Coronary Artery Disease

Fritz J. Baumgartner and Matthew Budoff


The patient who presents with chest pain needs to be thoroughly evaluated. A complete history and physcial is first undertaken, taking special care to note the presence of cardiac risk factors: history of premature family history of CAD, hypertension, diabetes, obesity, hypercholesterolemia and smoking. A physical examination should focus on the cardiovascular system, followed by laboratory assessment of cardiac enzymes (troponin, CPK and MB), a chest x-ray and electrocardiogram. Suspicion of an acute coronary syndrome (unstable angina or acute myocardial infarction) requires oxygen therapy, nitrates and aspirin therapy (unless contraindicated), blood pressure therapy (first line therapy of acute coronary syndromes is beta-blockers) and serial electrocardiograms and cardiac enzymes. Evidence of an acute myocardial infarction by either enzyme analysis or electrocardiogram usually requires immediate therapy with either thrombolytics or angioplasty. Currently there are several thrombolytics on the market, and utilization varies depending upon multiple factors including the location of infarction. Furthermore, studies demonstrate reduced morbidity and mortality with other antiplatelet agents (clopidrogrel and IIb-IIIa inhibitors) as well as heparin, either unfractionated or fractionated. The patient, depending upon their status, may be admitted to a chest pain unit (myocardial infarction unlikely) or a coronary care unit (present or likely infarction).

The patient is observed on bedrest and medical therapy. For continued pain or evidence of ischemia, urgent revascularization , either with angioplasty or bypass, is usually indicated. If myocardial infarction can be ruled out on the basis of normal serial enzymes and no evoluiton of EKG, the patient most often is tested with cardiac stress testing (treadmill, stress echocardiogram or nuclear testing). See Chapter 2 for cardiac testing. Patients who pass this noninvasive evaluation (no ischemia or chest pain) are most often discharged with a diagnosis of non-cardiac chest pain.

If the patient has a positive stress test (ST depression or chest pain), the patient is most often referred for cardiac catheterization (see Chapter 2).


Survival Without Surgical Treatment According to Anatomy

For one vessel disease, the survival after 5 years is the same as normal (except for isolated proximal LAD lesions).

For two vessel disease, there is a 75% 5 year survival compared to 95% of the general population. For three vessel disease, there is a 50% 5 year survival compared to 95% survival for the age matched general population. For left main coronary artery disease, the survival without treatment is similar to triple vessel disease.

Survival Without Treatment According to Left Ventricular Function in Coronary Artery Disease

In patients with coronary disease, for normal ejection fractions, the 5 year survival is 92%; for ejection fractions between 30-50% the 5 year survival is reduced to 75%.

As a general rule, the number and severity of atherosclerotic lesions progress with time. Patients with unstable angina have a decreased life expectancy compared to stable angina. One can therefore conclude that coronary revascularization will best help those with reduced ejection fractions and those with unstable angina. Although the presence of reduced ejection fraction in coronary patients is the best prediction of those whose cardiac function will be most benefitted by surgery, this factor also has the greatest chance of resulting in an operative mortality. In terms of relief of angina after coronary artery bypass grafting, 80-90% of patients remain relieved of their angina at 5 years; 50% are relieved of their angina at 10 years. After medical treatment, 3% of patients are relieved of their angina at 10 years showing the superiority of coronary revascularization compared to medical treatment for relief of angina.


Unstable angina is a condition of chest pain which is rapidly progressive or alternatively is pain at rest and frequently progresses to myocardial infarction. The Prinzmetal's variant angina is coronary artery spasm usually superimposed on atherosclerotic vessels but may occur in normal vessels. Unlike stable or unstable angina, Prinzmetal's angina may not necessarily be brought on by anxiety or effort. ST segments in Prinzmetal's angina are elevated. The pain is often relieved by myocardial infarction while pain in stable angina is often increased after myocardial infarction.

Soon after the onset of symptoms in Prinzmetal's angina, the natural history is often a catastrophic event, i.e. myocardial infarction or death soon after the onset of symptoms. Patients with Prinzmetal's angina are treated with nitrates. Ergot alkaloids for headaches are avoided as is exposure to cold. Calcium channel blockers are very helpful in addition to nitrates. Coronary revascularization may be useful for medically refractory patients who have atherosclerotic disease with superimposed Prinzmetal's angina but is not useful if there is no significant atherosclerosis present.

