Myocardial infarction in patients with previous coronary artery bypass surgery

An increasing proportion of patients hospitalized with myocardial infarction have previously undergone coronary artery bypass surgery. To define this subgroup, 77 patients with acute infarction occurring 2 or more months (mean 52.8) after bypass surgery were compared with 77 control patients with infarction. Baseline characteristics of the groups were similar except that post-bypass patients were more often men (p = 0.02) and more likely to have had a previous infarction (37 versus 21, p = 0.008). Infarct size was smaller in the post-bypass group as assessed by peak creatine kinase (CK), peak CK-MB, maximal number of electrocardiographic leads with ST elevation, maximal summed ST elevation and QRS score measured 7 to 10 days after admission (p less than 0.001 for each variable). Five control patients but none of the post-bypass patients died in the hospital (p = 0.06). Serious complications (death, acute heart failure, ventricular fibrillation, second or third degree atrioventricular block) occurred in 24 control patients but in only 5 post-bypass patients (p less than 0.001). Angiography was performed after infarction in 45 of the 77 post-bypass patients. Occlusion of both a native coronary artery and its graft was found in 24 of the 45; these patients had had higher peak CK levels (p = 0.008) than the other 21 patients who had angiography. The probable causes of infarction in these 21 were disease progression in nonbypassed arteries or graft occlusion with arterial stenosis, or vice versa, and disease progression distal to a patent graft.(ABSTRACT TRUNCATED AT 250 WORDS)     

S-T segment elevation and coronary spasm in response to exercise

The prevalence rate of exercise-induced S-T segment elevation of 0.1 mV or greater in symptomatic patients is 3.0 to 6.5 percent in most studies. S-T segment elevation is associated with a more severe degree of myocardial ischemia than depression and frequently implies a high grade coronary stenosis in the vessel that supplies the site of ischemia. Leads V₄ to V₆ and bipolar lead CM₅ have been found to be relatively insensitive in detecting exercise-induced S-T segment elevation.

The pathogenesis of S-T segment elevation is different in three clinical patient subsets reviewed. In patients after infarction, the largest of the three subgroups, exercise-induced S-T segment elevation usually appears in leads with Q waves, is more common after anterior myocardial infarction and implies underlying akinetic or dyskinetic wall motion. Of patients with variant angina, 10 to 30 percent have during exercise S-T segment elevation that is most likely provoked by coronary arterial spasm. The natural history of variant angina is cyclic, and clinical observations and laboratory findings are dependent on particular phases in the disease process and treatment. Finally, 0.2 to 1.7 percent of symptomatic patiënts without infarction or variant angina have exercise-induced S-T segment elevation. Although most of the latter have fixed high grade coronary arterial stenoses at angiography, the exact pathogenetic mechanism of S-T segment shift in this patient group is not yet fully understood.     

Importance of coronary collateral circulation in interpreting exercise test results

The Importance of the coronary collateral circulation as a cause of false negative exercise tests was studied in 37 patients who had a 90 percent or greater isolated stenosis of the luminal diameter in one major coronary artery. Sixteen patients had large collateral vessels and 21 patients had either minimal or no collateral circulation. Myocardial scintigraphy was performed in 22 of the 37 patients. The final treadmill time was similar in both groups (521 ± 192 versus 554 ± 144 seconds [mean ± standard error of the mean]). The presence and depth of S-T segment depression was not influenced by the degree of collateralization. The sensitivity of the exercise electrocardiogram was greater for patients with disease in the left anterior descending than in the right or left circumflex coronary arteries (95 versus 60 percent, p <0.03). Among the 22 patients with thallium-201 scintigrams, myocardial perfusion defects were more common in patients without collateral circulation (100 versus 40 percent, p <0.01) and Involved more myocardial segments (p <0.005). The overall sensitivity of exercise electrocardiography for the detection of single vessel stenosis 90 percent or greater was similar to that of myocardial scintigraphy (81 versus 73 percent). In conclusion, large intercoronary collateral vessels are not a cause of false negative exercise electrocardiograms in patients with single vessel disease but are a common cause of false negative scintigrams. Large collateral vessels may limit the quantity and location of myocardial ischemia, but exercise etectrocardtography and thallium-201 scintigraphy may detect different aspects of ischemia.     

