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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.

A solution of 300 gm of glucose, 50 units of regular insulin, and 80 mEq of potassium chloride in 1,000 ml of sterile water infused at a rate of 1.5 ml/kg of body weight per hour can alter the availability of glucose and free fatty acids to the myocardium. Clinical studies of patients receiving this infusion less than 15 hours after the onset of symptoms of acute myocardial infarction suggest a reduction in mortality, an improvement in left ventricular mechanical performance, and a reduction in cardiac irritability as beneficial effects. Swan-Ganz catheterization for hemodynamic, electrophysiologic, and metabolic monitoring is recommended. Diabetics who require insulin and patients with impaired renal function are not candidates for the infusion. Further clinical studies are required before conclusions can be reached regarding the efficacy of glucose-insulin-potassium infusion in attempts to salvage damaged myocardium.

The effects of glucose-insulin-potassium (GIK) on hemodynamics and left ventricular (LV) function in patients with acute myocardial infarction (AMI) were investigated in a prospective randomized study. Patients who presented with suspected AMI were candidates for this study if prerandomization evaluation was completed within 12 hours from onset of chest pain. Patients over 75 years of age, insulin-dependent diabetics, patients with renal insufficlency, and comatose patients were excluded. Following completion of baseline hemodynamic measurements, patients were randomly allocated to 48-hour infusion of 300 gm G, 500 units I, and 80 mEq KCl per liter at rate of 1.5 ml/kg/hr or to conventional therapy. In addition to serial hemodynamic measurements, dextran LV function curves (LVFC) were constructed during the second and third days to assess extent of LV injury. Eighty-five of 118 patients who were initially randomized into this study had AMI documented by diagnostic rise and fall of CK-MB isoenzyme. Baseline characteristics and hemodynamics were similar for GIK and control patients with AMI. GIK patients who presented with their initial AMI had significant reduction in pulmonary arterial end-diastolic pressure from prerandomization value of 16 ± 1 to 10 ± 1 by day 3, compared to 18 ± 1 to 16 ± 1 mm Hg for control patients ( p 2 for control patients ( p p p

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.

Severe congestive heart failure secondary to myocardial infarction remains a difficult management problem. Although intravenous vasodilators and mechanical assist devices have been reported to improve the depressed hemodynamic function, these interventions are limited to the intensive care unit and cannot be used for long-term management. This study evaluates the hemodynamic and symptomatic response to sublingual administration to isosorbide dinitrate (5 to 10 mg) in seven consecutive patients with severe congestive heart failure after anterior wall myocardial infarction. Serial measurements of mean right atrial and pulmonary arterial end-diastolic pressure, mean blood pressure, heart rate and cardiac output were obtained during the control period and during the 4 hours after administration of isosorbide dinitrate. The peak response occurred approximately 30 minutes after drug administration with an 83 percent reduction in mean right atrial pressure (from 6 to 1 mm Hg, P less than 0.02), a 36 percent reduction in pulmonary arterial end-diastolic pressure (from 25 to 16 mm Hg, P less than 0.0001) and a 6 percent reduction in mean blood pressure (from 94 to 88 mm Hg (P less than 0.05). There were small but statistically not significant increases in cardiac index (from 2.3 to 2.6 liters/min per m2 and stroke work index (from 26 to 32 gm/beat per m2). The total systemic vascular resistance was reduced by 5 percent from 1,605 to 1,518 dynes sec cm-5 (P less than 0.10). The baseline heart rate of 105 beats/min was not significantly changed. The reduction in pulmonary arterial end-diastolic pressure became statistically significant (P less than 0.05) between 15 and 30 minutes after administration of isosorbide dinitrate and remained significant for 3 to 4 hours. This reduction of pulmonary arterial end-diastolic pressure to less than 22 mm Hg was associated with relief of the patients' pulmonary symptoms. The response to nitroglycerin (0.4 mg) was similar in magnitude but of much shorter duration (approximately 15 minutes for nitroglycerin versus 4 hours for isosorbide dinitrate in patients with and without congestive heart failure. The slope (calculated by dividing the change in cardiac index or stroke work index by the change in pulmonary arterial end-diastolic pressure) was significantly (P less than 0.05) depressed in the patients with congestive heart failure. These data demonstrate that the symptomatic pulmonary venous hypertension can be effectively relieved by isosorbide dinitrate without further compromising left ventricular function.

A man evaluated for disabling chest pain was found to have isolated anatomically corrected transposition of the great vessels. Angiography demonstrated right and left atrioventricular (A-V) valve prolapse and normal coronary arteries. Atrial pacing produced chest pain, ischemic electrocardiographic changes, abnormal myocardial lactate metabolism and marked elevation of the left ventricular end-diastolic pressure; all of these changes returned to normal on termination of pacing. The association of corrected transposition and bilateral A-V valve prolapse and the possible causes of myocardial ischemia in this patient are discussed.

