It is time to wash the linen.

The unethical practice of commissions in private healthcare requires an open debate since it leads to expensive and hazardous healthcare. Doctors are accused of being sales agents and law breakers, private hospitals resemble luxury hotels, the consumer has become fair game whenever he/she has money, and our profession and society are rendered insensitive to human suffering. At the root of this malaise is the unplanned promotion of healthcare as a free market product. This very complex product, which is required in times of stress and vulnerability, has been institutionalized as a business for profiteering in the absence of adequate checks and balances. The product is inherently unsuited for the free market because the consumer cannot be king unless he is empowered to choose wisely. Not enough has been done to address this deficiency. Efforts are required to strengthen non-profit health facilities; to make the consumer wise and minimize her/his exposure to doctored health information. The present unethical practices of our profession are not the fault of doctors or the Medical Council of India, and punitive measures would be inappropriate. We should start with the creation of a government health website which educates the public about modern healthcare, and by regulating advertisement of health products. Since health personnel, officials and news media are directly benefited by the present malpractices, corrective will require consumer participation.

Adverse interactions of rofecoxib with lisinopril in spontaneously hypertensive rats.

BACKGROUND: Hypertension and arthritis are frequent comorbidities. Nonsteroidal anti-inflammatory drugs (NSAIDs) are well known to produce hypertension or attenuate the effects of antihypertensive agents in a few patients. The influence of selective NSAIDs on blood pressure and the cardiovascular and renal effects of coxibs have still to be investigated. The purpose of this study was to test the hypothesis that rofecoxib interferes with antihypertensive activity and cardiorenal protective effects of lisinopril in spontaneously hypertensive rats (SHRs). METHODS: Twenty-one unanaesthetised, male spontaneously hypertensive rats (SHRs), 16 weeks old, were randomized to receive lisinopril (LS) 15 mg/kg/d or rofecoxib (RF) 20 mg/kg/d or combination of lisinopril (LS) and rofecoxib (RF) for 2 weeks. The arterial blood pressure changes were recorded each week. The Sodium Hydrogen Exchange (NHE) activity of erythrocytes was determined 2 weeks after the study. The surviving animals were sacrificed 24 h after the last dose, and the sections of their hearts and kidneys were assessed histologically for injury by a pathologist masked to the treatment. RESULTS: RF completely prevented the hypotensive effects of LS during the first week of treatment but the antihypertensive efficacy of LS was restored during the second week of treatment. The NHE in erythrocytes of 18-week-old SHRs was found to be significantly lower than the age-matched Wistar rats (P < 0.05), and LS treatment reversed these values to Wistar control in SHRs. RF was devoid of any effect on NHE of erythrocytes. The histological examination revealed that the myocardial and renal protection induced by LS was attenuated by concomitant RF therapy. CONCLUSIONS: These results indicate that COX-2 inhibitors should be used judiciously in patients with history of hypertension, ischemic heart disease, or chronic renal failure.

Platelet glycoprotein IIb/IIIa inhibition using eptifibatide with primary coronary stenting for acute myocardial infarction: a 30-day follow-up study.

The results of primary coronary stenting for acute myocardial infarction (AMI) have been reported to improve significantly with the concomitant administration of platelet glycoprotein IIb/IIIa inhibitor abciximab. There are, however, no data available with the use of eptifibatide, a more cost-effective, small-molecule GP IIb/IIIa blocker with a shorter half-life. In a prospective multicenter feasibility and efficacy study, we assigned 55 consecutive patients with AMI being taken up for primary stenting to receive eptifibatide just before the procedure (two boluses of 180 microg/kg 10 min apart and a 24-hr infusion of 2 microg/kg/min). Clinical outcomes were evaluated at 30 days after the procedure. The angiographic patency of the vessel with TIMI flow rates, TIMI myocardial perfusion (TMP) grade, and corrected TIMI frame counts were assessed at the end of procedure and before hospital discharge. At 30 days, the primary endpoint, a composite of death, myocardial infarction, and urgent target vessel revascularization (TVR) was seen in 12.7% of patients. The TIMI 3 and TMP grade 3 flow, which was seen in 93% and 86% of patient, respectively, at the end of the procedure, declined to 86% and 78%, respectively (P < 0.05) before hospital discharge. Corrected TIMI frame counts also decreased from 25.7 +/- 7.2 to 22.9 +/- 6.8 (P < 0.05). There were five (9.1%) instances of subacute thrombosis (SAT) presenting as AMI, needing urgent TVR in all, within 3-5 days of the primary procedure. No excessive bleeding complication, directly attributable to the use of eptifibatide, was observed. The study was terminated prematurely because of an unacceptable SAT rate. Administration of eptifibatide along with primary stenting for AMI is associated with a high TIMI 3 and TMP grade 3 flow acutely. However, these flows decline significantly before hospital discharge and lead to a high rate of SAT. The dosage and duration of infusion of eptifibatide in this setting needs further evaluation.