Relationship between regional ventricular asynergy and the anatomic lesion in coronary artery disease

The percentage of left ventricular (LV) asynergy was measured in patients with isolated narrowing or obstruction of the right coronary artery (RCA), the anterior descending branch of the left coronary artery (LAD), or a combination of these lesions.Incomplete obstruction of a vessel was not associated with important asynergy. Isolated obstruction of the LAD caused asynergy of the distal two-thirds of the anterior wall and apex of the LV and 46 per cent asynergy. Isolated obstruction of the RCA caused asynergy of the middle or basal thirds of the diaphragmatic surface and 15 per cent asynergy. Double-vessel disease produced a combination of the individual lesions, and total obstruction of both arteries caused extensive asynergy.In each patient the extent of asynergy was modified by the underlying coronary artery anatomy and the collateral circulation. Ejection fraction was related to the percentage of LV asynergy.     

Relation of left ventricular contractile patterns in coronary artery disease to the electrocardiogram and vectorcardiogram

Two hundred thirty patients with coronary artery disease (CAD) were studied with left ventriculography, coronary arteriography, electrocardiography (ECG) and vectorcardiography (VCG) to determine how well left ventricular (LV) contractile defects could be predicted from the ECG-VCG patterns and how this was related to the coronary disease location and severity. Of 124 patients with infarction patterns on ECG-VCG about 50% had LV contractile defects localized to the corresponding ECG-VCG abnormalities, i.e., antero-apical asynergy with anterior infarction patterns, inferior asynergy with inferior infarction patterns, or antero-apical plus inferior asynergy with anterior plus inferior patterns. About 20% in each infarction group had unexpected synergy on ventriculography except for patients with dorsal infarction patterns (synergy in 68%) who are discussed as a special problem. Another 25-30% of patients had more extensive contractile abnormality than indicated by the ECG-VCG patterns. In 106 patients with left ventricular hypertrophy, normal QRS-abnormal T and normal QRS-T on ECG-VCG, 65-70% had synergy. However, 30-35% had asynergy in various combinations not suspected from the ECG or VCG. Coronary artery disease severity was less pronounced in patients with synergy than with asynergy and single vessel disease was more common in the former, 47% versus 18-30% in the latter. However, coronary artery disease severity was the same for all ECG-VCG groups except for anterior plus inferior infarction patterns where it was most severe.     

Clinical, hemodynamic and angiographic aspects of inferior and anterior myocardial infarctions in patients with angina pectoris

Clinical, hemodynamic and angiographic findings were reviewed in 82 patients with isolated inferior, 55 patients with isolated anterior and 27 with combined inferior and anterior myocardial infarction and were compared with findings in 100 patients without electrocardiographic evidence of a prior transmural myocardial infarction. All of the 264 patients were referred and evaluated because of angina pectoris and found, on selective coronary angiography, to have coronary artery disease. There was no significant difference in the ages of the patients in each group studied. A history of heart failure, audible gallops and cardiomegaly were more prevalent in the two groups with anterior infarction (isolated and combined with inferior infarction) than in the other two groups. The mean left ventricular hemodynamic measurements (end-diastolic pressure, end-diastolic volume and ejection fraction) in the groups of patients with a normal QRS or an isolated inferior myocardial infarction were not significantly different from those of patients with a normal left ventricle. Patients with isolated anterior myocardia infarction had abnormal end-diastolic pressure (68 percent), end-diastolic volume (51 percent) and ejection fraction (67 percent). Similarly, the group with multiple infarctions had abnormal hemodynamic measurements, with 81 percent having an abnormal ejection fraction. For the entire group of patients studied, an abnormal end-diastolic volume was always associated with an abnormal ejection fraction. Cardiomegaly on X-ray film was associated with an abnormal end-diastolic volume and ejection fraction. An abnormal contractile pattern (asynergy) was noted in 42 percent of the patients with a normal QRS; inferior asynergy was observed in 88 percent with inferior infarction, and anterior or apical asynergy, or both, was found in 90 percent with anterior infarction. All the patients with multiple infarctions had asynergy. The right coronary artery was significantly involved in 90 percent of the patients with inferior infarction, while all the patients with anterio infarction had significant disease of the left anterior descending artery. More than 80 percent of the patients with an infarction pattern on electrocardiogram had double or triple vessel disease, as compared with 68 percent of the patients with a normal QRS pattern. This study represents a select group of patients referred because of angina pectoris and cannot be extended to the asymptomatic patient with coronary artery disease. The observations made on these patients indicate that an anterior infarction (isolated or combined with inferior) in patients referred because of angina pectoris is accompanied by significant impairment of left ventricular function, whereas an inferior infarction (isolated), although accompanied by asynergy, is usually associated with normal hemodynamics. The electrocardiogram is not sensitive enough to predict reliably in the individual patient the extent and severity of the coronary artery disease.     