Eighteen patients treated with glucose-insulin-potassium infusion for anaerobic support of acutely ischemic myocardial tissue were studied to ascertain the metabolic consequences of this therapy, for acute myocardial infarction. Twelve patients with acute myocardial infarction were treated in a conventional manner and served as control subjects. The glucose-insulin-potassium solution was composed of 300 g of glucose, 50 units of regular insulin and 80 mEq of potassium ion per liter, and was infused at a rate of 1.5 ml/kg per hour through the right atrial port of an indwelling Swan-Ganz thermodilution catheter. Serial measurements of serum electrolytes, cardiac and hepatic enzymes, glucose and osmolality were obtained every 4 to 6 hours for 4 days. Twenty-four urinary volume and potassium levels were measured daily. Pulmonary arterial end-diastolic pressure was measured hourly and the cardiac index daily for the duration of the study. Serum potassium increased to 5 mEq/liter during the infusion and to more than 6 mEq/liter after infusion in 28 percent of patients. No recognizable complications or arrhythmias accompanied this transient hyperkalemia. Potassium balance studies revealed a net total body potassium ion gain of 120 MEq during the study. The second most frequent finding was an elevation of serum glucose (mean 175 mg/100 ml); in all instances this was controlled with supplemental administration of insulin. The serum osmolality and fluid balance remained normal in all patients during the study. Serum glutamic oxaloacetic transaminase (SGOT) and fraction 5 of lactic dehydrogenase (LDH) were increased in 34 percent of the patients during the last 12 to 18 hours of the glucose-insulin-potassium infusion. Characterization of these enzymes suggested a hepatic origin for these changes. This study suggests that glucose-insulin-potassium infusion is a relatively safe procedure in which postinfusion hyperkalemia is the most serious potential complication.

During the past decade, coronary artery disease has been recognized as one of the major health issues in the adult population, and as a result, intense interest was devoted to the investigation and management of patients with acute myocardial infarction. Major developments in noninvasive and invasive technologies to monitor the electrical and mechanical disturbances of the heart have been achieved. 1–3 As the result of these investigations and techniques, the patient with acute infarction can be characterized by physiologic measurements of rhythm and mechanical function in the absence as well as in the presence of heart failure and cardiogenic shock. With such objective information available on cardiac performance in the individual patient, a variety of therapeutic strategies has become available. 4–6 Thus management of acute myocardial infarction can range from home care or early hospital discharge to intervention with agents to salvage ischemic myocardium and reduce infarction size. This review will describe physiologic measurements in patients with acute myocardial infarction and will include information during the acute phase and several weeks after convalescence. The therapeutic options available in the acute and early convalescent phase will also be discussed.

The authors describe the value of the caudal left-anterior-oblique view in visualizing the following arteries: left main coronary, proximal circumflex, early-arising first marginal, proximal left anterior descending, first diagonal, and anomalous septal perforators from the circumflex system. The technique involves movement of the parallelogram (x-ray tube--image intensifier combination) to the left 55-65 degrees and caudal angulation of 15-20 degrees. To promote additional profiling of the left coronary system, imaging is performed after full expiration. In our series of 100 patients, this view is indispensable in determining significant pathology in the arteries of the proximal left coronary system.

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 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.

Employment and income status of 96 patients randomized into the Alabama portion of the National Cooperative Unstable Angina Study were evaluated before the patients' admission to the study and in 1977. All patients had at least 12 months of follow-up study (mean 38 months). The ratio of patients fully employed at the time of follow-up to those fully employed at entry into the study (baseline) was 0.68 for medically treated patients, 0.53 for surgically treated patients and 0.53 for patients in whom medical therapy failed and who later underwent operation. The changes in annual family income were +$1,111 for medical patients, −$2,447 for surgical and +$875 for those later undergoing surgery. Regression analysis revealed that nonwork income, initial work status, initial income, severity of angina while the patient was in the unstable angina study and the procedural variable (that is, persistent medical, early surgical or late surgical treatment) were associated with return to full-time employment. Changes in family income were related to change in work status, the procedural variable, the patient's education, initial work status, the spouse's income, occurrence of a myocardial infarction after entry into the unstable angina study, duration of angina before entry into the unstable angina study, marital status and sex. Patients who underwent initial surgery had the largest reduction in family income, related to the change in nonworking status at the time of follow-up interview.

The ability to quantitate the amount of permanent left ventricular dysfunction in patients with unstable ischemic heart disease would have important clinical value. Left ventricular function curves were constructed in sixteen patients with acute myocardial infarctions and five patients with unstable angina pectoris syndrome at an average of 56 hours (+/- 8) after the onset of symptoms. Fifty ml increments of low molecular weight dextran were rapidly infused into the right antrium during constant monitoring of the pulmonary artery end-diastolic pressure (PAEDP) via a Swan-Ganz thermodilution catheter. An average of 400 ml (range 200-800) was infused to produce a significant change in the PAEDP (range 3-13 mm Hg). The cardiac index was measured before and after the dextran infusion. The slope of the left ventricular function curve was calculated by dividing the change in the cardiac index by the change in the PAEDP. The sixteen patients with acute myocardial infarction underwent left heart catheterization and left ventricular biplane angiography an average of six months later. The five patients with unstable angina pectoris were studied within one month. The slope value of the left ventricular function curve was compared angiographic ejection fraction by linear regression analysis and the correlation coefficient was 0.80. These data demonstrate 1) the slope of the left ventricular function curve in patients with acute myocardial infarction or unstable angina correlates well with the angiographically calculated ejection fraction; 2) as early as two days post myocardial infarction, the residual impairment of left ventricular function can be estimated.

