Incidence of new pulmonary perfusion defects after routine cardiac catheterization.

The incidence of pulmonary perfusion defects after routine cardiac catheterization was assessed in 57 patients by comparing ventilation-perfusion lung scans obtained before and 1 day after catheterization. Patients were prospectively randomized to two groups, one in which right heart catheterization was performed using an antecubital venous cutdown procedure and one in which the percutaneous femoral vein approach was used. Seven patients (12 percent) had new postcatheterization perfusion defects consistent with pulmonary emboli. These patients did not differ significantly from patients without new defects in clinical characteristics, duration of catheterization, hemodynamic variables or route of right heart catheterization. The data suggest that pulmonary embolism may be a more common complication of routine cardiac catheterization than previously appreciated.     

Prospective randomized trial of glucose-insulin-potassium in acute myocardial infarction. Effects on myocardial hemodynamics, substrates and rhythm.

Fifty consecutive patients admitted within 12 hours of the onset of symptoms of acute myocardial infarction were randomly assigned to treatment with intravenous glucose-insulin-potassium infusion (23 patients) or to a control group (0.5 N sodium chloride infusion) (27 patients). The glucose-insulin-potassium infusion consisted of 30 g glucose, 50 U regular insulin and 80 mEq KCl per liter infused at 1.5 ml/kg per hour for 2 days. Serial measurements were made of pulmonary arterial end-diastolic pressure, cardiac index, daily fluid intake and output, serum glucose, potassium, urea nitrogen, free fatty acids, osmolarity, creatine kinase-MB isoenzyme and cardiac rhythm. Although all patients admitted comatose died (three glucose-insulin-potassium recipients, one control subject), hospital mortality in patients admitted noncomatose was 0 percent (0 of 20) in glucose-insulin-potassium recipients versus 12 percent (3 of 26) in the control group (three deaths secondary to late pump failure). Glucose-insulin-potassium recipients experienced 4.9 ± 1.3 hours of three or more premature ventricular complexes/min compared with 11.1 ± 1.9 hours for control subjects (P < 0.02). Twelve control patients had 60 episodes of ventricular tachycardia compared with seven glucose-insulin-potassium recipients, who had 12 episodes of ventricular tachycardia. During glucose-insulin-potassium infusion, fluid intake and output, serum glucose and potassium were significantly increased compared with values in control subjects, blood urea nitrogen and free fatty acids were decreased, whereas osmolarity, pulmonary arterial end-diastolic pressure and cardiac index did not differ significantly from control values. Creatine kinase-MB infarct size averaged 124 ± 15 IU/liter in glucose-insulinpotassium recipients and 109 ± 14 IU/liter in control subjects (difference not significant).These data demonstrate that, in patients with acute infarction, glucose-insulin-potassium infusion (1) does not adversely alter hemodynamics, (2) reduces free fatty acids, (3) diminishes frequency of ventricular arrhythmias, but (4) has no demonstrable effect on infarct size as assessed with creatine kinase isoenzyme values. In this ongoing randomized clinical trial, the number of patients studied is too small to permit definite conclusions to be reached regarding the effect of glucose-insulin-potassium infusion on hospital survival.     

Quantitative coronary arteriography. Coronary anatomy of patients with unstable angina pectoris reexamined 1 year after optimal medical therapy

The effect of optimal medical therapy on coronary arterial anatomy was evaluated in 25 patients with unstable angina pectoris. Coronary arterial diameter and the extent of stenosis were exactly quantified in two successive coronary angiograms performed in each patient at approximately a 1 year interval (range 4 to 31 months, average 12.4 months). The measuring device was a vernier caliper with an accuracy of 0.05 mm. After 1 year of medical treatment 69 stenoses of the three major coronary branches showed no significant change: The average degree of area obstruction of 27 stenoses of the right coronary artery was 79 and 84 percent in the initial and second studies, respectively; that of 26 stenoses of the left anterior descending artery 78 and 77 percent, respectively, and that of 16 stenoses of the left circumflex artery 73 and 83 percent, respectively. In 11 patients, 14 stenoses showed a distinct progression of more than 20 percent area obstruction. All six stenoses showing more than 90 percent obstruction in the first angiogram progressed to complete obstruction within 1 year. In five other patients area obstruction in five stenoses regressed by more than 20 percent. The anatomy of vessel segments distal to obstructions remained unchanged within 1 year. It is concluded from these quantitative measurements that the distribution and severity of coronary lesions are similar in patients with stable and unstable angina pectoris. Coronary anatomy showed no significant change after 1 year of medical treatment. The rate of progression was substantially lower than previously reported in patients with stable angina pectoris.     