The normal electrocardiogram as a predictor of left ventricular function in patients with coronary artery disease.

Fifty-five consecutive patients with a normal resting electrocardiogram and coronary artery disease were examined to determine left ventricular function. Fifty-two (95%) had no evidence of left ventricular asynergy; 3 patients had only mild hypokinesis. Of this group of patients, 25 (47%) had one vessel disease, 17 (30%) had two vessel disease, and 13 (23%) had three vessel disease. Significant left ventricular asynergy was not found in patients with coronary artery disease and normal electrocardiograms. In addition, a normal electrocardiogram was not related to the number of coronary arteries involved.     

Right bundle-branch block in coronary artery disease: a hemodynamic and angiographic study

Thirty-four patients with right bundle-branch block (RBBB) and coronary artery disease (CAD) (RBBB was not pre-existent to clinical development of CAD) and 52 consecutive CAD patients without conduction disturbances were studied and compared to verify whether the presence of RBBB implies more severe and extensive left ventricular myocardial damage as well as more severe CAD. The two groups did not differ either in age or in New York Heart Association functional class. The incidence or location of previous myocardial infarction (MI) was not different in the two groups. No significant differences were found in left ventricular volumes or ejection fraction. Higher end-diastolic left ventricular pressure and more severe and diffuse left ventricular wall asynergy were present in RBBB patients. At coronary arteriography, more severe involvement of the right coronary artery in CAD patients without conduction disturbances was the only significant finding. The group of patients with CAD and RBBB without MI showed significantly less involvement of the left anterior descending coronary artery and significantly more severe damage of the inferior wall of the left ventricle than the group with CAD without RBBB and MI. Patients with inferior wall MI and RBBB had more severe asynergy of the posterobasal region of the left ventricle than did patients with inferior wall MI without RBBB. The group of patients with anterior wall MI and RBBB had a higher left ventricular end-diastolic pressure, a lower left ventricular ejection fraction, and a greater extent of myocardial damage compared to similar patients of the control group. The groups with MI and RBBB had the same Gensini's score as similar groups without RBBB. (ABSTRACT TRUNCATED AT 250 WORDS)     

Preload reduction with right ventricular pacing: Effects on left ventricular hemodynamics and contractile pattern

Studies were performed in 32 patients to evaluate left ventricular pressure-volume changes and contractile pattern during right ventricular pacing as compared to normal sinus rhythm. Coronary artery disease was present in 27 patients, while 5 patients (control group) had no evidence of coronary artery or left ventricular disease. Studies were performed during both normal sinus rhythm and right ventricular pacing at comparable heart rates, utilizing angiographic methods to determine heart volumes. Right ventricular pacing in all patients resulted in decreased left ventricular systolic (p< 0.01) and diastolic (p< 0.01) pressures and decreased stroke work (p< 0.001). In the control group, right ventricular pacing caused a decrease in left ventricular end-diastolic volume (p< 0.01) and stroke volume (p< 0.01), with no change in ejection fraction. The patients with coronary artery disease were divided into four groups, dependent on the left ventricular contractile pattern during normal sinus rhythm and the percentage of change in hemiaxis shortening during right ventricular pacing. In group A (six patients with asynergy) and group B (seven patients with asynergy), there was no significant change in the percentage of hemiaxis shortening during right ventricular pacing when compared to normal sinus rhythm. Ventricular volume studies in these patients (groups A and B) were similar to the control groups and no change in contractile pattern was observed during pacing. In group C, twelve patients had asynergy and a 10% increase in percentage of hemiaxis shortening during right ventricular pacing when compared to normal sinus rhythm. Right ventricular pacing resulted in decreased end-diastolic pressure (p< 0.01) and end-diastolic volume (p< 0.001), no change in stroke volume, and an increased ejection fraction (p< 0.01). Contractile patterns improved in all patients in group C during pacing. Group D consisted of two patients with asynergy and a 10% decrease in percentage of hemiaxis shortening during pacing, associated with a decrease in end-diastolic volume and ejection fraction with deterioration of left ventricular contractile pattern. These results indicate that right ventricular pacing in patients with coronary artery disease decreases preload, which may be accompanied by improved left ventricular contractile pattern (11/27) and in some patients (2/27) deterioration of left ventricular function.     

