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Ventricularization of pressure during coronary angiography has been said to identify the presence of left main coronary artery disease, but the hemodynamic features and the mechanism of this process have not been studied. Twenty consecutive patients with ventricularization were identified prospectively in our laboratory. Four patients had a discrete ostial left main stenosis and 16 patients had stenosis of the entire length of the left main coronary artery. The degree of pressure drop upon cannulation of the diseased left main coronary artery was highly variable; the systolic pressure decreased by 9 to 94 mm Hg, and the diastolic pressure decreased by 6 to 60 mm Hg. The morphology of the ventricularized pressure was distinct. It had a presystolic deflection resembling an a wave. The upstroke of this waveform was slower and the downstroke was steeper than that of the aortic pressure. An identical waveform was observed in dogs after partial occlusion of the left main coronary artery with a balloon-tipped catheter. The waveform of the so-called ventricularized pressure is derived from the aortic pressure, which is altered by its transmission across the left main coronary stenosis. The appearance of ventricularization is an important clue to the presence of left main coronary artery disease.

Electrocardiographic changes induced by ionic contrast media can cause complications during coronary angiography. A conduction delay through various parts of the heart is one factor in the genesis of asystole or ventricular fibrillation. Hypaque-76 (H76) and Renografin-76 (R76) are nearly identical ionic contrast media except that R76 binds more calcium than H76 because of the presence of sodium citrate and EDTA in R76. To determine whether the calcium binding additives in ionic contrast media contribute to the cardiac conduction abnormalities, we examined conduction time through the atrioventricular (AV) nodal tissue (via bipolar His bundle electrograms) and through the distal part of the conduction system (recording the QRS complex from the ECG) during coronary angiography. We injected 10 mL of H76 and R76 in 19 closed chest dogs in a blinded, randomized fashion during coronary angiography. The effects of H76 and R76 on heart rate, AH interval, HV interval, V interval and PR interval, and QRS complex duration were recorded. In 14 nonatrial pacing dogs, compared with H76, R76 produced a greater increase in the AV interval (32.9 +/- 6 milliseconds vs 12.4 +/- 2 milliseconds, P less than .01) and the PR interval (29.6 +/- 6 milliseconds vs 11.9 +/- 4 milliseconds, P less than .02). Additionally, the heart rate decreased 13.9 +/- 3.5 beats/minute from control with R76 compared with a decrease of 4.2 +/- 2.6 beats/minute from control with H76 (P less than .05). There was no significant difference between the prolongation of the HV interval and V interval, or QRS complex duration generated by R76 and H76.(ABSTRACT TRUNCATED AT 250 WORDS)

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.

Coronary angiography occasionally results in ventricular fibrillation. To compare the fibrillatory propensity of conventional ionic and nonionic contrast media, we measured QT intervals and performed programmed electrical stimulation during intracoronary injection of Renografin 76 (R76), Hypaque 76 (H76), and iopamidol (IOP) in 16 open chest dogs. In ten dogs the incidence of ventricular fibrillation following induction of a single premature ventricular beat after every fourth atrial paced beat was 19/20 with R76, 8/20 with H76, and 0/20 with IOP (P less than .001). When two premature beats were induced, the incidence of ventricular fibrillation was 20/20 with R76, 19/20 with H76, and 1/20 with IOP (P less than .001). In six additional dogs, the mean prolongation of the QT interval was 170 +/- 20 msec with R76, 105 +/- 14 msec with H76, and 63 +/- 9 msec with IOP (P less than .001). Thus, programmed electrical stimulation readily induces ventricular fibrillation during intracoronary injection of conventional ionic contrast media. The incidence of ventricular fibrillation parallels the amount of QT interval prolongation produced. H76, which lacks EDTA and sodium citrate, is less fibrillatory than R76. However, the nonionic medium IOP appears far less fibrillatory than either R76 or H76.

The Loyola Open-Heart Registry is a fully operational database that has hundreds of programs designed to input, modify, verify, maintain, update and analyze its raw data. It contains retrospectively collected data on approximately 4000 patients who underwent coronary bypass (CABG) or cardiac valve replacement (CVR) from January 1970 to May 1981. Since 1981 we have collected detailed information on approximately 1300 patients per year. The system is described in clinical and technical terms. The means of data acquisition and input are described and a flow chart for the collection of data is provided. The system's hardware is described briefly, and the nature and limitations of the software are discussed. Specific datasheets are described, and examples of output retrievals are provided. A few comments are made regarding the administrative aspects of database management. The entire paper is summarized, and our future plans and areas of development are described.

The effects of orally administered indomethacin or placebo on coronary hemodynamics were studied in 23 patients with coronary artery disease. After indomethacin administration the systemic arterial pressure increased by 12 +/- 4% and the myocardial oxygen consumption by 24 +/- 11%. Coronary sinus flow did not change and coronary vascular resistance increased slightly. Oxygen saturation of the arterial blood did not change, but coronary sinus saturation decreased substantially. Hemodynamic values returned to normal 150 minutes after administration of indomethacin. During rapid atrial pacing, coronary sinus flow increased 79 +/- 14% above the rest value when pacing was done before indomethacin administration; only a 56 +/- 12% increase was seen when pacing was repeated after indomethacin. Peak heart rate achieved during atrial pacing, severity of angina and the degree of ST-segment depression were not altered by indomethacin treatment. Orally administered indomethacin has a mild coronary vasoconstrictive effect that does not interfere substantially with the expected increase in myocardial blood flow during rapid atrial pacing. Anginal threshold is not altered by orally administered indomethacin.