Comparative sensitivity and specificity of exercise electrocardiographic lead systems

A comparison of current exercise electrocardiographic lead systems reveals differences in the sensitivity and specificity of S-T segment shifts diagnostic of obstructive coronary artery disease. The differences are explained in part by differences in population samples, lead systems and criteria for positivity. Multiple electrocardiographic lead recording in symptomatic patients during and after exercise improves sensitivity in detecting S-T segment shifts with only a small decrease in specificity. A review of population screening studies in asymptomatic subjects shows a wide selection of different exercise electrocardiographic lead systems and criteria for a positive test. Few screening studies have compared the prevalence of different S-T segment configurations in individual leads of a simultaneously recorded multiple lead system during or after exercise.

Data from animal studies of myocardial ischemia suggest why 100 percent sensitivity in detecting obstructive coronary disease is unlikely to be obtained with surface electrocardiographic recordings. Additional research is required to identify the optimal set of diagnostic exercise electrocardiographic leads and criteria for positivity so that maximal predictive accuracy can be obtained for different patient subsets.     

Progression of atherosclerosis in coronary arteries and bypass grafts: Ten years later

Progression of atherosclerosis in aortocoronary saphenous vein grafts is frequent and is the predominant cause of late graft closure after CABG. Only approximately 60% of grafts remain patent between 10 and 12 years after surgery. Of patent grafts, 45% show angiographie evidence of atherosclerosis between 10 and 12 years after surgery and 70% of the atherosclerotic lesions reduce the graft lumen diameter by 50% or more. Atherosclerosis of saphenous vein grafts does not appear to be related to age, sex or cigarette smoking, but is associated with abnormalities of cholesterol lipoprotein fractions. Progression of atherosclerosis in the native coronary arteries is also very significant after CABG. Progression of CAD between 10 and 12 years after surgery occurs in approximately 50% of nongrafted arteries. Between 10 and 12 years after surgery, the rate of progression of disease in nongrafted arteries is not different from that of grafted arteries with patent grafts; however, progression is more frequent in grafted arteries with occluded grafts. The rate of progression is not related to age, sex, risk factors or extent of disease at baseline coronary arteriography. Progression of preexisting stenoses is more frequent than appearance of new stenosis. Progression is related to the severity of the preexisting stenosis only in nongrafted arteries. Finally, progression is related to alterations of left ventricular function during follow-up.

Because of these progressive late changes, CABG should probably remain limited to patients with incapacitating anginal symptoms or to those with severe lesions for whom surgery might enhance long-term survival, such as patients with severe left main CAD and 3-vessel CAD.     

Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant or obstruction?

Of 5,250 patients undergoing coronary arteriography over a 5 year period, 27 (0.51 percent) had an intramyocardial segment of the left anterior descending coronary artery producing a milking effect or constriction of the artery during systole. Of these, 11 patients with otherwise normal coronary arteries were studied. Hemodynamic data, coronary sinus blood flow and myocardial lactate extraction were measured during atrial pacing at rates of 120 and 150 beats/min and during a 60 watt supine ergocycle exercise test. The degree of narrowing of the left anterior descending coronary artery during systole was graded 3 (greater than 75 percent), 5 patients; 2 (50 to 75 percent), 4 patients; and 1 (less than 50 percent), 2 patients. Four patients with a grade 3 milking effect had S-T depression in the electrocardiogram indicating anterior wall ischemia and lactate production during pacing at 149 ± 2 (mean ± standard error of the mean) beats/min. Three patients had severe angina during pacing. Two patients with a grade 2 milking effect had angina-like chest pain and electrocardiographic changes during pacing at 150 beats/min. However, lactate extraction was unchanged during pacing. Two patients with a grade 1 milking effect had no angina and no electrocardiographic or metabolic abnormalities. Coronary sinus blood flow increased significantly with pacing and ergocycle exercise in all patients (rest 118 ± 8 ml/min; pacing at 150 beats/min 219 ± 27 ml/min; ergocycle exercise 251 ± 17 ml/min) (P < 0.001). We conclude that a grade 3 milking effect observed at coronary arteriography can result in significant obstruction of the left anterior descending coronary artery with typical angina and anterior wall ischemia during tachycardia. Surgical periarterial muscle resection or bypass of the left anterior descending coronary artery might be considered in symptomatic patients with this rare anomaly.     

