Comparative study of mitral annular calcification (MAC) with cardiac arrhythmias in dialysis patients.

Cardiac arrhythmias and myocardial malfunction are very frequent in uremic patients. The pathogenesis and etiology of arrhythmias are very complex and still unknown. The sedimentation of calcium salt in myocardial structures is one of the reasons for emergence of cardiac arrhythmias (AV conduction defects, ectopic arrhythmias). The appearance of mitral annular calcification (MAC), as the expression of the speed up process of atherosclerosis, was noted in younger uremic patients especially during hemodialysis. The aim of our research was to compare the incidence of MAC and cardiac arrhythmias in patients on hemodialysis. Our study included 40 patients, 24 male and 16 female, in the age between 20 and 60. Patients were mostly from Zagreb and the Counties of Zagreb (35%), Karlovac (10%), Slavonski Brod (7.5%), Varazdin (5%) and Pozega (5%). All 40 patients received 24 hours of Holter monitoring and 2-D echocardiography of M-mode. The patients were divided in two groups: I MAC+ (N = 23) and II MAC- (N = 17). Frequency of cardiac arrhythmias in group I was: atrial fibrillation N = 0; conduction defects N = 2 (1%); ventricularectopy Lown grade 3-5 N = 15 (65%); supraventricular ectopy N = 8 (34%), while the frequency of cardiac arrhythmias in group II was: atrial fibrillation N = 0; conduction defects N = 0; ventricular ectopy Lown grade 3-5 N = 6 (35%), supraventricular ectopy N = 6 (35%). During statistical processing the significant connection of MAC+ and frequency of cardiac arrhythmias was noticed. For both groups we have not noticed statistical significance in cardiac arrhythmia compared to electrolytes, risk factors PTH, and age. The time of hemodialysis treatment is one of possible factors for incidence of cardiac arrhythmias influenced by MAC. We noticed statistically significant (p < 0.05) difference of rhythm disorders between group I and group II especially for the ventricular ectopic activity, the frequency of which was higher in group I than in group II. MAC has probably significant role in dialysis patients for the development of cardiac arrhythmias within the framework of series of complicated multifactorial patogenetic mechanisms.

Frequency of mitral annular calcification in patients on hemodialysis estimated by 2-dimensional echocardiography.

Mitral annular calcification (MAC) is a degenerative process associated with left ventricular hypertrophy (HLV) and progressive atherosclerosis, characteristic of the older age groups. Numerous investigations point to significantly earlier onset of atherosclerosis process in patients in final stage of chronic renal insufficiency. The aim of investigation was to determinate the MAC frequency in patients on hemodialysis and to try to find the correlation between MAC intensity and the duration of hemodialysis, age, sex, Ca/P, metabolism, level of parathormone and atherogenic factors. A group of 40 patients on hemodialysis (aged 20 to 67, 26 men and 24 women) were divided int two groups; group 1 without MAC, N = 17 (42.5%), X = 3.5, SD = 3.1; and group 2 with MAC, N = 23 (57.5%), X = 6.2, SD = 2.4. M-mode and 2-D echocardiography were performed in all patients. Group 2 was divided into three subgroups according to MAC quantitation: mild N = 16 (70%), severe, N = 4 (17%), moderate, N = 3 (13%). Study results showed positive correlation between MAC and serum values of Ca and P (p < 0.05). Increased values of HDL cholesterol, statistically significant at the level p < 0.05 were observed. Study results showed the correlation between MAC and time factor, i.e. duration of dialysis treatment to be statistically significant (p < 0.05). Cardiac calcified syndrome could be a sequela of MAC causing conduction disturbances, valvular stenosis or insufficiency, and arterial emboli or endocarditis.

The effect of intravenous nitroglycerin therapy on infarct size in patients with acute myocardial infarction.

The authors investigated the influence of glyceryl-trinitrate (NTG) given intravenously to the reduction of infarction size in 95 patients (71 men and 24 women) aged 36 to 75, with acute myocardial infarction (AIM) admitted to the Intensive Care Unit within six hours of the onset of pain. Infarction mass was calculated by mathematical model from the serial changes of CK and CK MB serum activities during 72 hours and expressed in CK and CK MB gEq. CK and CK MB were determined every four hours. The patients were divided into four groups according to the therapy they were receiving: I--NTG i.v. (n = 29); II SK + NTG i.v. (n = 29); III SK i.v. (n = 17) and IV ISDN per os (n = 20). Each group was divided into subgroups regarding the time interval from the onset of pain to the beginning of the therapy (within three hours and after three hours). Application of NTG i.v. in the early phase of AIM, 0-3 hours from the onset of pain, led to the significant reduction of infarction mass CK gEq and CK MB gEq (0-3 hours; middle rank = 11.35; 3-6 hours: middle rank = 17.7) (P < 0.05) and 0-3 hours: middle rank = 10.31; 3-6 hours: middle rank = 18.81 (P < 0.01). It was established that the "timing" factor was very important in the preservation of myocardial mass in AIM. It affirms the efficacy of NTG i.v., i.e., its direct effects on the coronary arteries and systemic effects that cause salvation of the myocardium. The influence of NTG iv to myocardial infarction size CK gEq did not depend on ECG localization. But it influenced the ECG localization when the infarction size was calculated from CK MB isoenzyme and expressed in CK MB gEq. Infarction mass CK MB gEq was statistically significantly smaller in the inferior than in the anterior localization (P < 0.05).

