Free fatty acid metabolism of the human heart at rest.

Myocardial substrate metabolism was studied in 13 subjects at the time of diagnostic cardiac catheterization by means of palmitic acid-(14)C infusion with arterial and coronary sinus sampling. Two subjects were considered free of cardiac pathology and all, with one exception, demonstrated lactate extraction across the portion of heart under study. Data for this single lactate-producing subject were treated separately.The fractional extraction of (14)C-labeled free fatty acids (FFA) (44.4+/-9.5%) was nearly twice that of unlabeled FFA (23.2+/-7.8%) and raised the possibility of release of FFA into the coronary sinus. FFA uptake, based on either the arterial minus coronary sinus concentration difference or the FFA-(14)C fractional extraction, was directly proportional to the arterial FFA concentration. Gas-liquid chromatography failed to demonstrate selective handling of any individual FFA by the heart. Fractional oxidation of FFA was 53.5+/-12.7%, accounting for 53.2+/-14.4% of the heart's oxygen consumption while nonlipid substrates accounted for an additional 30.0+/-17.3%. Determinations of both labeled and unlabeled triglycerides suggested utilization of this substrate by the fasting human heart. Direct measurement of FFA fractional oxidation as well as FFA uptake, exclusive of possible simultaneous FFA release, would appear necessary in studies concerned with human myocardial FFA metabolism.

Muscle and splanchnic glutmine and glutamate metabolism in postabsorptive andstarved man.

Arterio-venous differences across forearm muscle in man in both prolonged starvation and in the postabsorptive state, show an uptake of glutamate and a relatively greater production of glutamine. Splanchnic arteriovenous differences in the postabsorptive state show a net uptake of glutamine and lesser rate of glutamate production. These data suggest that muscle is a major site of glutamine synthesis in man, and that the splanchnic bed is a site of its removal. The relative roles of liver and other tissues in the splanchnic circuit were not directly assessed, only the net balance. These data in man are in conflict with most previous studies in other species attributing the major proportion of glutamine production to the liver and, pari passu, to the splanchnic bed.

Coronary circulatory dynamics before and after successful coronary angioplasty.

The hypothesis that successful percutaneous transluminal coronary angioplasty restores normal coronary circulatory dynamics was tested. Regional coronary blood flow, myocardial oxygen consumption and lactate extraction were measured at rest and during sustained pacing tachycardia. Before angioplasty, tachycardia stress was associated with an attenuated blood flow and oxygen consumption response and the induction of anaerobic metabolism. After successful angioplasty, blood flow and myocardial oxygen consumption increased during tachycardia stress and aerobic metabolism was sustained. The influence of basal alpha-adrenergic tone in modifying the time course of blood flow response to abrupt pacing was also assessed. Patients with normal coronary arteries demonstrated delayed increase in blood flow after alpha-adrenergic blockade. Alpha-adrenergic blockade did not affect the time course of blood flow response in patients with coronary artery disease, suggesting that alpha-adrenergic tone was chronically withdrawn. In patients undergoing coronary angioplasty, flow response before angioplasty was delayed, consistent with withdrawal of basal alpha-adrenergic tone. After coronary angioplasty, a brisk flow response was observed, indicating that basal alpha-adrenergic tone had been restored. Thus, successful coronary angioplasty restores the normal responsiveness of the coronary circulation.

Objective assessment of coronary angioplasty for multivessel disease: results of exercise stress testing.