Pathogenesis of paroxysmal hypertension developing during and after coronary bypass surgery: A study of hemodynamic and humoral factors

A prospective study of hypertension first appearing during and after saphenous vein bypass coronary surgery was performed in 28 patients to examine the incidence, hemodynamics and mechanism of this problem. In 15 patients (54 percent) new hypertension developed (mean arterial pressure greater than 107 mm Hg), characterized by increased peripheral vascular resistance and unchanged cardiac output within 1 hour after surgery. These 15 patients had a longer history of angina of greater severity, but also had relatively well preserved ventricular myocardium. Because plasma renin activity was depressed in patients in the hypertensive group, activation of the renin-angiotensin system was not important in the pathogenesis of this postoperative hypertension. The expected decrease in total peripheral resistance at the onset of cardiopulmonary bypass was observed in all patients, but later during bypass the peripheral resistance increased in all patients in association with a rise in plasma epinephrine levels. Patients who had hypertension postoperatively had a greater increase in arterial pressure and total peripheral resistance during cardiopulmonary bypass than did those with normal postoperative blood pressure. An elevation in plasma epinephrine and norepinephrine concentration, suggesting enhanced sympathoadrenal responsiveness to the challenge of cardiopulmonary bypass, was characteristic of the hypertensive group. This evidence of enhanced sympathetic activity during surgery may be a useful predictor of the development of postoperative hypertension.     

Hemodynamic evaluation of patients with combined mitral and aortic prostheses

Complete hemodynamic evaluation of patients with combined aortic and mitral mechanical valve prostheses presents a difficult technical problem. Yet such patients with cardiac symptoms postoperatively often require this evaluation to determine the diagnosis and the advisability of reoperation. A 4 year experience with 22 patients requiring such evaluation is reviewed. Eight patients (36 percent) required reoperation for malfunction of the prosthesis. Four (18 percent) had major complications of the cardiac catheterization study, but no fatalities or residual permanent defects resulted. In 17 cases transthoracic left ventricular needle entry was used. A standardized procedure of this type for both pressure measurement and angiographic studies has evolved, providing reasonable efficiency and a relative degree of safety. The patient is positioned in the right anterior oblique position for optimal needle entry into the left ventricular apex and angiographic visualization of mitral prosthetic incompetence and the myocardial contractile pattern. A 16 gauge needle with side holes but no end hole allows ventriculography to be performed after chamber entry using the prostheses as reference points under fluoroscopic guidance. Retrograde catheterization of the aortic prosthesis, transseptal left atrial catheterization with anterograde crossing of the mitral prosthesis and transapical pressure measurement with a smaller needle, combined with quantitative left atrial angiography, are alternative choices for study.     

Transient electrocardiographic changes in patients with unstable angina: Relation to coronary arterial anatomy

The relation between the spontaneous electrocardiographic changes and coronary arterial anatomy in unstable angina pectoris was examined in 97 patients with coronary artery disease and transient electrocardiographic changes during chest pain. Sinus rhythm was maintained during pain in all patients. Heart rate increased significantly in 61 percent (mean ± standard error of the mean 72 ± 2 to 93 ± 2 beats/min, probability [p] < 0.001) and was unchanged or decreased in 39 percent of patients (73 ± 2 to 72 ± 2 beats/min; p = not significant) during pain. S-T segment changes developed in 97 percent of patients, of whom 42 percent had S-T segment elevation and 55 percent S-T depression. The magnitude of the S-T segment shift was greater in patients with triple vessel disease (2.2 ± 0.4 mm) than in those with double (1.5 ± 0.1 mm) or single (1.4 ± 0.1 mm) vessel disease (p < 0.05). In 43 patients with single vessel disease S-T segment elevation developed in 78 percent of those with right coronary artery disease and in only 9 percent of those with left circumflex disease (p < 0.02). Maximal S-T segment changes were more frequent in the inferior leads in patients with right coronary artery disease (56 percent) and in the anterior leads in patients with left anterior descending (65 percent) and circumflex (64 percent) disease (p < 0.05).Thus, patients with coronary artery disease and unstable angina maintain regular sinus rhythm during chest pain, and the heart rate usually increases but may be unchanged or decreased in a significant proportion. S-T segment elevation is common in these patients and the magnitude of the S-T segment shift is related to the extent of the underlying coronary disease. This study suggests that the type and distribution of the repolarization changes are a reflection of the location and severity of the atherosclerotic process.     

