The pericardium is the most commonly involved part of heart in HIV/AIDS patients. In the early stage of HIV infection, pericardial lesions may occur, but being asymptomatic during his/her life time. HIV/AIDS related pericarditis caused by tuberculous mycobacteria infection is the most common. Staphylococcus and streptococcus are also the common causes of pneumonia and pericarditis. Others pathogens including Nocardia and Listeria can also cause pericarditis. HIV/AIDS related pericarditis has a poor prognosis, with the CD4 T cell count being lower than 100/μl.

AIDS and left ventricular dysfunction, valvular heart disease or cardiac shunt can cause pulmonary hypertension and pulmonary heart disease. Patients with AIDS complicated by pulmonary hypertension mostly sustain serious pulmonary infection, such as Pneumocystis carinii pneumonia and cytomegaloviral pneumonia. Progressive pulmonary pressure in AIDS patients is caused by hyperplasia of pulmonary endothelial cells resulted from stimulation of growth factors to pulmonary endothelial cells. It has been recognized that growth factors can be derived from infected T cells or directly derived from HIV. Therefore, occurrence of dyspnea in AIDS patients shows evidence of right ventricular dysfunction instead of left ventricular dysfunction. In such cases, possible occurrence of pulmonary hypertension should be considered.

HIV/AIDS related myocarditis plays an important role in progressive left ventricular dysfunction. About 80 % cases of myocarditis is idiopathic and about 20 % is opportunistic. The pathogen usually includes the complex of tubercle bacillus and mycobacterium avium, fungi including cryptococcus, aspergillus, Candida albicans, Histoplasma capsulatum and Coccidiodes, and protozoa including Cytomegalovirus, simplex herpes virus and HIV.

HIV/AIDS related dilated cardiomyopathy may be caused by diffuse weakened mobility of myocardium due to myocarditis. The diffuse weakened mobility of myocardium causes compensatory hypertrophy and dilation of the ventricles, and finally progresses into dilated cardiomyopathy.

In AIDS patients, some vascular diseases may occur. HIV/AIDS related cardiopathy is common and dilated cardiomyopathy can also occur as one of the cardiac complications of AIDS. The common cardiovascular diseases that complicate AIDS are myocarditis, cardiomyopathy, pericarditis and pericardial effusion, abnormal heart valves, vascular diseases and neoplasms. In cases of pulmonary infections, the pulmonary vascular intima responds to lesions, mostly caused by HIV under effects of inflammatory mediators and cytokines. The endothelial cells can release vasoactive substances or trigger proliferative response to growth factors to cause the increase of pulmonary vascular resistance. Calabrese et al. reported four cases of AIDS patients, with occurrence of necrotic vasculitis [5]. The lesions were reported to be nodular arteritis and acute inflammation of small and medium-sized blood vessels, resulting in lesions of the skin, muscles and nerve fibers. There were two cases with such lesions occurring in the nervous system, with their clinical and morphological manifestations being in line with those of neurologic granulomatous vasculitis. The pathogenesis of vasculitis is still unknown, and it may be related to the effects of virus (HIV, CNV, HBV and EBV) or immune complexes to cause vascular lesions, opportunistic infections, pulmonary diseases, drugs and nutritional status. Autopsy of AIDS patients found inflammatory and fiber calcified arterial lesions. The inflammatory arterial lesions are vasculitis and peripheral inflammation, while fiber calcified arterial lesions often involve medium sized artery to cause arterial intimal fibrosis, elastic fiber breakage, arterial medial fibrosis and calcification, possibly with accompanying varying degrees of stenosis. In addition, aneurysm can be found in some AIDS patients, with vascular wall fibrosis and calcification as well as endothelial cell proliferation, with accompanying arterial stenosis of different degrees. Changes in the microcirculation have been studied, but the abnormalities and their significance still need clarifying.

In cases of acute pericarditis, infections can be caused by bacteria, parasites, protozoa, viruses and fungi. The pathogens of bacterial infections are commonly streptococcus, staphylococcus and Gram-negative bacilli. The pathogens of virus infections in immunocompromised patients are commonly Echovirus, influenza virus, and Coxsackie B virus. AIDS can be complicated by pericardial effusion due to infections of tuberculous mycobacterium avium, actinomyces, fungi or virus, lymphoma and Kaposi’s sarcoma.

The common subtypes of chronic pericarditis are chronic constrictive pericarditis and chronic exudative pericarditis.