The efficacy of coronary angioplasty in multivessel coronary artery disease was evaluated in a series of 145 consecutive patients in whom angioplasty had been successful and in whom a follow-up exercise stress test was performed within 2 months. Exercise stress test results of these patients with multivessel disease were compared with those of 177 patients with single vessel disease after successful coronary angioplasty. The postangioplasty exercise test showed ischemia in 13% of patients with single vessel and 29% of those with multivessel disease, although only 7 and 13%, respectively, experienced angina. The mean exercise duration was comparable for patients with multivessel disease (453 +/- 174 s) and single vessel disease (476 +/- 166 s). To assess the impact of the degree of revascularization in patients with multivessel disease on the results of exercise testing, 48 patients with completely revascularized vessels and 97 with incompletely revascularized vessels were evaluated. The mean exercise duration (459 +/- 178 versus 450 +/- 173 s), mean maximal heart rate (132 +/- 31 versus 136 +/- 25 beats/min) and mean systolic blood pressure (174 +/- 25 versus 170 +/- 26 mm Hg) were similar in completely and incompletely revascularized groups. Exercise-induced angina occurred in 13% of both groups. Ischemic ST segments were more common in the incompletely revascularized group (34 versus 19%, p = 0.06). Thus, exercise stress testing provides evidence that successful angioplasty can relieve electrocardiographic manifestations of ischemia as well as anginal symptoms in the majority of patients with either single or multivessel coronary artery disease who are suitable candidates for the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Thrombolytic therapy for prosthetic cardiac valve thrombosis.

To determine the efficacy and safety of thrombolytic therapy for prosthetic valve thrombosis, a composite series of 41 patients who received either streptokinase or urokinase intravenously for this disorder were analyzed. The series comprised 3 patients treated at Rhode Island Hospital and 38 previously reported on. Short-term success was achieved in 32 patients (78%). Prosthetic valve thrombosis recurred in seven (22%) of the successfully treated patients, four of whom were retreated with thrombolytic therapy. A favorable clinical outcome was observed in each. Fever and venipuncture bleeding were the most frequent side effects. Systemic embolization occurred in 4 (15%) of 26 patients with either aortic or mitral prosthetic valve thrombosis. None of these latter patients experienced a permanent neurologic or circulatory deficit. It is concluded that thrombolytic therapy is of value in the treatment of prosthetic valve thrombosis.

Role of adenosine in mediating myocardial blood flow response to isoproterenol: observations in closed chest, sedated, domestic swine.

To test the hypothesis that adenosine is required to mediate the sustained increase in myocardial flow evoked by isoproterenol haemodynamic indices, myocardial blood flow (microspheres), and regional myocardial oxygen consumption were measured in eight closed chest, sedated pigs at control, after isoproterenol (6.9(2.8) ng X kg-1 X min-1 (mean (SD)) infused into the left anterior descending coronary artery, repeat control, and after a simultaneous infusion of the same dose of isoproterenol and adenosine deaminase (10 U X kg-1 X min-1). Data were acquired at one and 10 minutes after each infusion and compared with control measurements. Heart rate was held constant by atrial pacing. Peak left ventricular dP/dt (mm Hg X s-1) increased significantly (control 2190(32) mean (SD)) at both one (2900(302)) and 10 minutes (3010(391)) of isoproterenol infusion alone. At one minute of simultaneous infusion there was no change (control 1970(447)) in left ventricular dP/dt (2290(521)), although dP/dt was significantly increased at 10 minutes of simultaneous infusion (2790(483)). Transmural flow (ml X min-1 X g-1) increased significantly (control 1.49(0.46)) in the distal left anterior descending zone at one (1.94(0.48)) and 10 minutes (2.07(0.27)) of isoproterenol infusion alone. In contrast, flow failed to increase (control 1.65(0.27)) during the first minute of simultaneous infusion (1.73(0.38)), although it did increase significantly by 10 minutes (1.91(0.21). Finally, although myocardial oxygen consumption (ml X min-1 X 100 g-1) increased significantly (control 16.4(4.7)) at both one (20.1(4.7)) and 10 minutes (19.4(3.6)) of isoproterenol infusion alone, it failed to increase (control 18.2(3.8)) at one (19.3(4.6)) and 10 minutes (19.1(3.8)) of simultaneous infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Elevated coronary vascular resistance in the presence of reduced resting blood flow distal to a severe coronary stenosis.