Relation of graded exercise test findings after myocardial infarction to extent of coronary artery disease and left ventricular dysfunction

To evaluate the effectiveness of the graded exercise test in predicting the extent of coronary artery disease and the degree of left ventricular dysfunction in patients with prior myocardial infarction, 100 consecutive patients underwent both graded exercise testing and coronary and left ventricular angiography at a median of 4 months after infarction. The studies caused no complications. An equal number of patients had anterior and inferior infarction. Coronary artery disease, defined as 70 percent or greater stenosis of luminal diameter, was present in three vessels in 31 patients, in two vessels in 35 patients, in one vessel in 33 patients and in no vessel in one patient. With “diagnostic” electrocardiographic criteria of 1 mm or greater J point depression plus a flat or downsloping S-T segment, 31 patients had an electrocardiographically positive exercise test; 27 of these (87 percent) had two or three vessel coronary artery disease. Of the 21 patients with a negative exercise test, 62 percent had coronary artery disease in no more than one vessel, 33 percent in two vessels and 5 percent in three vessels. Fourteen patients had S-T segment elevation during exercise; these patients had a lower ejection fraction and larger angiographic scar size than the remaining 86 patients. Patients terminating exercise because of symptoms of left ventricular dysfunction (fatigue or dyspnea) showed correlation between duration of exercise and ejection fraction (r = 0.65) and between duration of exercise and angiographic scar size (r = ?0.62). Thus, several months after infarction, the graded exercise test can be performed safely and can be utilized to predict the extent of coronary artery disease and left ventricular dysfunction in selected groups of patients.     

Experimental studies on the pathogenesis of asystole after verapamil in the dog.

The effect of verapamil on automaticity and conduction in the atrioventricular (A-V) junctional region was studied in anesthetized dogs. In five normal dogs verapamil, 10 microgram/ml, was selectively perfused into the A-V nodal artery and caused first degree heart block, which progressed to second degree heart block in three of the five. Higher concentrations of verapamil, 25 microgram/ml, caused complete heart block in three of five other dogs, but no episodes of asystole (defined as a ventricular pause of 10 or more seconds). In six other dogs after beta receptor blockade with propranolol, 20 microgram/ml, perfused into the A-V nodal artery, verapamil, 10 microgram/ml, regularly caused second degree heart block; in four of the six dogs there was a transient episode of third degree A-V block, and in two of these there was a period of asystole. In each of the 10 dogs pretreated with reserpine, verapamil, 10 microgram/ml, caused third degree A-V block; in seven of these there was a period of asystole with ventricular standstill up to 30 seconds. Concentrations of verapamil that do not produce high grade heart block in the normal heart thus readily cause both high grade block and prolonged ventricular standstill after elimination of adrenergic influences in the A-V junction.     

Intracoronary nifedipine in human beings: magnitude and time course of changes in left ventricular contraction/relaxation and coronary sinus blood flow

Eight patients, all men, having at least 75% stenosis of the proximal, middle or both segments of the left anterior descending coronary artery, underwent intracoronary drug studies at the time of cardiac catheterization after saphenous vein bypass grafting. Nifedipine, 0.1 mg dissolved in saline solution, was infused into a left anterior descending graft that was the primary blood supply to each patient's anterior left ventricular wall and septum. High fidelity left ventricular pressure and its first derivative, dP/dt, and aortic pressure were sampled synchronously with coronary sinus blood flow by the thermodilution technique. The time constant of isovolumic pressure decay (T) was derived. In five patients, percent systolic shortening and mean shortening velocity were determined from myocardial markers implanted into the midwall of the myocardium at the time of cardiac surgery. In response to nifedipine, left ventricular systolic pressure decreased and end-diastolic pressure increased up to 60 seconds. Both positive and negative dP/dt also decreased up to 60 seconds, whereas coronary sinus blood flow increased up to 5 minutes. T was increased at 1 minute but returned to baseline by 3 minutes. Percent systolic shortening and mean shortening velocity were decreased at 1 minute but returned to control level by 3 minutes. Thus, although both left ventricular systolic and diastolic function were depressed by intracoronary administration of nifedipine, coronary sinus blood flow was augmented and remained increased long after changes in left ventricular contraction and relaxation had subsided. These temporal differences are consistent with animal studies showing a differential depressant effect of nifedipine on calcium uptake in smooth muscle and cardiac muscle.     

