Biomedical subjects

S Paradowski

Publications and source records attributed to S Paradowski.

At least 19 recordsLinked to original sources

PubMed1993

Hypertrophy or hyperplasia in cardiac muscle. Post-mortem human morphometric study.

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, and density of myocyte nuclei. The values of all histometric parameters correlated well with left ventricular (LV) weight up to 350 g. In heavier hearts these parameters remained approximately of the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g. The influence on LV weight of age, coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue was also evaluated. On the basis of a linear discriminant function, hearts were divided into three classes: (1) LV weight < or = 250 g (absence of hyperplasia, hypertrophy only); (2) LV weight 251-350 g (hypertrophy+signs of hyperplasia); (3) LV weight > 350 g (marked signs of hyperplasia). The percent of fibrosis increased proportionally to LV weight. Where LV weight was above 250 g there was a subsequent increase in the mean percent of fibrosis (approx. 26%). This phenomenon (plateau of percent fibrosis) is the result of an increased number of myocytes (myocyte hyperplasia). We suggest that, independent of aetiology, in all hearts above 350 g (patients with congestive heart failure) hyperplasia phenomenon exists.

Adult↗

PubMed1992

[Hypertrophy or hyperplasia of myocytes in heart hypertrophy?].

One of the most controversial problem in cardiac muscle pathology is the existence of myocyte hyperplasia. The term hypertrophy indicates an increase in size of the individual muscle cells without changing their total number, whereas in hyperplasia there occurs proliferation of the myocyte. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention it has received. Contemporary views concerning the cardiac muscle hyperplasia are presented. From clinical point of view the problem is significant for two reasons. The loss of the ability of muscle cells to proliferate is responsible for the irreversible myocardial destruction after injury. From another point of view, if the increase of the heart muscle is maintained, although a complete remission of cardiac hypertrophy becomes impossible. In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p < 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. From these parameters only coronary artery diameters significantly influenced on LV weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗

PubMed1992

[Confirmed and borderline hypertension found in 44% of men (aged 40-59 years) working at the H. Cegielski plant in Poznań].

Blood pressure was measured in 3317 men, aged 40-59, working in H. Cegielski Metal Works in Poznań. The average systolic pressure for the whole population was 130.9 mmHg (SE = 17.90). The average diastolic pressure was 83.7 mmHg (SE = 10.03). The systolic, diastolic and mixed systolic-diastolic hypertension was found in 539 men which makes 16.3% of the study group. The borderline systolic hypertension was found in 327 men i.e. 9.9%, borderline diastolic hypertension in 267 men i.e. 8.0%. Both systolic and diastolic borderline hypertension displayed 339 men i.e. 10.2% of the study group. So, borderline hypertension (systolic, diastolic and systolic-diastolic) was found in 933 men which makes 28.1% of the population under the study.

Adult↗

PubMed1991

[Coronary lumen diameter and cardiac mass in various forms of cardiac hypertrophy].

Morphometric evaluation of the epicardial arteries is described in detail in 103 patients with various forms of cardiac hypertrophy. Coronary lumen diameter increases with aging regardless of the cardiac mass. Such an increase is observed in some particular types of cardiac hypertrophy and presumably is caused by the changes of intramuscular vessels and diminished perfusion. In patients with so called myocardial atherosclerosis correlation between coronary lumen diameter age and cardiac mass is opposite. In some forms of cardiac hypertrophy the increment of coronary lumen diameter is accompanied by the increase of the cross sectional area of the artery. In this pattern the increase of lumen diameter is not due to passive vessel dilatation because significant thickening of its wall can be seen. Age appeared to be the most important factor influencing the coronary lumen diameter within the whole population, although this correlation can hardly be seen in patients with "myocardial arteriosclerosis".

Aging↗

PubMed1991

[Value of two-dimensional echocardiography in predicting the clinical course and fates of patients 2 years after myocardial infarction].

133 patients with acute myocardial infarction, admitted to hospital 24 hours or less from the beginning of chest pain were investigated. Two-dimensional echocardiography (ECHO 2D) was performed 1-2, 3-5, 7-10, 21-28 days and 3, 6, 9, 12, 18 and 24 months after myocardial infarction. Relations between ECHO parameters, clinical course and prognosis. 2 years after myocardial infarction were analysed. Worse clinical course and prognosis during 2 years after myocardial infarction predict high values of 1) asynergy index (greater than or equal to 1), 2) percentage of asynergy segments (greater than or equal to 50) and 3) percentage of left ventricular (LV) akinetic and (or) dyskinetic segments (greater than or equal to 37.5). Right ventricular asynergy and maintenance or increase of LV asynergy degree aggravate clinical course and prognosis too.

