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Rupture of the ventricular septum after acute transmural myocardial infarction occurred in four patients aged between 53 and 79 years. The rupture was verified by means of right-side cardiac catheterization. Only in two cases did two-dimensional echocardiography reveal the rupture; in both cases the rupture site located by echocardiography was confirmed at autopsy. In each of the four patients the left-to-right shunt could be identified by means of pulsed Doppler echocardiography which showed a turbulence in the right ventricle. Furthermore, the combination of two-dimensional echocardiography and Doppler echocardiography allowed a correct localization of the turbulent left-to-right flow in all cases. In view of these findings, the combination of Doppler echocardiography and two-dimensional echocardiography may be regarded as a suitable method for a readily available, non-invasive diagnosis of ventricular septum rupture in patients with acute myocardial infarction in an intensive care unit.

The value of persistent ST-T elevations in the standard 12-lead ECG for the diagnosis of left-ventricular aneurysm (VA) was retrospectively analysed for 200 patients (171 males and 29 females) who had sustained a myocardial infarction at least 12 weeks previously. 105 patients (group 1) had a left-ventricular aneurysm confirmed by ventriculography; in 95 patients (group 2) an aneurysm had been excluded by ventriculography. Persistent ST-T elevations were present in 98 patients of group 1 (sensitivity 93.3%) and in 26 of group 2 (specificity 72.6%). In the 26 patients without VA, ST-T elevations occurred in at most three leads, but in 60 with aneurysm in four to nine leads. In addition, the area under the ST-T elevations and its height 1 mm after onset of the elevation and its maximal height were measured. The sums of the values in the limb and chest leads were statistically significantly different between the two groups for all three parameters. These measurements thus contribute to a reliable differentiation between patients with and without VA. The results also emphasize the importance of the 12 standard leads in the diagnosis of VA.

SummaryThe purpose of the study was to evaluate alterations of the hemostatic system and the effect of anticoagulant therapy in nonvalvular atrial fibrillation. A set of molecular hematologic markers was measured prospectively in 69 patients with atrial fibrillation and 28 age-matched patients in sinus rhythm. Significantly elevated levels of thrombin-antithrombin III complex (8.5 ± 1.6 vs. 2.5 ± 0.3 αg/1; p

In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

BACKGROUND The present study was designed to evaluate the efficiency of a newly developed troponin T enzyme immunoassay for the detection of acute myocardial infarction. METHODS AND RESULTS The study comprised 388 patients admitted with chest pain and suspected myocardial infarction and 101 patients with skeletal muscle damage and additional suspected myocardial cell damage. Troponin T was elevated to more than twice the analytical sensitivity of the assay (0.5 microgram/l) in all patients with non-Q wave (range, 1.2-5 micrograms/l) and Q wave infarction (range, 3-220 micrograms/l). Troponin T appeared in serum as early as 3 hours after onset of pain in 50% of the patients and remained elevated in all patients for more than 130 hours, revealing release kinetics of both free cytosolic and structurally bound molecules. The diagnostic efficiency of troponin T was superior to that of creatine kinase-MB (98% versus 97%) and remained at 98% until 5.5 days after admission, if patients with unstable angina were excluded from analysis. In the 79 patients with unstable angina, troponin T was elevated (range, 0.55-3.1 micrograms/l) in at least one blood sample from each of 37 patients (56%). Circulating troponin T was correlated to the presence of reversible ST segment or T wave changes on the electrocardiogram (p less than 0.005) and to the frequency of in-hospital complications. In the 101 patients with skeletal muscle damage and suspected additional cardiac muscle damage, troponin T was the most useful test; its efficiency was 89% or 94% (depending on the discriminator value used) as compared with 63% for creatine kinase-MB. CONCLUSIONS Thus, the data of the study indicate that the newly developed troponin T test improves the efficiency of serodiagnostic tools for the detection of myocardial cell necrosis as compared with conventionally used cardiac enzymes.