Moderately electron-dense intramitochondrial inclusions occurred in the myocytes present in biopsies from akinetic or dyskinetic left ventricle from 8 of 10 patients with old myocardial infarction, and in biopsies from 1 of 2 patients having apparently normal left ventricles but presenting with unstable angina. These inclusions were classified according to their presence in necrotic or viable cells into two categoris: (1) The necrotic cell type inclusion occurred in aneurysmal ventricular wall. The inclusion material occupied enlarged matrix spaces, masked cristal membrane profiles and often invaded intracristal spaces of disrupted mitochondria. Cytochrome oxidase activity was shown to be absent in these mitochondria. (2) The viable cell type inclusion occurred in the presence of various focal ultrastructural changes, but myofibrils, glycogen, nuclei and sarcolemma did not show any of the changes described by others for the early irreversible phase of cell injury in animal models of myocardial ischemia. This type of inclusion, 100 to 600 mμ in diameter, developed in the matrix of about 15% of total mitochondrial profiles. Cytochrome oxidase was demonstrated to be active in most of these mitochondria, including those which contained the inclusions. In right ventricular biopsy controls from five of eight patients with old myocardial infarction and from one of two patients with unstable angina, viable cell type inclusions were only rarely seen (less than 1%). The two types of inclusions we found in human hearts are compared with the three distinct types of intramitochondrial densities described by others in animal models of acute myocardial ischemia.

Physiologic studies spanning fifty years suggest that glucose and insulin can be beneficial to cardiac performance under experimental conditions. In 1926, Visscher & Muller observed the positive inotropic effects of insulin on the isolated beating turtle heart (I). Bayliss et al (2) described in 1928 the action of insulin and sugar on the heart-lung preparation. The marked abnormality in carbohydrate metabolism attending fatal diphtheritic myo­ carditis was reported to respond to dextrose and insulin administration in 1930 (3). In his pioneering studies on coronary blood flow and myocardial metabolism, Bing identified extraction and utilization of glucose, lactate, pyruvate, fatty acids, and ketone bodies (4, 5). In experiments on glucose uptake by the perfused rat heart, Morgan and associates (6) found that anoxia increased glucose uptake, and anoxia plus insulin further accelerated glucose uptake. Brachfe1d & Scheuer (7) ob­ served that myocardial ischemia accelerated glycolysis as evidenced by in­ creased glucose consumption and lactate production. Scheuer & Stezoski (8) demonstrated that elevations in cardiac glycogen increased glycolytic reserve and improved resistance to hypoxia mainly by enhancing glycolytic and anaerobic ATP production.

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 During experimental infusion pulmonary arterial end-diastolic pressure decreased in the glucose-insulin-potassium group (17 ± 2 to 12 ± 2 mm Hg, p 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.

S IGNIFICANT EFFORT has been invested to use digital computers as a tool for data processing in several areas of clinical cardiology. From the mid 1960s efforts have been made to utilize computer systems for the analysis of data from cardiac catheterization. These efforts have led to the development of several commercial systems. More recently similar efforts have been made at automating the patient monitoring process in the Coronary Care Unit (CCU). This article presents several computer applications for the analysis of cardiac catheterization data. While some effort is made to present an overview of work done in this area by other investigators, the approach taken in this article is to present in some detail the features of cardiac catheterization systems developed at the University of Alabama in Birmingham Medical Center over the past decade. The intent was to focus on the computer processing techniques typical of catheterization laboratory applications.

A preliminary report is presented of a prospective randomized trial conducted by eight cooperative institutions under the auspices of the National Heart and Lung Institute to compare the effectiveness of medical and surgical therapy in the management of the acute stages of unstable angina pectoris. To date 150 patients have been included in the randomized trial, 80 assigned to medical and 70 to surgical therapy; the clinical presentation, coronary arterial anatomy and left ventricular function in the two groups are similar. Some physicians have been reluctant to prescribe medical or surgical therapy by a random process, and the ethical basis of the trial has been questioned. Since there are no hard data regarding the natural history and outcome of therapy for unstable angina pectoris, randomization appears to provide a rational way of selecting therapy. Furthermore, subsets of patients at high risk may emerge during the process of randomization. The design of this randomized trial is compared with that of another reported trial. Thus far, the study has shown that it is possible to conduct a randomized trial in patients with unstable angina pectoris, and that the medical and surgical groups have been similar in relation to the variables examined. The group as a whole presented with severe angina pectoris, either as a crescendo pattern or as new onset of angina at rest, and 84 percent had recurrence of pain while in the coronary care unit and receiving vigorous medical therapy. It is anticipated that sufficient patients will have been entered into the trial within the next 12 months to determine whether medical or surgical therapy is superior in the acute stages of 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.

