Figure 10.2 External landmarks for right mini thoracotomy incision.
Monday, April 19, 2021
Thursday, February 18, 2021
CARDIOVASCULAR EFFECTS OF AIR POLLUTANTS
The effects of air pollution on cardiovascular disease is a relative new area of research. Historically, air pollution has not been regarded a significant risk factor for cardiovascular disease, but the World Health Organization estimates that >7 million premature deaths each year can be attributed to urban outdoor and indoor air pollution. Short-term exposure to high levels of particulate matter (PM), especially fine particles of <2.5 µm, has been found to trigger cardiovascular mortality due to myocardial infarction and heart failure. Long-term exposure increases the risk of cardiovascular mortality and reduces life expectancy. Reductions in PM exposure are associated with decreases in mortality. A growing body of evidence has linked PM to increased systemic inflammation, oxidative stress, thrombosis, cardiac ischemia, and heart rate variability. Further investigation of PM and other air pollutants is required to better understand their effects on cardiovascular disease. This will allow development of treatment and optimized prevention strategies in the future.
DIABETES AND CARDIOVASCULAR EVENTS
Type 2 diabetes (T2DM) is common in adults and is characterized by insulin resistance that results in hyperglycemia. Diabetes increases the risk of microvascular and macrovascular events. As a result, patients with diabetes have a higher risk of dying from cardiovascular disease and are at a higher risk for developing heart failure. The duration of diabetes and degree of glycemic control with diabetes is a significant predictor of future events. Thus, identification of patients at risk for diabetes, prediabetes, and new-onset diabetes allows for intensified therapy that may reduce the chances of developing diabetes and mitigate the risk of complications from diabetes. Patients are considered to have diabetes if they have a fasting plasma glucose of ≥126 mg/dL, oral glucose tolerance test with a 2-hour postprandial glucose ≥200 mg/dL, glycosylated hemoglobin of ≥6.5%, or random plasma glucose ≥200 mg/dL. Exercise, weight loss, and metformin improve insulin sensitivity and are effective strategies to reduce the risk of developing diabetes in patients with prediabetes. Drugs from two different classes have been shown to be effective in reducing cardiovascular events specifically in patients with diabetes. The sodium/glucose cotransport-2 inhibitors, liraglutide, and semaglutide have been shown to reduce cardiovascular events in patients with diabetes. Because of the high degree of cardiovascular disease in patients with diabetes, efforts to use drugs with proven cardiovascular benefit, together with intensive cardiovascular risk factor modification, offer the ability to reduce the incidence of cardiovascular events in this high-risk population of patients.
MANAGEMENT OF LIPID ABNORMALITIES
The management of lipid disorders in reducing the risk of coronary heart disease (CHD) has evolved in the past few years. There are a number of factors that account for these changes the introduction of the 2013 American Heart Association/American College of Cardiology (AHA/ACC) guideline report on cholesterol management and a series of clinical trials on nonstatin therapies (notably, several trials involved the cholesteryl ester transfer protein inhibitors [CETPis] for high density lipoprotein [HDL] elevation), as well as the introduction of proprotein convertase subtilisin/kexin type 9 (PCSK-9) therapies. The aforementioned 2013 recommendations are a key resource because of their evidence-based approach to patient care. They have simplified both the treatment approach to lipids and challenging issues such as dose titration, as well as achieving a specific and perhaps unreachable “target” lipid value. Of great importance, they allow for discretion on the part of the provider to engage with the patient in shared decision making and as stated, “Guidelines attempt to define practices that meet the needs of patients in most circumstances and are not a replacement for clinical judgment.”
Saturday, October 31, 2020
Hypertension is a disorder of BP regulation that results from an increase in cardiac output, or most often, an increase in total peripheral vascular resistance. Cardiac output is usually normal in established essential hypertension, although increased cardiac output plays an etiologic role. The phenomenon of autoregulation explains that an increase in cardiac output causes persistently elevated peripheral vascular resistance, with a resulting return of cardiac output to normal. Fig. 15.1 shows mechanisms that can cause hypertension. Inappropriate activation of the renin-angiotensin system, decreased renal sodium excretion, and increased sympathetic nervous system activity, individually or in combination, are probably involved in the pathogenesis of all types of hypertension. Hypertension also has genetic and environmental causes; the latter includes excess sodium intake, obesity, and stress. The inability of the kidney to optimally excrete sodium, and thus regulate plasma volume, leads to a persistent increase in BP whatever the etiology.
VASCULOGENESIS AND ARTERIOGENESIS: ALTERNATIVES TO ANGIOGENESIS
New vessel growth in chronic ischemic syndromes is an attractive idea. Fortunately, more than one mechanism exists to create new blood vessels. Angiogenesis is the creation of blood vessels from sprouts off the existing vessels. In contrast, vasculogenesis is the creation of de novo blood vessels by differentiation of new blood cells. Endothelial cell precursors in the bone marrow and circulating in the bloodstream can integrate into developing vessels and contribute to vessel growth in a manner similar to the vasculogenesis of embryonic development. The therapeutic potential of these cells has not been tested, but they can be recruited from bone marrow and may be a means to accelerate endogenous revascularization in patients with ischemia.
MECHANISMS OF ANGIOGENESIS
Angiogenesis occurs by the budding of new blood vessels from existing vessels (Fig. 14.1). Inflammation and hypoxia are the two major stimuli for new vessel growth. Hypoxia regulates angiogenesis predominantly by activating transcription factors, hypoxia-inducible factors (HIF) 1 and 2, which, in turn, activate the angiogenesis gene expression cascades, including vascular endothelial growth factor (VEGF), platelet growth factor, angiopoietin 1 and 2, as well as stromal cell-derived factor 1α. Based on this concept, HIF-1 promotes sprouting of blood vessels and neovascularization by homing of stem cells and enhancing vascular endothelial cell proliferation. HIF-2 mediates vascular maintenance. Inflammation stimulates angiogenesis mainly by the secretion of inflammatory cytokines derived primarily from macrophages. In either of these events, the result is production of VEGF and other potent angiogenic peptides. VEGF interacts with specific receptors on endothelial cells that, in turn, activate pathways to break down the extracellular matrix and stimulate proliferation and migration toward an angiogenic stimulus and recruitment of stem cells, pericytes, and smooth muscle cells to establish the three-dimensional structure of a blood vessel. After making appropriate connections with the vascular system, the newly formed vessel is capable of maintaining blood flow and providing oxygen to the tissue in need.
LEFT HEART CATHETERIZATION
Left heart catheterization is distinct from coronary angiography, which involves the cannulation and interrogation of the coronary arteries. Patients who undergo coronary angiography or right heart catheterization typically also undergo left heart catheterization as part of a comprehensive hemodynamic evaluation. The common indications for left heart catheterization include the evaluation of LV hemodynamics, LV systolic function, cardiomyopathy, valvular disease (e.g., aortic stenosis or mitral regurgitation), and intracardiac shunts (e.g., ventricular septal defects). The absolute contraindications for left heart catheterization include patient refusal, known or suspected LV thrombus, and mechanical prosthetic aortic valves. The relative contraindications for left heart catheterization include active bleeding, severe thrombocytopenia, severe coagulopathy, active infection, severe peripheral vascular disease, pregnancy, and patient inability to cooperate.