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The ectopic atrial tachycardia is diagnosed in approx. 10 to 15% of supraventricular tachycardias. Since medical therapy is often shown to be ineffective, ablative procedures became especially important in this disease. Localization of the arrhythmia foci seems to be concentrated at anatomical preformations like the crista terminalis, right or left atrial appendage orifice or at the superior pulmonary veins. The P-wave vector in the surface ECG is predictive for focus localization: a positive or biphasic P-wave in a VL for right atrial foci, a positive P-wave in V1 for left atrial foci. Catheter ablation therapy is also shown to be very effective in this kind of supraventricular tachycardia.

For registration of delayed depolarizations 50 healthy persons (age: 49.4 +/- 6.2 years) and 43 patients with bundle-branch block (age: 65.1 +/- 11.8 years; 23 of them with right and 20 with left bundle-branch block) underwent high-resolution electrocardiography at the body surface using signal-averaging technique. The findings were compared with results obtained in the 24-hour long-term ECG. In 2 normal persons (4%), delayed depolarizations were recorded whose configuration, however, differed from that of pathological findings in patients with coronary heart disease. 2 other subjects evidenced repetitive ventricular arrhythmias. Detection of delayed depolarizations in patients with coronary heart disease is indicative of an increased risk of malignant or even fatal arrhythmias. The low prevalence in healthy subjects underlines the specificity of this finding and represents the prerequisite for identifying patients with an increased risk. Delayed depolarizations were found also in 3 patients with right and 4 patients with left bundle-branch block (16.3% in all). 8 patients had repetitive ventricular arrhythmias, and one of them with a left bundle-branch block also revealed delayed depolarizations. Thus delayed depolarizations can be registered in some patients with intraventricular conduction defects. The incidence rate corresponds to that found in patients with coronary heart disease, so that detection of delayed depolarizations in this patient group is not helpful in the assessment of prognosis.

In 11 patients (9 men, 2 women) with angiographically confirmed coronary heart disease, hemodynamics, myocardial blood flow, oxygen consumption and lactate extraction were measured at rest before and after administration of 0.3 mg diltiazem per kg body weight. There was a prompt and sustained drop in mean systolic arterial pressure from 141 mm Hg to 127 mm Hg along with a reduction in total peripheral resistance. The filling pressure of the left ventricle remained constant following a post-injection rise lasting up to 5 minutes. A marked sustained drop in heart rate from 82/min to 73/min was registered. Concomitantly, stroke volume index rose from 39 to 49 ml/m2. Due to the decrease in load and frequency, contractility parameters dP/dt and dP/dt/P dropped slightly. Myocardial blood flow did not change. On the other hand, a decrease in the difference between arterial and coronary venous oxygen content indicated a coronary dilatory effect. Fifteen minutes after injection, myocardial oxygen consumption had dropped from 11.6 to 10 ml O2/min and 100 g of tissue. There was no substantial change in lactate extraction. Through a drop in peripheral arterial resistance and heart rate, diltiazem leads to a measurable decrease in myocardial oxygen consumption while the patient is still at rest. At the same time, there are indications of a coronary dilatory effect.

Within 6 hours after the onset of acute myocardial infarction, 93 patients received a brief high-dose intravenous infusion of streptokinase, 49 patients received 500,000 IU within 30 min and 44 patients received 1,500,000 IU within 60 min. 26 patients had angiography in the acute phase, after 24 hours, and in the 4th week; 52 patients had angiography in the 4th week only; and 15 had no angiography. 7 patients died in hospital and 6 suffered a nonfatal reinfarction. There were no complications with bleeding. In 52% of cases, reopening of an occluded infarct vessel was achieved within 1 hour of the beginning of treatment. During the 4th week after infarction a patent infarct vessel was found in 84%, and 58% had a residual stenosis less than 70%. In contrast, in a control group that received no streptokinase treatment, 25% had a patent infarct vessel and 4% had a residual stenosis less than 70%. Indicative for salvage of ischemic myocardium are a significant improvement in local contraction disorders between the acute phase and the 4th week and a significant correlation between infarct size in the 4th week and beginning of treatment after onset of symptoms. 1. It may be concluded that: brief intravenous infusion of streptokinase results in restoration of blood flow in an infarcted coronary artery in a high percentage of cases; the shorter thrombus-lysis time with intracoronary streptokinase infusion could be made up for by the earlier initiation of intravenous streptokinase treatment; and a conclusive randomized trial is needed to ascertain the true impact of a brief high-dose intravenous infusion of streptokinase on mortality and morbidity following acute myocardial infarction.