To evaluate the relative thrombolytic efficacy and complications of intracoronary vs high-dose, short-term intravenous streptokinase infusion in patients with acute myocardial infarction, we performed baseline coronary arteriography and then randomly allocated 51 patients with acute myocardial infarction to receive either intracoronary (n = 25) or intravenous (n = 26) streptokinase. Patients getting the drug by the intracoronary route received 240,000 IU of streptokinase into the infarct-related artery over 1 hr, whereas those getting the drug by the intravenous route received either 500,000 IU of streptokinase over 15 min (n = 10) or 1 million IU of streptokinase over 45 min (n = 16). Angiographically observed thrombolysis occurred in 76% (19/25) of the patients receiving intracoronary streptokinase, in 10% (1/10) of the patients receiving 500,000 IU of streptokinase intravenously, and in 44% (7/16) of the patients receiving 1 million IU of streptokinase intravenously. Among patients in whom thrombolysis was observed, mean elapsed time from onset of streptokinase infusion until lysis was 31 +/- 18 min in patients receiving intracoronary streptokinase and 38 +/- 20 min in those receiving intravenous streptokinase (p = NS). Among patients in whom intravenous streptokinase "failed," intracoronary streptokinase in combination with intracoronary guidewire manipulation recanalized only 7% (1/15). Fibrinogen levels within 6 hr after streptokinase were significantly lower in the patients receiving intravenous streptokinase (39 +/- 17 mg/dl) than the levels in those receiving intracoronary streptokinase (88 +/- 70 mg/dl) (p less than .05) but were similar 24 hr after streptokinase in the two groups. Bleeding requiring transfusion occurred in one patient in each group. Thus, in this prospective randomized trial of intracoronary vs intravenous streptokinase, hemorrhagic complications were few, although both regimens produced a systemic lytic state. Although the thrombolytic efficacy of intracoronary streptokinase was superior to that of high-dose, short-term intravenous streptokinase, the higher-dose intravenous regimen (1 million IU over 45 min) achieved thrombolysis in a significant minority (44%) of patients and might be useful therapy for patients not having access to emergency catheterization.

Two hundred-three patients had -echnetium 99m (stannous) pyrophosphate myocardial scintigrams for the evaluation of chest pain and suspected acute myocardial infarction. In addition to routine imaging at 60--90 minutes after injection of the radio-pharmaceutical, the blood pool was imaged immediately in each patient for comparison with routine anterior, left anterior oblique, and left lateral views. Further delayed studies were obtained when residual blood pool activity was identified. Seventy patients had acute myocardial infarction by clinical, electrocardiographic, and enzymatic (CK-MB) criteria. Sixty-five of these 70 patients with acute infarction had positive myocardial scintigrams, with one technically unsatisfactory study. Only four of the 70 patients had negative scintigrams when imaged 18--72 hours after infarction in this study. Technically satisfactory scintigrams were recorded in 125 patients without evidence of infarction. Ninety-six had negative scintigrams at 60--90 minutes, while 19 patients (15%) had precordial activity at 60--90 minutes which was identical in distribution to early blood pool images and cleared with further delay. With these included, the true negative incidence was 92%. Ten of 125 patients had false positive scintigrams; two had recent cardioversion with resultant chest wall damage. The other eight patients had previous infarction 1 1/2 to 72 months earlier and had akinetic segments shown angiographically in the areas of the persistently positive scintigrams. Myocardial scintigraphy correlates well with the presence of other evidence of acute infarction, as well as with the absence of acute infarction when residual blood pool activity is identified. False positive scintigrams can occur following cardioversion and in patients with previous myocardial infarction and resultant ventricular wall motion abnormalities.

Although biplane right anterior oblique-left anterior oblique (RAO/LAO) quantitative left ventricular (LV) angiography is commonly performed, justification of LV volume calculation using the area length method (originally formulated from anteroposterior-lateral (AP/LAT) angiograms) has been limited. To assess whether RAO/LAO and AP/LAT LV volumes are similar when computed by the area length method formula, we performed biplane cine LV angiography in both RAO/LAO and AP/LAT projections in random sequence in 21 patients and four LV models of known volume. LV silhouettes were drawn independently by two trained observers. Calculated angiographic volume of the models correlated almost exactly with their true volume (r = 0.999), establishing the absolute accuracy of this system. Rotation of the LV models through 90 degrees of obliquity at 10 degree increments demonstrated a mean change from true volume of only -5.4 +/- 0.7% (p less than 0.001). In the patient studies, rotation to the 30 degree RAO/60 degree LAO position was associated with significant changes in magnitude of biplane areas and long axes, but area length volume estimates were unchanged. Excellent correlation was found between area length calculated AP/LAT and RAO/LAO volumes with r = 0.90, 0.97, and 0.91 for end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF), respectively. Furthermore, interobserver agreement in volume assessment was excellent, with r = 0.98, 0.99, and 0.94 between observers for EDV, ESV, and EF, respectively. Interobserver and inter-method variability for estimates of LV volume and EF ranged from 5--10%. We conclude that when using RAO/LAO LV angiography, volume calculation by the area length method is justified.

Since coronary revascularization improves prognosis in some patients with multivessel disease, can the potential benefits be extended to "prophylaxis" in selected postinfarction patients as well? These investigators sought the answer on the basis of patient characteristics, types of surgery, survival data, and mode of death in the postinfarction population of 129 patients who had early angiography.

