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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.

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Twenty-five symptomatic patients of chronic heart failure were subjected to spirometry to detect abnormalities of pulmonary function and to assess the effect of ipratropium bromide in reversing or minimising these abnormalities. All the patients exhibited abnormal pulmonary function manifesting as obstructive (15/25) or restrictive (10/25) ventilatory defect. There was overall improvement in lung functions with ipratropium bromide especially in those with obstructive ventilatory defects and mostly comprised of smokers. Forced expiratory volume in one second increased by 47.7 percent (p < 0.02), forced expiratory volume in one second/forced vital capacity ratio by 14.1 percent (p < 0.001) and maximal voluntary ventilation by 40.6 percent (p < 0.05) in these patients. It is concluded that ipratropium bromide can prove as a promising adjunctive therapeutic intervention in improving quality of life in patients of chronic congestive heart failure who are incapacitated by dyspnoea and have clearly documented ventilatory defects.

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Inflammatory response in the atherosclerotic lesions of coronary artery disease, mediated by cellular immune mechanisms is well appreciated. The significance of the immuno-inflammatory processes for the development of acute ischaemic sequelae of these lesions remains unsettled. Fifty patients of acute coronary syndromes were studied for complement components and immunoglobin levels by single radial immunodiffusion method. Twenty-eight patients of acute myocardial infarction showed significantly lower levels of complement components C3 and C4 at admission (C3--69.19 +/- 12.91 mg% compared to 82.40 +/- 9.26 mg% in controls, p < 0.01; C4--14.56 +/- 2.46 mg% compared to 18.53 +/- 2.69 mg% in controls, p < 0.01). Twenty-two patients of unstable angina did not show any significant change (C3--83.14 +/- 8.01 mg% and C4--19.07 +/- 4.47 mg%). Sixteen patients of acute myocardial infarction who were thrombolysed with streptokinase showed a steep rise in the levels of complement components immediately after thrombolysis (C3--69.19 +/- 12.91 mg% before and 100.56 +/- 17.09 mg% after thrombolysis, p < 0.001; C4--14.56 +/- 2.46 mg% before and 21.48 +/- 4.78 mg% after thrombolysis, p < 0.001). Plasma C3 and C4 levels in acute myocardial infarction showed no relationship with peak CPK levels. Plasma immunoglobulins remained unchanged in patients of acute coronary syndromes.

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OBJECTIVE: To evaluate the association of silent myocardial ischemia (SMI) with cardiac autonomic neuropathy in asymptomatic diabetic patients. MATERIAL AND METHODS: Two hundred asymptomatic patients of diabetes mellitus were assessed for evidence of cardiac autonomic neuropathy. Of these, 30 (15 males, 15 females; mean age 44.7 +/- 8.8 years) were found to have cardiac autonomic neuropathy. Thirty (30) age and sex matched diabetic patients (mean age 42.4 +/- 7.6 years) who had no evidence autonomic neuropathy were included in the study as control group. Both the groups of patients were evaluated for SMI by 24 hour ambulatory electrocardiographic (ECG) monitoring. RESULTS: Incidence of SMI was significantly higher in patients with autonomic neuropathy 12/30 (40%) compared to those without 3/30 (10%) p < 0.001. Duration of diabetes was more (13 +/- 1.59 years) in patients with autonomic neuropathy compared to the control group (8.66 +/- 1.55 years) p < 0.001. Serum cholesterol and triglyceride levels were significantly higher in patients with autonomic neuropathy in comparison to control group < 0.05 and < 0.01, respectively. There was no difference in the pattern of SMI in the two groups (p = N.S). CONCLUSION: Cardiac autonomic neuropathy predisposes patients with diabetes mellitus to SMI. Twenty four hour ambulatory ECG monitoring provides useful diagnostic information in early detection and evaluation of SMI in asymptomatic diabetic patients.

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Four hundred and sixty-six patients (277 males, 189 females; mean age 23.2 years) diagnosed as cases of infective endocarditis during the past 15 years were retrospectively analysed. Two-thirds of patients belonged to the 15 to 35 years age group. The most common predisposing cardiac lesion was rheumatic heart disease seen in 73.4 percent patients. Mitral valve prolapse and right-sided endocarditis were infrequent, seen in four patients each. Blood culture positivity was 28.7 percent in adults and 61 percent in children. Commonest organism isolated was staphylococcus aureus in adults (39.3%) and streptococcus viridans in children (48%). Salmonella typhi was detected in 17 patients and showed excellent response to ciprofloxacin and gentamycin. Overall mortality was 13.9 percent and resistant heart failure was the leading cause of death. Our study presents the clinical spectrum of infective endocarditis and highlights the comparison with western studies.

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The incidence, clinical disease and outcome of acute pancreatitis caused by ascariasis in an endemic area of Kashmir, India, was studied prospectively. Ascariasis was an aetiological factor in 59 of 256 patients (23.0 per cent) with acute pancreatitis. Worms had invaded the bile duct in 51 patients, the pancreatic duct in four and both ducts in four. Pancreatitis was mild in 46 patients and severe in 13. Associated pyogenic cholangitis was present in eight. Acute complications occurred in 11 patients. Endoscopic retrograde cholangiopancreatography (ERCP) was performed in all cases within 72 h of admission and delineated ascarides in the duodenum invading the ampullary orifice (44 patients), in the bile duct (55) and in the pancreatic duct (eight). At ERCP, worms were extracted from the ampullary orifice and removed via the mouth of 33 patients with intractable epigastric pain, leading to rapid relief of symptoms. The eight patients with pyogenic cholangitis underwent endoscopic nasobiliary drainage to decompress the bile ducts; worms were extracted from the bile duct of three of these patients using a Dormia basket. A total of 56 patients recovered from acute illness with a combination of conservative and endoscopic treatment; the other three required emergency surgery. At a mean(s.d.) follow-up of 19(7) months, ten patients showed symptomatic worm reinvasion of the biliary tree. The overall mortality rate was 3 per cent.

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Sonographic and cholangiographic appearances of confirmed intrabiliary rupture of a hepatic hydatid cyst were studied in 15 cases. Sonographic findings included liver cyst in all cases; nonshadowing echogenic structures in the dilated biliary tree representing hydatid material, such as fragmented membranes, sand, matrix, and daughter vesicles, in eight cases; and loss of continuity of the cyst wall adjacent to the bile duct representing the site of communication in seven cases. Cholangiographic findings were as follows: filling defects of varying size and shapes in the dilated biliary tree in 13 cases, and changing shape and position of these filling defects in three of them; and leakage of contrast medium into the cyst cavity in 12 cases. Intrabiliary rupture of hepatic hydatid cyst was suggested by sonography in 10 cases (66.7%) and at cholangiography in 13 cases (86.6%). We conclude that a joint application of sonography and endoscopic cholangiography is mandatory for proper preoperative evaluation of this disorder.

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