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In 18 out of 419 successive myocardial infarctions an increase in R-wave amplitude compared to the pre-infarction ecg had been observed. It concerned to leads III, aVF and II in posterior and inferior infarctions. The alteration of R-wave amplitude was accompanied by a dextroversion of electrical heart axis in the frontal plane. Direction of inscription of QRS loop changed in most cases. R-wave increase was demonstrated in the first ecg after the beginning of subjective symptoms and disappeared within few hours or days in general. Clinical course was rather serious in the cases described. As a pathophysiological mechanism of the phenomenon mentioned above either the influence of an injury potential upon ecg pattern or the presence of left posterior conduction defect is discussed.

Im Rahmen einer Doppelblindstudie mit niedergelassenen und Notarzten wurde die Wirkung einer vorstationaren Lidocaingabe auf Letalitat und Arrhythmiehaufigkeit bei akutem Myokardinfarkt untersucht. Anlasslich einer Zwischenanalyse, die einen signifikanten Letalitatsunterschied zwischen der Lidocain-und der Placebogruppe ergeben hatte, entzundete sich eine kontroverse Diskussion uber das weitere Vorgehen. Die Argumente fur eine Fortsetzung der Studie basierten vorwiegend auf sachlichen Uberlegungen, die Argumente fur ihren Abbruch mehr auf ethischen Bedenken. Der Abbruch wurde schliesslich durch die geringe Zahl der verbleibenden kooperationsbereiten. Arzte besiegelt.

Bei der Prufung von antiarrhythmischen Substanzen hat sich der Einsatz des His-Bundel-Elektrogramms als auserordentlich wertvoll erwiesen. Es ermoglicht eine topographische Analyse des Angriffspunktes verschiedener Antiarrhythmika. Unerwunschte Nebenwirkungen dieser Pharmaka infolge Uberdosierung konnen beim Menschen nur auf Grund einzelner klinischer Beobachtungen, z. B. bei Suizidversuchen (Larbig u. Mitarb., 1970) und gestorter Pharmakokinetik beob achtet werden.

In 27 patients presenting with angina pectoris at rest and normal serum creatine kinase (CK) activity, cardiac myosin light chains (CM-LC), myoglobin (MG), and CK-B isoenzyme were determined in 7 serial blood samples by radioimmunoassays. Measurable amounts of CM-LC were found in at least one serum sample in 13 patients. MG was found to be elevated in 9, and CK-B in 8 of these patients. In the 189 serum samples determined, CM-LC were found more frequently elevated (21.7%) than MG (13.2%, P less than 0.05) or CK-B (12.2%, P less than 0.05). Coronary angiograms were obtained in 21 of the 27 patients. Elevated marker protein concentrations were found only in patients with coronary artery stenosis greater than or equal to 70% of at least one coronary artery. The incidence of elevated serum concentrations of any of the 3 marker proteins determined was higher in patients with 3 vessel disease than in those with 1 or 2 vessel disease (33.9% vs 15.6%, P less than 0.05), and it was higher in patients with a history of previous myocardial infarction than in those without (34.5% vs 11.4%, P less than 0.001). The findings suggest that in a subgroup of patients with angina pectoris at rest but without evidence of acute myocardial infarction, ischaemic damage of small myocardial areas can be detected by serological assays of high sensitivity. Among the marker proteins studied, CM-LC were found the most sensitive.

A coronary artery-to-left ventricular fistula is a rare finding; to the best of our knowledge, a total of only 35 cases have been reported. Only 5 cases of a generalized arterio-systemic fistula with three vessel involvement have been reported in the literature. We describe another case involving all major coronary arteries. A review of the literature is presented and the data of the reported cases are analyzed. A 55 year old woman was examined because of recurrent chest pain which had persisted for 2 years. On physical examination, the only abnormal finding was a fourth heart sound. Exertional chest pain, a positive exercise stress test, and the results of a lactate extraction study suggested severe myocardial ischemia. Thallium myocardial scintigraphy showed no evidence of a perfusion defect. Cardiac catheterization revealed an irregular left ventricular endocardial pattern (Thebesian veins). Selective coronary angiography showed communicating fistulae of all three major coronary arteries with the left ventricular cavity. We assume that this vascular anomaly causes a coronary steal phenomenon and subsequent myocardial ischemia.

