DOI: 10.1148/rg.261055058
RadioGraphics 2006;26:213-231
© RSNA, 2006
Cardiovascular Complications of Human Immunodeficiency Virus Infection1
Carlos S. Restrepo, MD,
Lisa Diethelm, MD,
Julio A. Lemos, MD,
Enrique Velásquez, MD,
Ty A. Ovella, MD,
Santiago Martinez, MD,
Jorge Carrillo, MD and
Diego F. Lemos, MD
1 From the Departments of Radiology (C.S.R., L.D., J.A.L., T.A.O., S.M., D.F.L.) and Cardiology (E.V.), Louisiana State University Health Sciences Center, 1542 Tulane Ave, Room 212, New Orleans, LA 70112; and Universidad Nacional de Colombia, Hospital Santa Clara, Bogotá, Colombia (J.C.). Recipient of a Certificate of Merit award for an education exhibit at the 2004 RSNA Annual Meeting. Received March 21, 2005; revision requested May 2 and received June 3; accepted June 6. All authors have no financial relationships to disclose.
Address correspondence to C.S.R. (e-mail: crestr{at}lsuhsc.edu).
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Abstract
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The heart and great vessels are not the sites most frequently affected by opportunistic infections and neoplastic processes in patients with acquired immune deficiency syndrome (AIDS). However, cardiovascular complications occur in a significant number of such patients and are the immediate cause of death in some. The spectrum of cardiovascular complications of AIDS that may be depicted at imaging includes dilated cardiomyopathy, pericardial effusion, human immunodeficiency virus–associated pulmonary hypertension, endocarditis, thrombosis, embolism, vasculitis, coronary artery disease, aneurysm, and cardiac involvement in AIDS-related tumors. To aid accurate diagnosis and appropriate treatment planning, radiologists should be familiar with the imaging appearance of each of these complications.
© RSNA, 2006
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Describe the clinical signs of cardiovascular complications of acquired immune deficiency syndrome (AIDS).
- List the conditions associated with AIDS that cause cardiovascular complications.
- Identify the imaging features of cardiovascular complications of AIDS.
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Introduction
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The World Health Organization estimated that the number of people worldwide who were living with the human immunodeficiency virus (HIV) rose in 2004 to the unprecedented level of 39.4 million; the number of those infected with HIV increased in every region, and 4.9 million were newly infected that year. Acquired immune deficiency syndrome (AIDS) was responsible for the deaths of 3.1 million people in 2003. The number of those who have died since the epidemic began exceeds 32 million. In North America alone, 1 million are currently infected with HIV. The prevalence of the virus in the adult population of the United States is 0.6%. In 2004, 44,000 adults and children in North America were newly infected with HIV, and 16,000 died of AIDS (1,2).
Although cardiac involvement in HIV infection was recognized early in the AIDS epidemic, the incidence of this complication and its imaging manifestations have not been fully described in the radiologic literature. Cardiac involvement in HIV represents a diagnostic and therapeutic challenge for cardiologists, specialists in infective diseases, and radiologists, who should be aware of the resultant imaging manifestations.
According to reports of clinical and autopsy studies, the prevalence of myocardial abnormalities in HIV-positive patients ranges from 25% to 75% (3,4). The effect of antiretroviral therapy on the incidence and prevalence of HIV-related cardiovascular disease is not clear. Investigators in the Data Collection on Adverse Events of Anti-HIV Drugs Study, a prospective observational study of a cohort of 23,468 HIV-positive patients, found that the incidence of myocardial infarction increased by an average of 26% per year of therapy with combined antiretroviral agents (5). Not surprisingly, a further analysis of data from the same population indicated that these patients experienced an increased incidence and higher risk of other cardiac and cerebrovascular events (eg, stroke; death from end-stage ischemic heart disease other than myocardial infarction; and invasive cardiovascular procedures, such as angioplasty, bypass creation, and carotid endarterectomy) (6). However, not all reported data agree with these results. Despite fear that the use of new-generation anti-HIV drugs associated with metabolic abnormalities (eg, dysglycemia and hyperlipidemia) might accelerate the progression of cardiovascular and cerebrovascular disease, the results of a study of more than 36,000 patients at Veterans Affairs facilities in the United States showed decreased mortality, with no increase in the rate of cardiovascular or cerebrovascular events (7). Overall, the rate of deaths from cardiovascular or cerebrovascular events in the study population remained constant (two deaths per 100 patient-years of follow-up) (7). Therefore, the radiologic diagnosis of cardiovascular disease is increasingly significant in the HIV-infected population.