Forty eight patients with bilateral isolated non-stenotic coronary artery ectasia or aneurysm without associated cardiac defects ("dilated coronaropathy") were identified in consecutive diagnostic cardiac catheterizations between 1986-6/1994 (angiographic incidence 0.44%). Ectasia was defined as a luminal dilatation of the 1.5-2-fold, aneurysm of more than double the normal limits. In 16 patients a myocardial infarction (5 non-q-infarctions/11 q-wave-infarctions) was the indication for coronary angiography, a thrombotic occlusion of the infarct vessel was documented in 8/16 patients. In patients without myocardial infarction (study group) an evaluation of exercise-induced myocardial ischemia was performed by means of a coronary sinus lactate study, treadmill ergometry and Thallium-201-scintigraphy. A corresponding coronary insufficiency was objective in all tests in the study group. An exercise-induced myocardial ischemia was found in 21/31 in the coronary sinus study, 19/29 in the treadmill ergometry and 13/26 patients in the scintigraphy; significant differences were found in comparison to the results of a control group of patients without heart disease (n = 29, p0.001). After administration of 0.8 mg nitroglycerin (NTG) a further significant deterioration of myocardial ischemia was measured in the 21 patients with pathologic lactate metabolism developing a frank cardiac lactate production (p0.03). The extent of myocardial ischemia in the coronary sinus study was significantly correlated to the coronary diameters of the proximal and middle segments of the Ramus interventricularis anterior and the middle segment of the Ramus circumflexus (r = 0.87, p0.02). A differentiation between ectasia and aneurysm therefore seems to be of functional relevance. Angiographic stigmata of an impaired coronary blood flow such as a segmental to and from movement and a local deposition of dye were found significantly more often with increasing coronary diameters (p0.04). "Dilated coronaropathy" is an entity of non-stenotic, ischemic coronary artery disease. NTG was of no therapeutic benefit or led to an aggravation of the exercise-induced myocardial ischemia. Because of this potential adverse effect the administration of NTG should be avoided in "dilated coronaropathy".

This prospective cross-sectional study include 100 consecutive patients (56 males, 44 females, 29 to 86 (mean = 67.5 +/- 12.2) years) with ventricular inhibited demand pacemakers 0.1 to 94.7 (mean 23.3 +/- 25.4) months after pacemaker implantation. Fifty-two patients were free of symptoms, whereas 48 patients were still complaining of syncope, dizziness, or palpitations. After history, physical examination, and 12-lead standard ECG all patients underwent 24-h Holter monitoring. A computer-aided analysis of spontaneous arrhythmias was done first. In a second run computed-aided analysis of transient pacemaker dysfunctions was performed with a specially designed pacemaker module. There were no significant differences between asymptomatic and symptomatic patients with regard to the incidence of transient pacemaker dysfunctions, with regard to defined types of pacemaker dysfunctions, spontaneous ventricular arrhythmias, and with regard to supraventricular tachycardias. A significant difference between asymptomatic and symptomatic patients was found, however, regarding the Lown classification of ventricular arrhythmias, because asymptomatic patients showed class 0 and I/II arrhythmias more frequently (p0.025). In the 100 patients a total of 6609 pacemaker dysfunctions were observed, 5104 failures to sense and 1505 inappropriate inhibitions. Most patients showed up to 240 pacemaker dysfunctions per 24 h. There were no failures to capture. Different types of pacemaker dysfunctions were found with different clinical implications. Due to the Holter findings in nine patients pacemakers were reprogrammed or replaced. After pacemaker implantation the number of patients with severe symptoms significantly decreased compared to the number of patients before pacemaker implantation. Nonetheless, there was a number of patients still complaining of symptoms after pacemaker implantation. In only a few patients did pacemaker implantation worsen symptoms . Our data show that with use of long-term ECG transient pacemaker dysfunctions and spontaneous arrhythmias are more frequent than patients' history and common standard techniques in the pacemaker clinic may suggest Holter monitoring, therefore, is a useful diagnostic tool, not only in symptomatic, but also in asymptomatic pacemaker patients. It allows to obtain a reliable survey of the real amount of transient pacemaker dysfunctions in the individual patient, which is the base for further therapeutic decisions.