Unlabelled: We studied 58 consecutive patients, ages 37 to 78, who were given intravenous streptokinase (IV STK) early in the course of acute myocardial infarction (AMI) in three community hospitals served by the same mobile intensive care system. Forty-four patients (76%) received IV STK within 3 hours and 53 patients (92%) received it within 4 hours of onset of chest pain. Half the patients were brought to the hospital by paramedics. The average time from pain to administration of IV STK for paramedic patients was 100 minutes vs 198 minutes for those brought by other modes. Fifty of 58 patients (86%) showed clinical evidence of reperfusion. Forty-six of 54 patients (85%) studied with coronary angiography an average of 6 days post infarction had patent vessels subtending the infarcted region of the myocardium. The average angiographic ejection fraction was 47% for patients with reperfused vessels vs 34% for those with occluded vessels. The in-hospital mortality was 2 of 58 patients (3.4%). There was one late death at 8 months (total 5.2%). Twenty-one patients eventually had coronary bypass surgery and 5 patients had angioplasty. The remaining 29 patients had conventional therapy including 6 months of warfarin sodium. Fifty-four of 55 surviving patients (98%) are in functional class I or II and none have angina at 2 to 18 months of follow-up. Fifty-one of 55 patients are back at work., Conclusions: (1) IV STK is effective in coronary thrombolysis in a high percentage of AMI patients. (2) IV STK is safely administered in community hospitals.(ABSTRACT TRUNCATED AT 250 WORDS)

To examine the role of adrenergic influences on genesis of ischemic and reperfusion arrhythmias, the left anterior descending coronary artery (LAD) was cannulated and perfused by a shunt from the left carotid artery in 38 open-chest pentobarbital-anesthetized dogs. Ischemia was produced by shunt occlusion and retrograde diversion of collateral flow from the LAD. The diverted blood was collected and returned to the animal by intravenous (i.v.) injection. The shunt was opened and the ischemic myocardium reperfused after 30 min of ischemia. Microsphere injections in six dogs during shunt occlusion and retrograde bleeding showed that blood flow to the ischemic zone was less than 1.5% of normal zone flow. The remaining 32 dogs were randomized into four treatment groups. Dogs (n = 8) were treated before shunt occlusion with either saline, nadolol (1 mg/kg), prazosin (0.2 mg/kg), or bilateral stellate transection. As compared with saline treatment, nadolol and stellate transection significantly reduced heart rate (HR), and prazosin significantly reduced mean arterial blood pressure (MAP) (p less than 0.05). However, none of the antiadrenergic interventions significantly reduced the number or frequency of ectopic beats during either the 1a or 1b phases of ischemia. None of the 32 dogs developed ventricular fibrillation (VF) during ischemia, but all dogs fibrillated within 30 s of reperfusion. The size of the ischemic zone ranged from 21 to 38% of the left ventricle, and there were no differences among the four treatment groups. The results suggest that when ischemia is severe, the adrenergic nervous system does not play a significant role in genesis of ischemic-induced ectopy or reperfusion-induced VF.

The intracoronary injection of contrast media during coronary angiography occasionally results in ventricular fibrillation. Experimental studies have implicated the calcium sequestering agents, sodium citrate and EDTA in Renografin 76 (RG76), as contributing to this complication. Angiovist 370 (AV370) is a contrast medium similar to RG76 except that it contains disodium calcium EDTA instead of EDTA and sodium citrate. To determine if contrast media lacking sodium citrate and EDTA will result in a lower incidence of ventricular fibrillation in man, this investigation compared the incidence of contrast media-induced ventricular fibrillation in patients undergoing coronary angiography with RG76 to that with AV370. Group A consisted of 2,500 consecutive patients undergoing coronary angiography with RG76 and group B consisted of 2,000 subsequent consecutive patients in whom AV370 was employed as the contrast medium. There was no significant difference between groups A and B with respect to the volume of contrast media used per patient (153 +/- 49 ml vs 154 +/- 45ml), age (58.4 +/- 10 vs 58.6 +/- 10 years), sex (70% male vs 70% male), ejection fraction (59 +/- 17 vs 60 +/- 20), history of mitral valve disease (5.8% vs 7.1%), history of aortic valve disease (6.7% vs 6.5%), prior coronary artery bypass graft surgery (6.6% vs 7.3%), or extent of coronary artery disease. Fifteen episodes of contrast media-induced ventricular fibrillation occurred in group A (incidence 0.6%) whereas two episodes occurred in group B (incidence 0.1%) (p less than 0.02). Each patient was successfully defibrillated and no adverse sequelae resulted. Thus the present investigation suggests that the incidence of ventricular fibrillation during coronary angiography can be significantly decreased by using contrast media lacking sodium citrate and EDTA.