Patients who present in cardiogenic shock after an acute myocardial infarction require intensive management. Their airway is assessed and if necessary, they are intubated. IVs are started with blood drawn for enzyme analysis and electrolytes. Chest x-ray and EKG are done and a Swan-Ganz catheter and Foley catheter and arterial line are placed. The patient is managed pharmacologically with inotropes, afterload reducers and diuretics, as well as nitrates and calcium channel blockers. Beta blockers are used with caution because of cardiogenic shock.

If cardiogenic shock persists, the next line of therapy is an intra-aortic balloon pump. This is used for two reasons: 1) It decreases the afterload against which the heart must work by deflating just prior to systole. Thus, there is decreased myocardial oxygen utilization. The decrease in afterload results in improved ejection fraction and decrease in left ventricular end diastolic pressure and volume, and decrease in workload on the heart. 2) The balloon then inflates in diastole. The coronary artery perfusion pressure is increased, improving oxygen delivery to the myocardium. Thus at precisely the time that the heart needs it the most, there is decreased workload of the heart and increased myocardial oxygen delivery. There is no question that the balloon pump has saved the lives of many patients in car-diogenic shock. Patients in cardiogenic shock should have coronary and cardiac angiography. If a patient will not tolerate a dye ventriculogram because of possible volume overload, a transthoracic echocardiogram may be warranted. A decision is then made whether these patients should undergo coronary artery bypass surgery.


Angioplasty is the cardiologist's method of re-vascularization; unfortunately it is a poor second to coronary artery bypass surgery and this is now only coming to full light. It is suspected that after angioplasty, up to 50% of lesions are re-stenosed after 6 months. Angioplasty is said to be initially successful in up to 90% of cases. Angioplasty done on multivessel disease increases the mortality from 1-3%. The overall Q-wave infarction rate for angioplasty is 5%. Contraindications to angioplasty include proximal LAD lesions (proximal to the first septal perforator), left main disease, long segments of disease which would be difficult to get a balloon catheter across, chronic occlusions, circumferential lesions, heavily calcified lesions, bifurcations or the appearance of liquid cholesterol which may embolize. PTCA indications include significant angina or positive exercise test in the presence of 75% narrowing with single or double vessel disease refractory to medical treatment without any of the above contraindications. Acute myocardial infarction with or without prior thrombolytic therapy may be another indication.

It should be noted that a failed angioplasty resulting in the urgent need for coronary artery surgery is a major crisis. Emergency coronary artery bypass sur-

Fig. 5.2. Right anterior oblique left ventriculogram.

Fig. 5.2. Right anterior oblique left ventriculogram.

Angina Pectoris With Pph And Cpd


gery after failed PTCA significantly increases the risk of operative death and perioperative MI compared to elective CABG. The risk of operative death and perioperative MI after a de novo coronary artery bypass grafting (CABG) without prior PTCA is 1% and 6%; the mortality of a coronary artery bypass surgery after a failed PTCA increases to 5-10%, and the risk of perioperative myocardial infarction (Q-wave myocardial infarction) increases to 25%. After a PTCA, the chance of a failure requiring an emergency coronary artery bypass surgery is 5%.

There are several technical details regarding coronary artery bypass surgery after failed PTCA. These include the problems of dissection of the coronary artery due to the PTCA, problems of free rupture of the coronary artery, and problems of distal embolization. The dissection may be managed by being sure that the opened coronary lumen is in fact a true lumen. This can be determined by examining closely the back surface of the lumen. If it is concave, then it is most likely the true lumen; however, if it is convex, then it is most likely the false lumen and the convexed surface will need to be further incised to enter the true lumen. Pre-rupture of the coronary artery is managed by ligation of the artery at the site of perforation and distal coronary bypass grafting. Distal embolization is managed by angiographically being sure where the distal emb olization occurs and then performing the coronary bypass distal to this.

In terms of management of the patient in the angiography suite after a failed coronary angioplasty, the following points should be borne in mind:

1) The main cause of morbidity and mortality from coronary bypass surgery after failed PTCA is a delay in coronary bypass surgery after the PTCA. The main cause of delay is persistence on the part of the cardiologist to maintain an open vessel past the area of iatrogenic inj ury by further instrumentation. It is an important point that there should be no further delay. The only instrumentation that should be performed in the cath lab after a PTCA accident is to place a "bail-out" catheter which contains multiple holes proximal and distal in the catheter to perfuse past the site of obstruction.