Vascular reserve in underperfused myocardium has recently been described. This seemingly paradoxical observation conflicts with older concepts of the coronary circulation which hold that flow deficits do not develop until reserve is fully exhausted. To examine this phenomenon in greater detail in an animal model mimicking a fixed human coronary artery stenosis, we analysed the records of 25 carefully selected, sedated pigs all instrumented with a rigid intralumenal coronary stenosis (82% lumenal diameter reduction). Each animal satisfied the following criteria: 1) perfused myocardial mass beyond the stenosis was within a narrow weight range (16 to 24 g); and 2) post stenosis (distal) epicardial (Epi) and endocardial (endo) flows were less than or equal to 90% of respective flows in a region perfused by the non-stenosed circumflex (CX) coronary artery. Accordingly, distal flow was reduced compared to circumflex zone flow (p less than 0.01) in the Epi (173 +/- 51 to 113 +/- 32 ml . 100g-1 . min-1), Endo (146 +/- 39 to 116 +/- 27) and transmural (Tm) regions (164 +/- 45 to 124 +/- 31). Despite a flow deficit and constant severity of stenosis, distal zone Tm resistance (0.55 +/- 0.21 mmHg/ml . 100 g-1 . min-1) exceeded the minimum level achievable with intravenous infusion of adenosine (0.25 +/- 0.07) in a separate group of eight animals without a stenosis. Distal transmural resistance also varied over a five fold range (0.27 to 1.33) and in 20/25 animals exceeded the highest level (0.37) seen in non-stenosis animals during adenosine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of adenosine in mediating the coronary vasodilative response to acute hypoxia.

To test the hypothesis that adenosine is required to mediate the coronary vasodilative response to acute hypoxia haemodynamic indices, regional myocardial blood flow, and oxygen and lactate metabolism were measured in nine closed chest anaesthetised domestic swine at control, after 3-5 min of 100% nitrogen inhalation, at second control, and after 3-5 min of 100% nitrogen inhalation plus adenosine deaminase infusion in the left anterior descending coronary artery. Cardiac lymph adenosine deaminase concentration was also measured in a separate group of four animals previously reported on. Heart rate was held constant by atrial pacing during the study. Aortic mean pressure did not change. Changes in arterial and anterior interventricular vein pH, PO2, PCO2, and oxygen content were similar for each intervention. Transmural left anterior descending artery zone flow increased significantly (p less than 0.01) compared with control (1.22(0.23) ml.min-1.g-1; mean(SD)) in response to hypoxia (2.73(0.92)). Intracoronary adenosine deaminase infusion (167 nmol.s-1), however, failed to blunt the flow response to hypoxia (1.33(0.30) to 2.79(1.32); second control to hypoxia plus adenosine deaminase respectively, p less than 0.01). Mean adenosine deaminase activity (nmol.s-1) in cardiac lymph was 105(85) at the end of 10 min of intracoronary infusion (167 nmol.s-1) and 203 (148) nmol.s-1 at the end of 15 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Recovery of myocardial function following brief versus prolonged atrial pacing stress in the presence of coronary artery stenosis.

The ability of myocardium distal to a severe coronary artery stenosis to recover from brief (5 min) versus prolonged (30 min) atrial pacing stress was compared in this study. Eight closed chest pigs were prepared with a coronary artery stenosis (82% lumenal diameter reduction) in the left anterior descending artery and ultrasonic length sensors in left anterior descending endocardium. Extent of recovery of systolic function 5 min following a brief (5 min) period of ischaemia induced by rapid (175 to 190 min-1) atrial pacing (AP-1) was compared with that following a prolonged (30 min) period of ischaemia induced by rapid atrial pacing (AP-2). Regional myocardial blood flow (ml X min-1 X g-1) was measured at control, during, and following atrial pacing. Regional shortening (%) distal to the stenosis declined versus control at both 5 min of AP-1 (10.0 +/- 7.3 (mean +/- 1 SD) to 0.6 +/- 0.9, p less than 0.01) and 30 min of AP-2 (6.8 +/- 3.3 to 2.1, +/- 3.5, p less than 0.01). However, within 5 min of discontinuing both brief as well as prolonged pacing, regional segmental shortening (5.7 +/- 3.9 and 7.0 +/- 6.9, respectively) returned to 50 to 70% of initial control levels (10.0 +/- 7.3). Regional shortening was similar 5 min following brief and prolonged stress. Distal left anterior descending zone epicardial regional myocardial blood flow increased (p less than 0.01) versus control at AP-1 (1.05 +/- 0.24 to 1.39 +/- 0.24) and 30 min of AP-2 (0.99 +/- 0.21 to 1.40 +/- 0.23).(ABSTRACT TRUNCATED AT 250 WORDS)