Biplane axial left cineventriculography represents the most accurate diagnostic technique for evaluating acquired and congenital heart disease. However, data have accumulated to indicate that without angled views of the left ventricle, the diagnosis will be incomplete and inaccurate in a significant number of patients. Left ventriculography is the acknowledged standard for left ventricular performance. However, comparison of the conventional or nonangled left anterior oblique left ventriculogram with the angled views of the left ventricle obtained with either two dimensional ultrasound or radionuclide left ventriculography may in many cases be invalid because dissimilar views are compared. The cranial-left anterior oblique view allows more accurate assessment of the precise degree and extent of asynergy, left ventricular aneurysms and ventricular septal defects. Left ventricular outflow tract abnormalities such as discrete subaortic stenosis and the obstructive form of hypertrophic cardiomyopathy can easily be distinguished. Lesions involving the mitral valve, especially mitral valve prolapse, are readily evaluated. Lastly, comparison with noninvasive tests of left ventricular performance can be more accurately performed.

Tennant and Wiggers [1] were perhaps the first to demonstrate the phenomenon of segmental left ventricular dysfunction when, in 1935, they ligated a coronary artery in a dog and at once observed paradoxic motion of the underlying myocardium. Subsequently, Harrison [2] recognized disordered patterns of contraction in the kinetocardiograms of patients with ischemic heart disease and applied the term “asynergy,” and, later, “dyssynergy,” [3] to this condition. More recently, Herman et al. [4], in an elegant quantitative ventriculographic study of patients with coronary artery disease, introduced the now familiar terms “hypokinesis,” “akinesis,” and “dyskinesis” for description of left ventricular contraction abnormalities.

Three hundred patients were examined to determine the value of the caudocranial right anterior oblique view (RAO) in revealing or improving visualization of lesions in the proximal and mid-left anterior descending artery (LAD), the origins of the septal and diagonal arteries, and the distal branches of the right coronary artery (RCA). The proximal and mid-LAD were shown to greater advantage in 80% of cases, the diagonal arteries in nearly 75%, the septal vessels in more than 90%, and the posterior descending and posterolateral branches of the distal RCA in more than 80%; in addition, the cranial RAO view revealed previously unsuspected lesions in 7% of the proximal and mid-LAD arteries and 26% of the septal vessels. In addition to superior visualization, this view gives satisfactory exposure even in extremely large patients and may also be helpful in coronary angioplasty.

SUMMARY The usefulness of thallium-201 (Tl-201) exercise myocardial scintigraphy in identifying patients with multivessel coronary artery disease (MVCAD) and residual jeopardized myocardium after myocardial infarction (MI) was evaluated in 32 patients 3 weeks after MI. All patients underwent 1) limited multilead submaximal treadmill testing, 2) thallium-201 (TI) myocardial scintigraphy at end-exercise and at rest, and 3) coronary and left ventricular angiography. TI-201 perfusion defects were categorized as either reversible (ischemia) or irreversible (scar). The conventional exercise test was designated positive if there was ST depression 2 1 mm and/or angina. Jeopardized myocardium (JEP) was defined angiographically as a segment of myocardium with normal or hypokinetic wall motion supplied by a significantly stenotic major coronary artery. MVCAD was defined as two or more significantly stenotic coronary arteries. “Significant” coronary stenosis was categorized as either 50–69% diameter narrowing or 2 70% diameter narrowing, thereby yielding, respectively, two subgroups each of jeopardized myocardium (JEP-50 and JEP-70) and MVCAD (MV-S0 and MV-70). Clinical findings of angina, heart failure or ventricular arrhythmias during the late convalescent period after MI occurred in four of 10 patients (40%) with MV-50, five of 16 (31%) with MV-70, four of 10 (40%) with JEP-50 and five of 18 (28%) with JEP-70, and thus were insensitive for detecting MVCAD and JEP. Reversible ischemia and/or a positive conventional exercise test occurred in five of 10 patients (50%) with MV-50, 13 of 16 (81%) with MV-70, four of 10 (40%) with JEP-S0 and 15 of 18 (83%) with JEP-70. All eight patients with both TI-201 reversible ischemia and a positive conventional exercise test had JEP-70. In 30 of 31 patients (97%) with angiographic asynergy, TI-201 scar was detected. No complications were associated with exercise testing. Thus, 3 weeks after MI, Tl-201 exercise myocardial scintigraphy is a safe, useful, noninvasive tool for identifying patients with MVCAD and residual JEP and is much more reliable than clinical findings during convalescence after MI.

This presentation has described the modern approach to the patient presenting with chest pain suspected as acute myocardial infarction. Noninvasive and invasive methods have been applied to estimate the extent of the myocardial damage and to monitor the electrical, hemodynamic and metabolic changes during the acute phase. In addition to the use of standard analgesics and antiarrhythmics, measurement of the determinants of left ventricular function by noninvasive and invasive techniques provides a physiologic basis for administration of available pharmacologic agents that can alter the afterload, contractile state, preload, heart rate, metabolic state and infarct size. Information from the Swan-Ganz catheter can describe hemodynamic categories that can be optimally managed by regulation of the left ventricular filling pressure. Patients managed in this manner can be identified for early hospital discharge at 7–10 days. Other patients less than 50 years of age or those experiencing recurrent arrythmias, ischemic pain or evidence of left ventricular dysfunction may be candidates for coronary arteriography and left ventricular angiography before hospital discharge.