Effects of glucose-insulin-potassium on myocardial substrate availability and utilization in stable coronary artery disease: Studies on myocardial carbohydrate, lipid and oxygen arterial-coronary sinus differences in patients with coronary artery disease

To assess the metabolic effects of myocardial substrate alteration In patients with coronary artery disease, glucose-insulin-potassium solution was administered intravenously for 30 minutes to 14 men with stable angiographically documented coronary artery disease. The glucose-insulin-potassium solution (300 g of glucose, 50 units of regular insulin and 80 mEq of potassium chloride per liter of water) was infused at a constant rate in each patient, but individual infusion rates ranged from 0.013 to 0.032 ml/kg per min (4 to 10 mg glucose/kg per min) in the 14 patients. Simultaneous arterial and coronary sinus samples were obtained at 15 minute intervals during a stable 30 minute control period and again at 15 minute intervals during the infusion; samples were assayed for glucose, lactate, free fatty acid and oxygen content.

In all 14 patients, during the glucose-insulin-potassium infusion, arterial glucose and lactate increased and arterial free fatty acid levels fell; the magnitude of the changes in arterial lactate and free fatty acids as related to the rate of infusion. Arterial-coronary sinus differences (A-C_s) for glucose, lactate and free fatty acid levels correlated with the arterial concentrations of these substrates (r = 0.66, 0.87 and 0.79, respectively). Regression analyses demonstrated myocardial thresholds for the uptake of these substrates as follows: glucose 79 mg/100 ml; lactate 300 μmole/liter; and free fatty acids 100 to 200 μEq/liter. Finally and most importantly, the reduction in A-C_s oxygen values after glucose-insulin-potassium infusion correlated with the reduction in A-C_s free fatty acid levels (r = 0.64, P < 0.0001). This observation suggests that, in patients with coronary artery disease, glucose-insulin-potassium infusion may significantly diminish myocardial oxygen requirements by reduction of myocardial free fatty acid utilization and simultaneous enhancement of myocardial carbohydrate utilization.

Myocardial substrate availability may be an important determinant of myocardial oxygen demand in patients with coronary artery disease. Infusion of glucose-insulin-potassium solution has the potential to alter myocardial substrate availability, thus improving the balance between myocardial oxygen demand and supply.     

Coronary anatomy and arteriography in patients with unstable angina pectoris.

A prospective series of 188 patients with the syndrome of unstable angina pectoris undergoing coronary arteriography was reviewed to determine the spectrum of anatomic coronary artery disease, suitability for coronary revascularization and in-hospital morbidity and mortality. Thirty-two patients demonstrated normal to moderately diseased coronary arteries. None of these patients sustained myocardial infarction or died. Twenty patients (10.6 percent) had normal coronary arteriograms. Of the 156 patients having severe coronary artery disease (greater than 70 percent stenosis), 20 patients (13 percent) had left main coronary artery disease. One hundred forty-two patients (91 percent) were potential candidates for coronary surgery; 14 were not candidates because of distal vessel disease or poor left ventricular function. During cardiac angiography or in the subsequent hospital period 12 patients sustained a myocardial infarction and 7 of these died. Of these seven, six had left main coronary artery disease and one had three vessel disease. In three patients who died (1.9 percent of those with severe coronary artery disease) the death may have been related to cardiac catheterization because evidence of myocardial necrosis began within 24 hours of study. Thus, patients with the syndrome of unstable angina pectoris usually presented with severe coronary artery disease and were candidates for coronary revascularization. The anatomic severity of coronary artery disease appeared to be the most important factor contributing to myocardlal infarction or death after cardiac catheterization. Mortality after catheterization was primarily associated with left main coronary artery disease.     

