U. Fasim. West Texas A&M University. 2019.
However generic 40 mg imdur fast delivery, open pericardiocentesis with biopsy and creation of a pericardial 2 window are preferred for recurrences severe enough to cause tamponade discount imdur 40mg on line. Percutaneous balloon pericardiotomy and pericardioscopy have been employed to drain fluid discount 40 mg imdur mastercard, create 50,51 pericardial windows, and perform pericardial biopsy. Balloon pericardiotomy may be particularly useful for malignant effusions and other situations where recurrence is common and a definitive approach without a surgical procedure is desirable. These methods appear safe and effective, but experience is limited and confined to centers with a special interest in pericardial disease. Analysis of Pericardial Fluid 1 Normal pericardial fluid has the features of a plasma ultrafiltrate. Although routine analysis of fluid does not have a very high yield for disease etiology, analysis is rewarding with bacterial infections and malignant effusions. Although most effusions are exudates, detection of a transudate reduces diagnostic possibilities. Sanguineous fluid is nonspecific and does not necessarily indicate active bleeding. Chylous effusions can occur after traumatic or surgical injury to the thoracic duct or obstruction by neoplasms. Pericardial fluid should routinely be stained and cultured for bacteria, including Mycobacterium tuberculosis, and fungi and as much fluid as possible submitted for detection of malignant cells. If there is a suspicion of tuberculous pericarditis, at least one of these tests should be routine because of the difficulty in diagnosing this disorder and delays in making a diagnosis by culture. New and novel approaches for the analysis of pericardial fluid have been the subject of active investigation. As discussed below, there may be a role for measurement of tumor markers as a screen for 2,52 malignant effusion. Selected cytokine and related biomarkers measured in both pericardial fluid and serum have shown promise in distinguishing various types of inflammatory effusions, but their precise 53,54 roles have not been elucidated. Pericardioscopy and Percutaneous Biopsy Pericardioscopic-guided drainage of pericardial effusions was discussed earlier. When standard noninvasive methods of evaluating the cause of pericardial effusions are unsuccessful, extended pericardioscopically guided biopsies combined with a battery of immunologic and molecular methods applied to both fluid and tissue (e. However, experience is limited and it is not known whether such an approach will in fact improve long-term outcomes. Constrictive Pericarditis Etiology Constrictive pericarditis is the end stage of an inflammatory process involving the pericardium. In the developed world the disorder is most 1,2,56,57 commonly idiopathic or due to surgical complications or radiation injury. Constriction can follow an initial insult by as little as several months and occasionally less, but typically takes years to develop. The end result is fibrosis, often calcification, and adhesions of the parietal and visceral pericardium. Scarring is usually more or less symmetric and impedes filling of all heart chambers. In a subset of patients, constriction is transient and/or reversible by antiinflammatory drugs. This is observed early after cardiac surgery and in 1,59-62 other patients with intense pericardial inflammation (discussed below). Pathophysiology 1,2 The consequence of pericardial scarring is markedly restricted filling of the heart. This results in elevated and equal filling pressures in all chambers and systemic and pulmonary veins. In early diastole the ventricles fill rapidly because of markedly elevated atrial pressures and accentuated early diastolic ventricular suction related to small end-systolic volumes. During early to mid-diastole, ventricular filling abruptly ceases when the cardiac volume reaches the limit set by the pericardium. Systemic venous congestion results in hepatic congestion, peripheral edema, ascites, anasarca, and cardiac cirrhosis. Reduced cardiac output also results from impaired filling and causes fatigue, muscle wasting, and weight loss. The myocardium is occasionally involved in inflammation and fibrosis, leading to contractile dysfunction, which predicts a 63 poor result after pericardiectomy. Failure of transmission of intrathoracic respiratory pressure changes to the cardiac chambers through the thickened pericardium is an important contributor to the pathophysiology of constrictive pericarditis (Fig. On inspiration, the drop in intrathoracic pressure is transmitted to the pulmonary veins but not 1 the left heart. High systemic venous pressure and reduced cardiac output induce retention of sodium and water by the kidneys. During inspiration the decrease in left ventricular filling results in a leftward septal shift, allowing augmented flow into the right ventricle. Clinical Presentation The usual presentation consists of signs and symptoms of right heart failure, including lower extremity edema, vague abdominal complaints, and passive hepatic congestion. With progression, hepatic congestion worsens and can progress to ascites, anasarca, and jaundice due to cardiac cirrhosis. Signs and symptoms of left heart failure, dyspnea, cough, and orthopnea may also appear. Atrial fibrillation and tricuspid