Left ventricular hemodynamics and contractile pattern after aortocoronary bypass surgery. Factors affecting reversibility of abnormal left ventricular function

Left ventricular hemodynamics and contractile patterns were evaluated in 104 patients before and after aortocoronary bypass surgery. Patients were selected on the basis of referral for surgery because of angina pectoris and the demonstration, postoperatively, of all grafts being patent. Group I consisted of 47 patients with single grafts (LAD 33 and RCA 14). Mean left ventricular end-diastolic pressure, volume, and ejection fraction revealed no change after surgery. Twenty-four patients had asynergy prior to surgery; of these 24, 16 patients had a normal contractile pattern after surgery. Group II consisted of 47 patients with double vein grafts. Postoperatively, there was a significant decrease in left ventricular end-diastolic pressure (p < 0.005) and increase in ejection fraction (p < 0.001). Asynergy in 29 patients preoperatively revealed synergy after surgery in 15 patients. Group III consisted of ten patients with triple vein grafts. Ejection fraction increased postoperatively (p < 0.01). All but two of the eight patients with asynergy preoperatively showed synergy after surgery. In the entire group of patients, 43 with synergy preoperatively, with but one exception, had synergy after surgery. Asynergesis in 41 instances preoperatively revealed postoperatively that 38 patients (93 per cent) had normal wall movement. In 29 instances of preoperative akinesia of one wall, only 8 patients (28 per cent) showed a return to normal wall movement. Unstable angina pectoris alone did not influence reversibility of abnormal contractile patterns. Unstable angina pectoris with absence of abnormal Q-waves in the ECG was noted in 23 patients with asynergy; all but one of these patients had a normal contractile pattern after surgery. Patients with infarction pattern on the ECG, when accompanied by asynergy, were unlikely to have a normal contractile pattern after surgery (4 out of 23 patients). Reversibility of left ventricular function after surgery is common, not related to number of grafts, but is related to type of wall abnormality noted prior to surgery as well as the ECG and clinical state of the patient.     

Relation between the site of origin of ventricular premature complexes and the presence and severity of coronary artery disease

The clinical implications of ventricular premature complexes in patients with coronary heart disease have received increasing interest. It has been suggested that ventricular premature complexes of right ventricular origin have more benign implications than those that originate from the left ventricle. To define more precisely the relation between the site of origin of ventricular premature complexes and the presence and severity of coronary heart disease in patients with a chest pain syndrome, 39 patients with ventricular premature complexes of right or left ventricular contour who were undergoing cardiac catheterization and coronary arteriography for evaluation of chest discomfort were studied. Ninteen patients had left and 17 had right ventricular premature complexes and 3 had both. Of the 19 with left ventricular premature complexes, 15 had coronary artery disease (12 with two or three vessel obstruction and 3 with single vessel obstruction). Four had normal cardiac catheterization studies. Twelve patients had asynergy on ventriculography. The 17 patients with right ventricular premature complexes had similar angiographic findings. Eleven of the 17 had coronary artery disease (8 with triple vessel disease and 3 with isolated obstruction of the left anterior descending coronary artery). Six had normal arteries. Eight of the 11 with coronary artery disease and right ventricular premature complexes also had asynergy. All three patients with both left and right ventricular premature complexes had coronary obstructive disease. These findings indicate that in patients with a chest pain syndrome there is no relation between the site of origin of ventricular premature complexes and either the prevalence or severity of coronary artery disease.     

Ventricular premature beats and anatomically defined coronary heart disease.