2) Persistent ST segment elevation, persistent chest pain refractory to nitrates, calcium channel blockers and beta blockers, or hypotension after a failed PTCA warrants placement of an intra-aortic balloon pump (in the catheterization lab in preparation for surgery).

3) The most important factor to improve survival in patients undergoing a failed PTCA is urgent coronary bypass surgery.

Continuing ongoing unresolved debate exists between medical management versus PTCA versus coronary artery bypass surgery in patients with coronary artery disease. As mentioned, 50% of patients who undergo PTCA can be expected to develop recurrence of a hemodynamically significant lesion requiring re-angioplasty or surgery.

Studies in the past have revealed the following caveats regarding these three modalities of management also:

1) PTCA versus medical treatment in patients with stable and unstable angina and 1-2 vessel coronary artery disease (excluding proximal LAD lesions). PTCA significantly increases angina-free survival. No overall difference in survival exists between PTCA versus medical treatment, but survival is significantly better in two subsets undergoing PTCA: those with impaired left ventricular function and those with two-vessel coronary artery disease.

2) PTCA versus coronary artery bypass in patients with severe proximal LAD stenosis. Although no difference in survival between these two treatment modalities has been determined, PTCA of an important proximal LAD stenosis may be quite dangerous and may be better treated with CABG.



Coronary artery bypass surgery has, over the years, proven its efficacy in terms of improved patient survival and improved quality of life in terms of pain-free survival. The general indications for coronary revascularization include improvement in survival, both overall survival as well as increase in angina free survival. The specific indications for coronary artery bypass grafting are as follows:

1) Triple vessel disease with or without decrease in ejection fraction (but particularly with a decrease in ejection fraction). Patients with reduced ejection fraction with coronary artery disease have a 5 year survival of approximately 75%, this increases to 90% in patients undergoing coronary artery bypass grafting.

2) Double vessel coronary artery disease with reduced ejection fraction. Coronary artery bypass surgery appears to increase long-term survival compared to medical management. However, double vessel disease with normal ventricular function probably can be managed as effectively with angioplasty or medical management.

3) Angina refractory to triple vessel therapy including nitrates, beta blockers and calcium channel blockers.

4) Compelling anatomy; this includes left main coronary artery disease in which the patients have a propensity to sudden death; also proximal left anterior descending artery disease where there is calcification proximal to the first septal perforator. This instance is associated with a high incidence of sudden death and should be managed with angioplasty cautiously if at all.

Life threatening ventricular arrhythmias after myocardial infarction even without a left ventricular aneurysm is an indication for coronary artery bypass surgery. Some type of anti-arrhythmic surgery, either endocardial ablation or placement of an automatic implantable cardioverter defibrillator, should be done as well. Unstable angina, i.e. crescendo angina, is an indication for coronary revascularization on a semi-urgent basis if full medical therapy is ineffective for up to several days. If an EKG shows infarction, urgent coronary artery bypass grafting may be performed or preoperative thrombolytic therapy may be tried.

Conduits Used for Coronary Revascularization

The two most commonly used conduits for a coronary revascularization are the greater saphenous vein and the internal mammary artery. Over the years, there has been no question that increased use of the internal mammary artery results in improved survival and improvement of angina free survival. This is because of the superior patency of the internal mammary artery graft compared to the saphenous vein graft. The 10 year patency of a saphenous vein graft is on the order of 50%. The 10 year patency of an internal mammary artery graft is on the order of 95%. The saphenous vein graft loses patency for the following reasons: Initially, intimal hyperplasia occurs as a remodeling process for the vein to adapt itself to the artery. This can result in occlusion of the graft. Later on atherosclerosis occurs within the vein graft, and this ultimately leads to the majority of saphenous vein graft occlusions. The internal mammary artery graft has the advantage that it will not occlude by either of these methods since it does not undergo intimal hyper-plasia and it does not undergo atherosclerosis. The left internal mammary artery is used most often and may be placed typically onto the left anterior descending artery or onto the obtuse marginal arteries coming off the circumflex. The right internal mammary artery may be used for the anterior descending artery or may be brought to the right coronary artery. It may also be brought down through the transverse sinus to be placed onto the circumflex artery. The mammary artery may also be used as a free conduit by transecting it proximally and attaching it separately onto the aortic root. In general, caution regarding the use of the internal mammary artery should be used in the following situations:

1) Diabetic patients in general may have one internal mammary artery taken down, however, two internal mammary arteries would probably be dangerous because of the decrease in vascularity of the chest wall, resulting in suboptimal wound healing.