The purpose of the study was to evaluate alterations of the hemostatic system and the effect of anticoagulant therapy in nonvalvular atrial fibrillation. A set of molecular hematologic markers was measured prospectively in 69 patients with atrial fibrillation and 28 age-matched patients in sinus rhythm. Significantly elevated levels of thrombin-antithrombin III complex (8.5 +/- 1.6 vs. 2.5 +/- 0.3 micrograms/l; p0.001), fibrin monomers (27.1 +/- 3.2 vs. 13.4 +/- 3.7 nM; p0.001), D-dimers (788 +/- 76 vs. 405 +/- 46 micrograms/l; p0.005), and tissue-type plasminogen activator (9.6 +/- 0.5 vs. 7.2 +/- 0.5 micrograms/l; p0.05) were observed in patients with atrial fibrillation compared to those in sinus rhythm. In a subgroup of patients in whom anticoagulant therapy with oral coumadin or standard intravenous heparin was established after the initial study, hemostatic activation decreased significantly. In conclusion, molecular hematologic markers indicate a hypercoagulable state in atrial fibrillation which may characterized a group of patients at elevated risk of thromboembolic disease.

Regional wall motion abnormality is the best indicator for coronary ischemia. Myocardial wall motion is registrated by cardiokymography (CKG), a mechanocardiographic method. Because of the high incidence of artefacts, echocardiography and nuclear imaging technique have been preferred. Computer-assisted signal averaging CKG improves practicability and allows measurements during exercise testing. Exercise testing was performed in 54 patients with suspected ischemic heart disease without mitral or aortic valve dysfunction, myocardial infarction or prior cardiac surgery. The results of simultaneously recorded ECG and CKG were compared with coronary angiographic results. CKG sensitivity and specificity were higher than that of ECG (76 and 80% vs 71 and 52%). If diagnosis was based on pathological or nonpathological results of both CKG and ECG, sensitivity and negative predictive value increased to 87 and 83%, respectively. Sensitivity reached 93% when only one pathological result was required. CKG combined with signal-averaging techniques has advanced to become a specific and sensitive tool in the non-invasive diagnostic approach to ischemic heart disease.

The importance of the pacemaker follow-up clinic has markedly increased in the face of the currently available multiprogrammable pacemakers. In contrast to the common standard techniques in assessing pacemaker dysfunctions, Holter monitoring allows the detection of transient pace-maker dysfunctions during a long period of time. Especially computer-aided analysis provides a considerable progress, because different pacemaker dysfunctions can be detected during prolonged time periods, and--in contrast to visual analysis--a reliable survey of the real extent of transient pacemaker dysfunctions in the individual patient is assessed. The reliability of computer-aided analysis by a specially designed module was prospectively investigated in 100 consecutive patients with permanent ventricular inhibited demand pacemakers. It could be demonstrated that the positive predictive accuracy of this analysis was limited to 60.2% in detecting failures to sense and 63.2% in detecting inappropriate inhibitions, respectively. All detected failures to capture were false positive events. The positive predictive accuracy, therefore, was not calculated for this category of event. The overall positive predictive accuracy was 59.9%. In contrast, the sensitivity of computer-aided analysis was remarkably high. Possible causes of false positive and false negative findings are described. The reliability of pacemaker pulse detection was also investigated. Out of 100 analyzed Holter recordings five showed a temporary total loss of pacemaker pulses. Loss of single pacemaker pulses was found in 30 patients. False positive pacemaker pulses were seen in three patients. These results show that visual control and validation by an experienced physician are mandatory.(ABSTRACT TRUNCATED AT 250 WORDS)

We report on a 44-year-old male with primary cardiac angiosarcoma who died 11 months after onset of nonspecific symptoms (thoracic pain and general fatigue) of intracerebral metastases. A right atrial tumor mass and a pericardial effusion could be demonstrated by transthoracic and transesophageal echocardiography. Cardiac angiography showed a right atrial hemangioma, fed by the right coronary artery. In a review of 108 cases of primary cardiac angiosarcoma we summarize clinical features, diagnostic means, therapeutic approaches and life expectancy of this rare disease.

Characteristic signs of the pacemaker syndrome occurred in a 69-year-old woman with intermittent 3 degrees atrioventricular (AV) block after implantation of a dual-chamber AV-synchronized pacemaker. Cannon beats due to inappropriate atrial timing were the main haemodynamic finding. Their development and size depended on the programmed AV interval and AV-synchronized mode of stimulation. Very long AV intervals in the DDD mode at a heart rate of 100/min caused very unpleasant palpitations and pulsations in the upper thorax. The symptoms due to the cannon beats were avoided by changing to a short AV interval. The clinical and haemodynamic events were thus the consequence of preserved sinus node function with subsequent atrial triggering.

