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Ischemic heart disease is a broad term encompassing several closely related syndromes caused by myocardial ischemia, an imbalance between cardiac blood supply perfusion and myocardial oxygen and nutritional requirements.

Understanding the various types of cardiomyopathies is important for identifying individual patients’ conditions and developing appropriate treatment plans. Yet defining and categorizing “cardiomyopathies” has proved no simple task—starting in 1972 when Goodwin and Oakley defined them as myocardial diseases of unknown origin and proposed three types. In 1990, the World Health Organization and International Society and Federation of Cardiology expanded the definition to diseases of myocardium with myocardial dysfunction. This chapter adapts the American Heart Association’s genetic-based classification introduced in 2006. Within primary cardiomyopathy, we use genetic, nongenetic, and “acquired” disease categories—describing presenting symptoms and the use of imaging, biopsies, and the role of family histories, in some cases, for making a diagno sis.

This chapter presents a description and illustration of the anatomic features of the coronary vessels. It first deals with the typical course and important variations of each major artery and then with anatomy of the veins, both as seen anatomically and in imaging, pairing coronary arteriograms and CT angiograms. Understanding coronary vessels’ anatomy is foundational for the diagnosis and treatment of ischemic heart disease.

The primary goal of catheter-based coronary angiography is the identification, localization, and assessment of stenotic lesions present within the coronary arteries that will enable us to determine the pathophysiologic significance of the obstructive lesions in question regarding ischemia vs. nonischemia.

This chapter focuses on pathology of coronary atherosclerosis as well as on the various types of lesions of the coronary ostia.

Anomalous coronary arteries are a heterogeneous group of disorders which vary in clinical importance from benign to highly malignant, causing angina, syncope, or sudden death. They are the second-most-common cause of sudden cardiac death in young athletes. The interarterial artery, located between the aorta and pulmonary artery, is the most concerning type, especially for patients with an anomalous left coronary artery. The treatment approach depends on hemodynamic significance, symptoms, and high-risk features. New imaging modalities, including coronary computed tomography angiography, may be helpful in determining the optimal therapeutic approach.

Atherosclerosis predominates as the pathologic lesion in coronary artery disease. Less commonly, other nonatherosclerotic etiologic processes involve the coronary arteries, with or without symptoms. This chapter explores the nonatherosclerotic etiologies of coronary artery disease, from spontaneous and device-induced vasospasm to spontaneous coronary artery dissection, vasculitis, embolism, aneurysm, and microcirculatory coronary disease to the impact of chest irradiation, heart valve transplants, congenital conditions, and cocaine use.

This chapter describes and illustrates complications of acute myocardial infarction, including mechanical, arrhythmic, and embolic disturbances. Circulatory failure from severe left ventricular dysfunction or other mechanical complications of acute myocardial infarction accounts for most fatalities. Mechanical complications include left ventricular failure with cardiogenic shock, cardiac free wall rupture, ventricular septal rupture, papillary muscle rupture, and right ventricular failure.

RATIONALE AND OBJECTIVES A new vascular occlusion device was tested in canine femoral and iliac arteries and in an animal model of a patent ductus arteriosus (PDA). METHODS Four variations of the vascular plug were placed into 18 iliac or femoral arteries of 17 mongrel dogs. Follow-up angiography was performed 1 hour and, if necessary, 2 hours after placement in all animals, 14 of which were then killed. Three dogs were followed angiographically for 2 weeks to 3 months. The "butterfly" plug was then tested in a canine model of a PDA. RESULTS All plugs contained thrombi, and 12 of the 18 devices caused complete or nearly complete vascular occlusion within 2 hours. In one dog, one vascular plug had eroded through the vessel wall at 3 months without clinical sequelae. Successful PDA occlusion was achieved in 1 or 2 days in 6 of 8 dogs. Three misplacements occurred, one of which resulted in death. DISCUSSION The balloon-expandable vascular plug appears to be a promising device for occlusion of blood vessels. Migration has not been observed once the device is placed, thus, sizing of the device appears less critical than with coils. However, modification of the delivery system and considerably more experience with the device are necessary to reduce the risk of misplacement.

The tissue reaction to reexpanded, purified bovine collagen sponge placed percutaneously into the lung, pleural space, liver, kidney, and muscle was studied in dogs and rabbits. In addition, the biocompatibility and radiopacity of tantalum-treated collagen foam plugs was examined. No adverse effects were found. We believe that collagen plugs may be of use in occluding needle tracts from biopsy sites to prevent complications such as bleeding or pneumothoraces.