Ambulatory 24 hour electrocardiographic monitoring was performed in 124 patients before cardiac catheterization and coronary angiography. Ventricular premature beats were demonstrated in 83% of all patients. Ectopic activity persisted for at least 3 of the 24 hours in 75% of the 84 patients with coronary heart disease, 61% of 28 with other heart disease and in 24% of 12 normal subjects. The prevalence and grade of ventricular premature beats were increased in the 57 patients with multivessel disease compared with values in the 27 patients with one vessel disease (P less than 0.01). Findings in the latter group did not differ from those of normal subjects. The presence of elevated left ventricular end-diastolic pressure of asynergy was associated with increased ventricular ectopy. Of 15 patients having both asynergy and elevated left ventricular end=diastolic pressure (more than 19 mm Hg), 40% had paroxysms of ventricular tachycardia and 67% had coupled beats; these findings were present in 6 and 12%, respectively, of the 34 patients without asynergy or pressure abnormality (P less than 0.005). Repeat monitoring performed in 65 patients demonstrated greater reproducibility of advanced grades of ventricular premature beats among those with the most severe lesions. For the individual patient the prevalence and grade of ventricular ectopy may not always correlate with the severity of coronary artery disease or degree of left ventricular dysfunction.     

Coronary arteriograms and myocardial scintigrams in the electrocardiographic syndrome of septal fibrosis

Coronary artery disease (CAD) and myocardial perfusion were assessed by arteriograms and scintigrams (Technetium-99 microspheres alone or combined with Iodine-131 albumin macroaggregates) in 178 angina pectoris patients with and without the electrocardiographic (ECG) syndrome of septal fibrosis and with ≥70% obstruction in one or more coronary arteries. The ECGs of 96 patients without angiographic evidence of obstructive CAD were also examined for the ECG syndrome of septal fibrosis. Patients with the ECG syndrome of septal fibrosis have significantly higher incidences of positive exercise stress test, of ≥70% narrowing of the proximal left anterior descending (LAD) artery, of severe proximal LAD disease, and of more extensive left ventricular hypoperfusion than patients without the ECG syndrome. The fact that only 4% of patients without obstructive CAD have the ECG syndrome of septal fibrosis indicates the usefulness of the syndrome in identifying a subset of angina pectoris patients with advanced CAD of the proximal LAD and diffuse left ventricular hypoperfusion.     

Correlation of heart size with clinical and hemodynamic findings in patients with coronary artery disease.

The clinical, hemodynamic, and angiographic findings were correlated with the heart size in 207 patients with proved coronary artery disease. Cardiomegaly was noted in 34 patients and normal heart size in 173. In these two groups, the patients' age range, duration of disease, and history of myocardial infarction were similar. There was no statistical difference in incidence of shortness of breath, hypertension, left ventricular hypertrophy, or abnormal glucose tolerance. Patients with cardiomegaly had a significantly higher incidence of congestive heart failure (26 per cent) as compared to patients with normal heart size (2.9 per cent) (P less than 0.001). Patients with enlarged heart presented a high incidence of anterior wall or multiple myocardial infarction (73 per cent) (P less than 0.001). The cardiomegaly group had a high incidence of elevated end-diastolic volumes, elevated end-diastolic pressures, and diminished ejection fractions when compared to patients with normal heart size (P less than 0.01). Double and triple coronary artery disease was more frequent in patients with cardiomegaly and total coronary score was also higher in this group (P less than 0.005). Asynergy was present in 55 per cent of patients with normal heart size but in 82 per cent of those with enlarged hearts (P less than 0.01). The group of patients with cardiomegaly and documented congestive heart failure had ejection fractions less than 0.30. Cardiac catheterization is probably not advisable in these patients in the absence of associated significant mitral regurgitation, ventricular septal defect, or ventricular aneurysm.     

Echocardiographic and electrocardiographic aspects indicative of necrosis caused by isolated disease of the right and circumflex coronary artery

The value of 12-lead electrocardiogram (ECG) and two-dimensional echocardiography (2D-ECHO, wall motion abnormalities) in recognizing myocardial infarction due to left circumflex and right coronary artery disease was evaluated in 75 patients (aged 26-69 years, within 3 months of myocardial infarction) with single vessel disease (luminal stenosis greater than or equal to 70%). Twenty-five patients (pts) had left circumflex disease and 50 right coronary artery disease. In the group of pts with left circumflex disease, 13 (52%)--group I--showed asynergy limited to the postero-lateral wall and 12 pts (48%)--group II--had more extensive asynergy involving both the postero-lateral and the infero-posterior wall. No pts with left circumflex disease demonstrated asynergy of the interventricular septum. Good correlations were found between the site and extent of asynergy and the location of left circumflex narrowings: 9--group I pts--(69.2%) had obtuse marginal branch disease and 8--group II pts--(67%) had proximal left circumflex disease. Patients with right coronary artery disease were subdivided as follows: group I: 35 pts (70%) with asynergy of infero-posterior wall and posterior septum; group II: 11 pts (22%) with extensive asynergy of infero-posterior, postero-lateral walls and posterior septum; group III: 4 pts (8%) with asynergy limited to the infero-posterior wall. The location of right coronary artery narrowings had no relation to the site and extent of infarct asynergy in pts with single right coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mucocutaneous lymph node syndrome: clinical, hemodynamic and angiographic features of coronary obstructive disease

