenomenon in interventional cardiology and in cardiosurgery.

[Ischemic preconditioning: a new issue in cardiology. Part I: preliminary studies: a suggested mechanism of the phenomenon]. / Hartowanie lub uodpornianie niedokrwienne, czyli preconditioning niedokrwienny--nowe zagadnienie w kardiologii. Czesc 1--badania doswiadczalne, proponowany mechanizm zjawiska.

The aim of this paper is the presentation of scientific experiments dedicated to understanding the mechanisms of ischemic preconditioning. The information about numerous cellular receptors involved in this process is reported. Other elements, mediating in the cascade of biochemical changes leading to the increase in resistance of the heart to ischemia are also described.

[Genetic changes and clinical management in familial hypertrophic cardiomyopathy]. / Zmiany genetyczne a obraz kliniczny rodzinnej kardiomiopatii przerostowej.

Hypertrophic cardiomyopathy (HCM) is phenotypically and genotypically heterogeneous disease of heart. Nine chromosomal loci responsible for this condition have been identified: beta-myosin heavy chain, essential and regulatory myosin light chains, troponin T and I subunits, alpha-tropomosin, cardiac myosin binding protein C, cardiac actin and titin. These genes code for proteins involved in the contraction mechanism or in the control of contraction, therefore HCM has been classified as a disease of cardiac sarcomere. Over 107 mutations have been identified. More then half of them have been detected in the beta-myosin heavy chain gene (beta-MHC). Some mutations in beta-MHC gene are associated with a benign prognosis, other are associated with high incidence of sudden cardiac death (SCD) and severe hypertrophy. Mutations in myosin binding protein C are associated with mild, delayed expression of cardiac hypertrophy and benign prognosis. Mutations in cardiac troponinT are associated with a mild degree of hypertrophy but a high incidence of SCD. Study of genes responsible for HCM will assume role in the context of clinical management of HCM, in particular regarding diagnosis and prognosis patients and families with HCM.

[Viscosity of blood and plasma in patients with single- and multi-vascular coronary heart disease]. / Lepkosc krwi i osocza u chorych z jedno- i wielonaczyniowa choroba wiencowa.

The aim of this study was to establish a connection between rheological disturbances and extensiveness of atherosclerotic changes in coronary angiogram. Patients were classified into two groups: group I--with multivascular atherosclerotic lesions (45 subjects at age of 58 +/- 11 years), group II--with univascular atherosclerotic lesions (18 subjects at age of 55 +/- 9 years). Blood samples were drawn from the cubital vein prior to the angiogram. Blood viscosity measurements were performed using low-shear Contraves viscometer-100 at 0.116; 1.0; 4.59 s-1 shear rates and Brokfield Cone/Plate Viscometer at 150 s-1. The plasma viscosity was measured by means of Ubbelohde's capilary viscometer. Besides the viscometric examinations the total cholesterol. LDL-cholesterol, HDL-cholesterol, triglycerides, glucose and fibrinogen as well as blood morphology and ESR were determined. All rheological measurements were carried out at the temperature of 37 degrees C immediately after blood drawing. The results of studies indicate that in patients with multivascular coronary disease whole blood viscosity at all examined shear rates was significantly greater then in univascular patients. It was found that the LDL-lipoproteins concentration was significantly elevated in the I group. Other examined parameters did not differ significantly. The examinations indicate that there exists the connection between hemorheological disturbances and the extensiveness of coronary heart disease.

[Results of promoting fibrinolytic therapy for myocardial infarction in the Katowice Province from 1996-1998]. / Wyniki akcji promujacej leczenie fibrynolityczne zawalu serca na terenie województwa katowickiego w latach 1996-1998.

The action promoting fibrinolytic treatment of myocardial infarction and questionnaire-based follow up of the results was carried out over a four million people area. 5262 questionnaires, in which physicians answered a number of questions, were received. The poll revealed that 79% of patients received fibrinolytic treatment. The authors estimate the overall percent of patients, treated in hospital wards, at about 27.7%. The mortality rate in the group of patients, who received streptokinase, was 8.61% and in the group of patients, who did not receive the treatment, was 16.28%. The signs of reperfusion were present in 60.38% of patients. The authors conclude that the increase in the number of patients administered fibrinolytic treatment should be aimed, and the results obtained in this group of patients come close to published data. Exercise tests are performed in too small number of myocardial infarction patients and only little proportion of them undergoes further coronary angiography.