Clinical and angiographic factors associated with progression of coronary artery disease

To characterize the clinical and angiographic factors associated with progression of coronary atherosclerosis, 313 consecutive medically treated patients who had had two coronary arteriograms 3 to 119 months (mean 39 +/- 25) apart were studied. One hundred eighty-one patients underwent recatheterization for stable angina, 52 for unstable angina and 80 for various other reasons. In addition to the conventional angiographic features present at the first angiographic study (number of diseased vessels 1.5 +/- 0.8, ejection fraction 59 +/- 11%), an extent score was defined based on the number of coronary segments with 5 to 75% narrowings from a 15 segment coding system. Multivariate logistic regression identified four independent predictors of progression of coronary artery disease: the interval between studies (p less than 0.0001), unstable angina (p less than 0.0001), a high extent score (p = 0.0001) and young age (p = 0.0026). In a subset of 74 patients aged 50 years or younger with, at the time of the first evaluation, an extent score of 4 or more, the probability of progression between 2 and 4 years and after 4 years was, respectively, 80 and 90% compared with 50% for the other patients. Risk stratification for progression of coronary artery disease can thus be obtained.     

Coronary artery disease in young women: Clinical and angiographic features and correlation with risk factors

Coronary arteriography was performed because of suspected coronary disease in 239 women less than 45 years of age. Normal coronary arteries were found in 112 women, and a further 23 had insignificant stenosis (less than 50 percent narrowing of luminal diameter). Of the remaining 104 women, 56 had one vessel, 22 two vessel and 26 three vessel disease. Hyperlipidemia, hypertension, diabetes, smoking and a family history of coronary disease were significantly more frequent in women with significant stenosis than in women with normal arteries. Significant coronary disease was found in 55 percent (100 of 182) of women with more than two risk factors but in only 7 percent (4 of 57) of those with less than two risk factors (P <0.0001). Evaluation of symptoms and the resting electrocardiogram also discriminated between women with and without coronary disease, but exercise testing was of little value. Only 4 of the 46 women with previous myocardial Infarction had normal or near-normal coronary arteries. Among women with segmental wall motion abnormalities on ventriculography, the site was anterior in 90 percent (19 of 21) of women who used oral contraceptive drugs but in only 60 percent (21 of 35) of nonusers (P <0.05). However, in most respects, coronary artery disease in young women does not appear to differ from coronary disease in other patients.     

Angiographic evaluation of the natural history of normal coronary arteries and mild coronary atherosclerosis

Between September 1966 and September 1976, a group of 48 patients with normal coronary arteries or nonsignificant coronary atherosclerosis documented in a first coronary arteriogram underwent a second angiogram because of persistent or recurrent chest pain. The interval between studies was 13 to 108 months (mean 42 months). The indication for the first angiogram was typical or atypical anginal pain. The patients were separated into two groups according to the results of the first angiogram. Group I included 22 patients, 9 men and 13 women, with normal coronary arteries (mean age 49 years, range 28 to 62). Group II included 26 patients, 18 men and 8 women, with coronary stenosis of less than 50% of intraluminal diameter (mean age 49 years, range 38 to 63). The second angiogram revealed normal coronary arteries in all 22 patients in Group I but showed progression of diseases in 7 (27%) of the 26 patients in group II. The coronary arterial narrowings were greater than 50% in four patients and greater than 70% in only two patients. The clinical course, coronary risk factors and interval between angiograms were not useful predictors of progression of disease. The data suggest that coronary artery disease is unlikely to developed in adults with normal coronary arteries and that roughly 75% of adults with nonsignificant atherosclerosis will not show progression of disease over a 3 to 4 year period.     