Troponin T is a unique cardiac antigen which is continuously released from infarcting myocardium. Its cardiospecificity as a marker protein might be particularly useful in assessing myocardial cell damage in patients undergoing cardiac surgery. Therefore, circulating troponin T was measured in serial blood samples from 56 patients undergoing cardiac surgery and in two control groups--22 patients undergoing minor orthopaedic surgery and 12 patients undergoing lung surgery by median sternotomy. In both control groups no troponin T could be detected, whereas activities of creatine kinase were raised in all 12 lung surgery controls and activities of the MB isoenzyme were raised in five of the 12 patients in the lung surgery group and in four of the 22 patients in the orthopaedic surgery group, respectively. All the patients undergoing coronary artery bypass grafting (n = 47) and cardiac surgery for other reasons (n = 9) had detectable concentrations of troponin T. Five patients had perioperative myocardial infarction detected as new Q waves and R wave reductions. In these five patients troponin T release persisted and serum concentrations (5.5-23 micrograms/l) reached a peak on the fourth postoperative day. In the 51 patients without perioperative myocardial infarction serum concentrations and the release kinetics of troponin T depended on the duration of cardiac arrest. In patients in whom aortic cross clamping was short troponin T increased slightly on the first postoperative days; in patients with longer periods of aortic cross clamping troponin T concentrations were higher and remained so beyond the fifth postoperative day. In patients with non-specific changes on the electrocardiogram troponin T concentrations were significantly higher on days 1 and 4 after operation than in patients with normal postoperative electrocardiograms(11.2 (5) and 4.5 (2.6) v 8.2 (3.4) and 2.9 (1.6) 1microg/l). Serum concentrations of troponin T showed some myocardial cell damage in every patient undergoing cardiac surgery. The persistent increases that were more common in patients with longer periods of cardiac arrest must have been caused by damage to the contractile apparatus. These results suggest that perioperative myocardial cell necrosis may be more common than indicated by changes of the QRS complex on the electrocardiogram.

In anesthetized rats under artificial respiration, intravenous infusion of nisoldipine (0.1 mg/kg x min) caused significant decreases in blood pressure, heart rate, cardiac output and peripheral resistance. The animals died 54.7 +/- 11.1 min after initiation of the infusion. The electrocardiogram showed sinus bradycardia, increasing AV blockade and displacement of the pacemaker into the AV node or the bundle of His. Survival time under nisoldipine infusion increased more than two-fold with simultaneous infusion of calcium gluconate, isoprenaline (isoproterenol) or dopamine. Norepinephrine (noradrenaline) had no significant effect on survival time; the latter decreased to 19.4 +/- 1.6 min by plasma volume expansion with polygeline. All antidotes prolonging survival time also normalized the cardiac output diminished after nisoldipine. Electrocardiographic changes were antagonized only by isoprenaline. Suitable antidotes for intoxication or over-dosage of nisoldipine are calcium salts as well as beta-sympathomimetic drugs; sheer volume substitution and peripheral vascular constriction should not be resorted to.

The value of persistent ST-T elevations in the standard 12-lead ECG for the diagnosis of left-ventricular aneurysm (VA) was retrospectively analysed for 200 patients (171 males and 29 females) who had sustained a myocardial infarction at least 12 weeks previously. 105 patients (group 1) had a left-ventricular aneurysm confirmed by ventriculography; in 95 patients (group 2) an aneurysm had been excluded by ventriculography. Persistent ST-T elevations were present in 98 patients of group 1 (sensitivity 93.3%) and in 26 of group 2 (specificity 72.6%). In the 26 patients without VA, ST-T elevations occurred in at most three leads, but in 60 with aneurysm in four to nine leads. In addition, the area under the ST-T elevations and its height 1 mm after onset of the elevation and its maximal height were measured. The sums of the values in the limb and chest leads were statistically significantly different between the two groups for all three parameters. These measurements thus contribute to a reliable differentiation between patients with and without VA. The results also emphasize the importance of the 12 standard leads in the diagnosis of VA.

