The internal mammary artery is the premier conduit for initial and repeat coronary artery bypass grafting and should be used as either a pedicled or free graft whenever possible. Saphenous veins from the greater and lesser systems are distinctly second choices but can serve satisfactorily as aortocoronary grafts for many years. When neither the internal mammary arteries nor the saphenous veins are available, the cardiac surgeon today must choose from a wide variety of alternative conduits that have been used periodically over the past two decades for coronary artery bypass grafting.

Because of excellent long-term patency (greater than 90% at 7 years), internal thoracic artery (ITA) bypass grafts are preferred over saphenous vein grafts for myocardial revascularization. ITA grafts can be used for up to 70% of all distal anastomoses and in up to 95% of patients. ITA grafts are more technically demanding; inadequate length, traumatic arterial injury, torsion, separation of intima and adventitia, and anastomotic stricture are important pitfalls. Postoperative problems of bleeding, phrenic nerve injury, mediastinal infection, and arm paresis or paresthesia are complications attributed to ITA grafts, but they are uncommon if meticulous technique is used.

Occlusion rate of the saphenous vein is around 12-20% during the 1st year and 2-4% annually for the next 4 or 5 years. Subsequently, this rate doubles, so that at 10 years, approximately 50% of grafts become occluded due to the occurrence of graft atherosclerosis. A similar percentage of patent grafts show atherosclerotic changes at the end of the 1st decade. Sequential vein grafts probably suffer the same fate although late follow-up is lacking. Reoperation is estimated to be 30% at 10 years, as judged by angiographic criteria. The operative risk of reoperation is at least double that of primary operation; symptomatic relief appears to be of shorter duration. Recent technical changes to better preserve medial and endothelial function and to pharmacologically inhibit platelet function may lead to longer duration of the venous conduit.

Compared with isolated coronary artery bypass grafting (CABG), the combination of valve replacement or repair with coronary revascularization generally increases operative risk. However, complete revascularization is superior to no revascularization in patients with valvular and coronary artery disease (CAD). Patients who undergo aortic valve replacement and CABG have two unrelated disease processes; these patients only infrequently have ischemic cardiomyopathy, and the operative mortality is slightly increased to 4-7% for the combined procedure versus isolated aortic valve replacement. Patients who are operated on for mitral valve disease and CAD fall into two groups: 1) where CAD and mitral valve disease are not etiologically related, and 2) where mitral valve dysfunction is the result of ischemic changes. In the latter group, operative mortality significantly exceeds that for isolated mitral valve surgery, and surgical priority increases that difference (operative mortality 7-20%). Thus, the operative risk for a mitral valve procedure plus CABG exceeds that for isolated coronary revascularization or isolated valve replacement. In the combined procedure, risk increases if valve dysfunction is caused by CAD, if severe left ventricular function is present, if the patient has been assigned to Class IV, or if emergency operation is required.

The direct surgical techniques for the treatment of refractory ischemic ventricular tachycardia have now been available for 10 years. This report assimilates the first decade's experience with these direct procedures to clarify the present indications for ventricular tachycardia surgery, the preferred method for conducting the operative procedures, the clinical results that are to be expected, the subsequent prognosis, and the role of the automatic internal cardioverter-defibrillator in the contemporary management of refractory ischemic ventricular tachycardia.

Onset of cardiogenic shock in patients with various manifestations of acute myocardial ischemia has high mortality, but use of improved hemodynamic monitoring, the intra-aortic balloon pump, and early operation have improved previously dismal results. Review of published experience spanning the last 20 years indicates that 66% of patients survive after emergency myocardial revascularization for acute myocardial infarction and cardiogenic shock. If cardiac damage is overwhelming and irreversible, selected patients may be "bridged" with mechanical biventricular circulatory assist devices and transplanted. Infarctectomy for acute myocardial infarction remains controversial and unproven; successful repair of free left ventricular wall rupture is uncommon. In patients with cardiogenic shock, operations for acute postinfarction ventricular septal defect or mitral insufficiency have operative survival rates of 45% and 54%, respectively. Long-term (greater than 2-year) survival for patients after repair of acute postinfarction ventricular septal defect is 84%. However, 5-year survival after successful operation for acute postinfarction mitral insufficiency complicated by cardiogenic shock is only 40%.

Analysis of published reports indicates that ischemic mitral insufficiency is associated with higher operative mortality (10-30%) than is nonischemic mitral valve procedures. Probable incremental risk factors include emergency operation, acute myocardial infarction, hemodynamic instability, poor left ventricular function, pulmonary hypertension, advanced age, and renal failure. Early valve repair or replacement with myocardial revascularization improves survival in patients with circulatory insufficiency due to acute postinfarction mitral regurgitation. Although the technique of repair of nonacute ischemic mitral insufficiency is not standardized, repair with revascularization is preferred. Preliminary data suggest that long-term results are primarily related to the severity of left ventricular dysfunction.

At a time when hospital mortality for adult cardiac operations is continuing to fall, the ischemic mitral regurgitation subset remains at relatively high risk. Based on analysis of available data, efforts to improve results might be directed toward a more general application of mitral valve reconstruction in this population. Other promising therapeutic measures include the liberal use of reperfusion therapy in the acute papillary muscle dysfunction group, better selection of patients for operation, and, perhaps, operative recommendation to a greater proportion of the more stable patients who previously were treated medically. Incorporating these therapeutic concepts into routine clinical practice may improve the overall prognosis of this difficult subgroup.

Thirty-one published reports (366 patients) and 48 consecutive patients treated for postinfarction ventricular septal defect at four institutions in northern California were reviewed. Overall hospital mortality was 43% in the reviewed group and was not affected by age, concomitant myocardial revascularization, date of operation, presence of cardiogenic shock, or location of the defect. Mortality for the 48 consecutive patients, all of whom had surgery within 30 days of acute infarction, was 67%. Although there were no survivors over 65 years of age, mortality was not affected by age, location of the ventricular septal defect, or concomitant myocardial revascularization.

