Coronary arteriovenous fistula complicating aortocoronary bypass surgery

A coronary artery fistula complicating aortocoronary bypass surgery is reported in a patient. A continuous murmur heard on follow-up visits was the important clinical clue. The diastolic murmur was localized by intracardiac phonocardiography to the area of the tricuspid valve. A small left-to-right shunt was demonstrated in the right ventricle. Angiographic studies demonstrated a saccular structure arising from the left anterior descending artery, just distal to the anastomotic site and communicating with the right ventricle through a maze of vessels.     

Recurrent angina after bypass surgery: evaluation by early and late arteriography

Arteriographic correlates of recurrent angina pectoris were obtained in 98 patients undergoing both early (< 2 weeks) and late (five to 70 months, average 2.6 yrs.) postoperative angiography after coronary bypass surgery. All patients were discharged with arteriographic evidence of patency of all grafts (171 saphenous vein and six internal mammary artery) and all were asymptomatic during their early (< 3 month) postoperative follow-up. During late follow-up, recurrent angina occurred in 38 patients. The group with recurrent angina had significantly higher frequencies of progressive coronary disease (47% vs. 18%), incomplete surgical revascularization (35% vs. 15%), and graft closure (21% vs. 5%) compared to the asymptomatic group. In the total study group, 29 (30%) had progressive coronary disease with 16 (55%) having recurrent symptoms. Progressive coronary disease was present in 24% of ungrafted vessels compared to only 3% in native coronary arteries distal to graft anastomoses. The frequency of progressive coronary disease was directly related (p < 0.025) to the time interval between early and late arteriographic studies. The average annual rate of progressive disease was 10.7% of patients per year. Patients with progressive coronary disease had a higher (p < 0.05) cholesterol (264 ± 57 vs. 239 ± 37 mgm./dl.). Incomplete surgical revascularization was more common (61%) in patients operated on during the early (< 1.5 yrs.) experience with bypass surgery. Late graft closure occurred in 7.6% of all grafts and in 11% of patients. The average annual rate (attrition rate) of graft closure was 3% per year. Late graft stenosis occurred in 5% of patients but was related to angina pectoris in only one patient.The present study indicates that late recurrent symptoms may be anticipated after bypass surgery, since for the most part, they are due to progressive atherosclerotic process in the native circulation. Primary graft failure plays only a minor role in producing recurrent symptoms. Thus, continued control of risk factors, especially lipid abnormalities, is warranted after bypass surgery.     

Comparative study of the postoperative flow in the saphenous vein and internal mammary artery bypass grafts.

Postoperative coronary bypass flow was evaluated in two groups of randomly selected patients with grafts to the left anterior descending artery (LAD). Saphenous vein bypass grafts were placed in 27 patients and internal mammary artery grafts in 25 patients. Postoperative flow studies were performed in both groups with roentgendensitometric methods based on the transit time of radiopaque media along the graft plus the mean graft diameter. There was no significant difference between the two groups of patients for age, duration of symptoms, or the frequency of hypertension, diabetes mellitus, prior myocardial infarction, or cardiomegaly. Intraoperative bypass flows were 75+/-27 and 77+/-24 ml. per minute for the saphenous vein group (SVG) and internal mammary artery group (IMAG), respectively. There was no significant difference in the heart rate or mean aortic pressure at the time of the roentgendensitometric flow study. The mean graft diameters were 3.0+/-0.5 and 1.9+/-0.3 mm. for the SVG and IMAG, respectively (p less than 0.001). The ratios of graft diameter to LAD diameter were 1.9+/-0.3 and 1.2+/-0.2 for the SVG and IMAG, respectively (p less than 0.001). The roentgendensitometric postoperative flows were 68+/-27 ml. per minute in the SVG and 46+/-16 ml. per minute in the IMAG (p less than 0.01). The present study indicates that flow in significantly higher in saphenous vein than in internal mammary artery bypasses and that the difference in flow may in part be explained on the basis of the graft diameter.     