Adult↗

PubMed1991

[Dynamics of disorders of ventricular contraction studied by two-dimensional echocardiography 2 years after myocardial infarction].

Two-dimensional echocardiography (ECHO 2D) was performed in 133 patients 1-2, 3-5, 7-10, 21-28 days and 3, 6, 9, 12, 18 and 24 months after myocardial infarction. During 2-years observation after myocardial infarction a gradually diminishing occurrence of left ventricular (LV) systolic wall motion abnormalities, is seen mostly--akinesia. Dyskinesia is the most persistent form of asynergy appearing with similar frequency during the whole study period. Improvement, worsening or no changes of LV asynergy are found with similar frequency in hospital phase. Favourable asynergy changes predominantly++ in the ambulatory phase. Right ventricular (RV) asynergy is found rarely (5%) in transmural inferior infarction only. It coexists with enlargement of RV. RV asynergy is always associated with LV asynergy, mostly of its inferior or posterior wall.

Adult↗

PubMed1991

[The effect of intravenous streptokinase on selected echocardiographic and clinical parameters of patients followed up for 2 years after myocardial infarction].

54 patients (pts) aged 70 years or younger with acute transmural myocardial infarction and onset of chest pain less than 12 hours were assigned in a blind manner to streptokinase group (SK), 54--to control group, 34 pts received intravenous infusion of 1,500,000 IU of SK/hour, 14 pts--2,000,000 IU/hour, and 6 pts--3,000,000 IU/2.5 hours. Intravenous streptokinase reduced left ventricular (LV) asynergy during hospital phase, decreased LV thrombus formation, and limited myocardial necrosis size 2 years after myocardial infarction. Its effect on clinical course and prognosis after myocardial infarction was of small importance.

Aged↗

PubMed1991

[Comparative evaluation of coronary arteriosclerosis in arterial hypertension and ischemic heart disease. Morphometric analysis of 4062 coronary artery specimens].

We performed a postmortem study on 61 hearts from patients who died of acute ischemic heart disease (IA). Chronic ischemic heart disease (IB) and from hypertensive patients who died of heart infarction (IIA) and other hypertensive complications (IIB). Control group consisted of 16 pts. who died of non cardiac diseases. 4062 coronary artery specimens were estimated. Irrespective of the clinical course of ischemic heart disease the mean percent of coronary artery stenosis was similar in both ischemic groups and significantly higher than in control group. In hypertensive pts. who died of heart infarction it was also significantly higher and similar to ischemic pts. We found the highest percent of segments with critical stenosis in the left anterior descending coronary artery in group IA, IB, IIA. It was also significantly higher in the left main coronary artery in the group of ischemic pts. (IA, IB).

Adult↗

PubMed1991

[Value of exertional echocardiography and performance of transesophageal left atrial pacing done 3-4 weeks after acute myocardial infarction].

Two-dimensional echocardiography during exercise (ECHO W) and left atrial pacing (ECHO S) was done in 30 patients 3-4 weeks after acute myocardial infarction. Sensitivity of these methods to detect fresh myocardial ischemia was compared. Their prognostic value during 2 years after myocardial infarction was determined too. Both methods increase sensitivity of simultaneously performed ecg. Sensitivity of ECHO S (80%) was higher than ECHO W (67%). Sensitivity of the two methods altogether was higher (93%) then each method independently. Coexistence of worsening systolic wall motion abnormalities and a decrease in ejection fraction during both examinations may suggest worse clinical course and prognosis 2 years after myocardial infarction.

Adult↗

PubMed1991

[Comparison of the diagnostic value of echocardiographic, ecg and enzymatic investigations in acute myocardial infarction].

Two dimensional echocardiography (ECHO 2D) was performed in 133 patients 1-2, 3-5, 7-10, 21-28 days and 3, 6, 9, 12, 18 and 24 months after myocardial infarction. Standard ecg examination was carried out at the admission time, every 15 minutes during the first 2 hours, 3, 6, 12, 24 and 48 hours later, and afterwards in the same time as ECHO 2D. At the admission time and 4, 8, 12, 16, 20, 24, 36, 48, 60, and 72 hours later creatine kinase activity was determined. It is concluded that a relation exists between severity and extensiveness of myocardial infarction in ecg and severity and the asynergy area in the ECHO 2D study. In transmural anterior infarction large concordance exists in necrosis location estimated by both methods. In the inferior myocardial infarction asynergy concerns inferior, posterior and lateral LV wall and RV walls. V5-6 ecg leads appear of little value in infarct location. The lack of infarct evolution in ecg coexists with exacerbation of LV asynergy and extension of the LV asynergy area. Sensitivity of ECHO 2D in detecting myocardial infarction in the first day was 90%, ecg - 83%, enzymatic examination - 98%. 2 or 3 methods all together have high sensitivity (99%-100%).

