Cough is a common side effect of angiotensin converting enzyme inhibitor (ACEi) therapy. The incidence of ACEi-induced cough has been shown to correlate with genetic variation among different populations. This study aimed to determine the association of candidate genetic polymorphisms with ACEi-induced cough among Filipinos. Two hundred twenty (220) participants on ACEi therapy pressure-lowering in an unmatched case-control study (82 cases with ACEi-induced cough and 138 controls). Genomic DNA samples were extracted and genotyped for selected genetic variants. The association of genetic variants and clinical factors with ACEi-induced cough was determined using regression analyses. Univariate logistic regression showed that the BAG6 variant rs805303 is nominally associated with ACEi-induced cough among Filipinos, at a per-comparison error rate (PCER) of 0.05 (OR 2.10, p = 0.016). The association of the variant with ACEi cough was statistically significant after multiple regression analysis (adjusted OR 2.09, p = 0.022) while adjusting for confounding clinical factors (sex, alcohol intake, and diastolic blood pressure). Further studies are needed to validate these findings.
We report a case of a man aged 65 years presenting with chronic cough, haemoptysis and intermittent atrial tachyarrhythmias on ECG. On 2D transthoracic echocardiography, an incidental left atrial mass was seen, initially thought to be a thrombus predisposed by intermittent atrial fibrillation. Transoesophageal echocardiography confirmed that this left atrial mass originated from a fixed, non-homogenous, right superior pulmonary vein mass with an extracardiac extension. Because of this finding, a thorough search for a primary focus lead to the discovery of a contiguous posterior mediastinal mass, which was a round cell neoplasm on histology. Management was deemed palliative. Although rare, left-sided cardiac masses should prompt the physician to search for a malignancy in the lung in high-risk patients, as haematogenous spread via the pulmonary vein is a potential mechanism for spread.
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 (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.
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