Mechanism of closure of the mitral prosthetic valve and the role of atrial systole. Phonocardiographic and cinefluorographic study

Phonocardiographic and Cinefluorographic methods were used to study the mechanism of closure of the Starr-Edwards mitral prosthetic valve (model 6320) in 41 patients with a normal QRS interval. Atrial fibrillation was present in 23 patients and normal sinus rhythm in 18. The following intervals were measured: QRS to mitral closing click (Q-Mc), QRS to onset of closure (Q-Oc) and QRS to completion of closure (Q-Cc) of the prosthetic valve. Ball travel time was measured as Q-Cc minus Q-Oc. Mean Q-Oc was shorter in the group with normal sinus rhythm. In 8 patients in this group, Q-Oc occurred before ventricular systole and, in 2, completion of closure occurred before the QRS interval. Early closure in the group with normal rhythm was related to a prolonged P-R interval. In this group, values for Q-Mc and Q-Cc intervals did not differ significantly. Q-Cc in the groups with atrial fibrillation and normal sinus rhythm were not significantly different. Ball travel time was significantly longer in the latter group. Long R-R intervals in the group with atrial fibrillation may be associated with partial and occasionally complete premature closure of the valve. Q-Mc was inversely related to the R-R interval in this group.This study indicates 3 mechanisms for closure of the mitral prosthetic valve. Atrial or ventricular contraction alone may close the valve. The contribution of each is dependent on the time interval separating the contraction of these chambers. Spontaneous partial or complete closure may occur before ventricular systole during a prolonged R-R interval.     

Postextrasystolic aortic pressure pulse response in coronary artery disease.

The response of the aortic systolic pressure after an extrasystole was evaluated in 100 consecutive patients with coronary artery disease. The patients were divided into four groups depending on the response of the first postextrasystolic beat. Group IA (45 patients), had lower systolic pressure, whereas group IB (40 patients), had a similar systolic pressure in the postextrasystolic beat, as compared to beats preceding the extrasystole. Group IIA (12 patients) and group IIB (3 patients), demonstrated an increased systolic pressure in the first postextrasystolic beat with subsequent beats in group IIB, also demonstrating pulsus alternans. Congestive heart failure and cardiomegaly were significantly more frequent in group II, as compared to group I patients. In group IIA and IIB, triple vessel disease was present in 83 and 100 per cent, respectively, as compared to 44 per cent in group I patients. Left ventricular end-diastolic pressure (mm. Hg) was 14 ± 6 and 12 ± 7 in group IA and IB respectively, as compared to 19 ± 9 (p < 0.025) in group IIA and 31 in group IIB. Comparing groups IA and IB with each other for cardiac output, stroke volume, end-diastolic volume and ejection fraction, revealed no significant difference. The cardiac output (L./min./M.²) was 2.2 ± 0.6 for group IIA, as compared (p < 0.01) to 2.8 ± 0.5 and 2.9 ± 0.5 in groups IA and IB. Stroke volume (ml./M.²) and ejection fraction were 30 ± 10 and 0.30 ± 0.08, respectively, for group IIA, which is signficantly less, as compared to group I patients. The end-diastolic volume (ml./M.²) in group IIA was 102 ± 28, which is significantly (p < 0.001) higher, as compared to group IA and IB. All patients in group IIB had an abnormal cardiac output, end-diastolic volume and ejection fraction. Thus, the differences in response between group I and group II patients to an extrasystole clearly define two distinct hemodynamic groups. The responses observed to an extrasystole are best explained by variable response of each group to postextrasystolic potentiation and aortic impedance.     

Unusual complications of coronary bypass surgery.

Five patients after coronary bypass surgery developed unusual complications. Three developed new apical thrombi which are thought to be due to the trauma of the left ventricular vent or deterioration of the left ventricular contraction. Significant new mitral regurgitation in one patient probably is secondary to papillary muscle dysfunction as the result of stenosis distal to anastomoses. The leakage of angoigraphic material around distal anastomatic site is due to technical error. Although these unusual complications are very rare, however, they should be considered as potential source of morbidity in asymptomatic patients who leave the hospital after bypass surgery.     