The relationship between effective renal plasma flow (ERPF) and cardiac output was examined in 46 patients (22 with congestive heart failure and 24 following cardiac surgical procedures) by simultaneously measuring the global ERPF by the single-injection method and cardiac output by the thermodilution method. Of the patients in the heart-failure group, 21 also had pulmonary artery end diastolic pressure (PAEDP) recorded at the same time. ERPF and cardiac output were found to be related by the regression equation: cardiac output = 2.08 +/- 0.0065 ERPF (r, 0.80), with a SE of estimate of 0.81 l/min. ERPF and PAEDP were related by the regression equation: PAEDP = 45.02-0.0675 ERPF (r, 0.86), with a SE of estimate of 5.5 mm Hg. ERPF may be a useful noninvasive method of estimating cardiac output if it is known that no intrinsic kidney disease is present, and if the error of 0.81 l/min (1 SE of estimate) is within the range of clinical usefulness. The error is principally attributable to the determination of cardiac output by the thermodilution method.

A 39-year-old man developed cardiac tamponade with Dressler's syndrome four weeks after an inferior myocardial infarction. Treatment of the tamponade by pericardiocentesis on two occasions produced serous fluid. The pericardial effusion cleared with short-term therapy with corticosteroids and the prolonged use of indomethacin.

Debate exists over the most appropriate form of treatment for patients with unstable angina pectoris. This study examined 106 patients randomized at the University of Alabama in Birmingham as part of the National Cooperative Study Group and focuses on the phenomenon of patients who fail medical therapy and thus require late surgery, and the costs of therapy. Discriminant function analysis revealed that the significant predictors (p less than 0.01) of patients who would later require surgery were: total number of vessels diseased, angina severly, presence of congestive heart failure, hypertension, and number of years that the patient had had angina. By means of this analysis, 85% of the late surgery patients were correctly predicted. Late surgery patients averaged 2.4 diseased vessels vs 1.5 for persistent medical patients (p less than 0.01). Mean charges for the first 2 years in the study were $6,226 (SD $2,967) for persistent medical patients, $10,416 (SD $2,146) for surgery patients, and $20,059 (SD $10,748) for late surgery patients (p less than 0.001). These data indicate that surgery is clearly an expensive procedure; but that it is more expensive for late surgery patients, who have total costs that are twice as high as surgical costs and 3.5 times as high as persistent medical costs.

The value of the cranial-right anterior oblique view in uncovering or improving the arteriographic visualization of lesions in the mid left anterior descending coronary artery, the origin of its diagonal and septal branches and of the distal branches of the right coronary artery was analyzed in 300 consecutive patients. The cranial-right anterior oblique view was compared with standard and other angled views. In the mid left anterior descending artery the view provided improved visualization over the other views in 80 percent of cases and uncovered lesions in 7 percent. In the septal arteries, the view improved visualization in more than 90 percent of cases and uncovered lesions in 26 percent. In the diagonal branches, the view improved visualization in nearly 75 percent of cases. In the distal right coronary artery there was improved visualization of the posterior descending and posterolateral branch arteries in more than 80 percent of cases. The cranial-right anterior oblique view was also the most advantageous view from a technical standpoint, yielding satisfactory exposure factors in obese and extremely heavy patients.

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] 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.

Total and individual plasma free fatty acids (FFA) were measured on admission and over the next 4 days in 24 patients admitted to the hospital with chest pain and suspected acute myocardial infarction (AMI). In a prospective randomized fashion, the patients were either given an infusion of 300 gm of glucose, 50 units of insulin, and 80 mEq of KCl per liter at a rate of 1.5 ml/kg/hr over the initial 48 hours of hospitalization, or they served as controls receiving conventional therapy. Eleven patients were in the control group and 13 were in the glucose-insulin-potassium (G-I-K) group. Twenty-one of the patients had an AMI by CK-MB rise and ECG changes (in the G-I-K group three did not evolve AMI). The total plasma FFA were 840 +/- 134 microM/L in the controls and 933 +/- 160 microM/L in the G-I-K group initially (prestudy). Total FFA rapidly fell in the G-I-K group and then rebounded when G-I-K was stopped. In contrast, total FFA values fell gradually in the control group over the 4-day period. The individual FFA had similar percentages initially in the two groups. In the control group the percent of individual plasma FFA was unchanged over the period studied, although there was some mild random day-to-day fluctuation. In contrast in the G-I-K group linoleic acid fell both during and after the infusion was stopped (26.8% to 19.1% P less than 0.001). Arachidonic acid doubled in percentage of the total FFA value during G-I-K infusion (3.1% to 6.5%, P less than 0.002) and returned to the control value when it was stopped. Thus G-I-K infusion during AMI reduces the total level of plasma FFA while increasing the percent of arachidonic and decreasing the percent of linoleic acid, observations proposed to reflect improved membrane stability of the ischemic myocardium.

Accumulated creatine kinase MB isoenzyme release (sigma CK-MB) during acute myocardial infarction was correlated with biplane left ventricular (LV) angiographic estimates of percent abnormally contracting segment (%ACS) and ejection fraction (EF) in 35 patients who underwent diagnostic angiography at a mean of 33 +/- 4 days post myocardial infarction (MI). Of the 35 patients, 18 had no evidence of prior MI and their sigma CK-MB showed good correlation with %ACS (r = 0.84) and with EF (r = - 0.78). An additional two patients with first (inferior) infarct secondary to stenosis of the right coronary artery proximal to the origin of the right ventricular arterial blood supply had disproportionately large sigma CK-MB, suggesting a combination of LV and RV necrosis. In the 15 patients with prior infarct, there was no significant correlation between sigma CK-MB and %ACS or EF. However, in the subgroup of patients with anterior MI, %ACS correlated with sigma CK-MB, both in patients with no prior MI (r = 0.88, N = 12) and in patients with prior MI (r = 0.69, N = 9). These independent angiographic and enzymatic data suggest that enzymatic infarct size estimates utilizing accumulated CK-MB release may be a valid and reliable clinical measure for assessing the extent of LV necrosis in the setting of acute anterior myocardial infarction. However, limitations may exists in certain cases of inferior MI, probably because of concomitant right and left ventricle necrosis.