Clinical characteristics of patients with variant angina complicated by myocardial infarction or death within 1 month

Of 132 consecutive patients hospitalized during a 5 year period because of active variant angina, 18 died or had a myocardial infarction within 1 month. In 4 patients an episode of pain and S-T elevation unrelieved by calcium antagonist drugs and intravenous nitroglycerin persisted for more than 1 hour, inducing cardiogenic shock and death before the appearance of Q waves and elevated serum enzyme levels. In the other 14 patients myocardial infarction developed in the electrocardiographic leads in which S-T elevation had occurred during attacks of variant angina.Clinical features were not helpful in distinguishing the 18 patients with complications from the other 114. Angina at rest had been present for less than 1 month in 7 of the 18 patients with infarction compared with 31 of 114 in the other group (probability [p] not significant [NS]). Before infarction the artery presumed to be perfusing the involved territory contained a fixed stenosis of 70 percent or more of luminal diameter in 8 of the 14 patients with complications who had coronary arteriograms compared with 50 of 112 in the other group (p = NS). In 13 of the 18 patients, complications occurred in spite of large doses of calcium antagonist drugs. In 11 of these 13, attacks of variant angina were monitored for 3 to 17 days both before and during treatment. All 11 had fewer attacks with treatment and 5 had no attacks. Daily attacks per patient decreased from 4.6 ± 4.3 to 0.5 ± 0.7 (mean ± standard deviation) (p < 0.01). It is concluded that in variant angina of recent onset myocardial infarction occurs frequently and unpredictably. Myocardial infarction may occur in the absence of severe fixed lesions and in spite of apparent clinical improvement with administration of calcium antagonist drugs.     

Serial exercise testing in patients with effort angina: variable tolerance, fixed threshold

To investigate the frequency and mechanism of variable threshold angina, seven treadmill exercise tests were performed in each of 28 patients with stable effort angina and exercise-induced ST segment depression. Each patient had tests at 8 AM on 4 days within a 2 week period and on 1 of these days had three additional tests at 9 AM, 11 AM and 4 PM. Time to 1 mm ST depression increased from 277 +/- 172 seconds on day 1 to 319 +/- 186 seconds on day 2, 352 +/- 213 seconds on day 3 and 356 +/- 207 seconds on day 4 (p less than 0.05). Rate-pressure product at 1 mm ST depression remained constant. Similarly, time to 1 mm ST depression increased from 333 +/- 197 seconds at 8 AM to 371 +/- 201 seconds at 9 AM and to 401 +/- 207 seconds at 11 AM and decreased to 371 +/- 189 seconds at 4 PM (p less than 0.01). Again, rate-pressure product at 1 mm ST depression remained constant. The standard deviation for time to 1 mm ST depression, calculated as a percent of the mean for each patient's seven tests and then averaged for the entire group, was 22 +/- 11%. The standard deviation for rate-pressure product at 1 mm ST depression, calculated in the same way, was significantly less at 8.4 +/- 2.8% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive assessment of aortocoronary bypass graft patency using pulsed Doppler echocardiography.

To evaluate noninvasively aortocoronary bypass graft patency, pulsed Doppler echocardiography was performed at the time of postoperative coronary angiography in 120 consecutive patients. Ultrasonic examination of 163 vein grafts was possible. One hundred twenty-seven patent and 14 occluded grafts were correctly identified. Eleven patent grafts could not be recorded, and 11 occluded grafts were falsely diagnosed as patent. The method had an overall sensitivity of 92% and a specificity of 56%. This high sensitivity level may be increased to almost 100% by enhanced technical skill and experience. The low specificity level, although the method must be tested in a larger number of bypass grafts, stresses the importance of correctly identifying other sources of diastolic blood flow. Diastolic flows from the superior vena cava, internal mammary veins, tricuspid valve, mitral valve and right ventricle may be eliminated by careful adjustment of the depth, site and size of the pulsed Doppler electronic sampling gate. Standard echocardiographic landmarks for avoiding confusion with the coronary arteries are also described.     