Free fatty acids and arrhythmias following acute coronary artery occlusion in pigs.

The arrhythmogenic potential of elevated serum free fatty acids (FFA) was investigated in closed-chest pigs following acute coronary artery occlusion. Animals both with and without ventricular irritability before the FFA rise were studied. No significant increase in PVC frequency occurred and only 1 out of 17 animals developed ventricular fibrillation in the 60 min following acute FFA elevation. In this situation, FFA did not significantly influence the appearance of arrhythmias.

Influence of adenosine on basal myocardial function: observations in anaesthetised, domestic swine.

Data from experiments in isolated cardiac muscle preparations indicate that adenosine in high concentration (10(-3) mol X litre-1) exerts a negative inotropic effect on the myocardium under basal conditions. The following study was performed to test the hypothesis that adenosine exerts a similar negative inotropic effect when administered in an intact animal model in a dose sufficient to cause maximal coronary vasodilatation. Six open chest anaesthetised pigs were studied as follows. Ultrasonic length sensors were placed in the endocardium of the free wall of the left ventricle in a region perfused by the left anterior descending (LAD) coronary artery. Large increases in endocardial blood flow in response to adenosine administration, which could enhance segmental function ("garden hose effect"), were prevented by inserting an artificial stenosis (73% reduction in lumenal diameter) in the proximal third of the LAD. Measurements of haemodynamics, regional myocardial blood flow (microsphere technique), and regional systolic function were made at control 1, at the end of 10 min of intracoronary adenosine infusion (3.0 mumol X min-1) at a dose which exceeded that previously shown to cause maximal coronary vasodilatation and at second control 20 to 40 min after discontinuation of adenosine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of endogenous prostacyclin in myocardial blood flow regulation distal to a severe coronary stenosis.

To test the hypothesis that endogenous prostacyclin is required to maintain reduced arteriolar tone distal to a severe coronary arterial stenosis under basal conditions and during challenge with a vasoconstrictor eicosanoid such as thromboxane A2 10 closed chest, domestic swine were prepared with an artificial stenosis, which reduced the luminal diameter of the left anterior descending coronary artery by 80%. Haemodynamic variables, regional myocardial blood flow (microsphere method), and lactate metabolism were measured at control (1); after infusion of U46619 (thromboxane A2 mimetic) distal to the stenosis at 1 microgram.min-1 for 10 min and 5 micrograms.min-1 for 10 min; at control (2); after indomethacin infusion distal to the stenosis; and after repeat infusion of U46619. At the end of the study the animal hearts were removed and their coronary vessels harvested for in vitro determination of prostacyclin (PGI2) production. Regional myocardial blood flow in all layers of the heart distal to the stenosis did not change compared with control during the initial 1 microgram.min-1 dose of U46619 but was reduced significantly after the 5 micrograms.min-1 dose (approximately 20% vs control). Distal zone flow (all layers) returned to baseline at control (2) and remained unchanged after indomethacin infusion. Although distal zone flows were reduced significantly in response to the second 5 micrograms.min-1 dose, the reduction in each layer after indomethacin was comparable to that observed with the 5 micrograms.min-1 dose before indomethacin infusion. Finally, the in vitro production of PGI2 by coronary vessels was considerably impaired by indomethacin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis of left-ventricular mural thrombus by means of radionuclide ventriculography.

Radionuclide ventriculography was used to diagnose the presence of a left-ventricular mural thrombus in a patient with left-ventricular aneurysm. Diagnostic features of the radionuclide study are described and correlated with postmortem findings.