2) Immunocompromised patients and patients in chronic renal failure likewise should undergo one internal mammary artery takedown at the most.

3) Extremely old patients who would most likely expire within the next 10 years would most likely not benefit from an internal mammary bypass graft.

4) Patients who have atherosclerotic subclavian arteries would most likely not benefit from an internal mammary artery because of the atherosclerosis which may progress to the internal mammary artery, as well as the subclavian artery atherosclerosis which may impair flow to the mammary artery.

5) Patients requiring emergency surgery for cardiogenic shock generally should not be subjected to the increased time it takes for taking down the internal mammary artery.

6) Patients who have a severely calcified or extremely tiny target coronary artery generally would minimally benefit from an internal mammary artery graft because of severity of disease in the distal target.

7) Redo-coronary surgery patients who have had previous vein grafts should receive mammary arteries with caution. In particular, the situation in which a stenotic vein graft to a completely occluded large important coronary artery requires reoperation. In this case, it may not be wise to use the internal mammary artery since the entire blood flow to that large coronary artery depends on the vein graft, and the mammary artery may not be able to supply the large demand of the large coronary artery in the acute postoperative phase. It should be noted that one of the major problems with internal mammary artery grafts is the propensity for these grafts to go into spasm in the perioperative period which can result in acute infarction and hemodynamic destabilization. This is why nifedipine is given intraoperatively after an internal mammary artery is performed, as well as postoperatively.

Other possible conduits for coronary revascularization include the lesser saphe-nous vein and gastroepiploic artery, as well as inferior epigastric artery. The gas-troepiploic and inferior epigastric arteries seem to have comparable patency to the internal mammary artery. The lesser saphenous has a patency comparable to the greater saphenous vein. Arm veins have been used, however, have an extremely poor patency in the order of 50% after 2 years. Radial artery conduits are used as well.

The natural history of vein grafts is that at 2-1/2 years, about a third show significantly decreased flow (i.e. greater than 50% reduction in diameter); about a third show mild reduction; and a third are normal. By 10 years, about half of vein grafts are occluded. Intimal hyperplasia is a remodeling process starting in the vein grafts older than 1 month and results in decreased flow to approximate the caliber of vein with the caliber of recipient artery. The absence of cine-angiographically evident intimal hyperplasia at 1 year is a good sign because only 10% of these will later develop intimal hyperplasia on cineangiogram 5 years post-operatively. Part of the pathophysiology of graft closure is due to atherosclerosis causing 1-3% of grafts closing per year. The reason the internal mammary artery is superior to the saphenous vein graft is because no intimal hyperplasia occurs and little to no atherosclerosis occurs, hence the 10 year patency of the internal mammary artery is 95% compared to 50% for the saphenous vein graft.

To decrease the incidence of postoperative graft thrombosis, aspirin and persantine are useful. In one landmark study evaluating the efficacy of aspirin and persantine in decreasing graft occlusion, it was shown that 1 month after coronary artery bypass, patients who had aspirin and persantine had a reduction in their graft occlusion rate from 21-8%. Similarly, at 6 months, the graft occlusion rate was decreased from 38-10%. Aspirin and persantine are, therefore, very effective medications in decreasing graft thrombosis postoperatively because of their anti-platelet effect.

Sudden death may occur in CABG patients in the perioperative period because of spasm of a vein graft or particularly an internal mammary artery; 10 mg sublingual nifedipine is given and the intravenous nitroglycerin is increased. This event may require that the chest be opened in the I.C.U. or that 0.1-1.0 mg of nitroglycerin may be given directly down the bypass graft in the electrographic distribution of the ischemia. Coronary artery spasm may be a very important cause of postoperative sudden cardiac arrest for unexplained reasons. Nifedipine in these situations, if the patient survives, should be continued indefinitely postoperative. Internal mammary spasm has been shown to occur many months after the revascularization on occasion.

With regard to PTCA after prior coronary revascularization, PTCA of a vein graft is only 50% effective and is generally more effective closer to the distal anastomosis. Overall although PTCA is useful in patients previously undergoing coronary bypass, it is more useful in patients never having received CABG. Angiography generally underestimates the severity of atherosclerosis. In general, any vein graft greater than 5 years old should be replaced at the time of redo-coronary artery surgery.