Adult↗

PubMed1991

[Selected hemodynamic parameters in overweight patients with mild and moderate hypertension treated with low caloric diet].

Basic haemodynamic parameters - blood volume (BV), cardiac output (CO), stroke volume (SV), and total peripheral resistance (TPR) were studied in two groups of overweight patients with mild and moderate hypertension. Each group consisted of 15 subjects. The patients of the first group were kept on low caloric diet (1000-1100 cal per day). Patients of the second-control-group were treated with propranolol (120 mg per day). The duration of each study was 24 weeks. Blood pressure fell due to body weight reduction. BV, CO and SV decreased without changes in TPR. In the control group treated with propranolol in which the body weight did not change a fall in blood pressure, cardiac output, and stroke volume was seen without changes in blood volume and total peripheral resistance values.

Adult↗

PubMed1990

[Myocardial infarction in patients with arterial hypertension. Changes in the creatine kinase MB isoenzyme activity in relation to myocardial hypertrophy].

The aim of the study was to investigate the relationship of arterial hypertension coexisting with myocardial hypertrophy to the infarct size evaluated by serial CK-MB measurements. The group of 98 patients (72 males and 26 females) with the first Q-wave infarction was selected from 137 patients admitted to I Clinic of Cardiology of Poznan Medical School with acute myocardial infarction (AMIO). Age of the patients ranged from 35 to 82, mean 60 years. Time from the onset of symptoms to admission to the hospital varied from 1 to 8 hours, mean 4. Enzymatic tests were performed on admission, every 4 hours during the first 24 hours, every 6 hours during the second and the third day and every 8 hours during the 4th and the 5th day. Anterior infarction was diagnosed in 46 patients and inferior infarction in 52 patients. The type of CK-MB curve, maximal CK-MB activity and the mass of necrotic tissue was evaluated for every patient using Sobel formula modified by Norris. Total mass of the left ventricle was calculated from echocardiographic measurements (2-D and M-mode) and the ratio of LV mass per square meter of the body surface was was calculated according to Horton's formula. The subgroup of 44 patients (25 males and 19 females) with the history of hypertension was selected. Ophthalmic examination revealed angiopathic changes of I and II grade K-W. This group, as compared to remaining patients with AMI was characterised by higher left-ventricular mass (198.0 +/- 28.6 vs 151.0 +/- 16.9 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

[Myocardial structure in various forms of hypertrophy. I. Myocyte hypertrophy or hyperplasia? Pathophysiological aspects and the methods of study].

One of most controversial problems in cardiac muscle pathology is the existence of myocyte hyperplasia. The term hypertrophy indicates an increase in size of the individual muscle cells without changing their total number, whereas in hyperplasia proliferation of the myocyte occurs. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention in has received. Contemporary views concerning the cardiac muscle hyperplasia are presented. From clinical point of view the problem is significant for two reasons. The loss of the ability of muscle cells to proliferate is responsible for the irreversible myocardial destruction after injury. From another point of view, if the increase of the heart muscle is maintained, although a complete remission of cardiac hypertrophy becomes impossible. In the light of these controversies we undertook the attempt to solve this complicated problem. Morphometric evaluation of the cardiac myocyte is described in detail.

Anthropometry↗

PubMed1990

[Myocardial structure in various forms of hypertrophy. II. Myocyte hypertrophy or hyperplasia? Results of the study].

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p less than 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. Only coronary artery diameters significantly influenced on LV weight. On the basis of linear discriminant function, three classes of hearts were separated: 1) LV weight 250 g - absence of hyperplasia, only hypertrophy 2) LV weight 251-350 g - hypertrophy + signs of hyperplasia 3) LV weight 350 g - marked signs of hyperplasia Among 18 patients with the LV weight above 350 g (all patients with congestive heart failure), 11 suffered from valvular disease, 3 were postinfarction patients, 2 suffered from primary hypertension and 2 from primary congestive cardiomyopathy. It indicates that, irrespective to the etiologic factor, hyperplasia is a simple result of the cardiac muscle mass increase.

Adult↗

PubMed1988