The efficacy of OKT*3 monoclonal antibody in reversing acute cardiac allograft rejection was investigated in 10 cardiac transplant recipients aged 5 to 57 years (mean 34 +/- 18) and treated with the same induction and maintenance immunosuppression. Serial endomyocardial biopsies, right heart catheterization, and echocardiograms were performed for rejection surveillance. After intensified immunosuppression with equine antithymocyte globulins and steroids, nine patients showed persistent rejection (lymphocytic infiltration and myocyte necrosis). Conventional immunosuppression was contraindicated in one patient. OKT*3 (5 mg by intravenous push daily for 14 days) resulted in complete resolution of rejection in nine of 10 patients (90%). After therapy with OKT*3 mean right atrial and pulmonary arterial wedge pressure were significantly lower (9.1 +/- 4.0 vs 4.8 +/- 2.0 mm Hg and 13.4 +/- 4.3 vs 8.0 +/- 3.3 mm Hg, respectively; p less than .05). Cardiac index was doubled in two patients with rejection-induced cardiac dysfunction (1.5 vs 3.2 and 1.6 vs 2.7 liters/min/m2). Only two patients developed antibodies to OKT*3. Fever, nausea and headache occurred with the first three doses of OKT*3 and did not recur. One patient developed aseptic meningitis. OKT*3 effectively reverses refractory cardiac allograft rejection before the development of irreversible graft dysfunction. Patients who do not develop antibodies to OKT*3 can be retreated with this drug. Adverse reactions to OKT*3 are self-limited.

Concomitant coronary revascularization and implantation of the automatic cardioverter/defibrillator is an increasingly common procedure. To determine whether cardioversion/defibrillation thresholds measured after weaning patients from cardiopulmonary bypass are sufficient to justify immediate implantation of the pulse generator, we prospectively compared postpump values to those obtained 1 week later in five patients. R-wave amplitudes during both sinus rhythm and ventricular tachycardia, lead impedance, defibrillation thresholds and cardioversion thresholds remained stable or improved from the postpump to the 1 week values. Five other patients had the generator implanted at the time of revascularization. Immediate postbypass cardioversion thresholds (mean 10 +/- 8 joules) in these ten patients did not significantly differ from those of 20 nonpump implantations (VT mean 7 +/- joules; VF 15 +/- 4 joules and defibrillation thresholds mean 17 +/- 6 joules). These findings suggest that the residual effects of cardioplegia, core-cooling and operative ischemia have no significant effects on intraoperative testing of implanted defibrillators. This clinical experience supports the practice of immediate implantation of the pulse generator at the time of revascularization.

Fifty patients with idiopathic dilated cardiomyopathy were separated into two groups based on the presence of segmental or diffuse left ventricular wall motion abnormalities by radionuclide ventriculography. Investigation included a history and physical examination, electrocardiogram, chest X-ray film, M-mode echocardiogram, coronary angiogram and right ventricular endomyocardial biopsy. Patients with histologic evidence of myocarditis were excluded. Sixty-four percent of the patients had segmental and 36% had diffuse wall motion abnormalities. The group with segmental abnormalities showed significant differences in age (52.5 +/- 10.7 versus 37.8 +/- 14.6 years, p less than 0.001), New York Heart Association functional class III to IV (56 versus 89%, p less than 0.01), pulmonary capillary wedge pressure (14 +/- 9 versus 26 +/- 9 mm Hg, p less than 0.001), left ventricular end-diastolic dimension measured on echocardiogram (67 +/- 8 versus 77 +/- 11 mm, p less than 0.001), cardiac index (2.6 +/- 0.6 versus 2.0 +/- 0.5 liters/min per m2, p less than 0.01) and ejection fraction by radionuclide ventriculography (20 +/- 7 versus 13 +/- 5%, p less than 0.001). Patients with diffuse wall motion abnormalities had poorer histologic findings based on myocardial cell hypertrophy and nuclear changes (p less than 0.01) and a higher short-term mortality with a 1 year survival rate of 50% compared with 90% in patients with segmental wall motion abnormalities by life-table analysis (p less than 0.05). When data were reanalyzed excluding those patients with complete left bundle branch block, no significant change in any variable was detected. Segmental wall motion abnormalities, even when left bundle branch block is excluded, are common in dilated cardiomyopathy in the absence of coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to gain understanding of how percutaneous transluminal coronary angioplasty (PTCA) is taught and practiced in the United States, two questionnaires were devised to survey all adult cardiology training programs and all adult cardiac catheterization laboratories in this country. Of the 184 programs that responded to the training questionnaire, 102 (55%) teach PTCA, usually in the form of fellowship training and especially as a specialized year, and less commonly in the form of a preceptorship. Though many programs expose trainees to an adequate number of cases as defined by the program directors, at least 37% do not. Of 388 laboratories responding to the practice questionnaire, 74% perform PTCA. The total number of PTCA's in this country seems to be doubling yearly, but many laboratories do relatively few cases per year, and 79% of physicians doing PTCA do fewer than one case per week. Average laboratory success rate for PTCA is in the range of 80-85%. Though there is now a proliferation of PTCA training programs, 93% of those practicing angioplasty are self- or preceptor-trained, and have not learned the procedure as part of a fellowship.