Free fatty acids (FFA), the predominant myocardial energy substrate, are present in increased quantities immediately following acute myocardial infarction (AMI) and may cause deleterious alterations in cardiac rhythm, oxygen consumption, and mechanical performance. In an attempt to suppress FFA and simultaneously increase the availability of carbohydrate as a myocardial substrate, 70 patients with unequivocal AMI were administered a right atrial infusion of glucose-insulin-potassium (GIK) (300 gm. of glucose, 50 U. of regular insulin, and 80 mEq. of KC1 per liter of H2O) at a constant rate of 0.5 to 2.0 ml. per kilogram per hour for 48 hours. A dramatic fall in FFA (944 +/- 57 to 289 +/- 16 muEq per liter, p less than 0.0005) occurred during GIK infusion, and FFA rebounded to 420 +/- 39 muEq per liter (p less than 0.005) when GIK was discontinued. The hospital mortality rate in the 70 GIK recipients was compared to that of 64 untreated patients (controls) from the same coronary-care unit during the previous year. GIK and control groups had similar severity of infarction as assessed by prognostic scales of Killip, Peel, and Norris, respectively. The hospital mortality rate was reduced in the GIK recipients compared to the control group (11/70 vs. 19/64, p less than 0.05). In patients without history of prior myocardial infarction, the mortality rate was reduced four-fold in GIK recipients compared to controls (6 vs. 24 per cent, p less than 0.05). Complications of GIK infusion were infrequent and included chiefly hyperglycemia and hyperkalemia, both of which dictated meticulous monitoring of serum chemistries. The data suggest that suppression of plasma FFA with GIK infusion may be associated with a significant reduction in the hospital mortality rate of acute myocardial infarction.

An echocardiographic digital image processing system has been constructed to quantify left ventricular (LV) dynamics. The system utilizes a commercial 8 bit analog-to-digital convertor (ADC) that encodes A-scan information from the echo pulses. The high rate conversions are stored in a shift register buffer memory, and between echo pulses are transmitted at reduced rate to the computer. A scan convertor with 32 levels of grey scale is used to display raw and processed echo data, physiological signals and alphanumerics at a remote computer terminal.

This study compares the inpatient costs of therapy of patients with unstable angina pectoris randomized to surgical or medical therapy at the University of Alabama in Birmingham as part of the National Cooperative Study Group. For 74 patients followed up for 2 years, the mean inpatient charges were $4,728 for 22 medically treated patients, $9,528 for 34 surgically treated patients and $20,215 for 18 patients who crossed over from medical to surgical therapy. Differences among the three groups were statistically significant (P less than 0.001). Stepwise multiple regression analysis of total inpatient charges with medical and procedural factors as explanatory variables showed that a history of congestive heart failure, the number of infarctions during the period of the study, the duration of the longest anginal attack, the type of unstable angina and the type of treatment were significant predictors of total inpatient cost, with an R2 value of 0.829 (P less than 0.001). These variables explain the cost of treatment. One should not infer that they will also predict the appropriate type of treatment for patients with unstable angina. Although the cost of surgical therapy was double the cost of therapy for patients treated only medically, those medically treated patients whose therapy failed and who subsequently required surgery incurred mean costs twice those of the surgically treated patients and four times of patients who received only medical therapy. Reassessment of previous criticism of the high cost of surgical therapy is indicated.

The hemodynamic response to nitroglycerin administration, to sublingual or oral administration of isosorbide dinitrate, or to a placebo was evaluated and compared in 37 patients with unstable angina pectoris under resting, pain-free conditions. Patients with congestive heart failure were not included in this study. Serial measurements of mean arterial blood pressure (MAP), pulmonary arterial end-diastolic pressure (PAEDP), cardiac index (CI), and heart rate (HR) were obtained for one hour following nitroglycerin administration and for four hours following sublingual or oral administration of isosorbide dinitrate. Echocardiographic end-diastolic volume (EDV) measurements were obtained for the groups receiving isosorbide dinitrate or placebo. There was a significant (P less than 0.05 or less than 0.1) reduction of the MAP (5 to 10 mm Hg) that persisted for more than four hours following both sublingual and oral administration of isosorbide dinitrate. The changes in the PAEDP, HR, and CI following sublingual or oral administration of isosorbide dinitrate were small and not significant. In the group receiving isosorbide dinitrate sublingually, the EDV was reduced by more than 30 ml below the placebo group (P less than 0.1) for up to four hours. The effects of nitroglycerin administration were similar in magnitude but of much shorter duration (three to four hours for sublingual and oral administration of isosorbide dinitrate vs 15 to 30 minutes for nitroglycerin). These data demonstrate that the duration of the hemodynamic effects of sublingually and orally administered isosorbide dinitrate in patients with unstable angina pectoris and normal resting hemodynamics is 8 to 12 times longer than that of nitroglycerin.