The kinetics of cytosolic and structural marker protein release from myocardium were studied in 44 patients with acute myocardial infarction. After intracoronary infusion of streptokinase, there was early recanalization of the infarct-related artery in 8 patients and late recanalization in 18. In 18 patients the infarct-related artery remained occluded. Creatine kinase (CK) level peaked and normalized significantly earlier in patients with early reperfusion than in patients with late reperfusion, and in patients with late reperfusion earlier than in patients with permanent occlusion. Thus, the interval of absolute diagnostic sensitivity of CK depends on early infarct perfusion. In contrast, release of myosin light chains was not significantly changed by recanalization of the infarct-related artery compared with that in nonreperfused myocardial infarction. Thus, in patients with acute myocardial infarction, myosin light chains may be superior to CK as a diagnostic means and for estimation of infarct size.

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 end diastolic pressure, global and regional ejection fraction were measured immediately and 3 weeks after admission. Particularly 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.

The left ventricular (LV) cineangiograms of ten patients with apical hypertrophy (AH, group I) as a form of hypertrophic nonobstructive cardiomyopathy (HNCM) were analyzed. The left ventricular ejection dynamics, the extent and pattern of left ventricular contraction were compared with eight patients with secondary myocardial hypertrophy due to arterial hypertension (group II) and eight normal subjects (group III). End-diastolic, end-systolic and stroke volumes were significantly lower in group I. The analysis of left ventricular ejection dynamics with frame-by-frame-analysis revealed the typical ejection pattern of hypertrophic nonobstructive cardiomyopathy: Left ventricular ejection was completed within two thirds of the systolic ejection period. This ejection pattern is of diagnostic value when compared with the dynamics in group II. Although the apical segment in group I shows a good fiber shortening, the overall contribution to systolic performance is low; systolic function in apical hypertrophy is maintained by a compensatory increase in regional wall motion of the basal and midzonal part of the left ventricular free wall. There is no striking difference between apical hypertrophy with and without giant negative T waves with respect to the ejection pattern. Within these subgroups, the only difference was the greater left ventricular mass in patients with giant T wave inversion. Thus, the ejection dynamics in apical hypertrophy is typical of hypertrophic nonobstructive cardiomyopathy. Global parameters of systolic left ventricular performance revealed supernormal values even though systolic function is impaired. Segmental analysis of ejection phase was most sensitive in establishing the diagnosis.

To detect myocardial cell damage, serum samples of 42 consecutive patients with angina at rest were screened for cardiac myosin light chains, which were detected in 22 patients (52%). In 17 of these patients there was a persistent release of myosin light chains lasting until the 4th hospital day, whereas in 7 patients myosin light chains were only detectable during the initial 24 h after admission. The presence of myosin light chains correlated with signs of ischemia in the electrocardiogram (ECG) (p less than 0.05) and with the extent of coronary artery narrowing (p less than 0.05). Cardiac myosin light chains were elevated in serum only if there was a greater than or equal to 75% diameter narrowing in at least one major vessel. In all five patients who developed transmural myocardial infarction during the course of their hospital stay, myosin light chains were detectable greater than or equal to 28 h before the diagnosis of myocardial infarction could be established by ECG criteria and conventional serum enzymes. Thus the detection of circulating cardiac myosin light chains enables one to identify a subgroup of patients with angina at rest having more severe coronary artery disease with a worse outcome.

Hypertrophic cardiomyopathy (HCM) has various manifestations with respect to the localization of the hypertrophy. In this study we report clinical, electrocardiographic (ECG), echocardiographic (echo), and hemodynamic findings in midventricular obstruction (MO), an uncommon form of hypertrophic obstructive cardiomyopathy (HOCM) in 9 patients. The prevalence of systolic anterior motion of anterior mitral leaflet (SAM) in MO, an echocardiographic diagnostic hallmark in HOCM, was another purpose of this study. All patients had complete clinical, ECG, echo, and hemodynamic workup, including left ventricular (in 4 patients simultaneous biventricular, SBVA) and coronary angiograms. All patients had dyspnea and palpitations, chest pain, 2 had syncope. In the ECG, atrial fibrillation was present in 2, and left ventricular hypertrophy in 9 patients. Septal and left ventricular free wall thickening was significantly present in all patients in echo, and SAM in 1 patient. The intraventricular gradient (IVG) was 40-176 mmHg, in 1 case 40 mmHg by provocation, Brockenbrough was positive in all patients. Two patients had right ventricular IVG. A positive beta-blocking agent effect was present in 6 cases. The best localization of the obstruction was possible with SBVA and 2D-echo. We conclude that MO has all the signs of HOCM, but SAM in echocardiography is uncommon. SAM is occasionally present and is not a necessary factor to produce an intraventricular pressure gradient in HOCM, especially in MO. It seems that hypertrophic right ventricular obstruction is relatively common in MO (2 of 9 cases), and may have the same obstructive mechanism.