Infarct size can be estimated noninvasively by analysis of circulating CK-MB and/or cardiac myosin light chains. To investigate whether myosin light chains release is correlated with the impairment of left ventricular function in acute myocardial infarction, this marker protein was determined by liquid phase radioimmunoassay in serial blood samples of 25 patients. Likewise CK-MB was measured in the same blood samples. From the serum concentration changes the cumulative appearance was calculated as an estimate of infarct size. Left ventricular enddiastolic pressure, global and regional ejection fraction were measured immediately and 3 weeks after admission. Particularily during the chronic phase of myocardial infarction a close correlation was found between serological estimates of infarct size and impairment of left ventricular function. The cumulative appearance of myosin light chains was superior to CKMB in assessing the hemodynamic impact of myocardial infarction in the acute and chronic stage. Therefore, myosin light chains are an appropriate serological indicator for the hemodynamic significance of myocardial infarction during the acute and chronic stage and might allow an assessment of the patients' risk.

Lidocaine was supplied to 10 cats by 2 comparative infusions of 7.5 mg/kg respectively. Once the drug was dissolved in a physiological and the other time in a K-Mg-concentrated electrolyte solution. The sequence of both infusions alternated. Serum potassium remained constant during infusion of the physiological electrolyte solution, but increased by about 1 mEqu/1 under K-concentrated solution. Lidocaine caused an enhancement of ventricular fibrillation threshold to an absolutely identical degree in both groups. Increase in cardiac output and stroke volume and decrease of sinus rate was significant in both groups, but more pronounced under K-Mg concentrated solution. Mean arterial pressure, peripheral vascular resistance, PQ, QRS, and QT interval remained constant on the whole. We deduce from these results for antiarrhythmic therapy on normokalemic patients, that the addition of potassium and magnesium to lidocaine solution does not enhance its antifibrillatory effect. This statement is valid for doses up to 20 mEqu/h of magnesium and 40 mEqu/h of potassium.

Im Rahmen einer elektrokardiographischen Untersuchung wurden bei 100–105 herzgesunden Versuchspersonen die rechtsthorakalen Ableitungen V4r und V3r, die dorsale thorakale Ableitung v2 2 ICR tiefer und die hochthorakalen Ableitungen V1–6 2 ICR hoher aufgezeichnet. Aus dem gewonnenen Material wurden die Extrem- und Mittelwerte einschlieslich der mittleren quadratischen Abweichung samtlicher vorhandener Ausschlage bestimmt und z. T. graphisch dargestellt. Auserdem wurden die verschiedenen Formen der Kammerkomplexe beschrieben und es wurde die prozentuale Haufigkeit ihres Vorkommens errechnet. In der anschliesenden Diskussion wurden die Indikationen fur die Anfertigung zusatzlicher Brustwandableitungen besprochen. Insbesondere wurden die Grenzwerte des Normalen herausgestellt und mit den entsprechenden Daten der vorhandenen Literatur verglichen. Es wurde hervorgehoben, das die rechtsthorakalen Ableitungen in erster Linie der Feststellung einer Rechtsuberlastung des Herzens dienen, wahrend die ubrigen Ableitungen ihren Wert in der Infarktdiagnostik haben: die dorsale Ableitung V8 2 ICR tiefer fur die Erkennung von Hinterwandinfarkten und die hochthorakalen Ableitungen fur die Diagnose basaler Vorder- und Seitenwandinfarkte.

Bei 35 Patienten mit Vorhofseptumdefekt wurden die Beziehungen zwischen hamodynamischen und elektrokardiographischen Grosen untersucht. Ein Einflus des Shuntvolumens auf den Beginn der grosten Negativitatsbewegung im Bereich des rechten Ventrikels konnte nicht nachgewiesen werden. Dagegen fand sich eine deutliche-wenn auch im Einzelfall nicht verlasliche-Abhangigkeit verschiedener elektrokardiographischer Amplitudenwerte von der Hohe des systolischen Druckes im rechten Ventrikel. Die elektrophysiologische Bedeutung desrSR′-Komplexes wurde diskutiert. Abschliesend wurde zur Frage der elektrokardiographischen Aussagemoglichkeiten uber die Druck-bzw. Volumenuberlastungsform eines Herzabschnittes Stellung genommen.

