Platelet volume indices in patients with coronary artery disease and acute myocardial infarction: an Indian scenario.

AIMS: To study platelet volume indices (PVI) in the spectrum of ischaemic heart diseases. METHODS: A total of 210 cases were studied; 94 patients had unstable angina (UA) or acute myocardial infarction (AMI) diagnosed on the basis of history, characteristic electrocardiographic changes, and increased cardiac enzyme activities. Seventy patients had stable coronary artery disease (stable CAD) or were admitted for a coronary angiography or coronary artery bypass graft procedure. The third group comprised 30 age and sex matched healthy controls with no history of heart disease and a normal electrocardiogram. RESULTS: All PVI-mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (P-LCR)-were significantly raised in patients with AMI and UA (mean MPV, 10.43 (SD, 1.03) fL; mean PDW, 13.19 (SD, 2.34) fL; mean P-LCR, 29.4% (SD, 7.38%)) compared with those with stable CAD (mean MPV, 9.37 (SD, 0.99) fL; mean PDW, 11.35 (SD, 1.95) fL; mean P-LCR, 22.55% (SD, 6.65%)) and the control group (mean MPV, 9.2 (SD, 0.91) fL; mean PDW, 10.75 (SD, l.42) fL; mean P-LCR, 20.65% (SD, 6.14%)). CONCLUSIONS: Larger platelets are haemostatically more active and are a risk factor for developing coronary thrombosis, leading to myocardial infarction. Patients with larger platelets can easily be identified during routine haematological analysis and could possibly benefit from preventive treatment. Thus, PVI are an important, simple, effortless, and cost effective tool that should be used and explored extensively, especially in countries such as India, for predicting the possibility of impending acute events.

Comparison of action of beta-methyldigoxin and digoxin utilizing systolic time intervals.

The temporal course of orally and parenterally administered beta-methyldigoxin and orally administered digoxin was studied in a series of twenty patients who suffered from congestive heart failure due to a variety of causes. The parameters studied mainly were systolic time intervals. The incontrovertible conclusion was that beta-methyldigoxin acts almost immediately when administered intravenously and after 20 minutes when given by mouth. The peak action, however, by either route of administration was evident at the end of 45 minutes. Viewed in comparison, digoxin after oral administration acted after 2 hours, reaching its peak action after 8 hours. It must be admitted, however, that the magnitude of the response to both drugs, as measured by significant reduction in PEP/LVET ratio and increase in ejection fraction, was the same. Our study suggests that beta-methyldigoxin is as effective an inotropic agent as digoxin, with an additional characteristic of total and rapid gastrointestinal absorption, predictable and rapid onset and much shorter time interval for its peak action.