In this article, we review the pathophysiologic and imaging manifestations of HIV- and AIDS-related cardiovascular complications (Table 1).
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Pericardial Effusion
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Pericardial effusion is the most common cardiovascular complication of HIV infection. Prior to the introduction of highly active antiretroviral therapy (HAART), the frequency of this complication was estimated to be between 5% and 46% (3,8), with an incidence of 11%–17% per year (9,10). The prevalence of pericardial effusion in children with AIDS is particularly high (68%) and is often associated with cardiac disease (11). Echocardiograms showed pericardial effusion in 10% of the HIV-infected patients in one study (12), and fibrinous pericarditis has been identified at autopsy in 9%–62% of deceased AIDS patients (4,13). The origins of pericardial effusion in patients with HIV and/or AIDS are diverse (Table 2), but in most cases no etiologic agent has been identified, despite an extensive work-up (8). In an autopsy series, serous pericardial effusion was more common (59%) than fibrinous pericarditis (3%) (4). In children, serous pericardial effusion has been found more frequently (81.0%) than have serosanguineous and sanguineous (14.3%) or purulent (4.7%) collections (11).
Pericardial effusion in patients with HIV-related disease may be associated with an opportunistic infection or malignancy, but most often no definitive cause is found (14). An association between pericardial effusion, pleural effusion, and ascites has been reported (Fig 1) (11). The observed pattern may indicate the presence of a generalized serous-effusive process, or polyserositis, that involves pleural and peritoneal as well as pericardial surfaces. Patients with AIDS who are affected by pericardial effusion have a total T-cell count that is comparable to that in patients who are not affected by pericardial effusion, but they have a significantly lower serum albumin level and lower CD4 count (9).
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Figure 1. Pericardial fluid in a 32-year-old woman with AIDS and a history of recurrent pneumonia. Unenhanced axial computed tomographic (CT) scan demonstrates a medium-sized pericardial effusion (arrows), as well as bilateral pleural fluid collections and slight dilatation of the heart.
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Although spontaneous resolution of pericardial effusion has occurred in as many as 42% of those affected, the 6-month mortality rate among HIV-positive patients with pericardial effusion (62%) is higher than that among HIV-positive patients without that complication (7%) (9). In HIV-positive patients in whom cardiac tamponade develops, mycobacterial infection is the most common cause worldwide (44%) (Fig 2), followed by malignancy (16%) and other bacterial infection (11%). With regard to bacterial infection, Staphylococcus aureus is the most common causal agent (15). There are some differences, depending on the population of reference. In Africa, for example, in an estimated 70% of patients hospitalized for treatment of pericardial disease, that disease is related to HIV infection, with more than 90% of cases of HIV-related pericardial effusion caused by tuberculosis (16). Pericardial effusion and tamponade also may be manifestations of cardiac involvement in Kaposi sarcoma (15,16). The prognosis for patients with AIDS-related cardiac tamponade is poor, regardless of the method of treatment (17).
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Figure 2. Pulmonary and pericardial tuberculosis in a 23-year-old man with HIV who presented with cardiac tamponade. Contrast material–enhanced CT scan of the chest depicts a large pericardial effusion and a loculated pleural fluid collection in the anterior right hemithorax. The pericardium appears as a thin line of slightly higher attenuation (arrow) between the two fluid collections.
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Pneumopericardium is a rare complication of AIDS. It occurs when an infection or malignancy of the pericardium produces a fistulous connection to the adjacent esophagus, trachea, or bronchus. The condition may develop in patients with a pericardial infection by a gas-forming organism. Spontaneous pneumopericardium also has been reported (18).
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Myocardial Disease
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According to various publications, the prevalence of myocardial abnormalities among AIDS patients is 25%–75% (3). Myocardial abnormalities that may occur in HIV-positive patients include myocarditis, dilated cardiomyopathy, ischemic heart disease, and myocardial involvement in Kaposi sarcoma or lymphoma. Hypertrophy of the right ventricle may develop in response to AIDS-related pulmonary disease (4).
