Initial studies of diastolic cardiac function in hypertension demonstrated that slowing of the maximal rate of left ventricular filling occurred before alterations in either ejection fraction or cardiac output. The present study was undertaken to determine: 1) the relation between hypertension, increased left ventricular mass and impaired left ventricular filling, and 2) the correlation between abnormalities in left ventricular diastolic function and its systolic performance. Eleven normal subjects (Group 1), 5 hypertensive patients without evidence of left ventricular hypertrophy (Group 2) and 18 hypertensive patients with increased left ventricular mass by echocardiography (Group 3) were studied by M-mode echocardiography, radionuclide (technetium-99m human serum albumin) first pass technique and gated blood pool scintigraphy. Indexes of systolic function (ejection fraction, maximal rate of ejection and percent left ventricular shortening) were essentially similar in hypertensive and normotensive subjects. No correlation was found between systolic blood pressure and left ventricular mass (r = 0.20, not significant). Maximal rate of left ventricular filling (P dV/dt) and fast filling fraction decreased progressively from Group 1 to Group 3 (2.36 +/- 0.4 [mean +/- standard deviation], 2.17 +/- 0.3 and 1.97 +/- 0.4 s-1, respectively, for P dV/dt and 46 +/- 7, 48 +/- 9 and 38 +/- 11%, respectively, for fast filling fraction); the difference from values in normal subjects reached statistical significance in hypertensive patients with left ventricular hypertrophy. Left ventricular maximal filling rate correlated inversely with left ventricular mass and left ventricular end-systolic diameter (r = -0.74), but positively with left ventricular fractional shortening and ejection fraction (r = 0.70).(ABSTRACT TRUNCATED AT 250 WORDS)

Introduction: Chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality in the world. Systematic treatment of COPD decreases symptoms and reduces the frequency of exacerbations and hospitalisations because of the disease. It is estimated that only 50% of patients use prescribed drugs systematically. The aim of this study was to identify the factors which can influence adherence to treatment of the patients who were treated due to exacerbation of COPD. Material and Methods: A questionnaire probe was conducted on 49 patients hospitalised at the Regional Lung and Tuberculosis Hospital in Olsztyn, Poland due to COPD exacerbation. The assessed variables were: quality of life and adherence to treatment 30 days after discharge from hospital in relationship with demographic factors, social status, disease and hospitalisation course, and relief after systematic treatment. Results: Most of the patients assessed their health condition as poor and the disease as limiting their everyday social and occupational activity. 30 days after discharge from hospital the adherence rate to therapy was only 67%. There was an association between systematic treatment and the rate of exacerbations (p = 0.045) and hospitalisations (p = 0.005) but also clinical benefit after long-term treatment (p = 0.023). There were no associations between adherence to treatment and sex, place of residence, education or occupation. Conclusions: Lack of systematic treatment is the main risk factor for COPD exacerbations and hospitalisation rate. A subjective sense of relief after drugs is a factor improving patients’ compliance.

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We have previously presented evidence that the polymorphism of the FCGR3A gene, encoding the receptor for Fc fragment of immunoglobulin G IIIa (FcγRIIIa) plays a role in the enhancement of circulating immune complexes (CIs) with the occurrence of Mycobacterium tuberculosis heat shock proteins in patients with sarcoidosis (SA). The immunocomplexemia might be caused by decreased affinity of CIs to Fcγ receptors, with the subsequently decreased receptor clearance by immune cells. In the present study we examined whether the polymorphisms of other related genes (FCGR2A, FCGR2C, FCGR3B) encoding other activatory Fcγ receptors, could have a similar effect. To this end, we genotyped 124 patients with sarcoidosis and 148 healthy volunteers using polymerase chain reaction with sequence-specific primers. We revealed a significant decrease in the percentage of the FCGR2A and FCGR2C variants that ensure effective CIs clearance, with a concomitant increase of less functional variants of these genes in Stages I/II, compared with Stages III/IV of SA. There was no aberration in FCGR3B allele/genotype frequencies. We conclude that the FCGR2A and FCGR2C polymorphisms may also contribute to immunocomplexemia present in SA. The assessment of FCGR genes could become a tool in presaging a clinical course of sarcoidosis and in its personalized therapy.