Dilated cardiomyopathy is a heterogeneous group of disorders with a prognosis that is dependent upon the severity of presenting clinical and hemodynamic abnormalities. Although this condition is characterized by a high mortality, spontaneous improvement is noted in 25% of cases. Standard therapeutic modalities are nonspecific and consist of the therapy of congestive heart failure and ventricular arrhythmia. Recent studies suggest that beta blockade and cardiac transplantation may soon become accepted modalities in this condition. Acute viral myocarditis is a common disease that has a good prognosis, however occasionally progression to chronic myocardial disease has been identified. The therapy of acute viral myocarditis should be limited to symptomatic treatment, anti-coagulation, and bed rest. When chronic myocarditis is identified on endomyocardial biopsy in patients with heart failure of unknown cause, the treatment differs little from that of dilated cardiomyopathy with the exception that recognizing that efficacy has not been proven; immunosuppressive therapy may be added in life-threatening situations. Future studies will be directed at further clarification of the prognosis of each of these conditions with intensive evaluation of the role of beta blockade and immunosuppression.

The effect of esmolol on the ventricular fibrillation threshold (VFT) was determined in 11 open-chest dogs anesthetized with sodium pentobarbital. Since changes in VFT by antiarrhythmic drugs have been shown to depend on the method used to test vulnerability to fibrillation, two methods were studied. The vulnerable period was scanned with a train of pulses (100 Hz, 4 ms, 20 pulses) in nine experiments and a single pulse (10 ms) in eight experiments. Following control measurements, esmolol was administered as an intravenous bolus of 500 micrograms/kg followed by a continuous infusion of 300 micrograms/kg/min. After 15 min of infusion, the adequacy of beta-blockade was tested by the administration of 0.5 micrograms/kg of isoproterenol. Isoproterenol increased the heart rate by only 18 +/- 2 beats/min following esmolol administration which was significantly less than the control response (79 +/- 7 beats/min, p less than 0.01). Although the VFT measured with the single-pulse technique did not change in response to esmolol (14.1 +/- 1.1 mA vs. 14.3 +/- 1.2 mA), the VFT measured with the train-of-pulses technique significantly increased (3.7 +/- 0.5 mA to 14.5 +/- 2.8 mA, p less than 0.01). Twenty minutes after discontinuing esmolol, the VFT measurements were repeated and did not differ from control values with either technique. The increase in heart rate in response to isoproterenol also returned to control values (80 +/- 6 beats/min). The results suggest that the ability of esmolol to raise VFT as measured by the train-of-pulses technique is due to beta-adrenergic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Transthoracic cardiac pacing is frequently associated with simultaneous stimulation of skeletal muscle and nerves. We describe a patient in cardiogenic shock and complete heart block in whom the associated vigorous abdominal and chest muscle contractions caused by transthoracic cardiac pacing resulted in a marked augmentation of cardiac output and systemic blood pressure via a "CPR" effect.

Removing sodium from standard ionic contrast media markedly increases the incidence of ventricular fibrillation in patients undergoing coronary angiography. Newer nonionic contrast media, iopamidol, iohexol, and ioversol contain only trace amounts of sodium. To determine whether sodium attenuates or potentiates ventricular fibrillation from nonionic contrast media, we measured the prolongation in QT interval and performed programmed electrical stimulation with one, two and three extra ventricular stimuli in 40 dogs during 4-mL intracoronary injections of iopamidol, iohexol, and ioversol. Solutions of each contrast medium with added NaCl at concentrations of 0.225%, 0.45%, and 0.9% were compared with standard contrast media. The addition of NaCl markedly increased the amount of QT interval prolongation produced by each contrast medium. With iopamidol, the amount of QT interval prolongation was 40 +/- 11 msec with standard iopamidol, but was 58 +/- 11 msec with 0.225% NaCl/iopamidol, 84 +/- 17 msec with 0.45% NaCl/iopamidol, and 132 +/- 42 msec with 0.9% NaCl/iopamidol (P less than .001). Similar results were seen with iohexol and ioversol. Ventricular fibrillation was difficult to induce with standard solutions of these agents (even with three extra stimuli), but became progressively easier to induce when NaCl was added. Three extra stimuli produced ventricular fibrillation in zero of 11 dogs with standard iopamidol, zero of 11 with 0.225% NaCl/iopamidol, three of 11 with 0.45% NaCl/iopamidol, and eight of 11 with 0.9% NaCl/iopamidol (P less than .001). Similar results were observed with iohexol and ioversol. The addition of choline chloride or dextrose did not increase ventricular fibrillation and QT interval prolongation. It is concluded that standard preparations of nonionic contrast media have a very low fibrillatory propensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid volume expansion is a diagnostic procedure which can reveal typical hemodynamics of pericardial constriction in patients with pericardial disease who have normal hemodynamics in their baseline state. We studied 20 patients with previous coronary artery bypass surgery in order to determine whether this operation results in some degree of pericardial constriction which could be demonstrated by rapid volume expansion. After infusing 1 L of physiologic saline solution over six minutes, the right atrial pressure increased by 5 +/- 2 mm Hg, the right ventricular diastolic pressure by 4 +/- 3 mm Hg, the pulmonary capillary wedge pressure by 7 +/- 3 mm Hg, and the left ventricular diastolic pressure by 7 +/- 4 mm Hg (mean +/- SD). Equalization of the left and right cardiac pressures was not observed, and the normal respiratory variation of the pressures was not altered by rapid volume expansion. Thus, the pericardial manipulation associated with the performance of coronary artery bypass surgery does not commonly result in the development of subclinical pericardial constriction.