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Myocarditis
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Histopathologic evidence of myocarditis has been found in approximately one-third of AIDS patients at autopsy, but no specific cause was identified in more than 80% of the cases (19). Common pathogens found in patients with AIDS-related myocarditis include Toxoplasma gondii, Mycobacterium tuberculosis (Fig 3), and Cryptococcus neoformans. Other infective agents that have been reported are Mycobacterium avium-intracellulare complex, Aspergillus fumigatus, Candida albicans, Coccidioides immitis, cytomegalovirus, and herpesvirus types 1 and 2 (8,20). HIV itself has been implicated as a cause of myocarditis. Since cardiac myocytes do not possess CD4 receptors that would allow a virus to attach itself and enter the cell by the usual mechanism, it is not clear how a virus enters the myocytes. Reservoir cells (dendritic cells), as well as infection and injury of myocytes by other cardiotropic viruses, may facilitate the entry of HIV into CD4 receptor–negative cells (2,21,22). Lymphocytic myocarditis was present in 52% of patients who died of AIDS (19), and it frequently has been found in patients with left ventricular dysfunction (23,24). Autoimmune abnormalities and nutritional deficiencies have been implicated in AIDS-related myocardial disease, and cardiac-specific autoantibodies (anti-
myosin) have been found in 30% of patients with HIV-associated cardiomyopathy (25). An association between the use of zidovudine and cardiomyopathy also has been reported (26).
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Figure 3. Myocardial tuberculosis in a 42-year-old man with AIDS. Gross autopsy specimen of the heart shows diffuse myocardial involvement, with caseous material within the walls of the left ventricle (curved arrows), thickened pericardium secondary to granulomatous infiltration (straight white arrows), and vegetation in an aortic valve cusp (black arrow).
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Dilated Cardiomyopathy
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HIV-related disease is now recognized as an important cause of dilated cardiomyopathy, with a prevalence of 8%–30% (12,19,21,27). Prior to the introduction of HAART, the annual incidence of dilated cardiomyopathy was estimated at 15.9 per 1000 patients with HIV infection (21). Usually seen in the late stage of AIDS, dilated cardiomyopathy is associated with a low CD4 count (fewer than 400 cells per milliliter) (Fig 4) (3,8,21). Myocarditis due to HIV or another viral agent, such as a group B coxsackievirus (17%), cytomegalovirus (6%), or Epstein-Barr virus (3%), was found in 83% of patients with dilated cardiomyopathy diagnosed on the basis of histopathologic findings (21).
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Figure 4a. Dilated cardiomyopathy in a 43-year-old man with AIDS. (a) Conventional radiograph from July 1998 shows a normal cardiac silhouette. (b) Conventional radiograph obtained in December 2003 shows a significantly enlarged cardiac silhouette and severe enlargement of the right heart chamber.
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Figure 4b. Dilated cardiomyopathy in a 43-year-old man with AIDS. (a) Conventional radiograph from July 1998 shows a normal cardiac silhouette. (b) Conventional radiograph obtained in December 2003 shows a significantly enlarged cardiac silhouette and severe enlargement of the right heart chamber.
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Various studies have shown a correlation between dilated cardiomyopathy and a poor prognosis. In patients with dilated cardiomyopathy, the median survival period is reduced to 101 days, compared with 472 days for patients who are at a similar stage of AIDS but whose hearts are normal (28).
At gross pathologic examination, hearts with AIDS-related dilated cardiomyopathy reveal a constellation of findings. The left ventricular myocardium may show eccentric hypertrophy, with increased wall thickness and chamber dilatation. Conversely, there may be thinning of the ventricular wall, especially of the free wall. In the setting of ventricular wall thinning, endocardial fibroelastosis and apical mural thrombi are common. Pericardial effusion or infective endocarditis may be present, especially in intravenous drug users (3).
The features observed on echocardiograms and CT images acquired with helical scanning reflect the findings at gross pathologic examination and may include abnormal size and shape of the heart, ventricular dilatation, abnormalities of wall morphology and/or motion, and apical rounding (Fig 5). Secondary findings that may result from congestive pathophysiologic change include cephalization of the pulmonary vascular distribution and variable degrees of pulmonary edema and pleural effusion (Fig 6).
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Figure 5a. Dilated cardiomyopathy in a 45-year-old woman with AIDS. (a) Apical four-chamber echocardiographic view shows marked enlargement of all four chambers, as well as spontaneous echo contrast ("smoke") in the left-sided chambers because of a very low ejection fraction and sluggish flow. (b) Apical four-chamber view obtained with color Doppler flow imaging shows an eccentric jet of severe regurgitation through the tricuspid valve. LA = left atrium, LV = left ventricle, RA = right atrium, RV = right ventricle.
