Pulmonary Artery and Pulmonic Valve Vegetations in a Young Pregnant Filipino with Patent Ductus Arteriosus.

BACKGROUND: Infective endocarditis (IE) involving the pulmonic valve and/or the pulmonary artery is rare. An unrepaired patent ductus arteriosus (PDA) is a risk factor for IE. A previous IE is also a risk factor that predisposes to IE recurrence. Discriminating between IE recurrence and a persistence of a vegetation from a previously treated IE can be difficult. We present the case of a 19-year-old primigravid with an unrepaired PDA and a history of IE treated 7 years prior, with positive blood cultures and vegetations on the pulmonic valve and pulmonary artery seen on transthoracic echocardiogram (TTE). METHODS AND RESULTS: On TTE, a small-sized PDA with a Qp : Qs of 1.18 and vegetations on the pulmonic valve and pulmonary artery were documented. Despite the paucity of symptoms, she was empirically treated as culture-negative IE and given 2 weeks of ceftriaxone. Repeat TTE done after 2 weeks only showed a slight decrease in the vegetation size. Due to the paucity of symptoms of infection, lack of growth of the vegetation, and absence of embolic events, the vegetations were deemed to be persistent remnants from the previous IE rather than a recurrent IE. She was advised surgical PDA closure and harvest of vegetations after delivery, but the patient did not consent. The rest of her perinatal course was uneventful. CONCLUSION: Persistence of vegetations despite successful medical treatment occurs in some cases and has not been reported to be associated with increased morbidity. Therefore, a follow-up of IE after treatment should be guided by the clinical course and response to therapy as well as the echocardiographic morphology of vegetations over time.

Systolic Anterior Motion of Mitral Valve Subchordal Apparatus: A Rare Echocardiographic Pattern in Non-Obstructive Hypertrophic Cardiomyopathy.

Systolic anterior motion (SAM) of the mitral valve or chordate is one characteristic seen in hypertrophic cardiomyopathy (HCM) either in obstructive or non-obstructive phenotypes. More often than not, the obstruction is caused by valvular rather than chordal SAM. We describe the role of echocardiography in identifying the actual anatomical location of the mitral valve apparatus involved in SAM and in assessing consequent left ventricular outflow tract (LVOT) obstruction in an otherwise asymptomatic patient. We report a case of a 29-year-old male admitted for an elective non-cardiac surgery, presenting with a cardiac murmur and left axis deviation with biventricular hypertrophy on electrocardiogram. On 2D transthoracic echocardiography (TTE), an asymmetrically hypertrophied left ventricle with systolic motion of anterior mitral valve was incidentally seen. Continuous wave Doppler assessment across the LVOT showed some gradient of obstruction (peak gradient: 9 mm Hg). Transesophageal echocardiography (TEE) demonstrated a redundant anterior mitral valve with the subchordal apparatus mainly causing SAM and confirmed the gradient obtained on TTE, with a mild degree, yet non-significant, degree of LVOT obstruction (mean gradient: 10 mm Hg) documented. Because of this finding, patient was cleared for surgery. Management was deemed conservative with emphasis on close surveillance for signs and symptoms attributable to development of significant LVOT obstruction in patients with HCM. To our knowledge, this is the first reported case in our country of an echocardiographic pattern of systolic anterior motion primarily of the subchordal mitral valve apparatus causing some, though non-significant, degree of LVOT obstruction in HCM. Echocardiographic features such as asymmetric left ventricular hypertrophy and presence of some LVOT obstruction caused primarily by subchordal apparatus could impact management in asymptomatic patients.

A Rare Case of Pneumopericardium in the Setting of Tuberculous Constrictive Pericarditis.

A 28-year-old Filipino male was admitted due to high-grade fevers and dyspnea on a background of chronic cough and weight loss. Due to clinical and echocardiographic signs of cardiac tamponade, emergency pericardiocentesis was performed on his first hospital day. Five days after, chest radiographs showed new pockets of radiolucency within the cardiac shadow, indicative of pneumopericardium. On repeat echo, air microbubbles admixed with loculated effusion were visualized in the anterior pericardial space. Constrictive physiology was also supported by a thickened pericardium, septal bounce, exaggerated respiratory variation in AV valve inflow, and IVC plethora. A chest CT scan confirmed the presence of an air-fluid level within the pericardial sac. The patient was started on a quadruple antituberculosis regimen and IV piperacillin-tazobactam to cover for superimposed acute bacterial pericarditis. Pericardiectomy was performed as definitive management, with stripped pericardium measuring 5-7 mm thick and caseous material extracted from the pericardial sac. Histopathology was consistent with tuberculosis. This report highlights pneumopericardium as a rare complication of pericardiocentesis. We focused on the utility of echocardiography for diagnosing and monitoring this condition on a background of tuberculous constrictive pericarditis, ultimately convincing us that pericardiectomy was necessary, instead of the usual conservative measures for pneumopericardium.