Effective treatment of supraventricular arrhythmias with acebutolol.

To evaluate the antiarrhythmic efficacy of the new beta adrenergic blocking agent acebutolol, 15 monitored patients with supraventricular arrhythmias received, in double-blind fashion, an intravenous infusion of either acebutolol or saline solution after a control period. Patients treated with saline solution demonstrated no change (P greater than 0.05) in heart rate or arterial blood pressure or conversion to sinus rhythm. After administration of acebutolol, significant (P less than 0.05) reductions in heart rate were noted at 5 minutes. Peak reduction occurred at 10 to 30 minutes and correlated with maximal acebutolol plasma concentrations, antiarrhythmic activity persisted for 24 hours. Mild reductions in systolic blood pressure were observed in the majority of patients. Two patients with atrial fibrillation and one with multifocal atrial tachycardia had conversion to sinus rhythm. Frequent premature atrial complexes noted in one patient were greatly suppressed after administration of the drug. In the nine patients with clinical evidence of chronic obstructive lung disease acebutolol was well tolerated. Adverse reactions were limited to transient dyspnea in one patient with prior heart failure and a decrease in systolic blood pressure to less than 90 mm Hg in three patients who remained asymptomatic. In the patients studied, acebutolol was an effective agent for the treatment of supraventricular arrhythmias and appeared to be of special value in those with chronic obstructive lung disease.

Acute coronary occlusion in the pig: effect of nitroglycerin on regional myocardial blood flow.

Myocardial blood flow was studied in 10 closed chest, anesthetized pigs after an acute balloon catheter occlusion of the left anterior descending coronary artery. With use of radioactive microspheres (15 mu), myocardial blood flow was measured before and during an intravenous nitroglycerin infusion and during a combined nitroglycerin-phenylephrine infusion. A significant zone of ischemis (myocardial blood flow less than 50 percent of normal zone flow) was produced by the occlusion and involved 15 percent of the combined left ventricular and interventricular septal mass. More than 50 percent of this ischemic zone was intensely ischemic (myocardial blood flow 0 to 3 percent of normal). Nitroglycerin resulted in a 20 to 30 mm Hg decrease in systolic blood pressure. Myocardial blood flow was unchanged in intensely ischemic areas but varied directly with the product of heart rate and systolic blood pressure in the moderately ischemic area (myocardial blood flow 26 to 50 percent of normal). S-T segment elevation was significantly increased during nitroglycerin infusion and returned to control level with the added infusion of phenylephrine sufficient to restore the systemic blood pressure to prenitroglycerin values. No improvement in ischemic zone perfusion could be demonstrated during the infusion of nitroglycerin alone or with phenylephrine. The endocardial-epicardial flow ratio in moderately ischemic areas was slightly lower than the normal zone flow ratio and decreased slightly during infusion of nitroglycerin. With the addition of phenylephrine, the ratios rose slightly and no longer differed from prenitroglycerin values. Blood flow distribution in acutely ischemic pig myocardium differs considerably from that observed in the dog. Nitroglycerin was not shown to have any beneficial effects with or without its relative hypotensive effect. More extensive study in animal models other than the dog is needed.

Angiographic findings when chest pain recurs after successful percutaneous transluminal coronary angioplasty.

Angiographic and clinical characteristics of 102 consecutive patients who underwent coronary cineangiography for assessment of recurrent angina pectoris after successful percutaneous transluminal coronary angioplasty (PTCA) were reviewed. Based on angiographic findings, patients were classified as having restenosis (n = 63), development of new, significant coronary stenosis (n = 15), incomplete revascularization (n = 9) or no significant coronary artery disease (n = 15). Eighteen clinical and technical characteristics of the study group were analyzed as predictors of angiographic outcome. The groups did not differ in terms of age, gender, number of inflations performed, peak inflation pressure or in the pre- or post-PTCA stenosis or gradient. The time from PTCA to onset of recurrent angina was the most powerful predictor of angiographic outcome. Patients in whom symptoms developed within 1 month of PTCA usually had incomplete revascularization or no coronary narrowing. Restenosis was the most common explanation for chest pain 1 to 6 months after PTCA. Angina recurring more than 6 months after PTCA was usually due to development of new, significant coronary artery narrowings.