Chronic constrictive pericarditis is usually non-specific, but almost all subtypes of acute pericarditis can be its cause. The common cause is tuberculosis or other infection, rheumatoid arthritis, trauma and heart surgery.

Chronic exudative pericarditis is usually non-specific, but can be caused by mycobacterium tuberculosis, fungi or neoplasm. Among inpatients, the most common cause of large quantity pericardial effusion is the metastatic tumors or direct spreading of tumors, such as cancer (especially lung cancer or breast cancer), sarcoma (especially melanoma), leukemia, lymphoma and thoracic tumors.

Acute pericarditis can be serous, fibrinous, hemorrhagic or suppurative. It may involve surface of the sub-picardial myocardium. The quantity and quality of the cellular responses are determined by pathogens.

Chronic pericarditis can be serous, chylous or blood exudative. Alternatively, chronic pericarditis can be fibrinous, adhesive or calcified. And it can be constrictive and asymptomatic. In cases of chronic exudative pericarditis, the pericardial effusion fluid is about 50–1,000 ml (normally less than 25 ml). In the cases of less but rapid pericardial effusion, more but slow pericardial effusion, decreased accommodation of the pericardium due to fibrosis, calcification and neoplasm, the ventricular filling during its diastole can be restricted. Under such conditions, the terminal pressure of the left ventricular diastole is determined by the quantity of pericardial effusion and the thickness of the thickened pericardium. The diastolic pressures of ventricles, atria and venous bed are close, usually being 13–32 mmHg. Occurrence of venous congestion of systemic circulation causes too much body fluid effusion from the capillaries, resulting in postural edema and later ascites. The sign of surrounding tissue congestion is more obvious than that of pulmonary congestion, but pulmonary edema with obvious clinical symptoms is not common. However, pericardial effusion gradually progresses and the quantity of effusion being up to more than 1,000 ml may fail to cause pericardial tamponade due to its elasticity for adaptation.

Pathologically, pericarditis can be divided into two stages of the fibrinous stage and the serofibrinous stage. In the early stage of pericarditis, parietal and visceral pericardium has congestion, swelling and effusions of fibrin, leukocyte and some endothelial cells. The thick exudates can be restricted to a certain part of pericardium or diffuse across the entire surface of the heart. The surface of the pericardium can be coarse. In the cases of increased exudates, the effusion fluid can be serofibrinous effusions, with its quantity varying from 100 to 2,000–3,000 ml. The sub-epicardial myocardium often has inflammatory changes. After being cured, the exudates can be reabsorbed within 2–3 weeks or shorter time period. But in some cases, the exudates may remain for several days or even years, such as in the cases of tuberculous pericarditis. When pericardium recedes, varying degrees of adhesion may remain. Sometimes, both layers of pericardium can be obviously thickened and adhesive to completely fill the pericardial cavity. Therefore, thick and hard scars form to compress the heart and the major vascular roots. The cardiac diastole is therefore affected to develop into chronic constrictive pericarditis.

Acute pericarditis is manifested with symptoms of chest pain, difficulty breathing, fever, pericardial friction sound, pericardial tamponade, chest or retrosternal dull or sharp pain that radiates to the neck, trapezius (especially the left side) or the shoulder. The severity of the pain varies, commonly aggravating at conditions of chest motion, coughing and breathing and alleviating at the postures of standing up from sitting and leaning forward. Fever, chills and fatigue are very common. And the most important sign is three-phase or two-phase (systolic and diastolic) pericardial friction sound. For cases of large quantity pericardial effusion, the heart sound is low, with enlarged range of dullness sound. In such cases, the lungs can be compressed to cause dyspnea. About 8–30 % patients with pericarditis have symptoms of heart tamponade, with accompanying increased central venous pressure. Cardiac tamponade is fatal. Chronic pericarditis has symptoms of fever but with no chest pain.

For the cases of pericardial effusion, the imaging demonstrations include enlarged heart shadow in shape of a flask, the increased ratio of heart to chest, and the absence of outer line of the heart. Generally, when pericardial effusion reaches up to 300–500 ml or above, the heart shadow commonly expands to both sides, with different morphology of the heart shadow due to different posture. Superior vena cava obviously expands and the cardiophrenic angle becomes blunt. When pericardial effusion exceeds 1,000 ml, the heart shadow obviously expands in a shape of triangle or flask. In addition, normal limits of heart arches are absent, with weakened or no heart beat by X-ray.