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Figure 5b. Dilated cardiomyopathy in a 45-year-old woman with AIDS. (a) Apical four-chamber echocardiographic view shows marked enlargement of all four chambers, as well as spontaneous echo contrast ("smoke") in the left-sided chambers because of a very low ejection fraction and sluggish flow. (b) Apical four-chamber view obtained with color Doppler flow imaging shows an eccentric jet of severe regurgitation through the tricuspid valve. LA = left atrium, LV = left ventricle, RA = right atrium, RV = right ventricle.
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Figure 6a. Dilated cardiomyopathy in a 38-year-old man with AIDS. (a) Digital radiograph shows an enlarged cardiac silhouette with left ventricular configuration and right-sided pleural effusion. (b) Apical four-chamber echocardiographic view obtained with color Doppler flow imaging shows severe tricuspid valve regurgitation and marked dilatation of all chambers. (c) Apical four-chamber gray-scale echocardiographic view better depicts enlargement of the chambers, as well as a markedly decreased ejection fraction (6%). (d) Contrast-enhanced axial CT scan demonstrates significantly enlarged right and left ventricles and a dilated inferior vena cava (arrowhead) and coronary sinus (arrow), as well as pericardial fluid, right-sided pleural effusion, and parenchymal consolidation in the lower lobe of the right lung. (e) CT scan at a lower level depicts the dilated inferior vena cava (arrowhead) and hepatic veins (arrows), as well as contrast material reflux via the right atrium.
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Figure 6b. Dilated cardiomyopathy in a 38-year-old man with AIDS. (a) Digital radiograph shows an enlarged cardiac silhouette with left ventricular configuration and right-sided pleural effusion. (b) Apical four-chamber echocardiographic view obtained with color Doppler flow imaging shows severe tricuspid valve regurgitation and marked dilatation of all chambers. (c) Apical four-chamber gray-scale echocardiographic view better depicts enlargement of the chambers, as well as a markedly decreased ejection fraction (6%). (d) Contrast-enhanced axial CT scan demonstrates significantly enlarged right and left ventricles and a dilated inferior vena cava (arrowhead) and coronary sinus (arrow), as well as pericardial fluid, right-sided pleural effusion, and parenchymal consolidation in the lower lobe of the right lung. (e) CT scan at a lower level depicts the dilated inferior vena cava (arrowhead) and hepatic veins (arrows), as well as contrast material reflux via the right atrium.
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Figure 6c. Dilated cardiomyopathy in a 38-year-old man with AIDS. (a) Digital radiograph shows an enlarged cardiac silhouette with left ventricular configuration and right-sided pleural effusion. (b) Apical four-chamber echocardiographic view obtained with color Doppler flow imaging shows severe tricuspid valve regurgitation and marked dilatation of all chambers. (c) Apical four-chamber gray-scale echocardiographic view better depicts enlargement of the chambers, as well as a markedly decreased ejection fraction (6%). (d) Contrast-enhanced axial CT scan demonstrates significantly enlarged right and left ventricles and a dilated inferior vena cava (arrowhead) and coronary sinus (arrow), as well as pericardial fluid, right-sided pleural effusion, and parenchymal consolidation in the lower lobe of the right lung. (e) CT scan at a lower level depicts the dilated inferior vena cava (arrowhead) and hepatic veins (arrows), as well as contrast material reflux via the right atrium.
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Figure 6d. Dilated cardiomyopathy in a 38-year-old man with AIDS. (a) Digital radiograph shows an enlarged cardiac silhouette with left ventricular configuration and right-sided pleural effusion. (b) Apical four-chamber echocardiographic view obtained with color Doppler flow imaging shows severe tricuspid valve regurgitation and marked dilatation of all chambers. (c) Apical four-chamber gray-scale echocardiographic view better depicts enlargement of the chambers, as well as a markedly decreased ejection fraction (6%). (d) Contrast-enhanced axial CT scan demonstrates significantly enlarged right and left ventricles and a dilated inferior vena cava (arrowhead) and coronary sinus (arrow), as well as pericardial fluid, right-sided pleural effusion, and parenchymal consolidation in the lower lobe of the right lung. (e) CT scan at a lower level depicts the dilated inferior vena cava (arrowhead) and hepatic veins (arrows), as well as contrast material reflux via the right atrium.