Ergonovine testing in a coronary care unit

This study describes the results of ergonovine testing in 100 consecutive patients who underwent this procedure in a coronary care unit. All patients had recently undergone coronary arteriography. A bolus injection of ergonovine was administered at 5 minute intervals in the following doses (mg): 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4. The criterion for a positive test was the appearance of S-T elevation greater than 1 mm. The test was positive in all 17 patients known to have variant angina and in 18 (40 percent) of 45 patients who had a history of chest pain judged strongly suggestive of variant angina but who had no electrocardiogram recorded during pain. Of 38 patients with a history of chest pain classified as not entirely typical of variant angina, only 1 (2.6 percent) had a positive test.Of the 64 patients with a negative ergonovine test, 47 had chest pain and 25 had nausea but none had more serious complications. Ventricular arrhythmia accompanied S-T elevation in 18 of the 36 patients with a positive test but occurred in only 4 of the 64 with a negative test (p < 0.0005). No patient needed treatment with antiarrhythmic drugs. Four of the 36 patients with a positive test had serious complications: severe translent hypotension (2 patients), recurrent episodes of angina with S-T elevation (1 patient) and a subendocardial infarction (1 patient). Thus, ergonovine testing is useful in patients with a typical clinical history of variant angina but without an electrocardiogram recorded during pain. in this study, a small but definite incidence of serious complications occurred during a positive test.     

Ergonovine testing to detect spontaneous remissions of variant angina during long-term treatment with calcium antagonist drugs

A subgroup of 22 patients with variant angina who had responded well to calcium antagonist drugs were studied to determine if ergonovine testing could help assess the need for continued therapy. Before treatment all 22 patients exhibited angina with S-T elevation during ergonovine testing done in the coronary care unit according to a previously described protocol with sequential ergonovine doses of 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4 mg administered at 5 minute intervals. After 9.4 ± 4.7 (range 1 to 24) months of treatment (nifedipine 7 patients, diltiazem 3, verapamil 8, perhexiline 3, nifedipine and diltiazem 1), all patients were free from anginal attacks. Medication was discontinued and ergonovine testing repeated 24 to 48 hours later (3 weeks for perhexiline). In 12 of the 22 patiénts, angina or S-T segment shifts did not occur during the second ergonovine test to a maximal dose of 0.4 mg. Treatment was not restarted in these patients and all 12 remain free of variant anginal attacks 4.2 ± 2.9 (range 1 to 13) months later. In seven patients angina and S-T elevation occurred during the second ergonovine test, in the same electrocardiographic leads as during the test before treatment. In three patients the ergonovine test induced angina with S-T depression in the leads where S-T elevation had occurred during the previous test. Treatment was reinstituted in these 10 patients with a positive test. No complications resulted from ergonovine testing in any patient.We conclude that in many patients with variant angina, symptoms will disappear spontaneously and the ergonovine test will revert to negative. Treatment with calcium antagonist drugs can probably be safely discontinued in some patients with variant angina; ergonovine testing appears to be helpful in identifying such patients. Longer periods of follow-up are required to confirm that symptoms do not recur.     