Technique of Coronary Artery Bypass

The patient is brought to the operating room and an arterial line and Swan-Ganz catheter are placed for hemodynamic monitoring. The patient is induced under general endotracheal anesthesia. A Foley catheter is placed and the chest and legs are prepped and draped. A median sternotomy is performed. If the mammary needs to be taken, this is done with an internal mammary artery retractor. The vein is generally harvested from the right lower extremity during this time. The pericardium is opened. Heparin is given and pursestrings applied. The aorta is cannulated. The right atrial appendage is cannulated with a two-stage venous cannula with one port going into the inferior vena cava and the proximal port in the right atrium. An antegrade cardioplegia cannula/aortic root vent is placed in the aortic root, and a retrograde cannula is placed transatrially into the coronary sinus. Cardiopulmonary bypass is instituted, the aortic cross-clamp applied, and antegrade blood cardioplegia instilled through the aortic root until arrest occurs, then this is switched to retrograde. The chosen targets are then grafted with the saphenous vein graft. This includes grafting to the distal right coronary, posterior descending, posterolateral branches or acute marginal for the right coronary system. For the left anterior descending system, this may include branches of the diagonal as well. For the circumflex system, this may include branches of the obtuse marginal, as well as posterior ventricular branches in the case of a left dominant system.

The proximal coronary anastomosis onto the aortic root is performed either during the period of cross-clamping, or once the cross-clamp is released with an aortic side-biter clamp. Once the aortic cross-clamp comes off, 100 mg of Lidocaine is given to help limit the amount of arrhythmias. When the patient has gained a normal sinus rhythm, the bleeding has been controlled, and mixed venous saturation is adequate, weaning is instituted. At this point, the anesthesiologist venti

lates the patient. One gram of calcium is given by the perfusionist and the following drugs are administered to help limit the chance of a protamine reaction: 100 mg of Solu-Medrol, 300 mg of Cimetidine, and 25 mg of Benadryl. With weaning from bypass accomplished, the venous line is removed and protamine is given. Generally, 3 mg/kg of protamine is given (i.e. equivalent to the 3 mg/kg of heparin dose administered at the beginning of the case). The ACT which was initially greater than 400 prior to initiating bypass now comes down to approximately baseline, which is about 100 seconds.

In the event that the patient has difficulty weaning from bypass, then cardiop-ulmonary bypass is re-instituted and the inotropes need to be raised. Initially, weaning from cardiopulmonary bypass is performed with 1 mcg/kg/min of ni-troglycerin and between 2.5 and 5 mcg/kg/min of dopamine. This may need to be increased to higher levels of dopamine and/or epinephrine added. If epinephrine needs to be added, this is usually started at about 1 mcg/min and can be titrated up. If this fails, then other pharmacologic maneuvers may be in order. If the patient has an elevated pulmonary artery pressure and also has a low cardiac output, this may be helped with Amrinone, which has a positive inotropic effect, but also causes vasodilatation, particularly on the pulmonary circuit. The choice of drug used depends on the hemodynamic parameters, the systemic vascular resistance, the cardiac output, and the pulmonary artery pressures.

In the event weaning is still unsuccessful, an intra-aortic balloon pump may be necessary. If weaning is still unsuccessful, i.e. after two tries at weaning with elevated inotropic agents and a balloon pump in place, then additional mechanical support is warranted. This type of support depends on the findings. If there is elevated pulmonary wedge pressure yet a low cardiac index (less than 1.5 l/min/m2) and a low blood pressure (i.e. less than 90 mmHg), then it could be assumed that there is left ventricular failure and a LVAD is warranted. Conversely, if the patient has right ventricular failure, there will be elevated right atrial pressure and low left-sided filling pressures, as well as low cardiac output and low blood pressure, i.e. an inability to volume load the left heart despite an elevated right atrial pressure. In this event, an RVAD may be required.

The LVAD is a partial bypass circuit from the left atrium to a biomedicus vortex pump which then pumps the blood into the aorta. This bypass circuit can be used to achieve nearly full flow and requires only mild to moderate hepariniza-tion at approximately an ACT level of 150 seconds for flows below two liters. The LVAD is positioned in the left atrium via the right superior pulmonary vein via a pledget pursestring placed in the right superior pulmonary vein. The aortic cannula, already in place in the aorta, can be used as the outflow for the LVAD. An RVAD is placed via the right atrial cannula in place which then drains blood through the biomedicus vortex pump into a cannula positioned in the pulmonary artery. Placement of the LVAD can be life-saving, and several patients in our unit have successfully survived placement of the LVAD. Its use is basically to support a stunned heart which will eventually recover.

