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Electrocardiography is one of most classical methods of examination in medicine and in cardiology. After more than 100 years of practical use, it is indispensable in diagnosing arrhythmias as well as several, clinically important proarrhythmic states. In those, the heart with normal anatomy endangers the patient with the risk of serious, frequently life threatening arrhythmias (Long QT Syndrome, Brugada Syndrome, Wolff-Parkinson-White Syndrome, T-wave alternans). Further, electrocardiography is nowadays important in diagnosing the very fresh signs of myocardial ischemia. Present time electrocardiography is demanding for manufacturers of electrocardiographic machines, and requires precise, standard technique of examination. Despite automatic evaluation programmes of electrocardiogram, which are nowadays almost a standard, physicians should understand well the electrocardiogram, and must be able to correct frequent inaccuracies of the automatic evaluations.

Female phenotype, sexual infantilism, small stature and stigmatization are typical for patients with Turner's syndrome (TS). The most frequent cardiovascular manifestations in these patients are a bicuspidal aortal valve and coarctation of the aorta. In 5% patients dilatation of the aorta is found which can develop into a dissecting aneurysm. In the submitted case-history the authors describe a 34-year-old patient where the diagnosis of TS was proved only in adult age at the time when a dissecting aneurysm of the aorta was detected. The submitted case-history supports the recommendation of regular echocardiographic check-up examinations of patients with TS.

Background: The value of operation of atrial septal defect (ASD) in adults, especially after 40 years, is still discussed., Methods and Results: In 1994-95 57 adults with unoperated ASD were examined clinically, echocardiographically and in 75% by catheterization. Type primum was present in 11%, type secundum in 77% and sinus venosus in 11%. Group A comprised 28 patients aged 20 to 40 years (average 29), group B comprised 29 patients aged 40 to 62 years (average 51). The groups (B:A) did not differ in pulmonary to systemic flow (Qp/Qs) (2.4:2.2) or pulmonary arteriolar resistance (PAR) (group B 2 U.m2, group A 1.7 U.m2), the older patients had worse New York Heart Association (NYHA) classification, more frequent tricuspid regurgitation (group B 96%, group A 45%), significantly larger right ventricles and pulmonary arteries, higher mean pulmonary artery pressure (group B 26 mmHg, group A 17 mmHg) and right ventricle end-diastolic pressure (RVEDP group B 10, group A 8.8 mmHg). All defects larger than 10 mm by transesophageal echocardiography (TEE) had Qp/Qs 1.5 or more. Forty patients were operated with zero mortality, in three cases by minithoracothomy. Postoperatively, 50% of group A and 63% of group B felt better, NYHA classification was significantly better in both groups. Tricuspid regurgitation decreased in both groups as well as the size of right ventricle. The size of the left ventricle enlarged after operation in group A., Conclusion: This study suggests to operate adults with ASD larger than 10 mm by TEE with signs of right ventricle overload and/or Qp/Qs 1.5 or more, who have normal PAR. Operative mortality was zero in both age groups, the functional repair was better in younger patients (under 40 years).

Intensive research into the presence of endogenous digitalis-like factor (EDLF) started shortly after identification of the alpha subunit of the Na,K,-ATPase as being receptor for digitalis glycosides. After years of skepticism, present data testify EDLF really exists. Most probably, the EDLF has chemical structure of either ouabain or of one of its isomers. It is secreted by the adrenal cortex, and, under conditions of stress, it's secretion is regulated differently from the secretion of both gluco- and mineralocorticoids. The physiological role of the EDLF has not been fully understood yet. In the newborn's kidneys, the inhibition of the Na,K-ATPase may assist to increase elimination of surplus sodium from the organism. In individuals of any age, the inhibitory influence of EDLF upon Na,K-ATPase in the arterial wall smooth muscle cells increases peripheral vascular resistance and thus, blood pressure. In the tissue culture, direct positive inotropic influences of EDLF upon rat cardiomyocytes was observed. However, the importance of positive inotropic effect of the EDLF upon the heart in clinical medicine remains to be elucidated.

There was studied the effect of intravenously administered creatin phosphate (Neoton-drug with cardioprotective effect, Alfa Schiapparelli Wassermann) in the group of 98 patients affected by their first attack of myocardial infarction. In the course of the treatment there were observed the serum level of many biochemical indices, including the cardioselective enzyme activity. We concluded that the patients treated with Neoton, compared with the control group, revealed the significantly higher elevation of the CK, AST and LDH activity levels and the shift of the CK peak activity towards to the earlier hours after the onset of anginal pain.

