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SUMMARY We divised a method to determine tissue osmolality in intact beating hearts. After occlusion of the left anterior descending coronary artery (LAD) of isolated porcine hearts, tissue osmolality in the ischemic myocardium increased within 50 minutes by about 40 mOsm/kg. This rise in osmolality could be accounted for by metabolic processes, notably the conversion of glycogen into lactate, and the hydrolysis of high energy phosphates. Concomitant with the rise in osmolality, the ischemic myocardium during the 1-hour period of LAD occlusion took up fluid and increased tistue water volume by an average of 16.5%. We demonstrated that the osmolality of fixatives used for morphological studies markedly influences ischemic cell morphology. Thus, normotonic fixation of the ischemic myocardium accentuates cell swelling, whereas nearly normal cell volumes result from hypertonic fixation, adjusted according to the rise hi ischemic tissue osmolality. Normotonic reperfusion of the ischemic area after 1 hour of LAD occlusion resulted in the "no-refiow" phenomenon in the mldmural and subendocardial regions. Epicardial and intramural DC-electrograms showed persistent ischemic changes, i.e., T-Q depression, S-T elevation, and monophasic potentials. Tissue resistivity, which during ischemia had risen twofold, remained high. Lacate levels remained high, creatinephosphate (CP) and adenosinetriphosphate (ATP) levels remained low. Selective hypertonic reperfusion of the LAD, followed by a gradual return to normotonic perfnsion, resulted in a normalization of DC extracellular elcctrograms, restoration of electrical resistivity to near normal, low levels of lactate, and higher levels of CP and ATP although control values were not reached. Cell morphology was correspondingly normalized following this procedure. We conclude that ischemic cells become hyperosmotic and consequently take up additional fluid when exposed to normotonic blood. This increased cell swelling compresses capillaries, prevents reperfusion, and may be a major factor in causing reperfusion damage. This damage can be prevented to a large extent by selective hypertonic reperfusion. Circ Res 49: 364-381, 1881

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SUMMARY Paroxysms of ventricular tachycardia in which the amplitude and the direction of QRS complexes change periodically are defined as "torsade de pointes" tachycardias. The mechanism of this atypical ventricular arrhythmia has not yet been elucidated. The aim of our study was to induce "torsade de pointes" tachycardia experimentally, in order to gain insight into its possible mechanism. The experiments were carried out with isolated porcine hearts, perfused by the Langendorff technique. Epicardial electrocardiograms were recorded by unipolar leads. The specific pattern of "torsade de pointes" tachycardia could be induced by stimulation of the right and left ventricles in phase. From our experimental observations we conclude that a possible cause of "torsade de pointes" tachycardia is the interaction of two ectopic ventricular foci.Rapid ventricular tachycardias, with periodic change of amplitude and direction of the QRS complexes, are defined as "torsade de pointes" tachycardias.1 A detailed description of this serious arrhythmia has been given by Dessertenne,2 who also created the term "torsade de pointes" (twisted tips). The precise mechanism of this atypical ventricular arrhythmia has not been completely clarified. Prolongation of the QT interval and inhomogeneous repolarisation of neighbouring areas of the myocardium are believed to be of major importance for its genesis.' I "Torsade de pointes" has been recognised during hypokalaemia,F6 hypomagnesaemia,78 acute ischaemia,9 myocardial infarction,'0 myocarditis,' during the use of various antiarrhythmic agents, for example quinidine," I lignocaine,' mexiletine,'2 disopyramide,'3 14 and could be initiated by electrical ventricular stimulation.'5 Thus, aetiology of this rhythm disorder is diverse; its characteristic electrocardiographic appearance, however, suggests a specific mechanism. The aim of our study was to induce "torsade de pointes" tachycardias experimentally in order to gain insight into its possible mechanism. MethodsThe experiments were carried out in isolated pig hearts (n=7). The animals (weight 20±1 kg) were Supported by Deutsche Forschungsgemeinschaft. Accepted for publication 8 April 1982 anaesthetised by intravenous injection of sodium pentobarbitone (15 mg/kg). After intubation and artificial respiration the thorax was opened by a midsternal incision and the heart was rapidly removed and fixed to a heart lung machine where it was perfused with the blood of the same pig using the Langendorff technique. 16 The temperature was 37°C, and the coronary flow was set at 200 m/min. The hearts were paced electrically from the epicardium with two independent stimulation generators at one and a half times the diastolic threshold. Unipolar electrocardiograms were recorded by means of non polarisable cotton wick electrodes from the epicardium and were recorded on an Elema ink writer (Fig. 1). ResultsIf paced from the right ventricle the electrocardiogram recorded within the area of the left anterior descending artery showed a positive deflection (...

Several metabolic factors have been regarded as a cause of ventricular tachyarrhythmias in cardiac ischemia, i.e. hypoxia, acidosis, intracellular potassium loss, local catecholamine release as well as an increased catecholamine concentration and an evaluation of serum free fatty acids. The arrhythmogenic properties of anoxia and hypoxic acidosis, catecholamines as well as potassium depletion are well known. However, the relationship between elevated free fatty acids concentration and the occurrence of ventricular arrhythmias remain obscure. The micro-electrode technique was applied to examine the electrophysiological effects of free fatty acids in papillary heart muscle fibres. Both linoleate and palmitate cause a concentration-dependent decrease of action potential duration and a corresponding shortening of the functional refractory period in the presence of sufficient oxygen supply. The results suggest that a high concentration of free fatty acids may play an additional role in the genesis of ventricular tachyarrhythmias in cardiac ischemia.

A recently developed antitachycardic pacemaker was implanted into seven patients with drug-resistant tachycardias. The implantation was made after diagnosis of a tachy-arrhythmia by invasive techniques and after experimental determination of the effective site, optimal mode and effective frequency of stimulation, as well as the regulation and duration of impulse release. Thus the pacemakers were individually adapted to the particular arrhythmia. High-frequency stimulation and competitive stimulation were used as stimulation modes. The systems work automatically, triggered either by the ECG, the patient or externally. The frequency of attacks was significantly reduced in five patients, the duration of attacks in all.

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