A correlative study in 50 cases of healed myocardial infarction compared the 12 lead electrocardiogram with pathologic observations. The electrocardiogram was interpreted according to established Minnesota codes with some modifications. The following conclusions were reached: (1) The electrocardiogram underestimates the extent of myocardial infarction. (2) When a healed myocardial infarct at a specific location is recognized with electrocardiographic criteria, it is likely that there are unrecognized infarcts involving other areas of the left ventricle. (3) Infarctions involving the lateral and inferobasal areas are frequently unrecognized. (4) The electrocardiogram is more likely to miss myocardial infarcts in patients with multiple, than in those with single, electrocardiographically diagnosed infarcts. (5) Apical myocardial infarction does not appear to have specific electrocardiographic findings, other than those related to general infarct localization by electrocardiogram, particularly in patients with anteroseptal or anterolateral infarction. (6) Abnormal Q waves, generally thought to indicate transmural myocardial infarction, are frequently found in subendocardial infarction. (7) The simplified electrocardiographic classification of myocardial infarct site (anteroseptal, inferior, anterolateral) used in this study is preferable to more detailed classifications previously suggested by others.

Ablation of the kidney was attempted in 12 dogs by injecting 10-30 ml of heated (100 degrees C) contrast medium (Hypaque-60, diatrizoate meglumine) into the renal artery. Complete renal ablation without collateralization was demonstrated. Hot contrast medium is an effective embolic agent, and its use is associated with few of the drawbacks of presently used techniques.

Four patients with atherosclerotic disease were found to have a recanalized coronary arterial thrombus on angiography. The functional significance of this finding varied. In 2 cases, flow (judged by collaterals) was insignificant in spite of the recanalization. In the other 2, collateral supply had been shown to be absent during the initial stage of thrombosis. In one case, recanalization was confirmed pathologically.

A pathologic study was done on 53 patients who had received 86 saphenous vein grafts to bypass obstructive coronary arterial lesions. The periods of study after operation ranged from failure to survive the operation to three and one-half years. Of significance was the high incidence of residual obstructive disease in nongrafted arteries (38 of 53 patients) and in grafted systems (graft and distal artery) (55 of 86 grafts; 64 percent). The residual obstructive disease in the graft systems increased with time after operation. Obstruction was observed in 30 of the 86 grafts, and in 17 of these 30 the distal artery was also obstructed (usually by residual atherosclerosis). The characteristic basis for occlusion of a graft one month or less after operation was thrombosis. In longer range grafts, occlusion was most commonly caused by fibrous intimal proliferation, although in a small number, organized thrombosis alone or with fibrous intimal proliferation was the basis. In 28 of the 43 patients who survived one month or less, acute myocardial infarction was present at operation or afterward; that is, in 65 percent of the patients who died during the period of hospitalization. Of the 29 acute infarctions, after operation 23 were in a zone supplied by a grafted artery, and six were in a zone supplied by an artery not receiving a graft. In six of the 14 cases of acute infarction in the distribution of an obstructed graft system, the artery proximal to the graft was also occluded by a recent thrombus. Thrombosis in an artery proximal to a graft was observed in one or more vessels in 12 patients who survived the first month after operation. In these, there were ten acute myocardial infarcts, seven of which were in the distribution of the occluded artery.

A model was developed which allows the dilatation of iliac cadaver arteries under normal blood pressure conditions (mean pressure 100 mmHg). Segments of the iliac artery were put under pressure and dilated with balloons under similar conditions as in clinical practice. Purposely oversized balloons were used because most of the arteries did not contain severely stenotic plaques and consequently the commercially available balloons had no effect because of their comparatively small diameter. In spite of the use of oversized balloons, the cadaver arteries could not be significant dilated. Rupture of the intima and media was almost invariably present. Leakage of distending fluid through the adventitia occurred commonly. The "therapeutic range" between minimal dilation and partial or total rupture in postmortem studies is small.