Clinical, hemodynamic and angiographic features of coronary obstructive disease (greater than or equal to 90% diameter reduction) in Kawasaki disease were evaluated in 30 patients. The mean age at the onset of Kawasaki disease was 2.9 +/- 1.9 years and that at cardiac catheterization was 6.3 +/- 2.8 years. Obstructive lesions were observed in the right coronary artery in 12 patients (group 1), in the left anterior descending coronary artery (LAD) in 6 (group 2), in both right coronary artery and LAD in 10 (group 3) and in the left main coronary artery in 4 (group 4). Twenty-two patients (73%) had cardiac symptoms, including myocardial infarction in 10 (33%). Cardiac symptoms were observed in 41% in group 1, 100% in group 2, 80% in group 3 and 100% in group 4. Left ventricular (LV) end-diastolic pressure, end-diastolic volume and ejection fraction were abnormal in 32% of the patients in group 1, a frequency less than that in other groups (83% in group 2, 78% in group 3 and 100% in group 4). Fifty percent had mitral regurgitation and 73% had left ventricular wall motion abnormalities. No patient in groups 1 or 2 has died, but 8 of 14 patients in groups 3 and 4 have died. These observations indicate that coronary obstruction owing to Kawasaki disease can cause depressed LV function, mitral regurgitation and LV wall motion abnormalities in children.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of pharmacologic coronary hyperemia on echocardiographic left ventricular function in patients with single vessel coronary artery disease

To assess whether pharmacologic coronary vasodilation could provoke new left ventricular wall motion abnormalities in patients with single vessel coronary artery disease, systemic hemodynamics, coronary blood flow velocity and left ventricular wall motion were measured by two-dimensional echocardiography during administration of 10 mg of intracoronary papaverine in 14 patients before and again immediately after left coronary angioplasty (group 1). As a comparison with an intravenous method, left ventricular wall motion was analyzed after 0.56 mg/kg body weight of intravenous dipyridamole in a separate group of 13 patients with single vessel coronary disease (group 2). Heart rate-blood pressure product increased 3% to 6% in papaverine-treated patients and 14 +/- 11% (p = NS) in dipyridamole-treated patients. No angiographic collateral vessels were present in either group. Although intracoronary mean flow velocity measured in the 14 group 1 patients and in 5 normal control subjects during papaverine treatment increased from 125% to 400% of basal flow velocity, papaverine induced new left ventricular wall motion abnormalities in only 5 of the 14 patients before coronary angioplasty. In three of five patients, left ventricular wall motion abnormalities persisted after successful coronary angioplasty. Four of the 14 patients demonstrated augmentation of left ventricular wall motion with papaverine. After intravenous dipyridamole, only 3 of the 13 group 2 patients developed new left ventricular regional asynergy. These data suggest that selective (papaverine) and, most likely, global (dipyridamole) augmentation of coronary flow alone does not reliably identify potential ischemic left ventricular regions affected by critical single vessel coronary artery disease.     

Effect of coronary collaterals on left ventricular function at rest and during stress

