Coronary Artery Bypass Surgery
Surgical treatment of coronary artery disease should increase regional coronary flow reserve and not increase any early or late morbidity and mortality more than the other treatment modalities. In the past 50 years, surgical treatment of coronary artery disease has been adapted rapidly worldwide and several techniques have been developed to decrease total surgical risks and to improve early and late results with the highest level of quality of life. In spite of the last guidelines that offer stents for single or multiple vessels disease, the fact is that surgical revascularization has better outcomes in all groups of coronary artery patients. In the past two decades, the main target has been to limit or eliminate side effects of extracorporeal circulation and cardioplegia (off-pump), and general anesthesia (awake coronary bypass). The prime goal of surgical revascularization is to obtain complete revascularization by bypassing all severe stenotic coronary arteries having a diameter larger than 1 mm. Surgical revascularization with cardiopulmonary bypass through a full sternotomy remains the most widely used surgical technique. With the development of stabilization devices, off-pump procedures can be safely performed in most patients with single or multivessel disease. Minimal invasive and/or robotic surgery is an attractive procedure to catch invasive cardiology. The gold standard strategy involves single graft to single target vessel bypass, especially the left internal mammary artery to the left anterior descending artery. The early cumulative mortality rate is below 3%, but lower than 1% in lower-risk patients. There are some variables most predictive of early mortality: older age, female, reoperation, non-elective surgery, left ventricular dysfunction, accelerated atherosclerosis. The survival rate is higher than 65% for 15 years. Late mortality is dependent not only on non-use of internal mammarian artery, closure of grafts, progression of native arterial disease but also on comorbidities. Satisfactory quality of life after surgery depends on the long-term duration of the freedom from angina, heart failure, rehospitalization and reintervention, and improvement of the exercise capacity. Return of angina during the first 6 months depends on incomplete revascularization or graft failure, whereas progression of native-vessel disease and grafts are serious risk factors for the late recurrence of angina. Venous graft occlusion is the most common reason for reintervention, and native vessel disease is the second.
Part of the book: Coronary Artery Disease
Surgical Treatment in Diffuse Coronary Artery Disease
Diffuse coronary artery atherosclerosis can be defined as “consecutive or longitudinal” and “complete or partial” obstruction in coronary vessels. Most of the patients with diabetes, hyperlipidemia, chronic renal insufficiency, connective tissue disease, and multi-stented coronary arteries have diffuse atherosclerotic lesions in the coronary territory. Viable large myocardium without necrosis is the only coronary bypass indication in these patients, because it is very difficult to find any healthy area for anastomosis. This type of coronary occlusion frequently stimulates the formation of collateral vessels that protect against extensive myocardial ischemia. The choice of a surgical method also depends on the nature of the coronary artery, and multisegment plaques and healthy-area intervals simplify complete revascularization. On the other hand, a more aggressive treatment modality should be preferred when no soft site can be identified for arteriotomy or there is an extensively diseased area that is not amenable to grafting. The less invasive techniques are “don’t touch the plaque” techniques (jumping multi-bypass, sequential bypass, hybrid interventions). Sometimes an aggressive diffuse plaque formation needs to be treated with “touch the plaque” techniques (long-segment anastomosis, patch-plasty, endarterectomy ± patch-plasty). In simple forms, a limited long-segment anastomosis of conduits eliminates the occlusion of the limited atherosclerotic plaque where the whole lesion is opened and cross-covered by the graft. In the accelerated form of coronary arteriosclerosis, the atherosclerotic plaque appears widespread and the full-length lumen of the coronary artery can get very narrow or occluded totally. The long-segment lesion is usually calcified and it inhibits any kind of stitching; however, the plaque can be separated easily from the arterial wall in order to create an appropriate lumen in the total occluded coronary artery. Because the aggressive endarterectomy increases the operation risk, the arteriotomy should be extended until the normal lumen with normal intima in the distal segment of the coronary artery. In general, severity and distribution of coronary arteriosclerosis tend to increase with time but the rate of increase is highly variable and difficult to predict. Although diffuse atherosclerosis is severe enough, it is uncommon to render any patient unsuitable for surgery.