The nature and incidence of postoperative mural thrombosis of the septal and/or posterior walls of the left atrium were studied in autopsy specimens of hearts from patients in whom the mitral valve had been replaced by a prosthesis I day or longer before death. The cases were divided into length of postoperative period as follows: Group I, 1 to 60 days, 57 cases; Group II, 61 days or longer, 36 cases. In Group I mural thrombus of the septal and/or posterior walls of the left atrium was found in 35 of 57 patients (61%). Thrombi against the septal wall tended to be broad and flat. Thrombi involving the posterior wall tended to be multifocal. In Group II, lesions interpreted as old thrombi of the atrial septum were found in 23 of 36 subjects (64%). Grossly, the old lesions were represented by gray nodularity. Histologically such lesions were consistent with organized thrombi. Superimposed recent thrombosis occurred in some cases. Systemic embolism occurred in each group. In the cases in which left-sided thrombi were restricted to the septal and/or posterior walls of the left atrium, systemic embolism was observed in 10 of 23 cases in Group I (43%) and in two of seven cases in Group II (29%). Obstruction of the mitral prosthesis by bulky mural thrombosis originating at the septal wall of the left atrium was observed in one case. The study suggests that the process of postoperative mural thrombosis of the septal and posterior walls of the left atrium may result from trauma to these structures during the operative procedure.

To investigate the acute and long-term effects on the vasa vasorum after massive overdilation, canine aortic segments were dilated with Gruentzig balloon catheters to more than 100% over normal size. In the acute study, the significant lumen increase was the result of intimal and medial rupture with stretching and thinning of the adventitia. In these areas, the vasa vasorum were stretched and severed, causing adventitial hemorrhage. In the chronic study, areas of previous subtotal wall rupture with adventitial thinning were repaired by scar tissue. This repair included formation of a neomedia, hyperplasia of the adventitia, and proliferation of the vasa vasorum. No progression of luminal dilatation was seen. This study showed that in subtotal aortic wall rupture, even a severely damaged adventitia is capable of preserving the lumen from further dilatation and rupture until healing. Blood flow to the damaged vessel wall was reestablished by revascularization via capillary budding in the aortic wall.

Balloon dilatation of the ductus arteriosus was carried out in vivo in newborn pigs and on postmortem specimens from humans and piglets. The ductus was functionally closed in all newborn animals but patency resulted in all animals after balloon dilatation. Left-to-right shunts of 50% to 70% were found with anatomic lumen sizes of 3 to 5 mm. Patency was demonstrated up to 6 weeks after dilatation. Histologic examination showed splitting of the internal elastic layer and media, areas of hemorrhage confined to the media, and preservation of the adventitia. Mediastinal hemorrhage did not occur. This new technique is useful as an animal model of patent ductus arteriosus and could theoretically be used for palliative treatment of ductus-dependent congenital heart disease.

Diatrizoate (76%) contrast agent heated to 100 degrees C was injected into the veins of dogs and one human volunteer for the nonsurgical occlusion of the vessels. Follow-up venograms and histologic examinations, at intervals varying from one day to four weeks later, revealed thrombosis of the injected veins in all animals. Thrombosis occurred one to five days after injection of contrast agent. The authors conclude that hot contrast medium is a safe and convenient agent for inducing thrombosis. It is much easier to use than mechanical devices, tissue glues, and plastics, which involve complex procedures and specialized equipment. In contrast to other sclerosing agents, hot contrast agent is rapidly converted into a nonsclerosing agent by cooling. The new technique allows a more controlled thermal injury to the vascular wall and is under fluoroscopic control.

The histological changes found in the coronary arteries in 15 patients with coarctation of the aorta have been described. Qualitative and quantitative studies were performed and the results compared with the findings of a matched control group of patients without heart disease. Severe changes in the intima during early life and even the severe atheroma which appears in young persons are considered to be a reaction to coronary hypertension. The striking thickening of the media in the coronary arteries is also thought to be a reaction to the altered hemodynamic forces. In coarctation of the aorta the coronary arteries are of greater than normal capacity, and it is suggested that this histological feature parallels the increased metabolic requirements of the left ventricle.

This chapter concerns itself with the matter of correlating angiocardiographic and pathologic findings. The subject is logically subdivided into two parts: the coronary arteries and the left ventricle.

The ascending Ao may be divided into two parts, the sinus, or proximal, portion, and the tubular, or distal, portion. The junction between these two parts lies at about the level of the free edge of the aortic cusps. Deviation of a few millimeters in the level of origin of the coronary arteries with respect to the junction is common. When the origin is as much as 1 cm above the junction, a condition of congenital high takeoff or ectopic origin should be considered. Instances of congenital high takeoff of a coronary artery usually involve the RC. Variations within the normal range are shown in Figure 124, after which cases exhibiting high takeoff will be illustrated.