To study the effects of bretylium on the restoration of circulatory function after resuscitation from ventricular fibrillation, closed-chest anesthetized dogs were electrically fibrillated for 1 minute followed by defibrillation (direct-current shock). After one control episode of fibrillation and defibrillation, 16 dogs received a bolus of bretylium (10 mg/kg intravenously). A second episode of fibrillation and defibrillation was induced in eight dogs 3 minutes after bretylium and in eight dogs 4 hours after bretylium. Prior to bretylium, mean arterial blood pressure spontaneously recovered to exceed 200 mm Hg by 2 minutes after defibrillation in all 16 dogs. However, after bretylium, 13 of 16 dogs were in electromechanical dissociation 2 minutes after defibrillation (p less than 0.001). Despite external chest compression, epinephrine, and sodium bicarbonate, a stable blood pressure could not be restored in 6 of 16 dogs. Clofilium, a bretylium analogue lacking sympathetic influences, did not alter the pattern of hemodynamic recovery following defibrillation in five of five dogs. The results suggest that the effects of bretylium on the sympathetic nervous system may profoundly influence the outcome of cardiac resuscitation from fibrillation.

Magnesium-diltiazem cardioplegia was evaluated in the intact, perfused rat heart to determine whether the joint administration of these agents would adversely affect myocardial contractile and high-energy phosphate recovery following intermittent, normothermic global ischemic arrest. Sequential metabolic and functional analyses were performed on isolated perfused rat hearts during each phase of the experimental protocol: control (10 min), normoxic cardioplegia (10 min), intermittent global ischemic arrest (two 15-min periods separated by 2 min infusion of the normoxic cardioplegic perfusate), and normoxic postischemic control reperfusion (60 min). Four different cardioplegic solutions were evaluated: 30 mM KCl, 30 mM KCl with 2 mg diltiazem/liter, 20 mM MgCl2, and 20 mM MgCl2 with 2 mg diltiazem/liter. Myocardial phosphatic metabolite levels and intracellular pH were analyzed nondestructively in the intact hearts by phosphorus-31 NMR spectroscopy. Corresponding measurements of peak left intraventricular pressure, rate of peak pressure development (dP/dt), and contraction frequency were performed at the midpoint during each 5-min interval of 31P NMR signal averaging. Magnesium plus diltiazem-treated hearts were distinguished from all other groups by a marked delay in postischemic functional recovery consisting of a prolonged depression in contractility (34% of control, P less than 0.01) that persisted throughout the first 50 min of postischemic reperfusion. Diltiazem in combination with magnesium cardioplegia was detrimental to postischemic functional recovery, despite a rapid restoration of high-energy phosphate stores. The apparent adverse interactive effects of excess magnesium and diltiazem suggest that elective ischemic arrest with magnesium cardioplegia in combination with diltiazem may be contraindicated clinically. The mechanistic basis and drug specificity of this response require further clarification. The present findings appear to exclude ATP and PCr production, and structural causes as the basis for the observed aberrant functional recovery from global ischemia of magnesium plus diltiazem-arrested hearts.

In summary, the present examples illustrate how pacemaker malfunction can be simulated by the sources of artifact produced or detected by the monitoring equipment. This form of pseudopacemaker malfunction remains a common cause of mistaken diagnosis of pacemaker malfunction. A thorough understanding of the examples outlined above should help distinguish true pacemaker malfunction from pseudopacemaker malfunction produced by artifact.

Striking electrocardiographic abnormalities have been noted in some patients with central nervous system injury. To study the relationship between the electrocardiogram and intracranial pressure, intracranial pressure was elevated in 14 open chest pentobarbital-anesthetized dogs. The right vagus was stimulated to produce sinus slowing and the right atrium was paced at a constant cycle length fast enough to prevent arrhythmias and maintain heart rate constant (750 msec in 11 dogs and 600 msec in three dogs). In nine dogs, intracranial pressure was sequentially elevated to 100, 150, and 200 mmHg. Systolic arterial blood pressure consistently rose to exceed intracranial pressure (P less than 0.005). At a pressure of 150 and 200 mmHg, mean QT intervals shortened significantly in recorded leads II, X, Y, and Z from 0.01). T wave changes were also noted that consisted of increasing positivity in leads II, X, and Y and increasing negativity in lead Z. To delinate the role of the sympathetic nervous system, an additional five dogs were subjected to an intracranial pressure of 200 mmHg before and after bilateral stellate ganglionectomy and timolol (0.1 mg/kg IV). Elimination of sympathetic influences did not significantly alter the electrocardiographic effects of elevated intracranial pressure. Thus, intracranial hypertension results in significant QT shortening and T wave changes that are not entirely mediated by the sympathetic nervous system.

A patient with catecholamine-sensitive right ventricular outflow tract tachycardia refractory to pharmacological therapy underwent intraoperative mapping and cryoablation. Epicardial and endocardial mapping demonstrated earliest ventricular activation in the free-wall of the outflow tract, and cryoablation of the area resulted in surgical cure. No histologic abnormalities at the site of tachycardia origin were detected. Catecholamine sensitivity does not appear to result from a diffuse myocardial process, and permanent ablation of the tachycardia in this group of patients with a regional procedure is feasible.