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Figure 6e. Dilated cardiomyopathy in a 38-year-old man with AIDS. (a) Digital radiograph shows an enlarged cardiac silhouette with left ventricular configuration and right-sided pleural effusion. (b) Apical four-chamber echocardiographic view obtained with color Doppler flow imaging shows severe tricuspid valve regurgitation and marked dilatation of all chambers. (c) Apical four-chamber gray-scale echocardiographic view better depicts enlargement of the chambers, as well as a markedly decreased ejection fraction (6%). (d) Contrast-enhanced axial CT scan demonstrates significantly enlarged right and left ventricles and a dilated inferior vena cava (arrowhead) and coronary sinus (arrow), as well as pericardial fluid, right-sided pleural effusion, and parenchymal consolidation in the lower lobe of the right lung. (e) CT scan at a lower level depicts the dilated inferior vena cava (arrowhead) and hepatic veins (arrows), as well as contrast material reflux via the right atrium.
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Endocarditis
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Patients with AIDS may develop either infective endocarditis or nonbacterial thrombotic (marantic) endocarditis. Marantic endocarditis has been reported with increasing frequency in HIV-positive patients who are in the advanced or terminal stage of the disease, in whom it is frequently associated with malignancy, inanition, or HIV wasting syndrome (20). The prevalence of endocarditis in autopsy studies of patients with AIDS has been reported as 10%–17%. Any of the cardiac valves may be involved in endocarditis, with multivalvular disease being common and tricuspid involvement being strikingly frequent (4,29,30). The condition is not limited to the valves; it also may arise in or involve the endocardial lining or vascular endothelium (3,31,32).
The lesions in endocarditis occur singly or in multiples as masses of platelets and red blood cells combined in a fibrin mesh; inflammatory cells also may be present but are not a prominent feature (3). Autopsy has revealed pulmonary and/or systemic thromboembolism in at least 40% of HIV-positive patients with thrombotic endocarditis. In many cases, embolism is not clinically diagnosed but is found at autopsy. Symptomatic embolic disease may manifest as an ischemic event (in the cerebral, pulmonary, renal, splenic, or mesenteric vessels) or an abscess (3,29).
In patients with AIDS, infective endocarditis usually occurs in those who engage in nontherapeutic use of intravenous drugs; such drug use is a common risk factor among HIV-infected patients in western societies. Estimates of the prevalence of endocarditis among HIV-positive intravenous drug users vary, with reported values ranging from 6.3% to 34% (21,33). Patients with infective endocarditis and HIV generally have the same endocarditis-related clinical manifestations as patients without HIV and have a similar survival rate (85% vs 93% for patients with and without HIV, respectively). However, patients with late-stage HIV-related disease and with endocarditis have a 30% higher mortality than do asymptomatic HIV-positive patients (32,34). In a series of 34 patients with infective endocarditis, Staphylococcus aureus (75%) and Streptococcus viridans (20%) were the most common causal organisms (34). Less commonly found were Haemophilus influenzae, Candida albicans, Salmonella species, Aspergillus fumigatus, Histoplasma capsulatum, and Cryptococcus neoformans (35). The clinical symptoms may include fever, chills, sweating, weight loss, and septic emboli. The course and outcome of infective endocarditis are determined by the degree of damage to the heart, the site of infection (right- vs left-sided valves; aortic vs mitral valve), the presence of distant seeding of infection, and the presence of ischemic changes (Fig 7). Peripheral embolization may occur in the presence of any causal organism and in any organ. In left-sided endocarditis, the most serious possible complications are cerebral and myocardial embolization, and the progression of disease may be rapid. Acute valvular insufficiency may develop as the result of the perforation of valve leaflets or rupture of chordae tendineae or papillary muscle (3) and may cause heart failure with a rapid onset and a poor outcome (Fig 8). Right-sided endocarditis typically involves the tricuspid valve; the possible pulmonary sequelae include septic emboli, abscess, and infarction (Fig 9).
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Figure 7a. Bacterial endocarditis with tricuspid valve involvement secondary to an atypical mycobacterial infection in a 56-year-old man with AIDS and a history of intravenous drug abuse. (a) Contrast-enhanced chest CT scan at the level of the ventricles shows right atrial enlargement (black arrow), consolidation in the lower lobe of the right lung (arrowhead), and a foreign body (a ballistic weapon fragment) in the right lung base (white arrow). (b) Right parasternal long-axis four-chamber echocardiographic view shows marked right atrial enlargement and a large area of echogenicity adjacent to the tricuspid valve (TV), a finding consistent with vegetation. LA = left atrium, RA = right atrium, RV = right ventricle. (c) Transesophageal echocardiographic view obtained with color flow Doppler imaging shows the large area of vegetation attached to the atrial side of the tricuspid valve, with associated valvular flailing and severe regurgitation. Multiple septic emboli also developed in the vessels supplying the lungs. The infective agent in this case was Mycobacterium fortuitum. RA = right atrium, RV = right ventricle.
