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Angina pectoris is a common and important symptom affecting many patients with advanced coronary artery disease (CAD) spinal cord stimulation (SCS) provides a relief from symptoms equivalent to that provided by surgical therapy. Some studies have shown a decrease in myocardial ischemia and an increase in coronary blood flow.
Angina pectoris is a common and important symptom affecting many patients with advanced coronary artery disease (CAD) spinal cord stimulation (SCS) provides a relief from symptoms equivalent to that provided by surgical therapy. Some studies have shown a decrease in myocardial ischemia and an increase in coronary blood flow.
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Angina pectoris is a common and important symptom affecting many patients with advanced coronary artery disease (CAD) spinal cord stimulation (SCS) provides a relief from symptoms equivalent to that provided by surgical therapy. Some studies have shown a decrease in myocardial ischemia and an increase in coronary blood flow.
Copyright:
Attribution Non-Commercial (BY-NC)
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Als DOCX, PDF, TXT herunterladen oder online auf Scribd lesen
Abstract Progress in prevention as well as drug and interventional therapy has improved the prognosis of patients with cardiovascular disorders. Many patients at risk have advanced coronary artery disease (CAD), have had multiple coronary interventions, and present with significant co-morbidity. Despite adequate risk factor modulation and often several revascularization procedures, some of these patients still have refractory angina pectoris. Apart from advanced CAD and insufficient collateralization, the cause is often endothelial dysfunction. For this situation, one treatment option is neuromodulation. Controlled studies suggest that, in patients with chronic refractory angina pectoris, spinal cord stimulation (SCS) provides a relief from symptoms equivalent to that provided by surgical therapy, but with fewer complications and lower rehospitalization rates. SCS may result in significant long-term pain relief with improved quality of life. In patients with refractory angina undergoing SCS, some studies have shown not only a symptomatic improvement, but also a decrease in myocardial ischemia and an increase in coronary blood flow. Discussion is ongoing as to whether this is a direct effect on parasympathetic vascodilation or merely a secondary phenomenon resulting from increased physical activity following an improvement in clinical symptoms. Results from nuclear medical studies have sparked discussion about improved endothelial function and increased collateralization. SCS is a safe treatment option for patients with refractory angina pectoris, and its long-term effects are evident. It is a procedure without significant complications that is easy to tolerate. SCS does not interact with pacemakers, provided that strict bipolar right-ventricular sensing is used. Use in patients with implanted cardioverter defibrillators is under discussion. Individual testing is mandatory in order to assess optimal safety in each patient. Introduction Therapeutic options for the management of angina pectoris in patients with coronary artery disease (CAD) have improved over the past 2 decades. Nevertheless, angina pectoris is a common and important symptom affecting many patients with CAD, as well as some with endothelial dysfunction. Despite optimal drug therapy and no option for coronary revascularization procedures (percutaneous coronary intervention [PCI] or aortocoronary bypass [ACB]), some patients with CAD have persistent angina pectoris class III or IV according to the Canadian Cardiovascular Society (CCS). The treatment of these patients with non-responding angina pectoris presents a medical challenge. We have no accurate figures on the occurrence and frequency of refractory angina, nor is the prevalence of angina pectoris known in most communities. The overall prevalence of patients referred for coronary angiography with refractory angina varies from 5% to 15%. Various treatment concepts have been developed for patients with therapy- resistant angina pectoris and have been applied in clinical studies: long-term intermittent urokinase therapy, surgical and percutaneous transmyocardial laser revascularization, enhanced external counterpulsation, percutaneous in situ coronary venous arterialization, and transcutaneous electrical nerve and spinal cord stimulation (SCS). The latter has been established as the most applicable. It is recommended as the therapy of choice by the European Society of Cardiology Joint Study Group on the Treatment of Refractory Angina. In this article, we review the role of SCS in the management of severe angina pectoris in patients with ischemic heart disease and endothelial dysfunction. Stable and Refractory Angina Pectoris Endothelial dysfunction is usually diagnosed in the presence of angina pectoris without obstructive CAD and coronary artery spasm. Patients with such a diagnoses experience typical anginal chest pain and experience positive exercise stress testing. About 15-20% of patients undergoing cardiac catheterization for the assessment of typical chest pain have these characteristics, and most of them have a good prognosis. Endothelial dysfunction often marks the onset of atherosclerosis, stays with the patient for the rest of his or her life, and at the end-stages of CAD following PCI, causes higher rates of relapse and re-intervention. Endothelial dysfunction can be ascertained invasively and non-invasively. After excluding hemodynamically relevant epicardial stenoses by determining the fractional flow reserve (FFR), the functional status of a coronary artery can be determined by coronary flow reserve (CFR). As a non-invasive procedure, ammonia positron emission tomography (PET) and flow-mediated dilatation of the brachial artery (FMD) can be used. The survival of patients with CAD is increasing as a result of improved prevention and coronary intervention, which in turn is leading to an increase in the prevalence of patients with refractory angina pectoris. It is important to underline that angina pectoris is a clinic diagnosis. Imbalance in myocardial oxygen demand and supply can produce myocardial ischemia. This may cause angina pectoris and lead to a reduction in left- ventricular contractility, as well as cause arrhythmia, myocardial infarction, and possibly death. Angina pectoris is commonly due to atherosclerosis of the coronary arteries, but it can also occur in conjunction with endothelial dysfunction due to insufficient coronary vasodilatation. Anti-anginal drug therapy improves the imbalance of the myocardium by interacting with heart rate, cardiac pre- and