Nach dem Ergebnis der tierexperimentellen Synchronisationsversuche ist festzustellen, das eine „mechanische Kopplung“ von Vorhofund Kammeraktion sowohl am isolierten Froschherzen als auch am Saugetierherzen in situ als gesichert gelten kann. Die Adaptation der Sinusfrequenz an die Kammerfrequenz erfolgt am Ganztier offenbar nicht durch unmittelbare mechanische Einwirkung der heterotopen Ventrikelerregung auf den Sinusknoten, sondern indirekt uber eine Vorhofkontraktion gegen geschlossene AV-Klappen. Die am Kaltbluterherzen beobachtete, durch ausschlieslich elektrische Leitung bedingte Rhythmenverknupfung, die nach physikalisch-technischen Modellversuchen auch am Warmbluterherzen eine Rolle spielen konnte, lics sich bisher am Ganztier nicht bestatigen.

Bei 13 Patienten mit verschiedenen Herzfehlern ohne Kurzschlusverbindungen wurde mit Hilfe des Kalte- bzw. des Farbstoffverdunnungsverfahrens nach Indikatorinjektion in die V. cava sup. das Herzzeitvolumen in der A. pulmonalis und der A. iliaca simultan registriert. Statistisch signifikante Unterschiede zwischen den beiden Messtellen konnten nicht festgestellt werden. Man kann auf diese Weise das Herzzeitvolumen des rechten und des linken Ventrikels getrennt bestimmen.

The case of acute purulent group B streptococcal myocarditis in a 29-year-old Turk is described, no similar case having previously been published. He fell ill suddenly with gastro-intestinal symptoms, high fever and pain in arms and legs. The ECG had low voltage in the limb leads and signs of a large acute myocardial infarct. The sedimentation rate was slightly raised, an initial leukopenia was followed by leukocytosis and high enzyme activity. He died in cardiogenic shock on the third day of illness. The post-mortem examination revealed acute purulent myocarditis, and numerous group B streptococci (Strept. agalactiae) were found in the myocardium.

The rare case of pericardial effusion with starting tamponade in post-myocardial infarction syndrome (Dressler's Syndrome) is described. Diagnosis and comment: The consequential steroid therapy improves the cardial situation dramatically. There is no echocardiographic differential diagnostic criteria, but in the case of the symptoms of Dressler's Syndrome (fever, pleuritis, pneumonia, serologic changes and pericarditis) allows the diagnosis of this pericardial disease. A latent period of several weeks to some months after myocardial infarction is possible.

A 20-year-old woman, admitted to an intensive care unit in ventricular fibrillation, had marked QT prolongation in the ECG after successful defibrillation. Family study revealed ECG signs of QT prolongation, as seen in the Romano-Ward syndrome, in four generations. Syncopal attacks only occurred in the third generation, affecting four siblings. In the described patient the intraventricular ECG revealed additional depolarizations (after-potentials) during and following repolarization (ST-T) in the surface ECG. The patient died later as a result of irreversible hypoxic cerebral damage. Invasive ECG studies in the mother also revealed after-potentials. In the patient, morbid-anatomical examination revealed, in addition to fibrosis and lipomatosis around the sinus and AV nodes, focal round-cell ganglionitis in both sympathetic trunks, but predominantly on the right. These infiltrations have not previously been described in this disease and could be of significance in the pathogenesis of the prolonged QT syndrome.

The effectiveness of the calcium-antagonist Ro 11-1781 (Tiapamil) was investigated in 23 patients with extrasystoles of different origin using continuous ECG recordings. Two 24-hour ECG recordings were registered without antiarrhythmic medication, one of these as a placebo period, and 3 during oral application of 3 x 200 mg/day Ro 11-1781, if the state of the health of the patients allowed it. No positive effects of Ro 11-1781 in supraventricular and ventricular extrasystoles were demonstrable, supported by 8 premature terminations of the study. The missing antiarrhythmic effectiveness of Ro 11-1781 corresponds to Verapamil in oral application.