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Figure 7b. Bacterial endocarditis with tricuspid valve involvement secondary to an atypical mycobacterial infection in a 56-year-old man with AIDS and a history of intravenous drug abuse. (a) Contrast-enhanced chest CT scan at the level of the ventricles shows right atrial enlargement (black arrow), consolidation in the lower lobe of the right lung (arrowhead), and a foreign body (a ballistic weapon fragment) in the right lung base (white arrow). (b) Right parasternal long-axis four-chamber echocardiographic view shows marked right atrial enlargement and a large area of echogenicity adjacent to the tricuspid valve (TV), a finding consistent with vegetation. LA = left atrium, RA = right atrium, RV = right ventricle. (c) Transesophageal echocardiographic view obtained with color flow Doppler imaging shows the large area of vegetation attached to the atrial side of the tricuspid valve, with associated valvular flailing and severe regurgitation. Multiple septic emboli also developed in the vessels supplying the lungs. The infective agent in this case was Mycobacterium fortuitum. RA = right atrium, RV = right ventricle.
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Figure 7c. Bacterial endocarditis with tricuspid valve involvement secondary to an atypical mycobacterial infection in a 56-year-old man with AIDS and a history of intravenous drug abuse. (a) Contrast-enhanced chest CT scan at the level of the ventricles shows right atrial enlargement (black arrow), consolidation in the lower lobe of the right lung (arrowhead), and a foreign body (a ballistic weapon fragment) in the right lung base (white arrow). (b) Right parasternal long-axis four-chamber echocardiographic view shows marked right atrial enlargement and a large area of echogenicity adjacent to the tricuspid valve (TV), a finding consistent with vegetation. LA = left atrium, RA = right atrium, RV = right ventricle. (c) Transesophageal echocardiographic view obtained with color flow Doppler imaging shows the large area of vegetation attached to the atrial side of the tricuspid valve, with associated valvular flailing and severe regurgitation. Multiple septic emboli also developed in the vessels supplying the lungs. The infective agent in this case was Mycobacterium fortuitum. RA = right atrium, RV = right ventricle.
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Figure 8. Severe mitral insufficiency in a 32-year-old woman with AIDS who presented with acute onset of shortness of breath. Conventional radiograph shows an enlarged cardiac silhouette, with left ventricular enlargement and asymmetric pulmonary edema that is more prominent in the right lung.
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Figure 9a. Bacterial endocarditis with multiple septic emboli in a 40-year-old man with AIDS and a history of intravenous drug abuse. Axial chest CT scans obtained with lung window settings demonstrate cavitary and noncavitary nodules (arrows in a) in both lungs, as well as an osteolytic lesion in the L1 vertebral body (curved arrow in b) and a left-sided paraspinal abscess (straight arrow in b).
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Figure 9b. Bacterial endocarditis with multiple septic emboli in a 40-year-old man with AIDS and a history of intravenous drug abuse. Axial chest CT scans obtained with lung window settings demonstrate cavitary and noncavitary nodules (arrows in a) in both lungs, as well as an osteolytic lesion in the L1 vertebral body (curved arrow in b) and a left-sided paraspinal abscess (straight arrow in b).
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The lungs are commonly affected by septic emboli in HIV-positive patients who use intravenous drugs, because of the higher frequency of right-sided valve involvement in such patients. Imaging findings include nodules with diameters ranging from 0.5 to 3.5 cm, distributed throughout both lungs, often with basilar predominance. Nodules may be well delineated or poorly defined, and cavitation is present in approximately 50% of them. If the nodules are located at the end of a pulmonary artery (67%), the "feeding vessel" sign will be observed on CT images (36,37). Focal areas of consolidation are depicted in 50% of cases; these areas are commonly wedge shaped and subpleural (Fig 10). After an intravenous contrast medium is administered, a rimlike pattern of peripheral enhancement may be seen along the edges of an area of consolidation. Additional findings that are both common and important are pleural effusion (67%) and hilar or mediastinal lymph node enlargement (27%) (36,37).
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Figure 10. Bacterial endocarditis secondary to atypical mycobacterial infection in the tricuspid valve in a 56-year-old man with AIDS and a history of intravenous drug abuse. Contrast-enhanced chest CT scan obtained with lung window settings at an infrahilar level shows parenchymal consolidation and areas of cavitation (arrow) secondary to septic emboli caused by M fortuitum.