The influence of coronary collateral vessels on resting left ventricular function was investigated in 87 consecutive patients with complete coronary artery occlusion of at least one of the three major coronary vessels. The morphology of coronary and collateral circulation was evaluated by coronary arteriography. Left ventricular function was assessed by biplane ejection fraction and segmental wall motion was evaluated by hemiaxes shortening. Collaterals to occluded arteries were graded as good or poor, according to the caliber of the distal vessel segment. Patients were divided into those with good collaterals (n =35), and those with poor or absent collaterals (n = 52), furthermore, these two groups were subdivided according to the location of coronary artery occlusion. Collateralized single vessel occlusions were found more frequently than collateralized multiple vessel occlusions. Ejection fraction and segmental wall motion was significantly better in well collateralized occlusions than in poorly collateralized occlusions of LAD or RC and was normal or depressed only slightly if compared to 17 patients without heart disease. In contrast, total and regional myocardial function was severely depressed in poorly collateralized LAD or RC occlusion. Ventriculography after rapid ventricular pacing was performed in 12 of 87 patients with well collateralized or poorly collateralized LAD occlusion to evaluate to what extent coronary collaterals protect anterior wall motion during increased oxygen demand. Pacing induced a drastic fall of anterior wall motion in well collateralized segments whereas no change was found in poorly collateralized segments. Reviewing clinical data of two patient groups with comparable numbers and locations of occlusions revealed in the well collateralized group more severe angina (p < 0.001) and ST-segment changes during exercise (p < 0.01) than in the poorly collateralized group. The latter showed more severe dyspnoe (p < 0.01) and more histories of previous infarctions (p < 0.001). We conclude that well-developed collateral vessels to a complete occluded artery prevent severe asynergy at rest but not during stress.     

Single vessel disease of the anterior interventricular branch as a cause of combined anterior and posterior wall infarct in comparison with 2-vessel disease of the RIVA and RCA

Only few studies deal with the problem of an isolated stenosis of the left anterior descending coronary artery (LAD) leading to a combined anterior and inferior myocardial infarction in the ECG and VCG. In the present study patients with electrocardiographic signs of anterior and inferior myocardial infarction and either one-vessel disease of the LAD branch (n = 27; group I) or two-vessel disease including the LAD and the right coronary artery (RCA) (n = 29; group II) were investigated. Due to the anterior myocardial infarction present in all patients, unequivocal signs of posterior and posterolateral infarct location were missing in the ECG and VCG. There was a distinct variability with regard to Q-wave duration and amplitude in the inferior leads of the ECG and of the Q/R-relation in the scalar lead Y of the VCG (Frank-leads) in patients with isolated LAD disease when compared to those with combined LAD and RCA disease, but no reliable parameter was found in the ECG and VCG which allowed to allocate patients to one of the two groups. On the other hand, there were significant differences in hemodynamics and left ventricular function between the two groups. Group I patients showed a significantly higher left ventricular ejection fraction (mean 49 +/- 15%) than patients with two-vessel disease (group II) (mean 42 +/- 12%) (p less than 0.05). Left ventricular end-diastolic pressures at rest (13 +/- 7 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular function in patients with and without myocardial infarction and one,two or three vessel coronary artery disease

Ninety-six patients with chest pain were studied to determine the relation between left ventricular function and severity of coronary artery disease in patients with and without a history of myocardial infarction. Coronary arteriography was performed obtaining cineangiograms (60 frames/sec) and large roll film angiograms (2 to 6 frames/sec) for precise definition of the coronary anatomy. The criteria for diagnosis of myocardial infarction were a typical history, a rise and fall in serum glutamic oxaloacetic transaminase levels and evolutionary S-T segment changes associated with Q waves of at least 0.03 second. Left ventricular function was assessed by measurement of left ventricular end-diastolic pressure and volume, and left ventricular ejection fraction, mass and compliance. Fifteen patients had normal findings; 81 were classified according to number of diseased vessels and presence or absence of myocardial infarction. There were no group differences in age or heart rate. Left ventricular end-diastolic pressure was abnormally increased in patients with three vessel disease and myocardial infarction. Left ventricular end-diastolic volume was increased and the ejection fraction was reduced in patients in each vessel disease group with myocardial infarction. Although ejection fraction was reduced in patients with three vessel disease without myocardial infarction, it was further reduced when infarction occurred. Left ventricular mass increased in patients with three vessel disease with or without myocardial infarction. Values for ventricular compliance were reduced in all patients with myocardial infarction and were lower in those with two and three vessel disease and infarction than in those with two and three vessel disease without infarction. These findings suggest that a previous history of myocardial infarction needs to be considered together with anatomic abnormalities of the coronary arteries in assessing cardiac performance in patients with ischemic heart disease. In patients with one, two or three vessel coronary artery disease, a previous myocardial infarction significantly alters left ventricular performance; the ejection fraction is a more sensitive measurement of left ventricular function than left ventricular end-diastolic pressure or volume.     