An additional note should be made on the use of the intra-aortic balloon pump. As stated previously, this is useful to decrease afterload, thus decreasing the

workload on the heart and increases coronary artery perfusion pressure by inflating in diastole. There are some patients who cannot have an intra-aortic balloon pump. Such patients have extremely atherosclerotic aorta-iliac disease which precludes placement of even a guidewire, let alone a balloon pump into their aorta. In these patients, an alternative route can be placement of the balloon pump directly into the ascending aorta, and then threading the balloon pump distally past the left subclavian into the descending aorta. This is done through pursestrings placed as for the aortic root cannula.

There may be vascular complications related to the balloon pump. These include lower extremity ischemia and necrosis. It is important to document lower extremity pulses preoperatively and, of course, to continue to follow pulses closely postoperatively when a balloon pump is positioned. If there is evidence of ischemia, then a decision must be made whether the patient can tolerate weaning from the balloon pump or if the balloon pump must be replaced to the contralateral extremity. Alternatively, a femoral-femoral bypass with 8 mm Dacron graft may be necessary.

Redo-coronary artery surgery is much more hazardous than first time coronary surgery. An oscillating saw is used to enter the sternum. Caution must be used to avoid injuring the heart. When dissecting the heart from surrounding tissues, caution must be taken that the old vein grafts are not excessively manipulated because they may release emboli into the heart resulting in a trash heart which can result in ischemia and infarction.

In general, after cardiopulmonary bypass is instituted, retrograde cardioplegia is very useful to flush atheromatous emboli out of the old vein grafts. These can be transected, the distal limb tied off, and the proximal limb used for the proximal anastomoses of the new vein grafts. Because of the increased risk of atheromatous emboli going down patent old grafts, these anastomoses are done first. After giving the initial dose of retrograde cardioplegia the old grafts are transected distally and proximally and the distal anastomosis is performed followed by the proximal anastomosis. Since it may be difficult to place a side-biter clamp for construction of proximal anastomosis with the cross-clamp off, the proximal anastomoses are generally performed during the period of cardiac arrest.

Left Ventricular Aneurysm

Left ventricular aneurysm is, on occasion, an indication for surgery. The indications for operating on a left ventricular aneurysm are large size with decrease in cardiac output and congestive heart failure, and predisposition to ventricular arrhythmias. Ventricular aneurysms are seen to have a paradoxical outward motion in ventricular systole (i.e. the ventricle is dyskinetic rather than akinetic). The dyskinetic ventricle results in decrease in ejection fraction by sequestering the cardiac output within the paradoxically moving aneurysm sac. The dilated aneurysm causes an increase in wall stress by the law of La Place, resulting in increased myocardial oxygen utilization and worsening ischemia. This may result in congestive heart failure. The aneurysm and surrounding scar tissue predispose to arrhythmias and this too is an indication for surgery. Ventricular aneurysms are

usually located anterolateral^, although 20% of the time they may be located posteriorly (Fig. 5.1). The posterior defects are much more dangerous, and half of these are false aneurysms, i.e. the aneurysms have ruptured and have been contained. The mortality of operating on posterior aneurysms is much higher than that of anterolateral aneurysms. Cardiopulmonary bypass is instituted and the aneurysm is incised after cross-clamping and cardioplegia solution has been given. The aneurysm is resected (Fig. 5.2a,b) and its margins can be noted by the smooth margin of the dead tissue compared to the rough trabecular surface of viable myocardium. Organized thrombus is frequently evident within the aneurysm (Fig. 5.2c). Coronary bypass is performed in standard fashion. The ventricular resection is repaired with felt strips and 3-0 or 4-0 Prolene horizontal mattress sutures. Deairing maneuvers are done as previously described (10 cm pressure on the lungs to fill the left heart; aspiration of the LA and LV with a needle and syringe). Only then is the cross-clamp released.