We evaluated 198 consecutive survivors of acute myocardial infarction and performed selective coronary angiography in 117 of 131 (89 percent) patients who were deemed candidates for angiography by clinical criteria. Overall, left main CAD (greater than or equal to 70 percent stenosis) was found in ten patients (8.5 percent), three vessel CAD in 41 patients (35 percent), two vessel CAD in 37 patients (31.5 percent), single vessel disease in 27 patients (23 percent) and zero vessel disease in two patients (2 percent). Factors suggesting multivessel disease included older age, history of prior myocardial infarction, and post-infarction convalescence complicated by angina pectoris. Factors not discriminating between single and multivessel disease were sex, infarct extent (transmural vs non-transmural), (3) infarct location (anterior vs inferior), and post-infarction convalescence complicated by late arrhythmia or heart failure. This study demonstrates that multivessel coronary artery disease is common in survivors of myocardial infarction and is suggested by the occurrence of post-infarction angina and by the history of an antecedent myocardial infarction. Coronary angiography can be performed safely within 30 days after myocardial infarction in patients with an uncomplicated convalescence and with mild risk in those with a complicated convalescence.

We report our experience with the use of a standard left Amplatz coronary catheter and a guidewire to cross the aortic valve in 34 patients being evaluated for valvular aortic stenosis. A number of 2 Amplatz left coronary catheter inserted via the femoral artery was positioned above the noncoronary aortic valve cusp with the tip aligned toward the aortic valve. This catheter allowed a soft-tipped, Teflon-coated guidewire to be guided through the aortic valve orifice. The catheter was then advanced over the guidewire into the left ventricle. This technique was successful within six minutes in 32 of 34 patients (94%). The stenotic aortic valve was crossed in less than two minutes in 15 patients (42%) and in less than four minutes in 31 (91%). The aortic valve was not crossed in two patients. Twenty-one patients (62%) had an aortic valve area of less than 0.75 cm2. There were no complications. We conclude that this technique provides a method for safe, rapid transaortic left ventricular catheterization in patients with aortic stenosis of all degrees of severity.

The data from 88 patients (pts) with aortic stenosis (AS) were reviewed to determine relationships between angina pectoris (AP) and coronary artery disease (CAD). Results of surgery performed in 81 of these pts was analyzed. All pts had coronary arteriograms, and lesions greater than or equal to 50% were considered significant. Fifty-nine pts had an aortic valve gradient measured at catheterization greater than or equal to 40 mmHg, and in 29 pts, AS was confirmed at operation. Sixty-eight pts (77%) experienced AP, and 32 had coexisting CAD (47%); 9 of 20 pts without AP had CAD (45%). There were no significant differences in the incidence of AP in pts divided into subgroups by the aortic valve gradient (40-50, 51-100, 101-200 mmHg) or age (40-59, 60-81 years). Also, no significant differences were found in the incidence or extent of CAD between the two age groups; the extent of CAD was similar regardless of the presence or absence of AP. In pts with AP (1) CAD was more likely in pts greater than or equal to 60 years of age; (2) CAD was less likely when the aortic valve gradient was greater than 100 mmHg, suggesting that AP in these pts was due to hemodynamically severe AS. All pts with 3-vessel CAD experienced AP, and the aortic valve gradient was less in these pts than in those with no CAD or less extensive CAD. In 19 pts with combined AS and CAD who had both the aortic valve replaced and a revascularization operation only 1 of pts died in the hospital, while 3 of 19 pts with combined AS and CAD who had aortic valve replacement alone died. In this study a significant number of pts with AS experienced AP, and the presence or absence of AP did not predict coexisting CAD. Coronary arteriography is recommended in the evaluation of pts greater than or equal to 40 years of age with AS. The operative mortality appears to be decreased in pts with AS and CAD who have combined surgery.

Despite the development of trained mobile rescue squads, cardiopulmonary collapse outside the hospital continues to carry a poor prognosis. We examined retrospectively the clinical courses of 19 consecutive coronary unit patients who had experienced prehospital cardiopulmonary resuscitation. Seven patients received basic life support from bystanders within five minutes. Cardiopulmonary resuscitation in the other 12 patients was delayed beyond five minutes pending the arrival of rescue personnel. Six of seven early-resuscitated patients survived compared with six of 12 late-resuscitated patients (P less than 0.01). The early-resuscitated patients were more alert on admission and had lower pulmonary pressures and higher cardiac outputs compared to the late-resuscitated patients. The early-resuscitated patients also had less residual central nervous system and myocardial damage on discharge than the late-resuscitated patients. On follow-up, three early-resuscitated patients had returned to full-time work compared with none in the late group. Training laymen to initiate early basic life support can benefit the cardiopulmonary collapse victim.

This paper discusses the practical aspects of incorporating an indexed sequential file structure into a large time sequential data base, which includes the sequence of intervals between heartbeats measured from the electrocardiogram (ECG). First, the paper describes the time sequential data base. Secondly, the paper presents uses made of the time sequential file. Finally, the paper describes the indexed sequential data structure developed to support this application.