Lidocaine was supplied to 10 cats by 2 comparative infusions of 7.5 mg/kg respectively. Once the drug was dissolved in a physiological and the other time in a K-Mg-concentrated electrolyte solution. The sequence of both infusions alternated. Serum potassium remained constant during infusion of the physiological electrolyte solution, but increased by about 1 mEqu/1 under K-concentrated solution. Lidocaine caused an enhancement of ventricular fibrillation threshold to an absolutely identical degree in both groups. Increase in cardiac output and stroke volume and decrease of sinus rate was significant in both groups, but more pronounced under K-Mg concentrated solution. Mean arterial pressure, peripheral vascular resistance, PQ, QRS, and QT interval remained constant on the whole. We deduce from these results for antiarrhythmic therapy on normokalemic patients, that the addition of potassium and magnesium to lidocaine solution does not enhance its antifibrillatory effect. This statement is valid for doses up to 20 mEqu/h of magnesium and 40 mEqu/h of potassium.

Noninvasive and invasive diagnostic procedures permit a differentiated insight into the hypertrophic cardiomyopathies. For a better understanding of the disease, classification according to morphologic and functional criteria was introduced. It has proven useful to subdivide hypertrophic obstructive cardiomyopathy into two types: idiopathic hypertrophic subaortic stenosis and midventricular obstruction; hypertrophic nonobstructive cardiomyopathies can be subdivided into two forms designated as asymmetrical septal hypertrophy and apical hypertrophy. Combined forms can also be recognized. With a high degree of accuracy, it is possible to differentiate between hypertrophic obstructive and hypertrophic nonobstructive cardiomyopathy by means of noninvasive procedures such as clinical examination, electrocardiography, mechanocardiography and, above all, echocardiography. Experience has shown that two-dimensional echocardiography, in particular, has assumed an especially important role, the value of which approaches that of cardiac catheterization. In this overview, emphasis is placed on the diagnostic peculiarities of idiopathic hypertrophic subaortic stenosis as well as the findings in midventricular obstruction and apical hypertrophy. In the past, only relatively little attention has been focused on the latter subgroups even though they can be diagnosed with a high degree of accuracy with noninvasive as well as invasive procedures.

Tierexperimentelle Untersuchungen uber den antiarrhythmischen Effekt von Brufacain® wurden zuerst 1971 von Zetler und Strubelt, spater von uns mit der von Diederich beschriebenen Methodik zur Bestimmung der Flimmerschwelle an Katzen durchgefuhrt [3]. Auch klinische Erfahrungen mit Brufacain® liegen bereits vor [1, 2].

The aging heart differs in several aspects from the heart in younger people: Cardiac muscle mass, systolic and diastolic wall stress increase, the velocity of electrical conduction decreases in different anatomical structures. Supraventricular and ventricular arrhythmias appear more frequently than in younger people. Heart rate and cardiac index tend to diminish, especially under work load. Work capacity is reduced. In the treatment of coronary heart disease drugs are preferred which lead to a reduction of preload. Nitrates and molsidomine are followed by calcium channel blockers and--afterwards--by beta-blockers. Bypass surgery is performed in elderly patients more often for therapeutical than for prognostic reasons, similarly in the case of valvular surgery. Typical tachyarrhythmias are treated only in case of hemodynamic relevance, whereas pacemaker therapy is not limited by greater age. The choice of the most suitable pacemaker model, however, has to be based upon the overall circumstances in each individual case. For the treatment of congestive heart failure, vasodilators, especially angiotensin-converting enzyme inhibitors, seem to be superior, in elderly patients, to diuretics and digitalis glycosides.

The role of delayed potentials in ventricular arrhythmias occurring in connection with acute myocardial infarction has been of increasing interest in recent years. In order to obtain further information about delayed electrical activity, we studied a group of 51 patients in the acute phase of myocardial infarction, and intracardiac recordings were made using bipolar electrodes. In 31 of the 51 patients we recorded delayed potentials 150-200 ms after the beginning of QRS. 14 patients showed delayed electrical activity in diastole even after the T wave. The same potentials as those obtained by intracardiac recording techniques were also recorded from the body surface using a signal-averaging technique. In several cases we were able to show that these delayed potentials initiated premature ventricular beats. In 1 patient a sustained ventricular tachycardia induced by delayed potentials was recorded. We found that delayed potentials could be abolished by antiarrhythmic drugs. There thus appears to be an important relationship between delayed electrical activity and the occurrence of ventricular arrhythmias.