The authors present a case of a dissecting aneurysm of the aorta type A which affected also the insertions of visceral and renal arteries, and in addition to renal ischaemia and impaired renal function caused also ischaemia of the liver parenchyma with a rise of transaminases and bilirubin. This led to temporary hospitalization at the infectious department where the patient was referred to rule out hepatitis. In the discussion the authors draw attention to the pathogenesis, differential diagnosis and contemporary therapeutic methods of the disease.

The existence of endogenous ligands of opioid receptors prompted research of a potential endogenous digitalis-like factor (DLF) and of endogenous clonidine-displacing substance (CDS). Within eleven years of research, endogenous ouabaine was identified as DLF. It originates in the adrenal cortex. Its physiological role is not yet clear. Most probably, endogenous ouabaine is primarily active in regulation of natriuresis and of blood pressure. The CDS originates in the brain and is active in regulation of blood pressure as well. Its chemical formula was recently identified as agmatine. The potential presence of further autacoids like, e.g. endogenous quinidine-like substance remains to be clarified.

Methods of molecular cardiology have extended our knowledge of cardiomyopathies. In hypertrophic cardiomyopathy the existence of at least nine beta-myosin heavy chain gene mutations on the arm of the 14th chromosome were detected. The latter cause substitution of amino acids in the molecule of this protein with subsequent slowing of the actin shift against myosin during muscle contractions. The presence of beta-myosin heavy chain gene mutation is strictly specific for hypertrophic cardiomyopathy, the mutations cause not only familial cases of the disease but also its sporadic incidence. There exists carriership of mutations, carriers can be quite healthy from the clinical aspect. Individual mutations differ by their penetrance and a different risk of sudden cardiac death. 100% penetrance and a high risk of sudden cardiac death are caused in particular by the mutation with substitution of glycine by arginine in position 403. In addition to possible point mutations there are also mutations with deletion of a portion of this gene and also mutations on chromosomes 1, 11 and 15; so far, however, genes with these mutations were not identified. In dilated cardiomyopathy gene mutations are the cause of familial diseases which account for cca 20% of all these diseases. Mutations can affect also the dystrophin gene on chromosome X, and genes of the mitochondrial genome which code in particular the primary structure of polypeptides participating in oxidative phosphorylation. Mutations as the cause of cardiomyopathies will probably call for a changed definition of these diseases.

Background: Infective endocarditis still remains a cardiological menace. However, the type of predisposing diseases has changed: the incidence of rheumatic heart disease in advanced countries has declined, advances made in the surgical and medicamentous treatment of inborn heart disease are the reasons why we are encountering, with increasing frequency, infective endocarditis which develops on their background., Methods and Results: The objective of the investigation was to assess the frequency of infective endocarditis and predisposing diseases. During the time interval between 1987 and 1991 16 patients (50% younger than 50 years) were hospitalized with the diagnosis of infective endocarditis. Rheumatic valvular damage and inborn heart disease were the predisposing factor in 25%. All patients were younger than 30 years (mean 24, range 18-30), and half the patients suffered from defects of the ventricular septum. Other defects were tetralogy of Fallot and inborn aortic stenosis. In 10% of the patients infective endocarditis developed on the background of a mitral valve prolapse with regurgitation. Echocardiographic examination confirmed the diagnosis in almost 70% by revealing vegetation. Bacteriological examination revealed the agent in 60%, most frequently it was Streptococcus viridans. The mortality rate in the group was 13%., Conclusions: The recorded incidence of infective endocarditis, 1.5 pro mille, is consistent with data in the literature. Corrected and not corrected heart disease plays an important role as predisposing disease. Despite the opportunity of intensive antibiotic treatment, the mortality remains high--13%.

Congenital heart disease of adults is a new area of cardiology with specific diagnostic, therapeutic, social and economic problems of these patients. The First Medical Clinic of the Second Medical Faculty, Charles University assembled so far data on more than 1200 adult patients with congenital heart disease from different districts in Bohemia and Moravia. Atrial septal defects are recorded most frequently (25.7%), followed by ventricular septal defects (25.0%) and coarctation of the aorta (12.4%). 50.3% of the patients were treated by surgery, most frequently patients with a patent ductus arteriosus--in 83.8%, with coarctation of the aorta (82.8%) and an atrial septal defect (60.5%). The authors review reasons why for the care of these patients in other countries specialized centres developed and the foundation of such a centre in the Czech Republic is discussed.

