Immunological analysis of pleural fluid in post-cardiac injury syndrome

Shrivastava, Rahul; Venkatesh, Sundar; Pavlovich, Branko; Bharadwaj, Jyoti; Vaz, Anthony J.

doi:10.1136/pmj.78.920.362

Cited by 16 publications

(12 citation statements)

References 6 publications

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“…Here in a case of acute pulmonary infection, the inflammatory reaction is well confined by the pleura (top). [206][207][208][209][210] Drug-induced (nitrofurantoin, bromocriptine, methysergide, procarbazine) 74,75,211 Trauma (external, esophageal rupture, intraabdominal abscesses) 209,212 Pancreatitis 213,214 Thoracic irradiation 215 Postcardiac injury syndrome 216 Pneumoconioses (asbestosis) 102,217 Metabolic disease (uremia) 218,219 Metastatic tumor 162,163 THE PLEURA IN HEALTH AND DISEASE/MURALI ET AL Worldwide, the most common etiologic agents of pleural infection are bacteria and tuberculosis. Fungal and protozoal infections are less common.…”

Section: Figurementioning

confidence: 99%

The Pleura in Health and Disease

Murali¹,

Park²,

Leslie³

2010

Semin Respir Crit Care Med

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A wide variety of local, regional, and systemic diseases may have pleural manifestations. The scope of this pathology encompasses a wide spectrum ranging from minimal inflammatory changes to highly malignant neoplasms. An overview of the normal structure of the pleura is provided, along with the diseases that may be encountered. Pleural specimens from patients with pneumothorax are rarely encountered by pathologists. In contrast, pathologists frequently receive pleural specimens showing evidence of inflammation, repair, or neoplasm. In these circumstances, an awareness of less common (and often clinically highly important) conditions such as epithelioid hemangioendothelioma and primary pleural malignant mesothelioma is essential. Knowledge of the clinical setting (e.g., disease tempo) and radiological picture (e.g., laterality) is often of great value to the pathologist in arriving at a correct diagnosis. Similarly, knowledge of the normal anatomical considerations and familiarity with the expected pleural histopathology for the most clinically relevant pleural diseases are critical assets for pulmonary physicians in providing optimal care for their patients.

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Section: Figurementioning

confidence: 99%

The Pleura in Health and Disease

Murali¹,

Park²,

Leslie³

2010

Semin Respir Crit Care Med

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“…14 Nevertheless, as we have already discussed, the absence of AHA does not exclude the possibility of PCIS. 15 It is also possible that prednisone accelerated the disappearance of AHA, which once appeared in the serum shortly after the onset of PCIS in this case. The clinical features of the present case were mostly consistent with the diagnostic criteria of PCIS.…”

Section: Discussionmentioning

confidence: 76%

“…Although AHA was detected only in the sera of 3 patients who had PCIS, AHA was undetectable at the onset of PCIS in all the patients and appeared afterward in the sera. 14 Moreover, AHA are not always detectable in PCIS patients 15 and the presence of the antibodies could just be a non-specific findings. 16,17 Thus, the role of AHA in the pathogenesis of PCIS still remains unclear, although the association of these antibodies with PCIS has been repeatedly shown.…”

Section: Discussionmentioning

confidence: 99%

Acute Pleuropericarditis After Coronary Stenting A Case Report

Setoyama

Furukawa

Abe

et al. 2006

Circ J

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leuropericarditis has a variety of causes, which include viral or bacterial infections, autoimmunity, malignant neoplasm, and other cardiac insults, such as myocardial infarction and surgery or trauma to the heart. The syndrome of pleuropericarditis with fever, pleuritic chest pain, and elevated inflammatory markers secondary to cardiac injury is referred to as post-cardiac injury syndrome (PCIS). PCIS is an inflammatory process involving the pleura and pericardium and includes 2 distinct entities: post-myocardial infarction syndrome secondary to myocardial infarction and post-cardiotomy syndrome secondary to cardiac surgery or trauma. 1 PCIS after open-heart surgery is rather common and the incidence is reported as 10-50%. 2 Recently, a few reports have described PCIS occurring as a rare complication after endovascular procedures such as percutaneous coronary intervention (PCI) and trans-venous temporary/permanent pacing. [3][4][5][6][7] We present a case of acute pleuropericarditis which occurred after successful coronary stenting with atypically early onset for PCIS. Case ReportA 72-year-old male hypertensive patient was admitted to hospital because of stable effort angina pectoris which appeared 2 months before admission. Treadmill stress test reproduced his chest symptoms, accompanied with reversible significant ST-segment depression in an electrocardiogram (ECG). Echocardiogram showed concentric left ventricular hypertrophy and mild left ventricular asynergy in the inferior wall. Coronary angiography revealed total occlusion in the middle right coronary artery (RCA) and 75% stenosis in the proximal RCA (Fig 1), and the distal RCA was filled through collateral circulation from the left coronary artery. The patient subsequently underwent PCI for the RCA. A 0.014 inch Miracle 3 g guidewire (Getz Bros) and a 0.014 inch PT Graphix guidewire (Boston Scientific) were used to cross the total occlusion lesion, with the aid of a microcatheter (Excelsior; Boston Scientific). The guidewire was replaced by a more flexible 0.014 inch BMW guidewire (Guidant Corporation) through the Excelsior. The lesion was predilated using a 2.0×15 mm Victo-X balloon catheter (Nippon Sherwood). Because the intravascular ultrasound examination indicated a large volume of plaque causing moderate stenoses in almost the full length of the proximal to middle RCA, 3 Cypher stents (2.5× 28 mm, 3.0×33 mm, 3.5×23 mm; Johnson & Johnson) were used from the distal to the ostium of the RCA. Adjunctive postdilatation was performed with 3.0 mm and 3.5 mm stent balloons. Thus, the 75% stenotic and total occlusion lesions were successfully dilated to 0%. There were not any immediate clinical or angiographic signs of complications throughout the procedure.Four hours after PCI, the patient complained of a mild chest pain which was augmented by deep breathing. However, his blood pressure, pulse pressure, and arterial oxygen saturation were maintained stable and ECG indicated no significant changes from his reference ECG before PCI. Thus, he was given non-s...

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“…However, even though active fixation leads cause more microtrauma than passive leads, why this presents a greater chance of causing an immune response in the atrium as opposed to the ventricle is unknown. Laboratory studies in two patients with PCIS following cardiac surgery documented low complement levels and the presence of immune complexes in the pleural fluid [15,16]. One patient had elevated antimyocardial antibody levels in both the serum and the pleural effusion [16].…”

Section: Resultsmentioning

confidence: 99%