regurgitation, which further exacerbate venous pressure elevation, are common at this stage. At the end stage, effects of a chronically low cardiac output are prominent, including fatigue, muscle wasting, and cachexia. Constrictive pericarditis can be mistaken for any cause of right heart failure, as well as end-stage liver disease. Physical Examination Physical findings include markedly elevated jugular venous pressure with a prominent, rapidly collapsing y descent. This, combined with a normal x descent, results in an M- or W-shaped venous pressure contour. In patients with atrial fibrillation, the x descent is lost, leaving only the prominent y descent. The latter can be difficult to distinguish from tricuspid regurgitation, which, as noted above, may also be 1 present. The Kussmaul sign, an inspiratory increase in mean venous pressure, is usually present, or the pressure may simply fail to decrease on inspiration. The Kussmaul sign reflects loss of the normal increase in right heart venous return on inspiration, even though tricuspid flow increases. These venous pressure abnormalities contrast with tamponade, where the y descent is lost. A paradoxic pulse occurs in perhaps one third of patients, especially with an effusive-constrictive picture. It is probably best explained by the aforementioned lack of transmission of decreased intrathoracic pressure to the left heart. The most notable cardiac physical finding is the pericardial knock, an early diastolic sound best heard at the left sternal border and/or the cardiac apex. It occurs slightly earlier and has a higher frequency content than a third heart sound and corresponds to early, abrupt cessation of ventricular filling.
Thus cheap 40 mg imdur free shipping, information from the two testing modalities may be complementary in refining the risk assessment of future coronary events discount imdur 40mg without a prescription, thereby curtailing the aggressiveness of primary prevention discount imdur 40 mg on line. Moreover, in a coronary segment that is heavily calcified, stenoses are particularly difficult to detect, to rule out, or to quantitate. After an average of approximately 2 years of follow-up, there was essentially no difference in the primary endpoint outcome composite, suggesting that the initial assessment strategies were associated with similar outcomes. A severe inferolateral resting perfusion defect (arrow, all images) suggests ischemia at rest or infarction in that territory. Upper left, Normal study findings, associated with a low risk of cardiac events during follow-up, suggesting that such a patient can be managed conservatively without catheterization but with aggressive secondary preventive strategies. Despite the stabilization of symptoms, extensive reversible perfusion abnormalities in the inferior and lateral walls suggest high risk of cardiac death or myocardial infarction, or both, during follow-up. This patient would therefore be managed more aggressively with catheterization and intervention. Contemporary guidelines suggest that noninvasive assessment of the presence and extent of inducible ischemia is indicated (class I recommendation) for patients who have not already had coronary angiography and do not have other high-risk features that would drive a decision to perform 45 angiography. Besides the fixed defect representing the infarct in the anterior wall and apex (arrowheads), extensive inducible ischemia is evident both within and remote from the infarct territory (septum and inferior walls, arrows), involving 25% of the ventricle. Role of adenosine thallium-201 tomography for defining long term risk in patients after acute myocardial infarction. As noted earlier, after a regional ischemic insult, abnormalities in fatty acid metabolism may persist long after perfusion has returned to normal, a finding termed ischemic memory. Imaging of fatty acid metabolism may therefore allow assessment of recent ischemia. Future studies will determine whether such techniques can help guide management decisions. Subsequent angiography demonstrated a severe stenosis of the left circumflex coronary artery. In a meta-analysis of outcome 48 studies after viability imaging, patients with evidence of preserved myocardial viability who underwent revascularization had a substantial reduction in the risk of cardiac death during long-term follow-up compared with those treated medically (Fig. Revascularization conferred no advantage in patients without substantial myocardial viability. These data suggest that noninvasive imaging of viability and ischemia can potentially play a role in selecting patients for revascularization, with the expectation of ameliorating symptoms and improving natural history. However, this analysis was based on 24 retrospective studies in which there may have been inadequate adjustment for comorbidity and in which the medical management would not be considered adequate in terms of current guidelines recommendations. In this study of more than 600 patients, viability status did not influence the intervention effect on outcome. Among patients determined to have predominantly viable myocardium, treatment with medical therapy is associated with a 16% annual risk of cardiac death. By contrast, patients with predominantly nonviable myocardium exhibit no difference in outcome whether they are treated with medical therapy or with