Recent evidence suggests that depression may be the most powerful predictor of cardiac events post-MI. The mechanism of enhanced cardiac events due to depression remains unclear. We speculate the post-MI depression and platelet activation may be casually related through serotonin or some other pathway. This interaction between depression and platelet activation may be also explain higher incidence of coronary disease in patients with depression. Serotonin-reuptake inhibitors besides being effective antidepressants also inhibit platelet serotonin re-uptake and may therefore have an inhibitory effect on platelet function. These drugs as well as psychological counseling may have an independent effect on catecholamine-mediated platelet activation. This would translate into decreased platelet aggregability and hence decreased cardiac events in depressed post-MI patients who are treated pharmacologically. Patients who have had AMI within 4 weeks and without exclusion criterion. The Co-Investigator will carry out structured baseline modified version of Hamilton Davis Depression Scale interview. Patients meeting the criterion of depression will be enrolled in this double blind randomized study. Baseline platelet function studies and plasma serotonin assays will be performed. Patients will be randomized in two groups: a) Psychiatric counseling + placebo b) psychiatric counseling + paxil 20 mg. At the end of 4 months, patients will be crossed over between placebo and treatment arms for another 4 months. Psychiatric counseling would be performed at 4 weekly intervals and platelet function studies and plasma serotonin essays will be repeated at 4 weeks and at 4 months in all patients after each randomization.