Effect of therapeutic interventions on CK and CK MB serum activity kinetics during acute myocardial infarct.

Determination of serum creatine kinase (CK) activity, especially the CK MB, isoenzyme is becoming the main diagnostic criterion for acute myocardial infarct (AMI). The aim of this study was to assess the kinetics of the release CK and CK MB in AMI patients on various therapeutic regimens. The study included 75 AMI patients (within 6 hours from the pain onset). They were divided into three groups according to therapy: 1.NTG i.v. (glyceryl trinitrate, N=29), 2.SK + NTG i.v. (streptokinases + glyceryl trinitrate, N = 29); and 3. SK i.v. (N = 17). Samples for CK and CK MB determination were taken every 4 hours in the course of 72 hours, until serum enzyme values returned to normal. The time interval between the introduction of therapy and CK and CK MB peak values expressed in rankes was the shortest in group 3 and longest in group 1. The difference in maximal CK release in to peripheral blood (chi 2 = 9.5270, p = 0.0180) was statistically significant, while difference in CK MB was not (chi 2 = 2.2733, p = 0.2875--NS) (Kruskal Wallis one way test). Comparing CK release time the CK MB within each group by means of rankes, statistical significance in favour of CK MB (1. NTG i.v. p = 0.0000, 2. SK + NTG p = 0.0001, 3. SK p = 0.0180) was obtained. The rate of CK and CK MB elimination from the circulation, expressed as fractional level of losing kd, did not statistically differ in the three groups. Authors' results showed the therapeutic procedures used in the treatment of AMI patients to differently influence the CK and CK MB kinetics. Thrombolytic therapy changed the CK and CK MB kinetics, due to reperfusion and explained by the washout phenomenon from the infarcted zone of the myocardium.

A case of McLeod syndrome with chronic renal failure.

A 50-year-old man with the rare McLeod syndrome, associated with glomerular lesion to the end stage of chronic renal failure and death, is reported. McLeod syndrome is an X-linked recessive disorder on the basis of abnormal expression of the Kell blood group antigens and absence of erythrocyte surface Kx antigen. Most often the clinical and pathological findings are retinitis pigmentosa to blindness, progressive chronic neuropathy, cortical atrophy, dilated cardiomyopathy, and glomerular lesion with chronic renal failure. Among the laboratory parameters the most important are very low level of cholesterol and triglycerides, then various numbers of acanthocytes in peripheral blood smears and sometimes in urine (as in our case).

Secondary hyperparathyroidism and brown tumor in dialyzed patients.

Secondary hyperparathyroidism is one of the most common complications of chronic renal failure (CRF). Its pathogenesis is multifactorial and still not completely understood. Pathological mechanism of hypocalcemia, hyperphosphatemia and calcitriol deficiency are basic characteristics of CRF and main reason for morphological changes in parathyroid glands and hyperparathyroidism (HP). We present a case of a female patient born in 1975. At the age of 10, a urinary infection was diagnosed for the first time and treated. Six years later, as nausea and vomiting started, CRF based on bilateral reflux was diagnosed and the patient was included in the hemodialysis treatment. The patient was again examined in 1997, when biochemical parameters, including the level of parathyroid hormone, ultrasonography of the neck, scintigraphy of the skeleton and densitometry revealed secondary HP. Parathyreoidectomy was perfomed in 1998. During the follow up period, a tumefaction on a ramus mandibulae dex. was noticed, which was cytologically diagnosed as osteitis fibrosa, "brown tumor", a rare complication of the secondary HP. Surgery was performed and PHD was granuloma gigantocelulare. Prevention and therapy of secondary HP is a problem that demands early actions to avoid possible complications.

[Kinetics of leukocytes in patients on hemodialysis]. / Kinetika leukocita u bolesnika na hemodijalizi.

The total numbers of leukocytes and relevant fractions of granulocytes in 51 patients on chronic intermittent hemodialysis were determined. The leukocytes were counted before the beginning, during the third hour of and one to two hours after the hemodialysis. Along with the kinetics of leukocytes the levels of C3 and C4 components of the complement were tested. A decrease of total numbers of leukocytes was observed as well as that of all the fractions of granulocytes during the third hour of dialysis. The intensity of leukopenia depended on the structure of dializer membrane. Observing the components C3 and C4 along with the values of leukocytes there was no association between these two alterations. The authors concluded that leukopenia during the hemodialysis is not caused by complement activation in the contact of plasma with the membrane of the dializer but by the mechanical effect of adhesion or microaggregation of leukocytes on the membrane of the dializer.