[Left Bundle Branch Block in Unstable Angina. Mortality and Rate of Myocardial Infarction].

AIM: to study mortality and adverse outcomes in patients with unstable angina (UA) and left bundle branch block (LBBB). MATERIAL AND METHODS: We included in this study UA patients with (n=56) and without LBBB (n=310). Period of observation was 14 days (from admission to discharge). The following events were considered as adverse outcomes: death, myocardial infarction, carcinogenic shock, and stroke. RESULTS: Combination of UA with LBBB was associated with increases of risk of death (3.4-fold) and myocardial infarction (2.6-fold), shortening of in-hospital mean duration of life and survival time by 1 day.

[THE FEATURES OF STRUCTURE-FUNCTIONAL HEART CONDITION IN OLDER PATIENTS WITH UNSTABLE ANGINA AND LEFT BUNDLE BRANCH BLOCK].

The structural and functional parameters of echocardiography in 56 older patients with UA and LBBB were analyzed in comparison with these parameters in 186 patients with UA without LBBB. The median age of patients with UA and LBBB was 75 (67-81) years, without LBBB - 74 (65-80) years. The procedure was carried out in the first day of hospitalization in cardiology department on the UA. LBBB in patients with unstable angina is associated with remodeling of the heart with an increase the diameter of the aorta, the LVID (s) and (d), thickening of the IST and PWT and increasing the RWT, as well as a decrease of LP and RV cavities. We revealed the signs of left ventricular dysfunction without evidence valvular obstruction in the patients with UA and LBBB. The hemodynamic of patients with UA and LBBB was characterized by large LV DV and SV, as well as by decrease FS, FJ, MFS and gradients MV, AV, PV, and TV than at UA without LBBB. The echocardiographic symptoms of diastolic dysfunction with delayed relaxation were found in patients with UA and LBBB. The mitral regurgitation occurred more frequently in 2,4 times more in patients with UA without LBBB.

[Cardiorenal syndrome and prerenal azotemia in patients with acute hypertensive encephalopathy].

AIM: To estimate changes in renal function in patients with acute hypertensive encephalopathy (AHE) during standard inpatient antihypertensive therapy. SUBJECTS AND METHODS: Patients were selected for the trial in the cardiology and admission units of a Perm hospital. The group included 60 patients with AHE. The patients received inpatient antihypertensive therapy for 10-14 days. Within the first 2 hours, enalaprilate 1.25 mg was intravenously injected, by monitoring blood pressure. After 6 hours, the patients were given enalaprilate tablets 20 mg b.i.d. plus hydrochlorothiazide 12.5 mg (Subgroup 1) or nifedipine 60 mg plus hydrochlorothiazide 12.5 mg (Subgroup 2). The laboratory parameters of kidney function were measured twice: on admission to and before discharge from hospital. Plasma creatinine and urea concentrations were estimated. Glomerular filtration rate (GFR) and urea/creatinine ratio were calculated. The patients were found to have proteinurea, low GFR, high plasma creatinine concentrations, and increased urea/creatinine ratio. RESULTS: Transient proteinuria was observed in 25% of the patients with AHE within the first 24 hours of the disease. The proportion of patients with lower GFR was unchanged during a 2-week treatment period (20 and 16%, respectively; p = 0.22). There was a rise in the proportion of patients with higher urea/creatinine ratio (83 and 95%, respectively; p = 0.006). CONCLUSION: The course of AHE is complicated by cardiorenal syndrome (CRS) with transient proteinuria and low GFR, as well as by prerenal azotemia (PRA). The number of patients with PRA increased after 2-week conventional inpatient antihypertensive therapy (enalaprilate + hydrochlorothiazide 12.5 mg or nifedipine + hydrochlorothiazide 12.5 mg).

[Cognitive functions and extracranial circulation in patients with hypertonic crisis].

We studied effects of enalaprilate and infedipine therapy on the cognitive functions and extracranial circulation in 60 patients with chronic AH complicated by acute encephalopathy. 10% of them had predemential disorders on day 1 of hospitalization and 90% mild cognitive problems. Half of the patients suffered reduced circulation in the common carotid artery. The contribution of impaired extracranial circulation to cognitive dysfunction in the acute period of hypertonic crisis was higher than that of high SAD and DAD. Antihypertensive therapy improved bloodflow in extracranial vessels, decreased their systolic and diastolic indices but failed to eliminate mild cognitive disorders in 65% of the patients. Visual-spatial orientation was restored more frequently than verbal auditory memory. Enalaprilate and infedipine had similar angio- and cerebroprotective effects but the latter had more pronounced favourable effect on verbal auditory memory than the former. The degree of recovery of cognitive function 2 weeks after hypertonic crisis depended not only on the form of cognitive disorder and therapeutic modality but also on the patient's age. Hemodynamic parameters and age 2 weeks after antihypertensive therapy are predictors of residual cognitive dysfunction soon (2 weeks) after recovery.

[Cognitive impairment in elderly patients with acute hypertensive encephalopathy].

Acute hypertensive encephalopathy in elderly patients appears reversible mild cognitive impairment. The erythrocyte sedimentation rate and blood creatinine measured during a hypertensive crisis are predictors of decline of visual-spatial orientation after two weeks of treatment.

Iliopsoas bursitis: diagnosis by MRI.

Iliopsoas bursitis is an unusual cause of hip pain. The condition may be due to athletic activity or may be secondary to a variety of inflammatory etiologies. An understanding of the anatomy and biomechanics of this structure is necessary to ensure prompt and appropriate radiologic diagnosis and clinical treatment. We report two cases of iliopsoas bursitis diagnosed with MRI and review the anatomy, pathophysiology, and treatment of this condition.