In 20 infarct patients, whose age varies from 43 to 78 years (m 59.6), continuous hemodynamic measurements were made to determine the cardiovascular effects of propranolol without and during a simultaneous infusion treatment with nitroglycerin. In cases of compensated ventricular function and pulmonary wedged pressures of 15 mm Hg or less (N = 10), a mean intravenous propranolol dose of 6.1 +/- 1.3 mg led to a significant reduction of the LVSWI and a simultaneous increase of the PCP by 31% of the control value (P less than or equal to 0.005). A simultaneously performed infusion treatment with nitroglycerin at a mean dose of 3.0 +/- 1.6 mg/h resulted in totally cutting off the propranolol-induced PCP increase, whereas a decrease of the heart rate and the LVSWI due to a beta-receptor-blockade remained completely unchanged. In the case of pre-existing congestion insufficiency of the left ventricle (N = 10) and of a pulmonary wedged pressure of above 15 mm Hg, the administration of a mean dose of propranolol of 5.8 +/- 1.1 mg for protection of the myocardium resulted in a partly disquieting decrease of the volume of cardiac output (P less than or equal to 0.005) which was 28% of the control value for the CI an 12% for the SVI. Correspondingly the left ventricular stroke work decreased to 18%. Nitroglycerin has a reducing influence on these changes, but not down to the initial level. In cases of sufficient ventricular function, propranolol has a favorable influence on the myocardial O2-metabolism via its depressor effect on heart rate and contractility. By means of nitroglycerin, an increase of the pulmonary wedged pressure occurring under this condition can be inhibited. However, in the case of a pre-existing congestion insufficiency, propranolol can lead to a partly disquieting depression of the circulation, which, apart from the hemodynamic risks, makes a rather unfavorable influence on the myocardial O2-metabolism seem likely.

The acute hemodynamic effects of the Ca-antagonist Diltiazem were measured in the course of diagnostic cardiac catheter examinations in 10 patients with coronary heart disease. After initial step-wise ergometric stress, Diltiazem (D) was applied intravenously for 5 min at a dose of 0.3 mg/kg. The effects on right and left ventricular performance as well as on arterial pressure and heart rate were registered 1, 3, 5, 10 and 15 min after termination of the infusion. Then, a second period of ergometric exertion under identical stress conditions was performed. The results under resting conditions show that D effects a significant increase in left ventricular filling pressure (p greater than 0.005), which, however, only lasts a few minutes. After D, the systolic and mean arterial pressure decreases significantly (p greater than 0.001); there is no reflex-induced increase in the heart rate, which on the contrary is significantly lower (p greater than 0.005) 15 min after termination of the infusion than the initial value. The stroke volume index increases from 40 to maximally 48 ml/m2 after D. Comparison of the hemodynamic parameters under ergometric stress before and 20 min after D shows that, on termination of stress, the filling pressure of the left ventricle is reduced. This behavior can largely be attributed to the reduction of the systolic pressure after D (maximal value before D 181, after D 167 mm Hg). Also, the stress-induced increase in the heart rate takes a flatter course after D than before it. The results obtained thus provide evidence that, at a dosage of 0.3 mg/kg, D has no significant negative inotropic effect and probably leads to a decrease of the myocardial oxygen consumption reducing the systolic pressure and, to a lesser degree, heart rate.

In the acute stage of transmural myocardial infarction, 22 patients ranging in age from 34 to 76 (mean 61.6) were given propranolol- because of its alleged myocardium-protecting properties - intravenously at a dosage of 0.03 to 0.1 mg/kg body weight under conditions of continuous hemodynamic control. Subsequently, the influence of digoxin, administered i. v. at a dosage of 0.01 my/kg body weight, on the negative-inotropic propranolol effects was examined. A hemodynamic comparison was made of the effects of propranolol before and after digitalis administration. In patients with compensated cardiac function (group 1, 16 patients), the propranolol-induced drop in the left ventricular stroke-work-index and rise in the left-ventricular filling pressure was completely compensated again by digitalis. The frequency-decreasing propranolol effect was nor influenced by digitalis. In patients with cardiac decompensation (group 2, 6 patients) digitalis only led to a renewed compensation of the left-ventricular stroke-work-index, the rise of the left-ventricular filling pressure remained unaffected. It follows from that, in cases of myocardial infarction without cardial decompensation, propranolol requires concomitant digitalisation. In cases of already existent myocardial insufficiency, propranolol can produce an unfavorable increase of the decompensation signs.