The optimal treatment for recurrent coarctation of the aorta remains undefined. Recurrent stenosis following surgical repair occurs in 6-48% of cases involving the thoracic aorta. Because of the high morbidity and mortality associated with surgery, an alternate approach such as transluminal angioplasty is desirable. To evaluate this possibility, the authors created several experimental lesions to test their capability for dilatation, using the percutaneous transluminal technique. The results indicate that balloon dilatation of coarctation after end-to-end anastomosis is difficult or impossible. Dilatation of other types of suture lines may also be difficult due to the large amount of fibrous tissue at the anastomotic site, which is not amenable to balloon dilatation. Thus surgery remains the preferred form of therapy.

Obliteration of varicoceles in men with infertility has been shown to improve semen quality and increase fertility rates. Many current techniques involve complex procedures and specialized equipment and may be associated with adverse effects. Transcatheter thermal vessel occlusion was utilized for spermatic vein obliteration in dogs. Diatrizoate (76%) contrast medium at a temperature of 100 degrees C was injected into canine spermatic veins. Follow-up venography and histologic examination revealed thrombosis of the injected veins without damage to the surrounding tissues in all cases. Clinical and laboratory examination of the animals revealed no adverse systemic effects. It is concluded that transcatheter thermal venous occlusion is an effective technique for spermatic vein occlusion in a canine model.

When there is a single coronary arterial ostium in the Ao, two anatomic possibilities exist. The first is that the entire coronary arterial system arises from the Ao, a condition that may be termed single coronary artery.

In adults, the LC normally runs for about 1 cm before branching into its terminal branches. According to Lewis et al, (1970), the length of the LC in 25 patients selected at random from the series of 354 arteriograms ranged from 7.5 to 20.5 mm (mean, 12.8 mm). These findings are similar to those reported from the pathologic studies of Baroldi and Scomazzoni (1967) who observed a range of 3 to 23 mm (mean, 13.5 mm). Green, Bernstein, and Reppert (1967) studied the length of the LC in 50 consecutive specimens. In 12 of these, the length was 5 mm or less. Fox, Davies, and Webb-Peploe (1973) performed angiographic and pathologic studies on the LC. One hundred cases were present in each group. In their pathologic study, they observed a mean length of 5.5 mm, while in their angiographic study, the mean length was 9.5 mm. The LC is considered to be short when it is less than 5 mm long.

An introducer-sheath dilator is described, which was modified to protect the leading lip of the sheath during insertion, thus reducing arterial damage. The new sheath and a standard sheath were inserted into the femoral arteries of six dogs. Subsequent histologic examination of the arteries proved the new sheath to be both safe and effective.

Balloon dilatation of the ductus arteriosus was carried out in vivo in eight piglets that were 12 to 16 days old. The ductus was functionally closed in all animals before dilatation. Long-term patency for periods of up to 6 months after the procedure was demonstrated in six animals by angiography, Doppler ultrasound examination, and at autopsy. The presence of hemodynamically significant shunts was indicated by clinical development of heart failure, pulmonary infections, and left ventricular hypertrophy. These results confirm the value of this laboratory preparation to create left-to-right shunts at the ductus level.

The authors describe an experimental model for the study of nephrotoxicity induced by contrast media, based on a standardized injection combined with occlusion of the renal artery so as to expose the kidney to a high concentration of contrast medium for ten minutes. Iopamidol, ioxaglate, and both isosmolar and hyperosmolar saline were well tolerated, but diatrizoate caused marked radiological and pathological changes. This model may be helpful in studies of the mechanisms underlying contrast medium nephrotoxicity and evaluating differences in toxicity between contrast agents.

The two main coronary arteries, the right and the left, originate from the aorta (Ao); in about half the population, a third artery, the so-called conus artery (CA), also originates from the Ao.