Attenuation by magnesium of the electrophysiologic effects of hyperkalemia on human and canine heart cells

Because magnesium (Mg⁺⁺) has been shown to promote maintenance of a negative resting potential it might oppose the depolarizing effect of potassium (K⁺) in cardiac cells. To test this hypothesis the electrocar diographic changes that occur during hyperkalemia were prospectively studied in 11 patients, 4 of whom had hypermagnesemia. Action potential studies were carried out in single atrial and ventricular cells isolated from 11 canine hearts using similar extracellular concentrations of Mg⁺⁺ _° and K⁺ _° to elucidate further the relative effects of these cations. Hyperkalemia was associated with a marked reduction in P wave amplitude and marked prolongation of the QRS complex. However, normal P waves and normal QRS durations were recorded in hyperkalemic patients with excess Mg⁺⁺ (2.5 mEq/liter or more). Mg⁺⁺ also antagonized some effects of K⁺ in the isolated atrial and ventricular tissues. With elevated levels of [Mg⁺⁺] the K⁺-induced depolarization of the resting potential was less than half as much as when [Mg⁺⁺]was normal (9 versus 21 mV in ventricular cells and 18 versus 40 mV in atrial cells). Furthermore, the fall in linear conduction velocity that accompanied elevated [K⁺]levels in ventricular cells failed to occur when the level of [Mg⁺⁺]was high. Mg⁺⁺-K⁺ antagonism helps to explain the preservation of a normal P wave because the onset of K⁺ effects in isolated atrial cells was delayed when [Mg⁺⁺]was high and action potential amplitude was improved. It is concluded that the heart cells of patients with high serum levels of [Mg⁺⁺]were less sensitive to an increase in [K⁺]than were those of patients with lower [Mg⁺⁺]and, accordingly, that Mg⁺⁺ attenuated the electrophysiologic response to elevated [K⁺].     

Fine structure of cells and their histologic organization within internodal pathways of the heart: clinical and electrocardiographic implications.

The fine structure of the normal internodal pathways was studied in 1 human and 2 canine hearts and correlated with histologic observations on more than 100 human and 10 canine hearts. From the electron microscopic studies six different kinds of myocardial cells were classified from two locations: the Eustachian ridge (posterior internodal pathway) and the Bachmann bundle (anterior internodal pathway). Five of the six kinds of cells (working myocardial cells, Purkinje-like cells, either broad or slender transitional cells and P cells, all previously described) were present in both locations. A sixth cell, pleomorphic and dark in appearance, with a special intertwined relation to P cells, is newly designated as an ameboid cell. It was found solely in the Eustachian ridge. In the same area a rare direct contact between a nerve and a myocardial cell was observed. The importance of these different kinds of cells, their respective cell connections, and their topographic locations inside the internodal pathways are discussed relative to certain functions such as rapid conduction and subsidiary pacemaking. The possible influence of these factors on clinical electrocardiographic changes is considered.     

Method for quantitative analysis of regional left ventricular function with first pass and gated blood pool scintigraphy

The ability of radionuclide angiocardiography to quantitatively assess regional left ventricular function was studied in 33 patients undergoing biplane left ventricular cineangiography (45 ° right anterior oblique projection, and 60 ° left anterior oblique projection with 25 ° caudocranial angulation), and first pass (30 ° right anterior oblique projection) and multiple gated equilibrium (35 ° to 45 ° left anterior oblique projection with 20 ° to 25 ° caudocranial angulation) left ventricular scintigraphy within 48 hours. End-diastolic and end-systolic silhouettes of contrast angiograms were superimposed, and five segments were defined in each plane by radial lines originating from the end-diastolic center of mass. Segmental angiographic ejection fraction (end-diastolic area — end-systolic area/ end-diastolic area) was calculated for each segment by computerized planimetry. Similar segments were defined in the end-diastolic and end-systolic regions of interest of the first pass and gated left ventricular scintigrams, and the segmental scintigraphic ejection fraction (back-ground-corrected end-diastolic counts — background-corrected end-systolic counts/background-corrected end-diastolic counts) was obtained for each.A good correlation was observed between segmentai angiographic and scintigraphic ejection fraction in the segments corresponding to the anterobasal (r = 0.74), anterolateral (r = 0.70), apical (r = 0.77), diaphragmatic (r = 0.71), distal septal (r = 0.66), posterolateral (r = 0.71) and inferolateral (r = 0.60) left ventricular regions. The poor correlation in the posterobasal (r = 0.39), basal septal (r = ?0.02) and superolateral (r = 0.05) segments was probably related to difficulty in defining the aortic valve, overlap of the left atrium and the left ventricle, and inability to visualize the high septum with these scintigraphic techniques. The reproducibility of scintigraphic segmental ejection fraction was studied in 13 patients in whom a second gated scintigram was performed 2 hours after the initial one. Excellent agreement (r = 0.93) was observed for scintigraphic segmental ejection fraction in the distal septal, posterolateral and inferolateral segments. Segmental scintigraphic ejection fraction enables accurate quantitative evaluation of the function of the anterobasal, anterolateral, apical, diaphragmatic, distal septal, posterolateral and inferolateral left ventricular regions with high reproducibility.     