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Coronary Artery Disease
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Coronary artery disease and ischemic heart disease have been reported in patients with HIV infection (38,39). Both the prevalence of ischemic heart disease and the mortality associated with it apparently are increased among HIV-positive patients (40,41). The increased prevalence could be, at least in part, related to an improvement in the overall survival of HIV-positive patients, especially since the introduction of HAART. The origins of the disease appear to be multifactorial and related to the higher incidence of infection with herpesvirus, cytomegalovirus, or HIV-1, as well as to the inclusion in HAART of protease inhibitors, which have been reported to produce lipodystrophy, hyperlipidemia, and hyperglycemia (41–43). In a retrospective analysis of data from the Frankfurt HIV cohort, which included almost 5000 patients, a fourfold increase in the annual incidence of myocardial infarction among HIV-infected patients was found after the establishment of HAART with protease inhibitors, compared with the incidence among patients who underwent treatment before the institution of HAART (41). Histopathologic examination of coronary arteries generally reveals eccentric atheromatous and fibrous plaques, with variable degrees of chronic inflammation and accelerated arteriosclerosis. Unusual proliferation of smooth muscle cells with abundant elastic fibers, as well as diffuse and circumferential involvement of the coronary arteries without any intervening healthy segments, also have been reported (3,44,45).
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Vasculitis
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A range of inflammatory vascular diseases, both infective and noninfective, may occur in the setting of HIV. These include polyarteritis nodosa, Henoch-Schönlein purpura, and drug-induced hypersensitivity vasculitis (14). In a series of 34 patients with biopsy-documented transmural inflammation of blood vessels, the histopathologic findings included necrotizing arteritis, nonnecrotizing arteritis, neutrophilic inflammatory vascular disease, mononuclear inflammatory vascular disease, and other small-vessel inflammatory changes (46). Features similar to those in Kawasaki syndrome, coronary arteritis, and Takayasu arteritis also have been described (44,47,48).
Large-vessel disease may be aneurysmal or occlusive. Aneurysms may be single or multiple and may affect vessels such as the aorta (Fig 11) or the common carotid, common iliac, femoral, or popliteal arteries (49). As many as seven aneurysms have been reported in a single patient. Occlusive disease has been reported in Africa in young HIV-positive patients and is less common than aneurysmal dilatation (49,50). In both processes, the main histopathologic features are found in the adventitia, with leukocytoclastic vasculitis of the vasa vasorum and periadventitial vessels, chronic inflammation, and fibrosis (50). Accelerated atherosclerosis also was found responsible for aortic aneurysm in a young man who had undergone several years of HAART for AIDS (51).
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Figure 11a. Abdominal aortic aneurysm and bilateral common iliac artery aneurysms in a 60-year-old woman with AIDS who developed severe dyslipidemia while undergoing HAART. (a) Contrast-enhanced CT scan of the abdomen shows the dilated aorta with a mural thrombus (arrow). (b) Contrast-enhanced CT scan of the pelvis shows an aneurysm of the right common iliac artery (arrow), also with a mural thrombus, as well as a dissection of the left iliac artery (arrowhead). (c) Contrast-enhanced CT scan at a level caudal to b shows the aneurysms of the right and the left common iliac arteries (arrows), both with mural thrombi.
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Figure 11b. Abdominal aortic aneurysm and bilateral common iliac artery aneurysms in a 60-year-old woman with AIDS who developed severe dyslipidemia while undergoing HAART. (a) Contrast-enhanced CT scan of the abdomen shows the dilated aorta with a mural thrombus (arrow). (b) Contrast-enhanced CT scan of the pelvis shows an aneurysm of the right common iliac artery (arrow), also with a mural thrombus, as well as a dissection of the left iliac artery (arrowhead). (c) Contrast-enhanced CT scan at a level caudal to b shows the aneurysms of the right and the left common iliac arteries (arrows), both with mural thrombi.
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Figure 11c. Abdominal aortic aneurysm and bilateral common iliac artery aneurysms in a 60-year-old woman with AIDS who developed severe dyslipidemia while undergoing HAART. (a) Contrast-enhanced CT scan of the abdomen shows the dilated aorta with a mural thrombus (arrow). (b) Contrast-enhanced CT scan of the pelvis shows an aneurysm of the right common iliac artery (arrow), also with a mural thrombus, as well as a dissection of the left iliac artery (arrowhead). (c) Contrast-enhanced CT scan at a level caudal to b shows the aneurysms of the right and the left common iliac arteries (arrows), both with mural thrombi.