Coronary ectasia: incidence and results of coronary bypass surgery.

Coronary angiograms were performed in 1,660 patients between the ages of 27 and 84 years. Coronary ectasia was noted in 42 (2.5 per cent) patients. These 42 patients were compared with an equal number of patients with coronary artery disease, matched for age and sex. There were no significant differences in numbers of vessels involved with significant disease, coronary score, main left or left anterior descending artery disease, coronary calcification, hypertension, or abnormal glucose tolerance test in patients with or without ectasia. A family history of coronary artery disease, diabetes mellitus, and hypertension did not separate the groups, neither did serum cholesterol level. The serum level of triglyceride was higher in the coronary ectasia group (p < 0.025). The location of infarction by electrocardiogram or abnormal left ventricular contractility was similar in both groups. Of 64 ectatic vessels, 34 (53 per cent) occurred in the right coronary, 16 (25 per cent) in the left anterior descending, and 14 (22 per cent) in the left circumflex artery. Thirty patients with ectasia and 26 in the control group underwent bypass surgery. Nineteen of the ectasia group and 17 of the control group had post-bypass graft angiograms. In the ectasia group, two out of 47 and, in the control group, five out of 41 grafts were closed. The postoperative course was similar in both groups. An 18 month (mean) follow-up of the 42 patients with coronary ectasia revealed no late deaths, whereas one death occurred in a control patient who did not have surgery. In conclusion, coronary ectasia is more common in the right coronary artery. The presence of coronary ectasia does not indicate more severe or widespread coronary disease than in controls. Short term follow-up of patients with ectasia, with or without bypass surgery, does not differ from control patients.     

Significance of new Q waves after bypass grafting: correlations between graft patency, ventriculogram, and surgical venting technique.

New postoperative electrocardiographic Q waves have been described in eight of 40 per cent of patients undergoing bypass grafting for coronary artery disease. Various theories have been proposed to explain these new Q waves. Correlations of new Q waves to vein bypass occlusion, prolonged pump time or aortic cross-clamping time are controversial. Indeed, whether or not the appearance of new postoperative Q waves means real transmural myocardial infarction is not clear. We report herein our experience with postoperative Q waves in 56 patients with vein bypass grafts and the relationship of new Q waves to ventricular venting, graft patency, and the postoperative ventriculogram. Our observations indicate that: (1) Not all Q waves are due to occlusion of the saphenous bypass grafts (as noted by others). (2) A certain percentage of new Q waves may not reflect true transmural myocardial infarction, especially when all the vein grafts are patent and the postoperative ventriculograms show improvement. (3) Some new Q waves reflect true transmural infarction due to occlusion of grafts or of distal coronary arteries with deteriorated left ventriculograms. (4) The high incidence of new Q waves in patients with ventricular vents is probably due to direct myocardial trauma at the apex of the left ventricle.     

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.     

Clinical and hemodynamic aspects of single vessel coronary artery disease

Two-hundred consecutive patients with arteriosclerotic heart disease underwent complete clinical and hemodynamic evaluation. Fifty-two patients (26 per cent) had significant single vessel coronary artery disease and were compared to 148 patients with more extensive coronary artery disease and to a group of 14 normal patients. The single vessel disease group, when compared to the diffuse disease group, was characterized by a shorter duration of angina pectoris, lower frequency of a history of congestive heart failure or cardiomegaly, and a lower frequency of electrocardiographic (ECG) evidence of a transmural myocardial infarction. The combination of angina pectoris for three or more years with cardiomegaly was the only factor which completely separated the two coronary disease groups. Cardiomegaly, when present in single vessel involvement, was always due to left anterior descending (LAD) disease, together with an anterior infarction on ECG and left ventricular asynergy. The single vessel disease group included 32 patients with LAD disease, 17 with RCA, and 3 with circumflex artery involvement. Resting hemodynamics in these 52 patients (other than a higher left ventricular end-diastolic pressure and wall stress) were not significantly different from hemodynamics in a normal group. Patients with diffuse disease were characterized by many hemodynamic alterations and by left ventricular (LV) asynergy, when compared to the single vessel disease or normal groups. The diffuse disease group had a lower ejection fraction (EF) and an increased frequency of LV asynergy and coronary collateral circulation than did the LAD group. In the single vessel disease group LV asynergy did not correlate with the ECG. LV synergy, however, was not found in any patient in the LAD group with abnormal Q waves on ECG. The single vessel disease group included only five patients with increased end-diastolic volume (EDV) and all had LAD involvement, increased LV end-diastolic pressure, and decreased EF. The remaining 47 patients with normal LV-EDV revealed that the LAD group had abnormal pressure-volume relationships, indicating a decreased compliance of the left ventricle.     