Part of the book: Coronary Artery Disease
Isolated Aortic Root Aneurysms
The aortic root has a complex anatomy due to a combination of several anatomical structures based on simple and consistent work in it. It is a hollow cylinder with three bulges, which have the main functional effect on the aortic valve opening-closing cycle and coronary circulation. Aneurysm is defined as a dilation of a blood vessel segment having ≥50% increase in diameter, whereas annuloaortic ectasia represents a diffuse dilation <50% of the normal diameter of the related vessel segment. Aortic root aneurysms mostly occur by degenerative processes as compared with primarily atherosclerotic changes in the descending and abdominal aortas: medial fragmentation, smooth muscle cells necrosis, and elastic fiber fragmentations with cystic spaces in the media filled with mucoid material. Because of the elevated mortality risk associated with complications, an effective aortic root aneurysm management depends on reduction the risk of death, rupture, and dissection. Conventional open heart surgery is the essential procedure for isolated aortic root replacement and a type of procedure (valve replacement or sparing) could be selected due to the pathology. An extensive aortic root replacement technique is the only option to rebuild the left ventricular outflow tract due to the reconstruction of the neo aortoventricular continuity in the aortic root abscess.
Part of the book: Aortic Aneurysm
Pathophysiology in Heart Failure
Heart failure syndrome is defined as the inability of the heart to deliver adequate blood to the body to meet end-organ metabolic needs and oxygenation at rest or during mild exercise. Myocardial dysfunction can be defined as systolic and/or diastolic, acute or chronic, compensated or uncompensated, or uni- or biventricular. Several counterregulatory mechanisms are activated depending on the duration of the heart failure. Neurohormonal reflexes such as sympathetic adrenergic system, renin-angiotensin cascade, and renal and peripheral alterations attempt to restore both cardiac output and end-tissue perfusion. An adequate stroke volume cannot be ejected from the left ventricle, which shifts the whole pressure-volume relationship to the right (systolic failure). Adequate filling cannot be realized due to diastolic stiffness, which shifts the diastolic pressure-volume curve upward without affecting the systolic pressure-volume curve (diastolic failure). Left ventricular heart failure is the dominant picture of heart failure syndrome, but the right heart can develop isolated failure as well. Biventricular failure is mostly an end-stage clinical situation of the heart failure syndrome. More recently, the rise in the incidence of right ventricular failure can be seen after the implantation of a left ventricular assist device. This chapter clarifies and presents pathophysiologic alterations in heart failure syndrome.
Part of the book: Cardiomyopathies
Invasive Treatment in Advanced (Stage-D) Heart Failure
Heart failure is a complex, true pandemic clinical syndrome and is responsible for 5% of hospitalizations globally. Severe heart failure can manifest as two lethal clinical entities: (1) acute cardiac decompensation with cardiogenic shock after large acute myocardial infarction with mortality rates approaching 50% or after cardiac surgery with mortality rates higher than 65% and (2) chronic destructive cardiac remodeling or acute decompensative exacerbations of cardiomyopathies with one-year mortality of approximately 80% (worse than most types of cancer). Interventional therapies aim first to improve symptoms and life expectancy in patients with severe heart failure syndrome, second to prevent left ventricular remodeling, and third to bridge patients to long-term mechanical circulatory support or transplantation. Several treatment options can be used to stabilize patients. In particular, new percutaneous mitral valve interventions and short-term circulatory support devices open up a new temporary treatment area in symptomatic Stage-D heart failure. The durable or curable surgical destination treatment will be only permanent ventricular assist devices or heart transplantation. This chapter focuses on the treatment steps and new approaches in hospitalized Stage-D heart failure patients.
Part of the book: Cardiomyopathies
Focus on Coronary Atherosclerosis View all chapters
Atherosclerosis is a vascular disorder consisting of thickening of arteries and lack of elasticity. Result of atherosclerosis is that arteries become narrowed and hardened due to an excessive buildup of plaque around the artery wall. The disease disrupts the flow of blood around the body, posing serious cardiovascular complications. Arteries contain what is called an endothelium, a thin layer of cells that keeps the artery smooth and allows blood to flow easily. Endothelial damage starts the first step of atherosclerosis. After this, low-density lipoprotein (LDL) cholesterol accumulates in the artery wall. Inflammatory process starts after this accumulation, and macrophages reach the endothelium to clean up cholesterol. But some macrophages are stuck in the affected part of the artery wall in this process. Over time, this results in plaque being built up, consisting of cholesterol and macrophage white blood cells. The plaque clogs up the artery, disrupting the flow of blood. This potentially causes blood clots that can result in life-threatening conditions such as heart attack and other cardiovascular diseases. Atherosclerosis can be seen in all arteries in the body. Atherosclerosis is the most common cause of death in the western countries. Some risk factors are as follows: age, sex, familial predisposition, hyperlipidemia, hypertension, diabetes mellitus, smoking, obesity, insufficient physical activity, etc. Whatever the main reason or the risk factor is, once atherosclerosis is formed, several life-threatening cardiovascular disorders can be seen. So, it has to be revealed.
Part of the book: Atherosclerosis