The authors investigated a group of 95 pregnant women with congenital heart disease. In two induced abortion was indicated fur cardiac reason (major left-to-right shunt in ASD II and in a patient with a non-corrected TOF with a significant right-to-left shunt). In the remainder the course of pregnancy was not complicated. From the total number of 132 deliveries only six were by Caesarean section, five times on obstetric grounds. One infant died, delivery during the 29th week by Caesarean section on account of premature escape of amniotic fluid--mother with a history of radial correction of TOF. Other relevant data are summarized in a table. In the conclusion the authors summarize basic provisions indicated in pregnant women with congenital heart disease.

The heart muscle is critically dependent on energy supply from oxidative phosphorylation, which in turn requires an adequate oxygen supply. Its greatest proportion (80%) is used by mechanical work of the heart, followed by the ion pumps and protein resynthesis. Global ischaemia of the isolated heart leads within two seconds to the electron transport arrest in mitochondria and at the same time glycogenolysis, an alternative energy source, is accelerated. The content of macroergic phosphate declines rapidly, in particular that of creatine phosphate and within 10-15 seconds mechanical activity stops. The subsequent fate of ischaemic tissue depends on the degree and period of ischaemia. Very brief ischaemia (1-2 min.) does not cause any functional sequelae after restoration of the arterial blood supply. Longer ischaemia (10-15 min.) leads during reperfusion to postischaemic dysfunction (stunned myocardium, G. R. Heyndrickx) which is completely reversible. Prolonged hypoperfusion lead to mechanical dysfunction, which may last weeks and months but is reversible (hibernated myocardium--S. H. Rahimtoola). Only prolonged critical ischaemia (30-60 min. and perfusion as low as 0.15 ml/min./g tissue) leads to necrosis of muscle cells. Its development is enhanced in particular by an extensive drop of macroergic phosphates with inhibition of anaerobic glycolysis, excessive amounts Ca++ in cardiomyocytes and cumulation of catabolites, such as lactate, H+ and free radicals.

25 adult asymptomatic patients with Turner's syndrome were evaluated by clinical examination, ECG, M-mode and two-dimensional echocardiography and 24 h Holter monitoring. Patients with Turner's syndrome had a significantly higher resting heart rate (83.3 versus 73.7/min in controls, p < 0.01) and a shorter PQ interval (122.3 ms versus 147.1 in controls, p < 0.01). The short PQ interval was not associated with the karyotype (45,X vs. mosaic karyotypes and structural abnormalities of X and Y chromosome), hypertension, estrogen treatment, or congenital valvular abnormalities. No significant arrhythmias were present. On 24 hours ambulatory ECG monitoring the frequency of ectopic supraventricular and ventricular activity was identical as in published controls. The congenital heart abnormalities were detected in 8 (32%) women with T.sy, however, during the follow-up they became significant in only two (8%) of them.

The authors investigated in a group of 106 patients with a first myocardial infarction treated by thrombolysis the effect of i.v. administration of creatine phosphate (a new drug with cardioprotective action--Neoton Alfa Schiapparelli Wassermann Co). In the course of treatment electrocardiographic changes were recorded and the presence of arrhythmias examined by the Holter technique. The Neoton group displayed a statistically insignificant but nevertheless obvious trend of electrocardiographically less serious forms of infarction and a lower incidence of infarctions, as compared with the control group.

Quinidine-like immunoreactivity (Abbott TDx Quinidine fluorescence polarization immunoassay) was measured in control, sham-operated, abdominal aorta stenotic and hyperthyroid (thyroxine feeding 0.1 mg/rat/day rats. The mean quinidine levels (mumol quinidine/1 serum) were 0.07, 0.14, 0.13 and 0.25, respectively. The elevation in experimental hyperthyroidism was statistically (analysis of variance, Duncan's test) significant. The possibility of the existence of an endogenous antiarrhythmic, immunologically cross-reacting in quinidine immunoassay, is discussed.

In chronic heart failure, dysregulation of sympathetic nerve system activity and of release of several neurohormones is present. Increased plasma levels of circulating hormones together with other factors have a negative influence on myocardial beta adrenergic receptors and induce cardiac hypertrophy with myocardial fibrosis. ACE inhibitors possess an ability to reverse these phenomena. An endogenous factor with an ACE inhibitory ability was isolated from the bovine left ventricular myocardium.