We have reviewed the literature and supplemented it with our own experience to provide a current viewpoint on emergency coronary bypass in three settings in which cardiogenic shock did not exist preoperatively. Acute failure of coronary angioplasty led to emergency operation in 701 patients with 25 (3.6%) deaths. There was a 37.6% incidence of perioperative infarction. Thrombolytic therapy for acute myocardial infarction, sometimes followed by angioplasty, led to emergency operation within 8 hours in 145 instances with four (2.1%) deaths. Emergency coronary bypass was primary therapy for 1,051 patients with acute myocardial infarction with 51 (4.9%) hospital deaths. Emergency operation for failed angioplasty is frequently mandated in the setting of surgical standby and iatrogenic ischemia although some operations could be postponed to an elective status. Emergency operation after thrombolytic therapy has been used for unsuccessful angioplasty of the infarct vessel, left main stenosis of greater than 50%, left main equivalent, multivessel disease with complex lesions not amenable to angioplasty, or failure to restore patency of the infarct vessel with thrombolysis. Operation within 12 hours of thrombolytic therapy is associated with a coagulopathy causing increased bleeding, the need for transfusion, and a greater incidence of reoperation for perioperative bleeding.

Restenosis after successful PTCA remains a major problem limiting the efficacy of the procedure. The pathophysiologic mechanism of restenosis has been enigmatic so far, but accumulated evidence strongly suggests that intimal hyperplasia is the major mechanism. Based on current understanding of the process of intimal hyperplasia, one unifying concept may be that there are at least two major local biologic determinants influencing this process, lesion characteristics and regional flow dynamics. Lesion characteristics include the plaque structure and the quantity of smooth muscle. These may provide the anatomic substrate that determines the extent of injury and the degree of smooth muscle cell proliferation. The amount of smooth muscle cells in the stenotic lesion activated by injury to undergo proliferation may determine the eventual bulk of the restenotic lesion. In addition, low wall shear stress could promote intimal hyperplasia and cause structural change of vessels to decrease the lumen, whereas high wall shear stress exerts the opposite effects. Intimal hyperplasia after balloon injury is a complex process involving platelets, growth factors, endothelial cells, smooth muscle cells, mechanical injury, wall shear stress, and probably other unknown factors. Platelets not only contribute growth factors such as PDGF but also cause organized thrombus. Different growth factors may be involved in initiating smooth muscle cell proliferation and may come from many different sources, including smooth muscle cells, endothelial cells, and macrophages. Intact confluent endothelial cells may produce heparin sulfates and inhibit intimal proliferation; however, regenerating endothelial cells may have the opposite effect. Thus, the proliferative potential of smooth muscle cells, endothelial recovery, extent of injury, wall shear stress, and other unknown factors may all influence this process. Based on these concepts concerning the biology of restenosis, some research directions concerning potential forms of therapy are proposed.

At this time, endomyocardial biopsy has proven validity as a diagnostic method in few circumstances. However, it is overused. In the near term, the extent of its use should be modified by knowledge of its therapeutic relevance in patients with myocarditis. In the long term, numerous new techniques for studying pathophysiology at the subcellular and molecular levels will demand a central role for endomyocardial biopsy in the diagnosis, treatment and fundamental understanding of myocardial diseases. We believe that endomyocardial biopsy will serve as an indispensible link between basic scientists and clinicians in the effort to describe disease mechanisms.

Information obtained during the past decade suggests the need to reexamine the possibility that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering onset of coronary thrombosis is supported by the findings that 1) the frequencies of onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations with parallel increases in the period from 6:00 AM to noon, 2) transient myocardial ischemia shows a similar morning increase, and episodes are often preceded by mental or physical triggers, 3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi, 4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state or coronary vasoconstriction, are accentuated in the morning, and 5) aspirin and beta-adrenergic blocking agents, which block certain of these processes, have been shown to prevent disease onset. The hypothesis is presented that occlusive coronary thrombosis occurs when 1) an atherosclerotic plaque becomes vulnerable to rupture, 2) mental or physical stress causes the plaque to rupture, and 3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of onset of acute disease suggests the need for pharmacologic protection of patients during vulnerable periods, and provides clues to mechanism, the investigations of which may lead to improved methods of prevention.

In 1904, Marchand recognized the consistent association of fatty degeneration and vessel stiffening and introduced the term "atherosclerosis" to indicate this combination. Current research is focused principally on the lipid component, but there is evidence that both aspects are reversible. Atheromatous lipids add significantly to the volume of lesions and thus contribute to vascular obstruction and end-organ damage. Reversal of atherosis has been observed in all the major species used in atherosclerosis research; rabbits, swine, dogs, chicks, pigeons, and subhuman primates. Direct evidence for reversal in humans is based on angiographic trials and is less extensive. One femoral artery and one coronary artery trial indicate that the lesions can be stabilized. CLAS, the largest angiographic trial to date, indicates that coronary lesion reversal is possible. Clinical effects of sclerosis are more subtle, and there is little evidence that sclerosis alone leads to end-organ damage. However, it should be noted that atherosclerotic lesions producing end-organ damage invariably have a major fibrous component. Sclerotic vessels have reduced systolic expansion and abnormally rapid pulse wave propagation, which can be measured noninvasively. Primate studies indicate that sclerosis is induced by hypercholesterolemic diets and is reversible when these diets are withdrawn. Changes in sclerosis may be another useful indicator of the formation and reversal of lesions and may involve changes in EDRF. Future studies of atherosclerosis reversal should use a combination of measures to evaluate both atherosis and sclerosis.