afterload, as well as coronary vascular tone. Hemodynamically significant coronary stenoses with and without angina pectoris may be dilated (PCI) or operated on (ACB). Refractory angina pectoris (CCS class III and IV) is a chronic condition characterized by the presence of angina due to coronary insufficiency in the co-presence of CAD that cannot be controlled by a combination of medical therapy, angioplasty, and coronary bypass surgery. Patients with endothelial dysfunction can also experience refractory angina. Before selecting patients with refractory angina for SCS, a re-evaluation of their medical therapy is required in order to ensure an optimal treatment regimen. Myocardial ischemia should be present, and other causes of chest pain, such as musculoskeletal pain, esophageal reflux, gastrointestinal disorder, pericardial disease, vascular disease (aortic dissection, pulmonary embolism), infection, panic disorder, and pulmonary conditions that cause chest pain, must be excluded. Pharmacologic Therapy The therapeutic options for endothelial dysfunction and stable CAD are comparable and aim at correcting the imbalanced redox potential. Treating the classical risk factors with lifestyle modification and drug therapy has facilitated the successful prevention of clinical cardiovascular events and has prolonged life expectancy. In many randomized studies, a reduction in increased low-density lipoprotein cholesterol and triglyceride, as well as an increase in reduced high-density lipoprotein cholesterol have contributed to stabilizing plaque, have frequently demonstrated a regression of coronary atherosclerosis, and have improved endothelial function. Controlling hypertension, cessation of smoking, increasing physical activity, and reducing weight all help to halt the progress of atherosclerosis and to reduce acute events. Lifestyle changes in the form of increased physical activity with or without weight reduction frequently lead to a reduction in angina pectoris and improved myocardial perfusion. In randomized studies, it was possible to show that, compared with coronary intervention (PCI), increasing physical activity resulted in a better event-free survival rate, a higher exercise capacity, and a higher oxygen uptake, and was more cost effective; it achieved clinical improvement in CCS class I at half the total cost of the interventional strategy. Effect on Cerebral Blood Flow. Non-invasive techniques for determining cerebral perfusion and measuring functional activity (e.g. PET, functional MRI, or magnetoencephalography) have contributed to a better understanding of cerebral function in healthy subjects and in those with various diseases and the ways in which cerebral function can be influenced through interventions. Changes in regional blood flow in areas involved with nociception and cardiovascular control have been documented in patients treated with SCS for refractory angina. The cerebral areas demonstrating a relative increase or decrease in CBF could possibly be determined by the underlying disease (pain during clinical examination, one-sided or two-sided for paired organs) and the measuring methods, as well as the type of intervention. In patients with documented CAD, typical anginal and ischemic electrocardiographic changes can be triggered during dobutamine infusion. Dynamic PET examinations during induced ischemia reveal increased and decreased regional CBF. During SCS, increased and decreased regional CBF can also be observed with and without stimulation in patients with refractory angina. In these two different patient groups, there are correlations within the following regions: increased CBF in the hypothalamus, and in the periaqueductal grey area and bilaterally in the thalamus, and decreased CBF in the posterior insular cortex, an area that modulates sympathetic effects. The well supported effects of SCS are possibly attained by influencing central structures within the area of pain perception and processing. The thalamus may act as a filter for afferent pain signals. Effect on Coronary Blood Flow. SCS has repeatedly demonstrated an anti- anginal effect by reducing angina pectoris and the use of short-acting nitrates, increasing exercise tolerance, and decreasing ST-segment depression on the electrocardiogram. Discussion about the effect of SCS on myocardial blood flow is ongoing. Angina pectoris is a projected pain that is caused by insufficient perfusion of the myocardium due to significant coronary stenoses or reduced vasodilatatory capacity, particularly of the microcirculation. CAD is frequently accompanied by endothelial dysfunction. In the majority of patients with significant coronary stenoses and exercise-induced ischemia, pain relief can be achieved following revascularization and/or through risk factor modulation with improvement in endothelial function. TENS and SCS are recognized therapies in patients with refractory angina pectoris. In many clinical studies, the effectiveness of these therapies have been demonstrated in patients (approximately 2500) with CAD and endothelial dysfunction: fewer angina pectoris episodes and less short-acting nitroglycerin (glyceryl trinitrate) or mononitrate intake per time period; increase in exercise tolerance, time to angina, and the appearance of ST-segment depression; extended walking distance in the 6-minute walk test before onset of angina; improvement in quality of life; and fewer stays in hospital as well as visits to the physician due to cardiac-related symptoms.
Refractory angina pectoris during end-stage CAD and with endothelial
dysfunction is a specific coronary syndrome that is chiefly caused by microcirculatory disturbances. Already receiving the best use of evidence- based therapies and with no interventional options, these patients can benefit from SCS. SCS is safe and effective for treating refractory angina pectoris - reducing both the number of anginal episodes and the intensity of the angina pectoris. With SCS the dosage of short-term effective nitrates per time period is reduced. The work period during exercise tests is significantly prolonged. SCS leads to a significant reduction in hospital admission for cardiac causes, without masking myocardial ischemias or myocardial infarction. The implantation costs are balanced out by savings in aftercare (fewer consultations and hospital stays). SCS is an excellent alternative for patients at an increased risk of requiring operative revascularization. For patients with refractory angina who are waiting for heart transplantation, SCS is also a good bridging option. In small studies, an improvement in myocardial blood flow in vital ischemic myocardial areas has also been proved. It has yet to be investigated whether SCS, in addition to a proven improvement in symptoms, also reduces mortality.