Failure of hyaluronidase to alter the early course of acute myocardial infarction in pigs.

The effect of hyaluronidase on the early course of acute myocardial infarction was evaluated in closed chest anesthetized pigs. One hour after balloon catheter occlusion of the left anterior descending coronary artery, hyaluronidase (500 units/kg body weight) was rapidly infused in 10 animals while 9 received no treatment. The animals were than observed over the next 4 hours. Cardiac output, heart rate, mean arterial pressure and left atrial pressure were not significantly affected by treatment. Heart rate increased and arterial pressure decreased in each group to a comparable degree of 5 hours, but left atrial pressure and cardiac output were unaffected. Precordial S-T segment mapping revealed no significant difference between the two groups. S-T segments rose to a comparable degree in each group and peaked before 1 hour. Hyaluronidase had no acute effects on the S-T segment map in the first 30 minutes after infusion or during the subsequent return of the map toward control level. Slightly lower S-T segments in the hyaluronidase-treated group at 5 hours was of borderline significance but was attributed to factors other than the drug intervention. Changes in ventricular wall motion were assessed angiographically, and all animals manifested akinetic or dyskinetic segments. A significant reduction in shortening fraction of involved segments was seen after occlusion, but no difference was observed between the two groups at 5 hours. Shortening fraction of the combined anterior and anteropical segments decreased from 66 +/- 10 to 20 +/- 6 percent at 5 hours in the hyaluronidase group (no. = 7) whereas in the control group (no. = 6) it decreased from 68 +/- 6 to 28 +/- 9 percent. Comparable increases in end-diastolic volume were also present at 5 hours in each group. Volumes increased from 80.6 +/- 5.1 to 97.5 +/- 6.4 ml3 at 5 hours (P less than 0.05) in the hyaluronidase-treated group (no. = 10) compared with 86.9 +/- 8.9 to 104.8 +/- 11.0 ml3 (P less than 0.05) in the control group (no. = 8). Hyaluronidase did not alter the early course of acute myocardial infarction in pigs. Species differences may contribute to different results reported to date.

Assessment of coronary flow reserve using digital angiography before and after successful percutaneous transluminal coronary angioplasty.

Important alterations of coronary blood flow and coronary flow reserve occur during percutaneous transluminal coronary angioplasty (PTCA). This study evaluated these alterations using digital subtraction angiography. Coronary flow reserve was determined before and after successful PTCA in 20 patients with 1-vessel coronary artery disease (CAD). Ten other patients with angiographically normal coronary arteries, normal exercise electrocardiographic responses and normal cardiac structure also were evaluated. Coronary flow reserve was calculated as the ratio of papavarine-induced hyperemic flow to basal flow. Flow reserve for the stenotic artery in patients who underwent PTCA was 1.6 +/- 0.2 (mean +/- standard error of the mean) (range 0.9 to 3.9, n = 20). After successful PTCA, flow reserve for this artery increased to 3.1 +/- 0.2 (range 1.7 to 5.2, n = 20) (p less than 0.0001 vs before PTCA). Flow reserve for adjacent nonstenotic, nondilated arteries was 2.6 +/- 0.2 (range 1.4 to 4.5, n = 13). Coronary flow reserve in the stenotic arteries before PTCA was far below normal. In addition, both successfully dilated arteries and nondilated, nonstenotic arteries in these patients with CAD had flow reserve values smaller than those in the patients with normal arteries (4.8 +/- 0.6, range 2.3 to 12.6, n =22) (p less than 0.01). These findings suggest that digital angiographic determinations of coronary flow reserve can reveal important alterations of individual artery vasodilatory capacity. The data suggest that although an epicardial coronary in a patient with CAD may appear angiographically normal, flow reserve remains impaired due to abnormalities as yet undefined.