Thirty-nine patients underwent coronary arteriography 1 to 20 months (mean 7 months) after percutaneous transluminal coronary angioplasty (PTCA). At the time of the repeat study, 35 patients (90%) had recurrent angina or myocardial infarction, and 4 patients (10%) were asymptomatic. Restenosis, defined as greater than 50% loss of PTCA gained diameter, was found in 19 patients (49%). In addition, 20 patients had new lesions or marked progression of existing lesions (defined as greater than 20% or increasing greater than 20% obstruction in coronary diameter) in the previously normal or mildly diseased coronary segments. The new or progressive lesions occurred both in patients with restenosis at the PTCA site (nine of 19) and in patients without restenosis (11 of 20). New or progressive lesions tended to occur more commonly in the artery on which PTCA was performed (13 of 40) than in the artery that did not have PTCA (10 of 77) (p less than 0.02 by chi 2). In arteries that had PTCA, new or progressive lesions occurred more often in the segment proximal to the angioplasty site (seven of 13 or 54%) than in the peri-PTCA segment (two of 13 or 15%) and in the segments distal to it (four of 13 or 31%), but this observation did not reach statistical significance. No other clinical, angiographic, or PTCA procedure variables affected the occurrence of new or progressive lesions. In patients with recurrent angina or myocardial infarction after PTCA, both restenosis and new or progressive lesions are common. New lesions or marked progression of existing lesions tended to occur in the vessel subjected to PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)

We have operated on 62 consecutive patients for postinfarction ventricular aneurysm since coronary bypass grafting became available. Analysis of hemodynamic and angiographic data reveals that the prognosis of operation is favorable if mean pulmonary artery pressure is less than 45 mm Hg and cardiac index is greater than 2.0 L/min/m2; such factors as the preoperative New York Heart Association Functional Class, number of coronary grafts, aneurysm size, left ventricular end-diastolic pressure, and coronary score were not closely related to the outcome of operation. Hospital mortality was 6.5% (4 patients) and late mortality, with a mean follow-up of two years, was 11% (7 patients). The prognosis among survivors was good: 82% (46) achieved NYHA Class I or II status, whereas 87% (54) had been in Class III or IV preoperatively. Concomitant vein grafting with aneurysmectomy did not significantly enhance operative or late survival, nor did it add appreciably to the risk of operation. Long-term benefits of revascularization in addition to aneurysmectomy are expected but not yet proved.

Two cases of acute myocardial infarction occurred in association with myocarditis, which was confirmed by biopsy. The first patient suffered an anteroseptal and the second patient an inferior wall myocardial infarction shortly after an acute viral illness. In both patients, coronary angiography showed normal coronary arteries, and right ventricular endomyocardial biopsy confirmed myocarditis. Histological abnormalities attributable to ischaemic heart disease were absent. The first patient's condition became stable after immunosuppressive treatment. Myocarditis resolved spontaneously within three months in the second patient. Coronary artery spasm and myocardial involvement with a systemic disease were unlikely. Endomyocardial biopsy in patients with acute myocardial infarction and normal coronary arteries may be useful in identifying myocarditis associated with myocardial necrosis. Myocarditis in acute myocardial infarction in the absence of coronary artery obstruction has not previously been documented during life.

A total of 145 patients with greater than 50% obstruction of the left main coronary artery (LMC) were studied by coronary arteriography. Of the 140 who survived cardiac catheterization, 121 were considered operable by coronary arteriography, and 19 were inoperable. Of the 121 operable patients, 32 were treated medically, and 89 had aortocoronary bypass surgery. Surgical mortality was 11%. The follow-up was from 1 to 72 months with a mean follow-up of 15 months. A survival table was plotted over a 24-month period. At 90 days survival in surgical patients was 85%, medical patients 72%, and inoperable patients 64%. At one year 82% of surgical patients were alive compared with 61% of medically treated operable patients (P less than 0.05). Thereafter, the survival rate remained stable up to 23 months. Survival in inoperable patients was 38% at one year. Improved surgical survival was associated with the presence of preoperative collateral vessels and a left ventricular stroke index greater than 18 g-m/m2. The study demonstrates that survival is improved significantly by surgery in LMC patients. Since mortality occurs early after coronary arteriography, surgery should be offered early to operable patients.

Current standards for detection of myocarditis in a clinical setting rely on endomyocardial biopsy for accurate diagnosis. With this technique a subset of patients with dilated cardiomyopathy show unsuspected myocarditis histologically. Endomyocardial biopsy, despite its specificity, may lack sensitivity due to sampling error if the inflammation is patchy or focal. Therefore, inflammation-sensitive radioisotopic imaging may be a useful adjunct in the diagnosis of myocarditis. This study was designed to evaluate the applicability of gallium-67 (67Ga) myocardial imaging as an adjunct to endomyocardial biopsy in the diagnosis of myocarditis. Sixty-eight consecutive patients referred for evaluation of dilated cardiomyopathy underwent 71 parallel studies with 67Ga imaging and biopsies that served as the basis of comparison for this study. Histologic myocarditis was identified in 8% of biopsy specimens. Clinical and hemodynamic parameters could not be used to predict the presence of myocarditis. Five of six biopsy samples (87%) with myocarditis showed dense 67Ga uptake, whereas only nine of 65 negative biopsy samples (14%) were paired with equivocally positive 67Ga scans (p less than .001). The single patient with myocarditis and no myocardial 67Ga uptake had dense mediastinal lymph node uptake that may have obscured cardiac uptake. The incidence of myocarditis on biopsy with a positive 67Ga scan was 36% (5/14); however, the incidence of myocarditis with a negative 67Ga scan was only 1.8% (1/57). Follow-up scans for three patients showed close correlation of 67Ga uptake with myocarditis on biopsy. In conclusion 67Ga may be a useful screening test for identifying patients with a high yield of myocarditis on biopsy, and serial scans may eliminate the need for frequent biopsies in patients with proven myocarditis.

