Protozoa Chagas disease is one of the major causes of nonischemic cardiomyopathy throughout the world cheap prednisone 10 mg otc allergy zinc, although the incidence is changing generic prednisone 40mg free shipping allergy shot maintenance dose. In a remarkable tale of discovery at the beginning of the 20th century cheap 40 mg prednisone with visa gluten allergy symptoms uk, Carlos Chagas almost single-handedly identified the parasite, Trypanosoma cruzi, which causes the entity now known as Chagas disease. He also elucidated the relatively complex life cycle of the parasite in poor, 23 rural areas of Brazil. The parasite resides in and replicates in an infected host such as an armadillo or a domestic cat. The parasite then infects triatomine insects, including the hematophagous reduviid bug that feeds on the blood of infected vertebrate carriers. The triatomine acts as the vector of infection when it bites a human, depositing the parasite in its feces in the area of the bite wound, conjunctiva, or other mucous membranes. Once within the now-infected individual, the parasite replicates and infects target organs such as the heart. Parasitic infection of cardiac myocytes and activation of the associated immune function damage the heart and other organs and lead to the clinical manifestations of Chagas disease; Fig. Trypomastigotes can infect host cardiac, skeletal, smooth muscle, or neural cells, subsequently giving rise to the round amastigote form that can replicate intracellularly (C). Amastigotes and trypomastigotes released from dying cells can propagate the infection or reenter the circulation (E to G). Insects can pick up the parasite when consuming a blood meal (H); it develops into the epimastigote form that replicates in the insect gut (I). The distribution of Chagas disease is changing to include more urban and traditionally nonendemic areas because of migration of infected individuals from the rural to urban areas. Vector control initiatives in the endemic areas and aggressive screening of the blood supply has reduced the overall incidence of Chagas 25 disease. By 2010, it was estimated that the number of infected persons had dropped to nearly 5. Similarly, the number of annual deaths from Chagas disease has decreased, from 50,000 per year in 1990 24,26 to approximately 12,500 per year. However, at the same time that Chagas disease is decreasing worldwide, the incidence in the developed world is increasing because of immigration from endemic areas. It is currently estimated that approximately 238,000 people in the United States are infected with T. This has important implications in relation to blood transfusion and organ donation, because the infectious agent can be transferred from donor to recipient; this is a particularly important consideration in the immunocompromised transplant recipient. During the acute phase of parasite infection, most affected patients are either asymptomatic or have a mild, subacute febrile illness. Other potential manifestations include adenopathy, hepatomegaly, myocarditis, and meningoencephalitis. Death occurs from myocarditis or meningoencephalitis in less than 5% to 10% of symptomatic patients. Of these, approximately 60% to 70% never develop chronic Chagas disease manifestations even in the absence of treatment with trypanocidal drugs, but these patients will remain seropositive throughout life. The other 30% to 40% of patients ultimately develop more typical manifestations of the chronic form of Chagas disease. Treatment with antiparasite drugs such as benznidazole usually can cure 23,24 the patient during the acute illness. The 30% to 40% of patients with acute illness that go on to develop chronic Chagas disease usually manifest the disease within 5 to 15 years after the initial infection. However, less than 1% of patients with chronic Chagas disease report a history of symptoms of acute Chagas disease. The chronic form is characterized by myocardial fibrosis, destruction of the conduction system, ventricular dilation, thinning of the apex of the heart, and formation of a thrombus in the apex of the heart. These changes lead to heart failure, arrhythmia, atrioventricular and bundle branch block, and possible thromboembolism. It is reported that 50% to 90% of patients with chronic Chagas disease remain asymptomatic despite ongoing 23,24 pathologic processes. Congenital transmission of the parasite to a fetus from the mother is another important mechanism of transmission of the parasite. Conversely, the parasite can be passed from the mother to the infant at the time of birth. Congenital transmission occurs in 1% to 5% of pregnancies when the mother has chronic Chagas disease. Congenital transmission of this disease results in spontaneous abortion, premature birth, or infection of 23,24 organs in the fetus. The goal of treatment in all forms of Chagas disease is to eradicate the parasite. Antitrypanosomal treatment is strongly recommended for all patients with acute, congenital, and reactivated infections. Therapy should be offered to patients 19 to 50 years of age without advanced heart disease. Chagas disease is associated with both active persistent parasite infection and an immune response that may be directed 28 against the parasite or may be a response of autoimmune origin. Antiparasite treatment generally is not indicated in patients with advanced heart failure from Chagas disease. Helminths Echinococcosis (Hydatid Cyst) Echinococcosis is endemic in many sheep-raising areas of the world, particularly Argentina, New Zealand, Greece, North Africa, and Iceland; however, cardiac involvement in patients with hydatid disease is uncommon (<2%). The usual host of Echinococcus granulosus