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The effects of verapamil on the [K+]o rise produced by myocardial ischaemia were assessed in 26 open chest mongrel dogs. Ischaemia was produced by intermittent occlusion of the LAD artery (15 dogs) or by reduction of flow of the cannulated LAD (11 dogs). Specially constructed valinomycin K+ sensitive electrodes were inserted into the mid myocardium in the central zone of ischaemia (CZ); in the margin (MZ) and in the nonischaemic zone (NZ). Occlusion of the coronary artery under controlled conditions produced significant [K+]o rise, greater in the CZ than in the MZ. During the infusion of verapamil the ischaemic [K+]o rise was substantially reduced in both zones. During controlled 75% reduction of coronary flow the [K+]o reached a plateau that remained stable until reperfusion was re-established. During verapamil infusion, the plateau showed a steady decline, both in the CZ and in the MZ. The changes in [K+]o produced by verapamil, during myocardial ischaemia are probably due to: coronary dilatation of the marginal arteries and+or to a reduction of the late cellular K+ conductance due to a decrease in the intracellular Ca2+, produced by verapamil.

The heart rate can be controlled by an electrical pacemaker when its frequency of stimulation is greater than that inherent in the heart. 1 " 3 However, no method has been described, to our knowledge, by which a rapidly beating heart may be slowed by means of repetitive electrical impulses applied to the heart. The commercial pacemakers available for clinical application generate d-c electrical impulses with a duration of about 3 msec. Although the voltage and frequency of the impulses can be changed within certain limits, the duration of the impulses is kept constant. 2 " 4 While studying the control of heart rate in dogs by means of an intracardiac electrical pacemaker, we found that the frequency of effective ventricular contractions, namely those that produced an arterial pulse or at least a clearly visible ventricular pulse, could be reduced by almost 50% by increasing appropriately the duration of the electrical impulse of the artificial pacemaker. It was soon determined that this effect was due to proper spacing between the make and break of the repetitive impulses. Electrotonus was not involved in the change of ventricular rate. This decrease of the frequency of effective ventricular contractions could be reproduced with pairs of impulses, each 3 msec in duration, when the two impulses of the pair were properly spaced. A decrease in ventricular frequency could also be induced when the interval between break and make of successive long impulses fell in an appropriate range; in which case it was the break that became the first and the make the second stimulus-just the reverse of the usual sequence when long impulses were used.This finding was subjected to repeated tests in dogs with sinus rhythm and in several animals with experimentally produced arrhythmias. It was studied also in one patient with Stokes-Adams attacks due to intermittent A-V block, who had an intracardiac electrode catheter introduced to pace the heart. Our observations and a discussion of the mechanisms by which this reduction of heart rate is produced are the subjects of this communication. I. Ventricular Stimulation MethodsThirteen dogs, weighing 18 to 23 kg and anesthetized with pentobarbital (20 to 25 mg/kg iv), were used for these experiments. Unipolar right atrial intracavitary electrocardiograms (RA ECG), right atrial (RA), and right (RV) and left ventricular (LV) pressures were recorded simultaneously by catheters. The catheters in the right atrium and ventricle were introduced via the jugular vein; the one in the left ventricle was introduced via a femoral artery. A thoracotomy was performed after the catheters were in place and intermittent positive pressure breathing was maintained throughout the entire procedure. A pericardiotomy was then done and a pair of platinum electrodes was hooked into the free wall of the right ventricle for stimulation by the artificial pacemaker. In some dogs the left atrium (LA) was cannulated after the chest had been opened and left atrial pressure was also recorded.Electrocardiograms and pressures...

The hemodynamic and angiographic data of 147 individuals were analyzed in an attempt to assess the value of three techniques used in the diagnosis of mitral incompetence. One hundred patients had clinical evidence of mitral incompetence (group A) and 47 had normal hemodynamics (group B). The degree of mitral incompetence was assessed in all 147 individuals by two methods: determination of a regurgitant index (RI) using indicator dilution curves and determination of a regurgitant fraction (RF) using left ventricular volumes. In 26 patients of group A and 26 individuals in group B mitral incompetence was also assessed by cineangiocardiography. Each of these methods was compared with the clinical and hemodynamic evidence of mitral valvular incompetence. Both the determination of RI by dye dilution curves and RF by angiocardiography were found to be useful in separating normal individuals from patients with mitral valvular incompetence. Severe mitral incompetence is associated with an RI greater than 35% and with an RF greater than 55%. The degree of incompetence by either method was not well correlated with any independent hemodynamic variable. The use of cine angiocardiography to quantify the degree of mitral incompetence was found to be too subjective, depending on the observer, and thus less useful.

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