Erste klinische Untersuchungen von Bauch u. Mitarb. (1973) uber eine antiarrhythmische Wirkung des Lokalanaesthetikums Brufacain® hatten positive Effekte ausschlieslich bei ventrikularen Ektopien gezeigt. Der klinischen Erprobung waren tierexperimentelle Untersuchungen vorausgegangen, welche u. a. eine Verlangerung der Refraktarzeit an Meerschweinchenvorhofen, einen antagonistischen Effekt auf aconitininduzierte Arrhythmien bei Ratten (Zetler u. Strubelt, 1971) sowie eine Anhebung der ventrikularen Flimmerschwelle bei Katzen (Djonlagic, 1974) erkennen liesen. Siegers u. Mitarb. (1974) haben an Ratten bei einem Vergleich von Lidocain, Procainamid und Brufacain® im oralen Versuch eine Uberlegenheit von Brufacain® gegen aconitininduzierte Arrhythmien nachgewiesen. Die Halbwertzeit von Brufacain® war deutlich langer, als sie fur Lidocain und Procainamid angegeben wird. Die Ursache fur die unterschiedlich lange Wirkdauer wird in der chemischen Struktur von Brufacain® gesehen.

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 influence of 3-(2-diethylaminoethyl)-4-methyl-7-(carbethoxy-methoxy)-2-oxo-1,2-chromene-hydr ochloride (carbocromen, Intensaïn) on A-V-conduction and refractory period was studied by means of His-bundle-electrography on 12 anaesthetized cats. Immediately after application of carbocromen 6 mg/kg the A-H-conduction time was increased. In contrast to this, 12 mg/kg carbocromen caused significant prolongation of H-v interval. This study shows that carbocromen has effects on intraventricular conduction.

After the loss of membrane integrity cardiospecific myosin light chains are released as a result of proteolytic degradation of the insoluble myosin pool. Thus, as with cytosolic enzymes, the measurement of the serum concentration changes of myosin light chains may allow a non-invasive estimation of infarct size. A two compartment model was used to describe the serum concentration changes of myosin light chains after a bolus injection into awake beagle dogs. The initial distribution volume was 7.4% of body weight, whereas the second compartment accounted for 4.7% of body weight. The fractional disappearance rate of 0.0092.min-1 resulted in a serum half life of myosin light chains of 75 min. In 30 patients with acute non-reperfused myocardial infarction a close correlation was found between the cumulative appearance of myosin light chains and their maximal serum concentration. In these patients the cumulative appearance of myosin light chains correlated with serum creatine kinase estimates of infarct size, with impairment of left ventricular ejection fraction, and with mortality during hospital admission. Thus the maximal serum concentration and the cumulative appearance of myosin light chains allow a non-invasive estimation of infarct size and may serve as a serological indicator of the patient's prognosis.

In a double blind study performed in cooperation with 69 emergency doctors and general practitioners in the catchment areas of the university and of the city hospital in Lübeck the action of intramuscular lidocaine on mortality and on the incidence of arrhythmias was investigated in patients with acute myocardial infarction aged less than 70 years. The mortality in the lidocaine group was significantly lower than in the placebo group. The incidence of ventricular arrhythmias up to 120 minutes after the lidocaine injection was also lower than in the placebo group. However, the only case of primary ventricular fibrillation was in the lidocaine group. As the difference in mortality between the two groups appeared at a time when an antifibrillatory action of lidocaine can no longer be assumed one must question whether the positively beneficial effect was real or whether the lower mortality was in fact due to primarily milder disease in the lidocaine group.

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.

Plasma levels of lidocaine were determined in either 10 patients following injection into the deltoid and lateral vastus muscle, respectively. We used an automatic injector containing 250 mg of lidocaine in a 10% solution. In the early phase after injection, plasma levels were higher, when the deltoid muscle had been chosen for administration. This was the same result as referred by other authors using normal injectors. Variance of single plasma values was smaller in the vastus group.

Bei Patienten mit frequenzstarren elektrischen Pacemakern schlagen Vorhofe und Kammern normalerweise unabhangig voneinander. Die Ventrikel werden vom kunstlichen Schrittmacher, die Vorhofe vom Sinusknoten aus erregt. Eine retrograde Erregungsleitung vom Reizort im Ventrikel auf die Vorhofe kommt vor, ist aber selten.