is the dog, but humans may serve as intermediate hosts if they accidentally ingest ova from contaminated dog feces. When cardiac involvement is present, the cysts usually are intramyocardial, located in the interventricular septum or left ventricular free wall. Rupture of the cyst is the most dreaded complication; rupture into the pericardium can result in acute pericarditis, which may progress to chronic constrictive pericarditis. Rapidly progressive pulmonary hypertension can occur with rupture of right-sided cysts, with subsequent embolization of hundreds of scolices, fragments of the tapeworm, into the pulmonary circulation. The liberation of hydatid fluid into the circulation can produce profound, fatal circulatory collapse as a result of an anaphylactic reaction to the protein constituents of the fluid. It is estimated that only approximately 10% of patients with cardiac hydatid cysts experience clinical symptoms. Chest pain usually is due to rupture of the cyst into the pericardial space with resultant pericarditis. The chest radiograph may show an abnormal cardiac silhouette or a calcified lobular mass adjacent to the left ventricle. The Casoni skin test or serologic evaluation for echinococcus has a limited role in cardiac diagnosis. In terms of therapy, despite the availability of effective drugs such as mebendazole and albendazole, surgical excision generally is recommended, even for asymptomatic patients. This is because of the significant risk of rupture of the cyst and its attendant serious and sometimes fatal consequences. Trichinosis Infection with Trichinella spiralis is common after ingestion of infected meat, usually pork.
The latter may result from vasoconstrictors released by platelets order genuine prednisone allergy testing nyc, from endothelial dysfunction (cardiac syndrome X; see Chapter 89) buy 40 mg prednisone free shipping allergy treatment center kelapa gading, adrenergic stimuli buy generic prednisone 20 mg line lidocaine allergy, cold, cocaine, or amphetamines (Chapter 80). Left, Plaque rupture of a necrotic core with an overlying thin ruptured cap represents the most frequent pathophysiologic process leading to an acute coronary syndrome. Center, Plaque erosion with a thrombus in direct contact with an intimal plaque that is rich in smooth muscle cells and proteoglycan matrix. There are breaks in the calcified plate of the plaque with bone formation and interspersed fibrin, with a disrupted fibrous cap and overlying thrombus. Activation of the coagulation cascade and platelets play central roles in the formation of thrombus following plaque disruption (see Chapter 93). In parallel, tissue factor expressed within the lipid-rich core of atherosclerotic plaque, when exposed to circulating blood, activates the coagulation cascade. The platelet and coagulation systems converge as thrombin also potently activates platelets. However, while coronary risk factors reliably assess risk in populations, they are less helpful in the assessment of individual patients. Radiation to the ulnar aspect of the upper left arm, either shoulder, the neck, or 11 the jaw is common, but symptoms may localize anywhere between the ear and epigastrium. Symptoms such as diaphoresis, nausea, abdominal pain, dyspnea, and syncope may accompany the discomfort. Features that support the diagnosis include exacerbation of symptoms by physical exertion; precipitation by severe anemia, infection, inflammation, fever, or metabolic or endocrinologic (e. Atypical manifestations, such as dyspnea without chest discomfort, pain limited to the epigastrium, or indigestion, represent “anginal equivalents. Chest pain that is pleuritic, positional, or described as “stabbing” is generally not caused by myocardial ischemia. Physical Examination Findings on physical examination may be normal, although patients with large territories of myocardial ischemia may have audible third and/or fourth heart sounds or pulmonary rales. Findings such as pulse deficits, tachypnea, and tachycardia in the presence of clear lung fields and pulsus paradoxus with jugular venous distention may lead to alternative life- threatening diagnoses, such as aortic dissection, pulmonary embolism, or cardiac tamponade. These include markers of myocyte necrosis, hemodynamic stress, vascular damage (particularly renovascular), acceleration of atherosclerosis, and inflammation (Fig. However, although troponin elevation in the presence of ischemic discomfort often signifies myocardial necrosis, there are numerous other mechanisms of troponin release, including apoptosis, cellular release of proteolytic degradation products of troponin, increased cellular 15 wall permeability, and normal myocyte turnover. As high-sensitivity troponin (hsTn) 17 assays that can detect ultralow concentrations of troponin in approximately 90% of healthy individuals become increasingly available, consideration of the clinical context of a troponin elevation will become even more important in avoiding misdiagnosis and improper triage in management of patients. Future of biomarkers in acute coronary syndromes: moving toward a multimarker strategy. Fourth-generation cTn assays currently used in the United States are less sensitive than hsTn assays available in some European countries. Several other biomarkers may be useful to determine prognosis and help guide care. Circulating levels of interleukin-17 and cardiovascular outcomes in patients with acute myocardial infarction. Heart-type fatty acid–binding protein predicts long-term mortality and re-infarction in consecutive patients with suspected acute coronary syndrome who are troponin-negative. Elevated levels of systemic pentraxin 3 are associated with thin-cap