We describe the long-term follow-up of 25 patients treated with murine antihuman mature T cell (OKT3) monoclonal antibody at Loyola University Medical Center. After OKT3 rescue therapy, 12 patients were monitored for 16.5 +/- 6.5 months. Twenty-two moderate and three severe rejection episodes occurred 11 to 469 days (166.8 +/- 126.0) after OKT3 therapy in nine of 12 patients. During the follow-up period three patients died, and one required retransplantation because of recurrent rejection. The coronary arteries of three failed allografts had severe intimal thickening and infiltration with lymphocytes. Thirteen patients received OKT3 for prophylactic immunosuppression, and their course was compared to that of 13 patients who underwent transplantation during the same period but were given prophylactic horse antihuman thymocyte globulins (HATG). There were no differences between the two drugs with respect to long-term incidence and severity of rejection and infection, cardiac allograft function, and survival. Our results indicate that, despite successful reversal with OKT3, heart transplant recipients with refractory rejection remain plagued by recurrent rejection. Cardiac allografts in recipients who die as a result of recurrent rejection show evidence of immune-mediated vasculitis, which results in severe and diffuse coronary luminal narrowing. OKT3 and HATG appear to be equally effective for rejection prophylaxis.

In order to compare the effects of acute and chronic beta-blockade on infact size, the left circumflex coronary artery was occluded for 6 hours in 33 anesthetized dogs. The dogs (18 to 22 kg) were divided into three groups; group 1 (N = 10) served as controls, group 2 received intravenous nadolol (average dose 1.25 mg/kg) just prior to coronary occlusion, and group 3 received oral nadolol (80 mg) twice daily for 16 days prior to coronary occlusion. To ensure equivalent degrees of beta-blockade at the time of occlusion, group 2 and 3 dogs were given incremental doses of intravenous nadolol to abolish the chronotropic response to isoproterenol (2 mu/kg IV). Left ventricular pressure, its first derivative (dP/dt), and heart rate were monitored. The anatomic risk region was determined antemortem by Evan's blue staining while the infarct zone was delineated postmortem by tetrazolium staining. Compared to Group 1, heart rate was 22% lower in group 2 and 15% lower in group 3 dogs 6 hours after occlusion (p less than 0.05). There were no differences among groups in peak left ventricular systolic pressure or mean arterial pressure. Infarct size as a function of the area at risk was 68 +/- 3% in group 1, 52 +/- 7% in group 2, and 44 +/- 8% in group 3. A significant difference was found only between groups 3 and 1. The data suggest that chronic beta-blockade provides greater protection against ischemic-induced necrosis than does acute beta-blockade. The greater protective effect of chronic beta-blockade may be due to chronic adaptive changes in either blood flow or metabolism.

It has been suspected that the increased sympathetic activity seen in patients with chronic congestive heart failure from dilated cardiomyopathy may be harmful. We therefore tested the long-term effect of metoprolol on eight patients in a double-blind, randomized protocol and 12 patients in an unblinded, crossover protocol who were treated for 12 months (range 10 to 24), and compared them with 16 similar subjects who were treated with placebo for 10 months (range 6 to 12) in a double-blind, randomized protocol. Patients were followed by serial clinical assessment, treadmill testing, radionuclide ventriculography, and echocardiography. Metoprolol-treated patients had an improvement in mean exercise capacity by 3 mets (p less than .0001) while experiencing a significant improvement in functional classification (p less than .001) during both the double-blind and open-label crossover studies and had an improved ejection fraction during the double-blind study (p less than .02). These improvements were not seen in matched control subjects receiving placebo. Seven of 20 patients receiving long-term metoprolol therapy had resolution of nearly all symptoms of heart failure, doubled their exercise capacity, and had progressive improvement in resting radionuclide left ventricular ejection fraction (12.6 +/- 3% to 26.9 +/- 6%) and echocardiographic left ventricular end-diastolic dimension (7.7 +/- 0.5 to 6.5 +/- 0.5 cm). Only one of 21 patients treated was intolerant of metoprolol. We conclude that metoprolol can be given safely to a select group of patients with dilated cardiomyopathy in doses that substantially reduce both resting and exercise heart rates. Long-term beta-blockade improved functional class and exercise capacity in 14 of 20 patients while producing an exceptional clinical response in seven that was accompanied by improved resting parameters of left ventricular function.

