A rare case of improved diastolic function following subxiphoid pericardiostomy for cardiac tamponade in a hypertensive patient with dressler's syndrome and non-tuberculous hemorrhagic effusive pericarditis.

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Title: A rare case of improved diastolic function following subxiphoid pericardiostomy for cardiac tamponade in a hypertensive patient with dressler's syndrome and non-tuberculous hemorrhagic effusive pericarditis.
Alternate Title: Un caso raro de mejoría de la función diastólica tras una pericardiostomía subxifoidea por taponamiento cardíaco en un paciente hipertenso con síndrome de Dressler y pericarditis hemorrágica efusiva no tuberculosa.
Authors: Grecia, Valerie1 valeriegrecia20@gmail.com, Pranata, Citoporta2 citoportapr@gmail.com, Putranto, Johanes Nugroho Eko3 nugicardio1@yahoo.com, Winarno, Dhihintia Jiwangga Suta4 dhihintiaji@gmail.com
Source: Revista Latinoamericana de Hipertensión. 2026, Vol. 21 Issue 3, p179-185. 7p.
Subjects: CARDIAC tamponade, PERICARDIUM surgery, PERICARDITIS, PERICARDIAL effusion, HYPERTENSION, STAPHYLOCOCCUS aureus infections
Abstract (English): This case report describes a 54-year-old hypertensive man with minor coronary artery disease (CAD; 30% stenosis in mid-LAD and RCA, managed medically with clopidogrel) and a recent history of non-tuberculous (Staphylococcus aureus) pneumonia who developed massive hemorrhagic effusive pericarditis (HEP) leading to cardiac tamponade. Hypertension, a major global cardiovascular risk factor, likely contributed to the underlying vascular and inflammatory milieu that predisposed the patient to this rare complication. Transthoracic echocardiography demonstrated a massive circumferential pericardial effusion (>20 mm diastolic separation) with tamponade physiology, including severely reduced left ventricular end-diastolic volume (LVEDV 52 mL, below the normal male reference range of 53--156 mL). Emergency subxiphoid pericardiostomy evacuated approximately 2000 mL of grossly hemorrhagic fluid, resulting in immediate hemodynamic stabilization. Post-procedure echocardiography confirmed complete effusion resolution and a significant 28.8% increase in LVEDV to 67 mL, documenting restoration of diastolic filling and normalization of previously impaired (restrictive-pattern) diastolic function. Pericardial fluid analysis revealed an exudative process (positive Rivalta test, protein 6.35 g/dL, LDH 1426 U/L, borderline ADA 26 U/L) with no bacterial growth on culture. Cytology and histopathology showed chronic inflammatory changes (dense lymphoplasmacytic infiltration) without malignancy. The patient improved clinically over an 11-day hospitalization and was discharged in stable condition. This rare presentation of cardiac tamponade secondary to HEP likely reflects overlapping mechanisms: autoimmune response consistent with Dressler's syndrome (post-injury pericarditis following minor CAD, occurring -4 weeks post-ischemic insult) and pericardial involvement from recent non-tuberculous pneumonia, exacerbated by antiplatelet therapy and the hypertensive state. The case underscores the reversibility of tamponade-induced diastolic dysfunction with prompt surgical drainage and highlights the need for advanced imaging (cardiac CT and MRI) to clarify etiology, monitor for recurrence (including constrictive pericarditis), and prevent future morbidity. [ABSTRACT FROM AUTHOR]
Abstract (Spanish): Este caso clínico describe a un hombre hipertenso de 54 años con enfermedad coronaria menor (EAC; estenosis del 30% en la arteria coronaria izquierda media y la arteria coronaria derecha, tratada médicamente con clopidogrel) y antecedentes recientes de neumonía no tuberculosa (Staphylococcus aureus), quien desarrolló una pericarditis hemorrágica efusiva masiva (PEH) que resultó en taponamiento cardíaco. La hipertensión, un importante factor de riesgo cardiovascular global, probablemente contribuyó al entorno vascular e inflamatorio subyacente que predispuso al paciente a esta rara complicación. La ecocardiografía transtorácica demostró un derrame pericárdico circunferencial masivo (separación diastólica >20 mm) con fisiología de taponamiento, incluyendo un volumen telediastólico