Sudden death while driving: Role of sinus perinodal degeneration and cardiac neural degeneration and ganglionitis

A young business executive was seen to slump over his steering wheel while driving, after which the automobile veered and turned over. Quickly taken unconscious to a nearby emergency room, he was pronounced dead on arrival. Because there was insufficient physical injury found to account for his death, and because atrial fibrillation had been detected for the first time on a routine physical examination 3 months previously, special examination of the cardiac conduction system was performed. A fibroma was present on the right side of the central fibrous body above the His bundle, similar to several fibromas on the mitral valve. Small foci of neuritis were present in the ventricular myocardium and the atrioventricular node. More extensive neural degeneration and ganglionitis were found near the sinus node, which also exhibited an encircling perinodal flbrosis. Ways in which these abnormalities could have caused a fatal electrical instability of the heart are discussed. Careful examination of the cardiac conduction system is warranted in other fatal automobile accidents under similar circumstances.     

Pulmonary arterial compression syndrome caused by false aneurysm of left ventricular outflow tract

A 29 year old man experienced exertional dyspnea and coughing 3 1/2 years after insertion of a Braunwald-Cutter aortic valve prosthesis. Clinical examination suggested pulmonary arterial hypertension, and cardiac catheterization revealed a saccular lesion apparently arising from the left ventricular outflow tract and producing compression of the right pulmonary artery. Origin from the left ventricular outflow tract just under the aortic ring was confirmed at operation. The lesion apparently arose from an anular excavation related to previous endocarditis with abscess formation. Reported cases of similar aneurysmal lesions are briefly reviewed, and other known causes of the pulmonary arterial compression syndrome are discussed.     

Enhancement of left ventricular function by glucose-insulin-potassium infusion in acute myocardial infarction

Twenty-eight patients admitted to the hospital with suspected acute myocardial infarction underwent baseline studies within 12 hours of onset of symptoms. Patients were then randomized to receive control infusion (0.45 percent sodium chloride at 20 ml/hour) (15 patients) or glucoseinsulin-potassium infusion (300 g glucose, 50 units regular insulin, 80 mEq KCl/liter water at 1.5 ml/kg per hour) (13 patients) for 48 hours. All patients received 0.45 percent sodium chloride for 2 more days. Coronary arteriograms and left ventriculograms were obtained in 26 (93 percent) of 28 patients 2 to 3 weeks after infarction.Radionuclide ejection fraction improved during glucose-insulin-potassium infusion (49 ± 4 to 55 ± 5 percent, p < 0.01). Before discharge, the angiographic ejection fraction was greater in the glucose-insulin-potassium recipients than in control patients (43 ± 3 versus 35 ± 3 percent, p < 0.05). Radionuclide ejection fraction decreased in all control patients during the study (42 ± 4 to 37 ± 3 percent, p < 0.0005) and did not change significantly in the treated group (49 ± 4 to 43 ± 5 percent, p = not significant [NS] by paired t test). Regional wall motion analysis revealed an increase in ejection fraction in the “infarcted zone” in the treated group only (44 ± 7 to 54 ± 8 percent, p < 0.01) during glucose-insulin-potassium infusion. There was also a significant decrease in ejection fraction in the “noninfarcted zone” in the control group only (50 ± 4 to 45 ± 4 percent, p < 0.01).During experimental infusion pulmonary arterial end-diastolic pressure decreased in the glucose-insulin-potassium group (17 ± 2 to 12 ± 2 mm Hg, p < 0.01) without changing significantly in the control group. Calculated end-diastolic and end-systolic volume indexes changed in opposite directions in the two groups during experimental infusion (end-diastolic volume index 80 ± 5 to 90 ± 9 ml/m² in the control group versus 70 ± 9 to 55 ± 6 ml/m² in the treated group, p < 0.005 for change from baseline value between groups and the end-systolic volume index 48 ± 6 to 55 ± 8 ml/m² in the control group versus 39 ± 8 to 26 ± 5 ml/m² in the treated group (p < 0.01 for change from baseline value between groups).These data suggest that glucose-insulin-potassium infusion after acute myocardial infarction in human beings (1) increases global ejection fraction, (2) Increases ejection fraction in the “infarcted zone” without changing ejection fraction in the “noninfarcted zone”, and (3) decreases pulmonary arterial end-diastolic pressure and end-diastolic and end-systolic volumes.     

