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Due to changing characteristics of infective endocarditis in the past two decades, we, retrospectively analysed 28 cases of infective endocarditis in children of age less than 15 years at Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar from December, 1983 to November, 1993. The incidence of disease was observed as 1.5 cases/1000 children admitted with a M:F ratio of 2:1. Three patients were of age less than 2 years (group I) as 25 were above 2 years of age (group II). The two groups had significant difference in portal of entry of infection, infective microorganisms, echocardiography and prognosis. Congenital heart disease was the commonest underlying cardiac lesion in 24 (85.71%) patients. Portal of entry of infection was apparent in 35.71% only; dental route being more frequent in group II. Streptococcus viridans (in 9 cases) followed by staphylococcus aureus (in 4 cases) were the two common organisms isolated. Patients were treated, for a period of 4-6 weeks with a over all mortality rate of 25%. Factors associated with poor prognosis were age < 2 years, staphylococcal infection ad negative blood cultures. Heart failure resistant to medical therapy was a leading cause of death.

Microalbuminuria can be present in 25–100% of patients with essential hypertension and is associated with increased incidence of cardiovascular events. Our goal was to evaluate the effect of a commonly used calcium channel blocker, amlodipine, and an angiotensin converting enzyme inhibitor, lisinopril on urinary albumin excretion in patients with mild to moderate essential hypertension. We screened 324 patients with essential hypertension for microalbuminuria and documented it in 120 patients. These 120 patients with microalbuminuria were randomly divided into two groups of 60 each, matched for age, sex, arterial pressure, creatinine clearance, and urinary albumin excretion so as to receive amlodipine or lisinopril. We prospectively measured their urinary albumin excretion and creatinine clearance prior to treatment and, four and eight weeks after treatment with amlodipine or lisinopril. Mean arterial pressure (mean ± SD) at baseline, after four weeks, and after eight weeks was 113.01 ± 4.38,104.93 ± 3.12, and 98.89 ± 1.75 mmHg (P < 0.0000); and 114.13 ± 7.11, 106.52 ± 3.50, and 100.89 ± 2.80 mmHg (P < 0.0000) in amlodipine and lisinopril groups, respectively. Urinary albumin excretion (mean ± SEM) at baseline, after four, and after eight weeks was 79.30 ± 3.74, 62.03 ± 3.61, and 52.02 ± 3.05 (P < 0.0000); and 73.96 ± 4.10, 72.39 ± 3.74, 66.12 ± 3.94 (P = 0.1742) in lisinopril and amlodipine groups, respectively. Lisinopril but not amlodipine, reduced the urinary albumin excretion significantly despite their similar antihypertensive efficacy. The clinical and prognostic significance of these observations need to be established.

An elevated hepatic venous pressure gradient (HVPG) has been associated with risk of variceal bleeding, and outcome and survival after variceal bleeding. In this pilot study, we measured HVPG in 40 patients with liver cirrhosis and studied its relationship with etiology of liver disease, esophageal variceal size, history of variceal bleeding or ascites, biochemical liver tests and Child-Pugh class. There was no procedurerelated complication. The mean (SD) HVPG was similar in patients who had history of variceal bleeding as compared to those who did not (15.4 [2.8] mmHg vs. 13.9 [2.7] mmHg, p=0.1); HVPG had no significant association with etiology of cirrhosis (p=0.4). HVPG levels were significantly higher in patients with larger esophageal varices (grade III/IV vs. I/II: 15.2 [2.7] mmHg vs.13.1 [2.8] mmHg, p=0.04), poorer Child-Pugh class (B or C versus A), and presence of ascites (p=0.04). Thus, HVPG correlated with variceal size, Child-Pugh class, and presence of ascites, but not with variceal bleeding status.

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