Forty-five patients were identified as having constrictive pericarditis after cardiac surgery. The mean patient age was 61 years (range, 40 to 77 years). Twenty-three of 37 patients with adequate clinical information were reported to have had a diagnosis of postpericardiotomy syndrome after the original surgery. The mean interval from original surgery to presentation with constriction was 23.4 months (range, 1 to 204 months). Computerized tomography was helpful in establishing a diagnosis of constriction in 23 of 29 patients (79%). Bypass graft patency was 93% (85 of 91 grafts). Severe pulmonary hypertension (pulmonary artery systolic pressure greater than or equal to 60 mm Hg) was present in nine patients; 8 had coexistent valvular disease (seven cases of mitral valve disease, and aortic valve disease in one). Thirty-seven of the 45 patients underwent pericardial stripping, 28 of whom experienced marked symptomatic improvement. One patient had persistent right heart failure, which was not documented to be secondary to constriction. Four patients had persistent constrictive physiologic conditions. Three of these patients had more extensive pericardial stripping and showed clinical improvement. Four patients (11%) died within 30 days of stripping. Eight patients received medical therapy alone. The decision to treat patients medically was based either on favorable response to medical therapy (five patients), or poor general clinical status.

Nonsteroid anti-inflammatory drugs are often used to treat myalgias and arthralgias in enteroviral infections, but their effects on acute viral myocarditis are unknown. The effect of the nonsteroidal anti-inflammatory drug, ibuprofen, on acute viral myocarditis was studied in 75 four week old male BALB/c mice infected with 1.75 X 10(7) plaque-forming units of Coxsackie virus B3 on day 0. Ibuprofen was given intraperitoneally at a dose of 15 mg/kg body weight daily. The mice were assigned to four groups--Group I, 18 uninfected mice given ibuprofen on days 1 to 14; Group II, 18 infected, untreated mice; Group III, 20 infected mice given ibuprofen on days 1 to 14; and Group IV, 17 infected mice given ibuprofen on days 7 to 14. Nine animals in Group I, eight in Group II and seven in Group III were killed on day 7; the remaining mice were killed on day 14. Heart viral cultures and histologic analysis were done. Cultures at days 7 and 14 were all negative. Inflammation and necrosis analyzed in each animal were graded 0 to 4, with grade 4 representing widespread inflammation and necrosis. The heart was histologically normal in all 18 uninfected mice (Group I) given ibuprofen only. Inflammation and necrosis were not significantly different in Group II (infected, untreated) and Group III (infected, treated beginning day 1) mice killed at day 7. Inflammation scores of mice killed on day 14 were 2.1 +/- 0.6 (Group II), 3.1 +/- 0.7 (Group III) and 2.9 +/- 1.0 (Group IV infected, treated days 7 to 14).(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to define the role of beta-adrenergic blockade and direct membrane effects in the ability of dl-propranolol to alter ventricular repolarization and refractoriness in the intact heart. The effective refractory period (ERP) and the local Q-T interval were measured at an epicardial site in the left ventricle in 14 open-chest dogs anesthetized with alpha-chloralose. Beta-adrenergic influences were eliminated in seven dogs (group 1) by stellate transection and nadolol (0.5 mg/kg IV), and enhanced in seven dogs (group 2) by stellate transection and stimulation of the left ansae subclavia. Each dog received an initial beta-blocking dose of propranolol (0.5 mg/kg) followed by a second, cumulative dose of 5.0 mg/kg. In group 1 dogs, there was no significant change in either the ERP or local Q-T interval in response to the first dose of propranolol. In group 2 dogs, left stellate stimulation significantly shortened the ERP (20 +/- 2 msec) and the local Q-T interval (17 +/- 4 msec). The first dose of propranolol prolonged these parameters to values not different from prestimulation control values. There was no change in the H-V interval, QRS complex duration, or diastolic threshold (DT) in either group after the initial propranolol dose. The second dose of propranolol significantly shortened the ERP (5 +/- 1 msec) and the local Q-T interval (11 +/- 2 msec) in both groups. This dose also significantly increased the DT, H-V interval, and QRS complex duration.(ABSTRACT TRUNCATED AT 250 WORDS)

Experiments were performed to determine the importance of sympathetic blockade vs a direct myocardial effect as a mechanism for the antifibrillatory action of bretylium. The ventricular fibrillation (VF) threshold was determined in open-chest, anesthetized dogs by scanning the vulnerable period with either a single electrical stimulus (10 ms) or a train of electrical stimuli (14 pulses, 4 ms, 100 Hz). Using the train-of-pulses technique, the VF threshold increased from 6.8 +/- 0.6 mA to 29.7 +/- 6.4 mA 15 minutes after a 10-mg/kg intravenous bolus of bretylium (p less than 0.001, n = 8). There was no further significant change in the train-of-pulses VF threshold at 2 or 4 hours. Beta-adrenergic blockade with timolol (0.2 mg/kg) increased the train-of-pulses VF threshold from 6.7 +/- 1.6 mA to 24.5 +/- 5.2 mA (p less than 0.01 n = 8) and prevented any further significant change in response to bretylium. When single electrical pulses were used to scan the vulnerable period, bretylium at doses of 10 mg/kg (n = 8) and 100 mg/kg (n = 6) did not alter the VF threshold over a 4-hour observation period. The administration of timolol, alone or in combination with bretylium, did not significantly alter the single-pulse VF threshold. The failure of bretylium to alter the single-pulse VF threshold was not dependent on the site of stimulation. Stimulation of the right sympathetic cardiac nerves showed that 15 minutes of bretylium treatment was sufficient to completely inhibit adrenergic neuronal transmission to the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)