Reflex heart block: Baroreflex, chemoreflex and bronchopulmonary reflex causes

Reflex heart block was studied in 20 dogs anesthetized with sodium pentobarbital and in 5 trained unanesthetized dogs. Three different vagal reflexes were produced: the Marey response during hypertension caused by administering methoxamine, a cardiogenic hypertensive chemoreflex activated by injection of serotonin into the left atrium and the Hering-Breuer reflex observed during normal respiration of unanesthetized dogs. In every dog during any of the three reflexes heart block was consistently observed after the normal slowing response of the sinus node had been selectively eliminated by the direct perfusion of 10 μg of atropine into the sinus node artery. This was a uniform response despite its being variously produced by a pressor reflex, a chemoreflex or an extracardiac bron-chopulmonary reflex. Transient heart block is therefore to be anticipated during reflexes with vagal efferent components if for any reason the sinus node is incapable of slowing suitably. The possible clinical relevance of these experimental observations is discussed.     

Total occlusion of the left main coronary artery: The Coronary Artery Surgery Study (CASS) experience

Total occlusion of the left main coronary artery was confirmed on review of the coronary angiograms in 12 (0.06 percent) of the 20,197 patients entered into the Coronary Artery Surgery Study (CASS) before coronary arterial surgery. Clinical features alone could not distinguish the patients with total occlusion of the left main coronary artery from those enrolled in the CASS with subtotal stenosis of this vessel. The right coronary artery had a stenosis greater than or equal to 70 percent of luminal diameter in 7 of the 12 patients. Collateral flow to the left coronary artery was defined as “substantial” or “limited” based on the presence or absence of clear visualization of the main channel of either the left anterior descending or left circumflex coronary artery during coronary angiography. Of the eight patients with “substantial” collateral flow, one (13 percent) had an aneurysmal or dyskinetic left ventricular wall segment, whereas all (100 percent) of the three patients with “limited” collateral flow had dyskinesia or an aneurysm (p < 0.05). Seven patients underwent coronary bypass graft surgery; 6 (86 percent) of these patients were living at their most recent follow-up, a mean of 46 months after entry into the CASS. Two of these patients continued to have angina pectoris. Five patients did not undergo coronary bypass grafting and 2 (40 percent) were still alive at their most recent follow-up, a mean of 45 months after entry into the CASS. One of these patients had angina pectoris. The difference in survival between the medical and surgical groups was not statistically significant.

This study indicates that patients with total occlusion of the left main coronary artery are uncommon and cannot be distinguished by presenting features alone from patients having subtotal stenosis of the left main coronary artery. “Substantial” coronary collateral blood flow is associated with better left ventricular wall motion than is “limited” collateral flow. Prolonged survival and lessening of symptoms may occur after coronary bypass grafting although long-term survival is possible without it.     

Primary and secondary cardioneuropathies and their functional significance

For most functions of the heart its nerves are as important as its coronary arteries, but this is particularly true concerning cardiac rhythm, conduction and repolarization. It is thus paradoxical that postmortem correlative studies of sudden death virtually always include careful scrutiny of the coronary arteries but only rarely of the cardiac nerves or ganglia. In this review, abnormalities of the cardiac nerves and ganglia, collectively termed cardioneuropathies, are examined from the dual standpoint of their structural appearance and functional significance. Some cardioneuropathies are found in the absence of any other significant structural abnormality detectable in the heart and these are designated as primary cardioneuropathies. A viral etiology or some heritable disorder must rank high among possible causes. Secondary cardioneuropathies are those observed in association with almost every disease that can affect the heart; examples include myocardial infarction, infections, amyloidosis and cancer, but there are many others. Because abnormalities of the heart's nerves and ganglia not only have their own unstabilizing influence on cardiac electrical activity but can also profoundly alter a patient's responses to pharmacologic treatment, it is hoped that future clinicopathologic examinations will more often include their careful study and thereby add to our meager knowledge about these important structures.