revascularization. These data suggest that noninvasive interrogation of myocardial viability can identify treatment strategies associated with more favorable long-term outcomes. Myocardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: a meta-analysis. Principles of Assessing Myocardial Viability by Radionuclide Techniques The radionuclide tracers and techniques most often used to assess viability have been evaluated for their relation to preserved tissue viability by correlation of tracer uptake with histologically confirmed extent 48 of tissue viability. Quantitative analysis of tracer uptake correlates directly with the magnitude of preservation of tissue viability, and tracer uptake represents a continuous variable—that is, the magnitude of tracer uptake directly reflects the magnitude of preserved tissue viability. For a dysfunctional segment or territory, the probability of functional recovery after revascularization is related to the magnitude of tracer uptake, representing the degree of preserved myocardial viability (extent of hibernation or stunning) within that territory. A dysfunctional territory with normal or only mildly reduced tracer uptake thus has a high likelihood of improved function after revascularization. By contrast, a territory with a severe reduction in tracer uptake would represent predominant infarction, and the likelihood of improved function after revascularization would be low (Figs. In contrast, column B demonstrates images from a patient with an occluded proximal left anterior descending artery and severe hypokinesis of the subtended territories, with symptoms of heart failure and some angina. There is normal uptake throughout the anterior wall and septum (yellow arrows) as well as in the apex (arrowheads), consistent with completely retained viability. The images suggest that revascularization of the territory would be associated with improved regional function and likely improvement in symptoms. Studies correlating tracer uptake with biopsy specimens have shown that the magnitude of uptake is related to the degree of retained myocyte viability within each territory. There is a severe defect in the inferior wall (white arrows), consistent with predominant infarct. There is a moderately severe defect in the anterior wall (white arrowheads), in which there is clearly more uptake compared to the inferior wall. This would be consistent with an admixture of viable myocardium and infarct in that territory. There is only very mild reduction in tracer activity in the septum (yellow arrows), consistent with predominantly retained viability. Because the 201 absence of Tl uptake on the redistribution images is not a sufficient sign of the absence of regional 201 4 viability, however, iterations of the standard Tl protocol have been investigated to optimize the 201 assessment of regional viability (eFig. The presence of a severe Tl defect after reinjection identifies areas with a very low probability of improvement in function. The initial thallium images demonstrate several areas of reduced blood flow at rest involving the septum, anteroapical wall, and inferior wall. Thallium redistribution imaging 4 hours later demonstrates substantial redistribution of thallium in the septal, anteroapical, and inferior regions of the left ventricle, indicating myocardial viability, with only the basal portion of the inferolateral wall representing irreversibly damaged myocardium. After the thallium redistribution image acquisition, stress 99m imaging with Tc-sestamibi demonstrates inducible ischemia in the septum and anterior wall. However, without the redistribution images, routine stress-rest imaging would have given misleading information about viability because of the apparently irreversible defects in the inferior and anteroapical walls. In such patients, 201 Tl reinjection after late redistribution imaging may provide further insight into defect reversibility and thus viability. The finding of a reversible resting defect may identify areas of myocardial hibernation (eFig. This finding appears to be an insensitive but specific sign of potential improvement in 4,51 regional function. The key finding to evaluate is the magnitude of tracer uptake in a dysfunctional region. Normal uptake is consistent with preserved viability; only mild reduction in uptake is consistent with predominantly preserved viability; moderate reduction in uptake is consistent with an admixture of viable and infarcted tissue; and a severe defect is consistent with predominant infarct. Administration of nitrates to improve blood flow at rest before injection of sestamibi appears to 4,51 improve slightly the ability of these tracers to detect myocardial viability. All these data suggest that differences between the imaging approaches to assess viability are small, and that choice of modality should be driven by the available expertise and experience. In some situations, subsequent noninvasive definition of regional viability and ischemia may be important to plan the revascularization strategy when the anatomy is known. Imaging in Inflammatory and Infiltrative Cardiomyopathies Myocarditis Inflammatory injury to the myocardium by infective agents, postinfective immune processes (e. The clinical manifestation of such an inflammatory process is acute myocarditis and cardiac allograft rejection (see Chapters 27 and 79).