The author presents a review of requirements of the American Heart Association, the American College of Cardiology and American College of Physicians to obtain qualification in the discipline of monitoring of haemodynamics, in echocardiography of adults, percutaneous transluminal coronary angioplasty and ECG loading tests. He mentions also requirements essential for maintenance of the acquired qualification. In the conclusion the author reflects on the possible application of these criteria under local conditions.

Patients with significant residual stenosis after thrombolytic therapy during acute myocardial infarction have higher risk of reinfarction, periinfarction ischemia and sudden death. Early revascularisation can prevent such complications. To find out patients who are at increased risk and are candidates for early angiography 74 patients undergoing angiography after thrombolytic therapy were reviewed. Significant residual stenosis (greater than or equal to 50% diameter reduction) of infarct related artery was present in 85%, high grade stenosis (greater than or equal to 75%) in 58% of patients respectively. The group of patients with preinfarction angina (Canadian class I to IV. 24 hours before infarction) had higher mean residual stenosis than patients without angina (76.5% vs 64%). There was significant difference in presence of preinfarction angina in patients with high grade stenosis and without high grade stenosis (79% and 21% respectively). Thus preinfarction angina can be used to identify patients with higher risk of reocclusion after thrombolytic therapy during acute myocardial infarction. Early coronary angiography and revascularisation can prevent serious complications in these patients.

The antianginal and anti-ischemic effect of isosorbide dinitrate (ISDN), 120 mg once daily, and nifedipine, 20 mg twice daily, both in slow-release formulations, were compared in 17 patients with variant angina pectoris in a randomized, double-blind trial. The design included a placebo run-in period and two 6-week crossover periods of active treatment. Mean frequency of angina decreased significantly from 43 attacks per week during the placebo period to 4 per week with ISDN and 8 with nifedipine (p less than 0.001). Sublingual nitroglycerin consumption decreased significantly from 37 tablets per week with placebo to 3 tablets per week with ISDN and 7 with nifedipine (p less than 0.001). Both drugs reduced the silent and symptomatic ST-segment deviations on ambulatory electrocardiographic recording and increased maximal exercise tolerance. Episodes of coronary spasm could be provoked, by hyperventilation, in all patients during the placebo phase but in no patient during therapy with either active drug. Thus, both ISDN and nifedipine, in their slow-release formulations, are effective in the treatment of variant angina pectoris.

Cardiac hypertrophy in heart disease is associated with a deterioration of the patient's prognosis. From experimental work it is known that hypertrophy can recede, sometimes it is, however, associated with an undesirable increase of fibrous tissue in the heart muscle. In clinical practice we can reduce cardiac hypertrophy (assessed mainly by echocardiography), at least in some patients, by reducing or eliminating the evoking cause (e.g. in sportsmen terminate training, in aortic valve disease by replacement of the valve, in hypertonic patients we reduce the pressure by drugs). After regression of hypertrophy later also the amount of fibrous tissue recedes and as a rule the function does not deteriorate. Lately we are trying to influence factors which directly participate in the hypertrophy of the myocytes, in particular in hypertonic subjects by preferential action on the adrenergic system and the renin angiotensin system.

Cardiac wet and dry weight, adrenal weights, blood pressure and food consumption were measured in control male rats, rats fed 0.2% dried thyroid powder in the food, rats fed metyrapone (an inhibitor of adrenocortical 11-hydroxylase, Metopirone CIBA, 50 mg/rat per day) and both metyparone + dried thyroid. Metyparone markedly inhibited thyroid-induced cardiomegaly as well as the increase in adrenal weight. Myocardial dry weight and blood pressure differences between the various groups were not significant. The results supply further evidence of the existence of a relationship between the adrenal cortex and thyroid-induced cardiomegaly. Metyrapone also completely inhibited the post-thyroid drop in body weight.

The effects of isosorbide dinitrate single dose 120 mg daily and nifedipine 20 mg twice daily were studied in 17 patients with variant angina pectoris due to coronary artery spasm. After a placebo phase the patients were randomized to treatment with either isosorbide dinitrate or nifedipine. After six weeks the patients were crossovered for another six weeks period of treatment. There was significant decrease of number of angina attacks during both treatment regimens. Using 24 hours Holter monitoring we also proved significant decrease of number of ST segment elevation or depression, either symptomatic or asymptomatic. There was increase of performed work during exercise tests after both treatment periods. The efficacy of Isoket 120 mg and Adalat Retard 2 x 20 mg daily in the treatment of patients with active variant angina pectoris was comparable in our study. 3 patients suffered untolerable headache during isosorbide dinitrate phase and had to terminate treatment after first day only.