fibroatheroma in coronary culprit lesions: assessment by optical coherence tomography and intravascular ultrasound. Prospective evaluation of pregnancy-associated plasma protein A and outcomes in patients with acute coronary syndromes. Elevated placental growth factor levels are associated with adverse outcomes at four-year follow-up in patients with acute coronary syndromes. Circulating secretory phospholipase A activity predicts recurrent events in patients with2 severe acute coronary syndromes. Prognostic utility of neopterin and risk of heart failure hospitalization after an acute coronary syndrome. Circulating osteoprotegerin levels and long-term prognosis in patients with acute coronary syndromes. The merits of various modalities of stress testing have been compared (see Chapter 13). Exercise stress myocardial perfusion imaging with nuclear isotopes and stress echocardiography with dobutamine have greater sensitivity than electrocardiographic exercise stress testing without imaging (see Chapters 14 and 16). A practical approach is to select the modality of stress testing based on individual patient characteristics and preferences, as well as local availability and expertise. In patients who cannot achieve a significant workload during exercise, pharmacologic stress testing with imaging is recommended. State-of-the-art evaluation of emergency department patients presenting with potential acute coronary syndromes. These detailed assessments can help guide coronary revascularization in several common clinical scenarios, as when the stenosis is of borderline significance, the culprit lesion is uncertain because of multivessel disease, or myocardial viability in a territory at risk is in question (see Chapter 17). Invasive Imaging Invasive coronary angiography has been the standard technique for imaging the coronary arterial tree for nearly six decades. These angiographic findings may represent disrupted atherosclerotic plaque or thrombus. Features suggesting thrombus include globular intraluminal masses with a rounded or polypoid shape; “haziness” of a lesion suggests the presence of thrombus, but this finding is not specific. Most have obstructive disease, including multiple epicardial arteries—approximately 10% with left main coronary artery disease, 35% with three-vessel disease, and 20% with two-vessel disease—whereas only approximately 20% have single-vessel disease. The remaining 15% have no significant coronary obstruction, a finding that is more common in women and minorities. Aggressive medical management of the remaining plaques and prevention of new ones is required to prevent recurrent 41 events. This simple, rapid assessment at the initial evaluation identifies high-risk patients who can derive benefit from an early invasive strategy and more intensive 45 antithrombotic therapy. It distinguishes 46,47 patients with greater absolute benefit with more intensive antithrombotic and lipid-lowering therapies. Blood specimens for cTn or, if possible, hsTn assay should be obtained with expedited assessment via either a point-of-care device or laboratory measurement that can provide results within 60 minutes. Additional laboratory studies, such as natriuretic peptide, a complete blood count, serum electrolytes, creatinine, and glucose, can help guide early management treatments and strategy. Anti-Ischemic Therapy Guidelines emphasize the early use of anti-ischemic therapies to improve the balance between oxygen 11,23 supply and demand. Effect of cyclosporine on left ventricular remodeling after reperfused myocardial infarction. Nonantithrombotic medical options in acute coronary syndromes: old agents and new lines on the horizon. Nitrates Nitrates are vasodilators that increase myocardial blood flow (coronary vasodilation of atherosclerotic and normal vessels), reduce myocardial oxygen requirements by lowering cardiac preload (systemic venodilation), reduce cardiac afterload (systemic arterial dilation) thereby diminishing ventricular wall stress, and may have a mild antiplatelet effect. In symptomatic patients without hypotension, the initial administration of rapidly acting nitroglycerin (sublingual or buccal, 0.
This complication significantly impacts the duration of hospital stay and related health care costs order 5 mg prednisone allergy testing elizabethtown ky. Certainly 40mg prednisone for sale allergy forecast galveston, toxic damage caused by the passage of iodine molecules in the interstitial kidney is one of the causes order prednisone in india allergy symptoms mouth sores. Another mechanism is related to the redistribution of flow in the kidney tissue secondary to contrast administration. In particular, after injection of contrast media, blood flow increases in the cortex and decreases in the medulla. Therefore, blood flow reduction in the medulla after contrast injection further decreases oxygen tension, leading to endothelial dysfunction. Other important elements affecting kidney function are the physical and chemical characteristics of the contrast agents, in particular osmolality and viscosity. Contrast agents with a high osmolality and viscosity significantly increase hypoxemia and tubular stress. In high-risk patients, prevention is crucial and consists of pharmacologic and nonpharmacologic measures. Individual risk/benefit ratios should be carefully estimated for each patient, and the utility of an alternative noninvasive diagnostic test should be evaluated. If the use of contrast medium is necessary for diagnostic purposes, the volume used should be minimized, and the use of monomeric low- or iso- osmolality contrast agents is recommended. Moreover, to obtain effective hydration, devices have been