Post-Infarction Ventriculoseptal Defect

Post-infarction VSD occurs through necrotic myocardium resulting from infarction and complicates in 1% of cases of acute myocardial infarction and usually occurs within 2 weeks following infarction. It is a true surgical emergency. About 25% of patients die within the first day and more than half die within the first week. After an acute myocardial infarction, if a patient develops a new systolic murmur or sudden congestive heart failure within 1-2 weeks, one should always be suspicious of either a post-infarction ventricular septal defect or postinfarction papillary muscle rupture. Either of these may result in the same type of symptoms and may be difficult to differentiate clinically because they both result in systolic murmurs and congestive failure. Swan-Ganz catheter is extremely useful in differentiating between these since an oxygen saturation step-up in the pulmonary artery is consistent with a post-infarction VSD but not papillary muscle rupture resulting in mitral regurgitation. The left-to-right shunt resulting from a postinfarction VSD is what leads to the pulmonary artery oxygen step-up.

After the patient has been resuscitated and a diagnosis inferred from Swan-Ganz catheterization, the patient is brought to cardiac catheterization and cineangiography. This confirms the diagnosis of either post-infarction VSD or papillary muscle rupture and helps assess myocardial function. Also, it allows one to see if there is a concomitant ventricular aneurysm which requires repair. Cineangiogra-phy is essential as a road map to determine which vessels should be bypassed and where at the time of definitive surgery.

The morphology of post-infarction VSDs is most commonly anterior or apical. About 20% of patients have a VSD in the posterior portion of ventricular septum. Posterior VSD is frequently associated with mitral valve regurgitation secondary to papillary muscle infarction. It should be noted that ventricular aneurysm may be associated with post-infarction VSD.

The conduct of the operation includes bi-caval cannulation with tapes. Car-diopulmonary bypass is instituted and after giving cold cardioplegic arrest, the VSD is approached through the left ventricle. In apical ventriculoseptal defects, the apical septum is approached via the anterolateral infarct that is almost always present. There may be an aneurysm associated with the infarction, in which case the incision is made directly through the aneurysm. The apical septal defect is repaired with a Dacron patch with pledgets on the right ventricular side and the suture is then brought up through the left ventricular side through the Dacron patch (Fig. 5.3a). If it is an apical infarction, one can amputate the apex to include the VSD and close with felt to include the septum and thus plicate the left ventricular free wall, the interventricular septum and the right ventricular free wall (See Fig. 5.3b).

For repair of a posterior septal VSD, the exposure is more difficult. This is done through the necrotic posterior left ventricular infarct. Pledgets are placed on the right ventricular aspect of the interventricular septum and attached to a Dacron patch located on the left ventricular side of the interventricular septum (Fig. 5.4).

In the case of posterior post-infarction VSD, there may be concomitant mitral regurgitation secondary to ischemia of the posterior medial papillary muscle. A patch may then be used to close the left ventricular infarction after it has been excised if necessary. It should be noted that operation early after rupture has a risk of death of about 50% compared to a risk of death of only 6% if the operation is done more than 3 weeks after rupture. One possible explanation for this is because the edges of the defect hold sutures better when an operation is delayed. Hence, if hemodynamically stable, some suggest delaying surgery, but usually the patient must go to surgery urgently because of the severity of their heart failure and hemodynamic compromise.

Ischemic Mitral Regurgitation Including Post-Infarction Papillary Muscle Rupture

As mentioned in the previous section, it may be clinically impossible to differentiate between post-infarction VSD and post-infarction papillary muscle rupture resulting in mitral regurgitation. Both present with systolic murmurs and congestive heart failure and require urgent surgery.

If the patient presents with severe congestive heart failure and coronary artery disease, the patient is resuscitated and is sent to the ICU for Swan-Ganz catheterization and measurement of left- and right-sided heart pressures. Saturation of the right atrium and pulmonary artery are assessed to look for a step-up in the pulmonary artery saturation indicating a post-infarction VSD. If this is not found and if the patient does have a systolic murmur, then the patient may well have severe ischemic mitral regurgitation based on Swan-Ganz catheter readings.

If the patient is hemodynamically unstable, pharmacological support may be indicated and if refractory, an intra-aortic balloon pump may be inserted. It should be noted that the balloon pump may be extremely useful to hemodynamically

Fig. 5.2a. Resection of apical aneurysm and resuspension of papillary muscle to free ventricular wall.

Fig. 5.1. Ultrafast CT scan demonstrating ruptured postinfarction ventricular aneurysm with fluid within pericardial sac.

Fig. 5.2a. Resection of apical aneurysm and resuspension of papillary muscle to free ventricular wall.

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