A deformable soft-tipped angiographic catheter has been designed and developed to reduce vascular trauma during coronary arteriography. In order to test the ability of the catheter tip glide over vascular endothelium, the coefficient of resistance was tested using fresh human aortic tissue. The mean frictional coefficients of resistance (FRc) for the soft-tipped catheter, as compared with two commonly used catheters (N = 10/group), were .78 +/- .08 units for the soft-tipped catheter and 1.10 +/- .10 (p less than .006) and .98 +/- .10 (p less than .034) for the conventional catheters. This demonstrates a significant 23% reduction in FRc with the soft-tipped catheter. The ease of penetration into a wax media was also measured using the soft-tipped catheter and compared with the same two conventional catheters. The indentation depths for the soft-tipped catheter and the two other catheter groups (N = 7/group) were 140 +/- 18 micron, 246 +/- 15 micron and 318 +/- 20 micron, respectively. This represents a 56% decrease in indentation depth with the soft-tipped catheter. Histologic studies in canines have demonstrated considerably less endothelial damage and subsequent intimal proliferation in the aorta and coronary ostia with the soft-tipped catheters compared with control catheters. It is concluded that a soft-tipped angiographic catheter is less traumatic to vascular tissue and may offer a safer approach to intravascular studies.

The term hypoplasia is applied to a coronary artery when it is uniformly narrow on the basis of its intrinsic structure and has a shorter course than usual. When a hypoplastic artery is present, the region of the heart usually supplied by this artery is perfused through branches from the other coronary arteries. As a rule, only one of the coronary arteries is hypoplastic, either the right or a branch of the left. While hypoplasia implies that there is an intrinsically narrow lumen, hypoplastic arteries may additionally harbor atherosclerotic lesions.

The term abnormal communication of the coronary arteries refers to the state in which the coronary arteries arise in normal fashion from the Ao but one or several branches connect directly with one of the cardiac chambers, the coronary sinus (CS), the PT, or the superior vena cava (SVC). The condition varies from a simple single fistulous connection to a complex angiomatous type with multiple communications.

Stenosis of the takeoff of a coronary artery from the Ao may result either from spasm or from organic lesions. Organic lesions involve the coronary artery intrinsically or, more commonly, are secondary to diseases of the Ao.

A new theory of the mechanism of percutaneous arterial angioplasty is advanced. For this study, abdominal aortas and coronary, renal, superior mesenteric, and iliac arteries were obtained from cadavers. In addition, the iliac arteries of dogs were dilated and studied. No evidence of significant compression or redistribution of plaques could be found, supporting the theory that atheromatous material is incompressible. Cracking of the intima and separation of it from the media were histologically demonstrated following angioplasty. It is proposed that the stretched media distends following dilatation, carrying with the intima and atheromatous material. Once the media is freed from the encasing effect of the intima, it adapts to the circulatory needs of the body. Beyond a certain point, the arterial widening becomes permanent, due to an overstretching of the muscle fibers, which is demonstrated by a corkscrew deformity of the muscle cell nuclei.

Infarctectomy with or without revascularization procedures has been reported for some cases with ventricular tachyarrhythmias or pump failure and cardiogenic shock. As the latter situation is usually associated with a large portion of Myo being destroyed, infarctectomy obviously would be at high risk and the principles underlying such an intervention debatable.

The reliable and safe production of myocardial infarction in closed-chest animals is of paramount research interest. To date, the injection of particulate matter and the introduction of occlusive solid plugs have been described. Because of the limited size of the catheter, only small branches could be occluded, which resulted in a high incidence of mortality. A new simple technique is described that allows occlusion of a major coronary artery at a preselected site. An Ivalon (polyvinyl alcohol) plug compressed around the tip of an introducing wire is advanced through a selectively placed catheter into the coronary artery. It is felt in place for 5 minutes and assumes its original size upon contact with blood. Once the plug is re-expanded, the wire is withdrawn. The new technique was carried out successfully on nine dogs with no immediate fatality and myocardial infarction as demonstrated by cine ventriculography and histopathologic examination.

Despite the terrible toll of death from acute myocardial infarction, the majority of patients reaching a hospital recover and can return to an active life. As a rough assessment of the problem, 75 percent or more will leave the hospital and 60 percent will be alive at the end of 1 yr. After the first year, the group without disabling symptoms or high risk factors have a mortality rate of about 6 percent per yr. It is clear that many patients have recurrent problems related to extensive myocardial loss including the formation of LV Aneus, arrhythmias, including those causing sudden death, and recurrent infarction. Associated conditions such as valvular disease, hypertension, and chronic pulmonary disease, may contribute to cardiac failure in patients who have recovered from acute myocardial infarction.