developed that balance the volume of infusion and fluids lost 24 through diuresis. In animal models of ischemia-reperfusion injury, the use of N-acetylcysteine significantly limited kidney 25 damage mainly through its antioxidant properties. However, the efficacy of N-acetylcysteine in humans 26 in clinical studies remains unclear, given the high heterogeneity in study protocols and populations. These findings were attributed to a potential reduction in the production of reactive oxygen species in the renal parenchyma. However, recent meta- 27,28 analyses did not show superiority of sodium bicarbonate over saline solution. For this reason, both N- acetylcysteine and sodium bicarbonate have minimal roles in the latest guidelines on prevention (i. Risks Related to Radiation Exposure Coronary catheterization may result in radiation-related injury, which although infrequent may be potentially serious. Stochastic injury can result in cancer, pregnancy complications, and inheritable diseases. However, the most common location of radiation-induced lesions in cardiac catheterization is the skin of the back, and common patterns include erythema, 29 telangiectasia, and plaques. The sensitivity of the skin to radiation exposure is differentiated by site; areas at risk in decreasing order of sensitivity include anterior neck, antecubital and popliteal areas, 30 flexor extremities, chest and abdomen, face, back, extensors, nape of the neck, scalp, palms, and soles. Although uncommon in contemporary practice, early reports from coronary catheterization indicate deep and extensive skin rashes and burns at the site of radiation exposure, some requiring skin grafting. For exposures of absorbed radiation greater than 5 Gy, patients should be advised to watch for areas of erythema; for those greater than 10 Gy, a medical physicist should be consulted to calculate the peak dose in 2 to 4 weeks; greater than 15 Gy is regarded as a hospital risk management event. From the perspective of occupational radiation exposure, operators should be cognizant of the need to wear protective personal equipment during catheterization procedures, including a lead apron, thyroid 33 drape, lead eyeglasses, and dosimeters. Table height and distance from the x-ray source are important, and radiation risk decreases as the inverse square of distance from the source. Operators should also optimally position lead shields and skirts and should be compliant with use of radiation dosimeters for monitoring exposure to the whole body (chest) and eye. Novel dosimeters providing real-time monitoring 34 and alerts can serve to decrease operator radiation exposure. Monitoring, reporting, and audit of radiation exposure can promote improved awareness and practice in the operator and catheterization laboratory staff. Coronary Arteriography Technique Patient Preparation Patients should receive a comprehensive explanation of the diagnostic angiographic procedure and of the coronary intervention potentially required. Risks of angiography should be discussed in-depth and weighed against both the clinical benefit and the risks related to refusal of the procedure. Patients are required to provide written informed consent before coronary angiography. Women of childbearing age should be questioned on their pregnancy status and advised on the additional risks of radiation exposure for pregnant women. A thorough medical history, including comorbidities, current medications, and allergies, needs to be obtained before the procedure. Patients may receive mild sedation with a benzodiazepine before the procedure according to the hospital 35 standard practice. In case of hemodynamic instability or respiratory distress, anesthesiologist support might be necessary. In most patients, however, general anesthesia and deep sedation are unnecessary for coronary angiography. Conscious sedation with short-term agents such as midazolam or fentanyl is most common. A venous access line should be readily available for the infusion of fluids or medications. Local anesthesia with topical anesthetic cream or subcutaneous injection of 1% lidocaine or mepivacaine (0. An adequate local anesthetic will not only make the patient more comfortable but, by reducing the pain during the arterial cannulation, also reduce the risk of peripheral artery spasm. Access Sites Possible access sites for coronary angiography are the femoral artery and the radial artery. Although the radial access approach is associated with fewer vascular and bleeding complications, femoral access remains the most commonly used in the United States. In addition, accessing from the femoral artery usually grants an easier advancement of the catheter to the aortic root due to the lack of tortuosity in the descending aorta. The head of the femur, visualized under fluoroscopy, can be used as a landmark (see Chapter 19, Fig. Puncture should be performed with the needle leveled at half the head of the femur. Multiple punctures should be avoided to reduce the risk of bleeding and vascular damage. The needle is then removed and a sheath advanced around the wire into the artery (see Fig. Once the sheath is fully advanced in the artery, the dilator 37 and wire are removed, and the sheath is flushed with saline. Verification of the correct position of the sheath in the vessel can be ascertained simply by drawing blood from the sheath. Radial access should always be considered first, before resorting to the femoral approach, especially 38 for diagnostic coronary angiography. The procedure for the sheath insertion is similar to that described for the femoral artery. However, when using radial access, a modified Allen test should be performed on both hands (see Chapter 19).