Multiple coronary arteriosystemic fistulas

A 58 year old man presented with angina pectoris and no heart murmur. On selective coronary angiography, multiple coronary arteriosystemic fistulas involving all three major coronary arteries were found. This is the first such case reported. It is speculated that this vascular anomaly represents persistence of embryonic intertrabecular vessels that permit the coronary arteries to communicate with the left ventricular chamber through the Thebesian vessels.     

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.     

Reappraisal of the functional significance of the coronary collateral circulation.

A review of data in 465 patients with complete obstruction of either the left anterior descending or right coronary artery was undertaken to evaluate the functional role of the collateral circulation. Complete obstruction of a dominant right coronary artery was observed in 288 patients, 83 percent with distal filling and visualization of the posterior descending artery by way of collateral vessels. Complete obstruction of the left anterior descending artery was noted in 177 patients, 71 percent with filling and visualization distal to the obstruction by way of collateral vessels. Among patients with obstruction of the left anterior descending artery, there was a significantly greater frequency of congestive heart failure and cardiomegaly in those without collateral vessels than in those with collateral vessels. The former also had a significantly greater frequency of both electrocardiographic evidence of an anterior wall myocardial infarction and angiographic findings of anterior wall asynergy. The frequency of inferior myocardial infarction and inferior wall asynergy was not influenced by the presence of collateral vessels. These observations indicate that the collateral circulation plays a significant protective role in the presence of obstruction of the left anterior descending artery, which is not apparent with obstruction of the right coronary artery.     

New Q waves after bypass grafting: Correlations between graft patency, ventriculogram and surgical venting technique

New Q waves were observed in 35 (11%) of 321 patients undergoing saphenous vein bypass grafting with an overall mortality rate of 1.1%. Twenty-eight (80%) had postoperative arteriograms and ventriculograms and are reported. Ventricular venting was used intra-operatively in 17 patients and atrial venting in 11. The incidence of new Q wave was 22% in patients with ventricular venting and 5.5% in those with atrial venting (p less than 0.05). Complete or incomplete revascularization did not affect the incidence of new Q waves. New Q waves appeared in a zone of myocardium supplied by a grafted artery in all except two patients with ventricular venting in whom Q waves occurred within the zone of myocardium supplied by diseased ungrafted vessels. In the ventricular venting group, seven (41%) demonstrated an improved or unchanged postoperative ventriculogram and ten (59%) had deteriorated ventriculograms. In 11 patients with atrial venting, nine (82%) showed improved or unchanged postoperative ventriculograms and two (18%) had deteriorated ventriculograms. Ventricular venting patients with improved or unchanged postoperative ventriculograms had 7% graft closure as compared to 5% of those with atrial venting (pNS). Graft closure rate was 44% in ventricular venting and 20% (pNS) of patients with atrial venting who had deteriorated left ventriculograms. These findings indicate poor correlation between new Q waves and graft closure. Improved postoperative ventriculograms corrleated well with graft patency despite new Q waves. The etiology of new post bypass graft Q waves are varied. They include ventricular trauma and conduction delays resulting from surgery or venting, as well as infarction. This may be due to compromised arterial inflow either in nonoperated vessels or in the vessels distal to the anastomosis with patent grafts, or due to occluded grafts.