Geometric and functional abnormalities of the left ventricle with a chronic localized noncontractile area

Thirty-one patients with coronary artery disease, 25 of whom had a chronic localized noncontractile area in the anteroapical region of the left ventricle, were studied at rest by means of left heart catheterization, left cineventriculography and selective coronary arteriography. The left ventricular volume, stroke volume, ejection fraction, left ventricular end-diastolic pressure, cardiac output and the surface area of the noncontractile area were measured.

The patients with a noncontractile area were classified in 4 groups according to the size of the noncontractile area relative to the end-diastolic left ventricular surface area. The relative size of the non-contractile area ranged from 5 to 47 percent. Six patients with uncomplicated coronary artery disease comprised the control group.

The critical size of the noncontractile area beyond which significant functional derangement occurred appeared to be 20 to 30 percent of the left ventricular internal surface area. The end-diastolic volume increased significantly and the ejection fraction was reduced to less than half of normal when the regional noncontractile area was larger than the critical size. Neither the cardiac output nor the left ventricular end-diastolic pressure correlated closely with size of the noncontractile area. In contrast, the ejection fraction was a more sensitive indicator and correlated well with the extent of regional contraction abnormality. In this study, double vessel disease was most common, followed by single vessel disease. Obstruction of the left anterior descending coronary artery was significant in the formation of anteroapical noncontractile regions.     

Localization of coronary artery disease with exercise induced ST segment depression: coronary angiographic correlation

Abnormalities of the 12 lead electrocardiogram (ECG) are often used to localize the anatomic site of myocardial ischemia and vessel involvement in patients (pts) with coronary artery disease. This study is to determine if ischemia of specific vascular segments can be identified by exercise induced ST segment depression (STD) on 12-lead ECG. One hundred and forty three pts with a positive treadmill stress testing (TST) who had coronary arteriography within one month of TST were reviewed. There were 114 men and 29 women, aged 34-74 years (mean 55 years). The Bruce protocol was used for TST. Significant coronary stenosis was defined as obstruction of 70% or greater of the luminal diameter. The pattern of STD on 12 lead ECG during exercise was similar in pts with single vessel disease involving the left anterior descending artery (LAD), right coronary artery (RCA) or circumflex artery (Cx). This pattern of STD in single vessel disease was also comparable to 2-vessel, 3-vessel or left main stem disease. Twenty-two percent of pts with LAD disease had isolated STD in inferior leads. Twenty-five and 29% of pts with RCA and Cx disease respectively had STD in the anterior leads alone during exercise testing. It is concluded that exercise induced STD in 12 lead ECG can not predict ischemia of specific vascular segments or specific vessel involvement.     

Left ventricular asynergy in patients with impending myocardial infarction: two-dimensional echocardiographic assessment

To determine the clinical significance of regional left ventricular asynergy in patients with impending myocardial infarction, we recorded two-dimensional echocardiograms (2DE) serially and performed coronary angiography immediately after the hospital admission in nine patients with initial impending infarction and their last anginal attacks were within 48 hours. Left ventricular asynergy on the first 2DE was observed in six of nine patients during symptom-free periods (Group A: LV asynergy group). Five of the six patients had significant coronary artery lesions (greater than or equal to 75% stenosis) in at least one major coronary artery. Intracoronary filling defects were detected in four of the five patients. Another three patients without asynergy (Group B) had significant fixed stenosis. Coronary artery spasm was observed in two patients during coronary angiography, but no patient had intracoronary filling defects. Intracoronary nitroglycerin (0.1-0.3 mg) reduced the severity of coronary artery narrowing in two patients. In addition, urokinase (240,000-480,000 IU) via the corresponding vessel (PTCR) in the remaining seven patients resulted in reduction in the severity of coronary artery stenosis in four patients, but not in the remaining three patients. Left ventricular wall movement in the asynergy group improved rapidly and no asynergy was observed by the seventh hospital day in five of the six patients. Successful PTCR treatment resulted in improvement of left ventricular wall movement. No asynergy was found in the non-asynergy group throughout their hospitalizations. These findings indicated that abnormal left ventricular wall movement is found in patients with impending myocardial infarction, even during symptom-free periods, but the wall movement gradually improves. The 2DE observations are useful for estimating the clinical status and for planning precise therapy for impending myocardial infarction.