del ventrículo izquierdo severamente reducido (VTDVI 52 mL, por debajo del rango de referencia normal masculino de 53-156 mL). La pericardiostomía subxifoidea de emergencia evacuó aproximadamente 2000 mL de líquido macrohemorrágico, resultando en una estabilización hemodinámica inmediata. La ecocardiografía posprocedimiento confirmó la resolución completa del derrame y un aumento significativo del 28,8% en el VTDVI a 67 mL, documentando la restauración del llenado diastólico y la normalización de la función diastólica previamente deteriorada (patrón restrictivo). El análisis del líquido pericárdico reveló un proceso exudativo (prueba de Rivalta positiva, proteína 6,35 g/dL, LDH 1426 U/L, ADA limítrofe 26 U/L) sin crecimiento bacteriano en el cultivo. La citología y la histopatología mostraron cambios inflamatorios crónicos (densa infiltración linfoplasmocitaria) sin malignidad. El paciente mejoró clínicamente tras 11 días de hospitalización y fue dado de alta en condición estable. Esta rara presentación de taponamiento cardíaco secundario a una EH probablemente refleja mecanismos superpuestos: una respuesta autoinmune compatible con el síndrome de Dressler (pericarditis postraumática tras una EAC leve, que se presentó aproximadamente 4 semanas después de la lesión isquémica) y afectación pericárdica por una neumonía no tuberculosa reciente, exacerbada por el tratamiento antiplaquetario y el estado hipertensivo. El caso subraya la reversibilidad de la disfunción diastólica inducida por taponamiento con drenaje quirúrgico inmediato y destaca la necesidad de imágenes avanzadas (TC cardíaca y RMN) para esclarecer la etiología, monitorizar la recurrencia (incluida la pericarditis constrictiva) y prevenir la morbilidad futura. [ABSTRACT FROM AUTHOR]
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Database: MedicLatina
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Abstract:This case report describes a 54-year-old hypertensive man with minor coronary artery disease (CAD; 30% stenosis in mid-LAD and RCA, managed medically with clopidogrel) and a recent history of non-tuberculous (Staphylococcus aureus) pneumonia who developed massive hemorrhagic effusive pericarditis (HEP) leading to cardiac tamponade. Hypertension, a major global cardiovascular risk factor, likely contributed to the underlying vascular and inflammatory milieu that predisposed the patient to this rare complication. Transthoracic echocardiography demonstrated a massive circumferential pericardial effusion (>20 mm diastolic separation) with tamponade physiology, including severely reduced left ventricular end-diastolic volume (LVEDV 52 mL, below the normal male reference range of 53--156 mL). Emergency subxiphoid pericardiostomy evacuated approximately 2000 mL of grossly hemorrhagic fluid, resulting in immediate hemodynamic stabilization. Post-procedure echocardiography confirmed complete effusion resolution and a significant 28.8% increase in LVEDV to 67 mL, documenting restoration of diastolic filling and normalization of previously impaired (restrictive-pattern) diastolic function. Pericardial fluid analysis revealed an exudative process (positive Rivalta test, protein 6.35 g/dL, LDH 1426 U/L, borderline ADA 26 U/L) with no bacterial growth on culture. Cytology and histopathology showed chronic inflammatory changes (dense lymphoplasmacytic infiltration) without malignancy. The patient improved clinically over an 11-day hospitalization and was discharged in stable condition. This rare presentation of cardiac tamponade secondary to HEP likely reflects overlapping mechanisms: autoimmune response consistent with Dressler's syndrome (post-injury pericarditis following minor CAD, occurring -4 weeks post-ischemic insult) and pericardial involvement from recent non-tuberculous pneumonia, exacerbated by antiplatelet therapy and the hypertensive state. The case underscores the reversibility of tamponade-induced diastolic dysfunction with prompt surgical drainage and highlights the need for advanced imaging (cardiac CT and MRI) to clarify etiology, monitor for recurrence (including constrictive pericarditis), and prevent future morbidity. [ABSTRACT FROM AUTHOR]
ISSN:18564550
DOI:10.5281/zenodo.19643237