Role of myocardial ischemia in the genesis of stress-induced S-T segment elevation in previous anterior myocardial infarction.

This study tests the hypothesis that myocardial ischemia is responsible for exercise-induced S-T segment elevation in patients with previous anterior myocardial infarction (MI). Exercise stress testing in conjunction with thallium imaging of the myocardium was performed in 28 patients with previously documented anterior MI. Thallium images were analyzed by computer for the presence of initial uptake defects and evidence of abnormal clearance of the isotope from the myocardium (that is, imaging evidence of ischemia). Total S-T segment elevation (sigma ST) in precordial leads V1 to V6 at rest was subtracted from sigma ST at peak stress in order to quantitate the extent of S-T elevation induced by stress (delta ST). Two groups of patients were identified; 1 with stress-induced S-T elevation (Group I, delta ST greater than or equal to 4.0 mm) and 1 without this abnormality (Group II, delta ST less than 4.0 mm). Evidence of abnormal thallium washout from myocardial scan segments occurred in 12 of 15 Group I patients versus 9 of 13 Group II patients (difference not significant). In addition, abnormal tracer washout from anterolateral or septal scan segments occurred in 5 patients in each group. Likewise, abnormal thallium clearance from inferior or posterior scan segments occurred in 8 of 15 Group I patients versus 7 of 13 Group II patients (difference not significant). The patient with the greatest amount of stress-induced S-T elevation (S-T 11.5 mm) had no evidence of ischemia during the stress test. However, Group I patients did have larger anterolateral plus septal initial thallium uptake defect scores than did those of Group II (10 of 15 with defect score greater than or equal to 350 in Group I versus 1 of 13 in Group II, p less than 0.002). Similarly, resting left ventricular ejection fraction greater than or equal to 30% was present in only 4 of 15 Group I patients versus 13 of 13 in Group II (p less than 0.001). Finally, multiple stepwise linear regression analysis demonstrated that delta ST correlated best with the extent of initial anterolateral plus septal thallium uptake defect score (F = 17.3, p less than 0.001) and to a lesser extent with resting ejection fraction (F = 5.2, p less than 0.05) and change in heart rate from rest to peak stress (F = 8.1, p less than 0.01; corrected multiple correlation coefficient = 0.76, p less than 0.001). Thus, in patients with previous anterior MI (1) exercise-induced myocardial ischemia occurs as often with as without S-T segment elevation, (2) myocardial ischemia is not required for the production of stress-induced S-T segment elevation, and (3) stress-induced S-T elevation primarily reflects the extent of previous anterior wall damage and to a lesser extent an increase in heart rate between rest and peak stress.

Precordial ST segment mapping. A sensitive technique for the evaluation of myocardial injury?

Myocardial ischemic injury was created acutely in pigs by a closed-chest technique utilizing an intracoronary balloon occluder for the interruption of flow in the left anterior descending coronary artery and ST-segment elevation was followed over a two hour period using an 18 lead precordial map. In an experimental group of 10 animals, occlusion was carried out within the left anterior descending coronary artery 8.3 plus or minus 0.5 cm distal to the origin of the main left coronary. Mean ST segment elevation (ST) showed a peak rise of 0.16 mV 10 minutes after occlusion. The balloon was moved proximally 1.6 plus or minus 0.2 cm giving a significant secondary rise of 0.16 mV within 5 minutes, despite indications of a generally small area of additional myocardial involvement, as judged from anatomic distribution of additional vessels occluded as well as a lack of significant change in hemodynamic parameters. In a control group of 5 additional pigs, a single distal occlusion at 6.4 plus or minus 0.9 cm from the origin of the main left coronary was produced by an identical technique. The ST rose to a peak of 0.20 mV at 15 minutes and was followed by a steady decline. Unlike the experimental group, no additonal rise in ST was seen. The technique of precordial mapping thus appears to be a sensitive index of myocardial injury. In addition, it appears from this study that the magnitude of ST elevation is a direct reflection of the extent of myocardial injury.