CONTEXT AND OBJECTIVE: Arterial thrombosis may occur consequent to hereditary thrombophilia and increased lipoprotein(a) [Lp(a)] and fibrinogen. Our aim was to study the prevalence of common thrombophilia markers in 85 consecutive cases of arterial thrombosis. DESIGN AND SETTING: A retrospective study was conducted from 85 consecutive young patients treated as outpatients or admitted due to stroke or myocardial infarction at a tertiary care hospital. METHODS: Eighty-five Indian patients (age < 45 years) presenting ischemic stroke (n = 48) or myocardial infarction (n = 37) and 50 controls were studied for seven thrombophilia markers including antithrombin (AT), factor V, protein C, protein S, activated protein C resistance (APC-R), fibrinogen and Lp(a). Functional assays for protein C, protein S, factor V and APC-R were performed using clotting-based methods. Semi-quantitative estimation of fibrinogen was done using Clauss's method and Lp(a) using immunoturbidimetry. Statistical analysis was done using the Epi Info 6 software. RESULTS: Thirty-three samples (38.8%) tested positive for one or more thrombophilia markers. The three commonest abnormalities were elevated Lp(a) (20%), fibrinogen (17.6%) and low APC-R (14.2%). Low levels of protein C, protein S and AT were present in 4.7, 9.4 and 7% of the patients, respectively. Overall, the risk factor profile was: smoking (33%), positive family history (15.3%), hyperlipidemia (7%), hypertension, diabetes mellitus and obesity (2.3% each). CONCLUSIONS: An association was found between low levels of protein C, protein S and AT and arterial thrombosis, but only elevated fibrinogen levels, smoking, positive family history and hyperlipidemia showed statistical significance.

We report an 8-year-old child presenting with classical features of hypertrophic obstructive cardiomyopathy and Noonan syndrome with New York Heart Association (NYHA) class III symptoms. Due to progressively worsening symptoms, the child was taken up for percutaneous transluminal septal myocardial ablation, which was successfully performed. Postextrasystolic gradient fell down from 125 to 35 mm Hg. Other than postprocedure bifascicular block, no complications were encountered till 1 year of follow-up.

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Background: Definitive diagnosis of pulmonary artery hypertension (PH) requires an elevated mean pulmonary arterial pressure (MPAP) of 25 mmHg at rest measured by right heart catheterization (RHC). As it is invasive mode of investigation, it is declined by many patients, echocardiography was thought to be an acceptable substitute to assess pulmonary arterial pressures. Whether there is a correlation between these measurements is controversial. The aim of this study was to assess PH by echocardiography and its correlation with RHC.Methods: Twenty-six patients aged ≥18 years with pulmonary artery hypertension with or without tricuspid regurgitation (TR) were included in this cross-sectional study. All the patients underwent a transthoracic echocardiography evaluation and were taken for RHC study within an hour.Results: The correlation between pulmonary artery acceleration time (PAAT) and pulmonary artery systolic pressure (PASP) and PAAT and MPAP was significant in all degrees of PH. In contrast, correlation between TR jet maximum velocity (TR Vmax) derived estimated pulmonary artery systolic pressure (EPASP) and PASP was significant in moderate and severe PH, while it did not correlate in mild PH.Conclusions: PAAT is easily measurable parameter and strongly correlates with the values of PASP and the MPAP obtained by right heart catheterization. Implementation of a novel method of determining EPASP from PAAT shall increase significantly the number of patients in whom TTE can be used for the assessment of pulmonary hemodynamic non-invasively.

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