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A vast array of pathogens are capable of producing infective vasculitis (52). Reports of infective arteritis or aortitis in HIV-positive patients are scarce in the literature. However, large vessels such as the aorta may become infected, and mycotic aneurysms may develop, especially in intravenous drug users. Causative agents include Salmonella species, Mycobacterium tuberculosis, and Staphylococcus aureus (50,53–55).
In children with AIDS, arteriopathy with aneurysm may occur in the cerebral circulation, a condition that produces diffuse dilatation of the major arteries of the circle of Willis. Medial fibrosis, loss of the muscularis, destruction of the internal elastic lamina, and intimal hyperplasia are the most common findings. The prognosis is poor, and death occurs shortly after diagnosis (56).
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Systemic Arterial Hypertension
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The prevalence of systemic hypertension among HIV-infected patients is much higher than that in the general population: It has been estimated as 20%–25% before the introduction of HAART (57) and as approximately 74% among patients who undergo HAART with protease inhibitors and who subsequently develop lipodystrophy and metabolic syndrome (58). The lipodystrophic syndrome is characterized by peripheral fat wasting in the arms, legs, and buttocks, as well as by increased fat deposition in the breasts, abdomen, and dorsocervical fat pads. Systemic hypertension in HIV-positive patients seems to have a significant effect on their risk of premature cardiovascular disease: Compared with normotensive HIV-positive patients, hypertensive patients have a higher frequency of coronary heart disease (16.1% vs 1.3%) and a higher incidence of myocardial infarction (8.1% vs 0.7%) (59).
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Thrombosis and Embolism
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HIV-infected patients tend to develop coagulation abnormalities due to increased levels of fibrinogen, d-dimer, plasminogen activator inhibitor-1, and tissue-type plasminogen activator antigen. A deficiency of protein S also has been identified. These hematologic abnormalities are associated with both arterial and venous thrombosis, especially in patients who are undergoing therapy with protease inhibitors (60,61). In a series of HIV-positive patients with venous or arterial thrombosis, deep vein involvement, most commonly in a lower extremity, and secondary pulmonary emboli accounted for 66% of all thrombotic events (Figs 12–15). In this cohort, persistent antiphospholipid antibodies were the most common abnormal serologic finding (62). An association between cigarette smoking and spontaneous thrombosis in HIV patients has been mentioned (61) and was reported to affect 77% of the patients in one series (62).
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Figure 12. Bilateral iliac vein thrombosis in a 32-year-old HIV-positive woman. Contrast-enhanced CT scan at the level of the aortic bifurcation shows filling defects as areas of abnormally low attenuation in both iliac veins (arrow).
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Figure 13. Venous thrombosis in a 40-year-old HIV-positive woman with miliary tuberculosis. Real-time gray-scale longitudinal ultrasonographic image shows an extensive thrombus (arrows) in the right common femoral vein.
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Figure 14a. Pulmonary embolism and infarction in a 50-year-old man with AIDS. (a) Conventional radiograph shows an abnormal pleura-based triangular parenchymal opacity in the left middle and lower lung zones (Hampton hump) (arrow), a finding that represented acute embolism. The patient died shortly after the examination. (b, c) Photomicrograph (original magnification, x10; hematoxylin-eosin stain) (b) and photograph (c) of a gross specimen depict a thromboembolus and a hemorrhagic infarct in the lower lobe of the left lung.
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Figure 14b. Pulmonary embolism and infarction in a 50-year-old man with AIDS. (a) Conventional radiograph shows an abnormal pleura-based triangular parenchymal opacity in the left middle and lower lung zones (Hampton hump) (arrow), a finding that represented acute embolism. The patient died shortly after the examination. (b, c) Photomicrograph (original magnification, x10; hematoxylin-eosin stain) (b) and photograph (c) of a gross specimen depict a thromboembolus and a hemorrhagic infarct in the lower lobe of the left lung.
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Figure 14c. Pulmonary embolism and infarction in a 50-year-old man with AIDS. (a) Conventional radiograph shows an abnormal pleura-based triangular parenchymal opacity in the left middle and lower lung zones (Hampton hump) (arrow), a finding that represented acute embolism. The patient died shortly after the examination. (b, c) Photomicrograph (original magnification, x10; hematoxylin-eosin stain) (b) and photograph (c) of a gross specimen depict a thromboembolus and a hemorrhagic infarct in the lower lobe of the left lung.
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Abstract
LEARNING OBJECTIVES