Effect of physical training on treadmill exercise capacity, collateral circulation and progression of coronary disease

The increased exercise capacity after physical training in patients with coronary artery disease has been attributed to improved oxygen supply to the myocardium by way of increased collateral circulation or reduction of myocardial oxygen consumption by extracardiac factors, or both. Fourteen patients aged 43 to 61 years (mean 51 years) with 50 percent or greater obstruction in one, two or three vessels (three, six and five patients, respectively) underwent 13 months of physical training. Clinical status was either stable or improved with training. Treadmill exercise capacity, as measured by oxygen consumption, increased 25 percent from 21.9 ± 4.8 (standard deviation) to 27.4 ± 4.1 ml/kg-min at heart rates of 154 ± 17 and 156 ± 12 beats/min, respectively. After training, new collateral vessels, apparently secondary to progression of the disease, were observed in 2 of 21 arteries significantly but not completely obstructed before training. These data are in contrast to those reported for trained dogs with incomplete obstruction. Coronary arterial lesions progressed in only 4 of 14 patients. Coronary arteriographic data from this laboratory do not support the hypothesis that the increased exercise capacity after training in patients with coronary disease can be attributed to the development of collateral circulation. It is possible that physical training may retard the progression of coronary artery disease.     

Circadian variation in variant angina

Thirteen hospitalized patients with variant angina were studied to assess circadian variation in disease activity. Over 48 hours, all angina attacks were noted, a continuous Holter electrocardiogram was recorded and 2 ergonovine tests were performed 12 hours apart, 1 at 4 AM and the other at 4 PM. Only 2 patients gave a clearcut history of more frequent nocturnal or early morning attacks. During the study period, 1.8 +/- 1.6 AM and 0.62 +/- 1.2 PM angina episodes per patient were reported (p less than 0.02), but a circadian pattern was apparent in only 4 patients. However, Holter analysis revealed 5.3 +/- 13.8 AM and 2.6 +/- 8.5 PM episodes of ST elevation per patient (p less than 0.05) and 8.1 +/- 13.9 AM and 3.2 +/- 8.5 PM episodes of ST elevation, ST depression or T-wave pseudonormalization (p less than 0.01). Ten of 11 patients with Holter abnormalities had more frequent AM than PM attacks (p less than 0.01). ST elevation developed during all 13 of the 4-AM and 12 of 13 of the 4-PM ergonovine tests. In 10 cases the ergonovine threshold at which the attack occurred was lower in the morning, in no case was it lower in the afternoon, and in 3 patients the morning and afternoon doses were identical (p less than 0.01). Thus, circadian variation in disease activity both for spontaneous and provoked attacks is present in most patients with variant angina, even though it is often not clinically apparent.     

Influence of partial sympathetic denervation on the results of myocardial revascularization in variant angina

Poor results of the aortocoronary bypass graft operation in the treatment of variant angina have been ascribed to recurrent vasospastic activity due to autonomic imbalance. Cardiac sympathetic denervation (plexectomy) may represent a rational approach in the prevention of vasospasm. To test the value of plexectomy in the treatment of variant angina, 31 patients were studied, 17 of whom (Group 1) underwent conventional coronary artery grafting whereas the remaining 14 (Group 2) underwent cardiac sympathetic denervation also. The 2 groups were similar with respect to age (54 +/- 8 versus 50 +/- 7 years), sex distribution (male/female ratio 12/5 versus 9/5), prevalence of coexisting effort angina (10 versus 12 patients), previous myocardial infarction (7 versus 4 patients), and duration of variant angina (3.3 +/- 5.4 versus 2.4 +/- 2.7 months). The left ventricular ejection fraction was comparable in both groups (60 +/- 11 versus 60 +/- 4%) as were left ventricular end-diastolic pressure (15 +/- 4 versus 13 +/- 5 mm Hg) and extent of coronary artery disease (65 versus 71% prevalence of multivessel disease). The average duration of follow-up was 23 +/- 15 months in Group 1 and 22 +/- 18 months in Group 2 (p = not significant [NS]). There were no operative deaths. Four patients, 2 in each group, had a perioperative myocardial infarction. Seven patients in Group 1 and 1 patient in Group 2 had recurrent variant angina. There was sudden death and 2 infarcts in Group 1. Actuarial curves showed the cumulative probability of recurrent variant angina to be significantly lower (p less than 0.05 and p less than 0.001 at 6 and 10 months, respectively) in Group 2. This study suggests that cardiac sympathetic denervation may prevent recurrent vasospastic activity in variant angina.