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To assess the results of a conservative coronary angioplasty strategy in unstable angina pectoris, the records of 1,421 consecutive patients without previous myocardial infarction undergoing a first percutaneous transluminal coronary angioplasty (PTCA) between 1986 and 1990 were reviewed. Of these patients, 631 had unstable and 790 had stable angina pectoris. Only after an intense effort to medically control symptoms, the unstable patients underwent PTCA at an average of 15.4 days (range 1 to 76) after hospital admission. Primary clinical success was achieved in 91.7% of patients with unstable and in 94.4% of those with stable angina pectoris (p = not significant). In-hospital mortality rates were 0.3 and 0.1%, respectively (p = not significant). Nonfatal in-hospital event rates for acute myocardial infarction, cerebrovascular accident and coronary bypass surgery were only slightly higher in patients with unstable angina pectoris; however, the difference from the stable group was significant when all events were combined (9 vs S.9%; p

To analyze the effect of the calcium antagonist diltiazem on coronary hemodynamics, epicardial coronary artery diameter, coronary blood flow and coronary blood flow velocity were assessed at baseline and after a 0.5 mg intracoronary bolus of diltiazem in nonstenotic coronary arteries of awake humans. Patients (n = 20) were first randomized to pretreatment with either placebo (n = 10) or isosorbide dinitrate (0.5 [Micro]g/kg/min infusion; n = 10), and coronary flow reserve was measured before and after administration of diltiazem. There were significant increases in epicardial coronary artery diameter (10%; p = 0.0001) and coronary blood flow (30%; p = 0.0001) in all patients after administration of diltiazem. Whereas basal coronary blood flow velocity increased only slightly (7%; p = not significant), there was a significant decrease in coronary flow reserve (10%; p = 0.004). Increases in coronary diameter and blood flow after diltiazem were comparable in patients pretreated with placebo or nitrates. However, the decrease in coronary flow reserve was significant only in patients pretreated with placebo (19%; p = 0.0008). This reduction in coronary flow reserve could be due to 'raising the floor' (increased baseline coronary blood flow) or 'lowering the ceiling' (reduction of maximal coronary blood flow). (Am J Cardiol 1991;68:1633-1637)

The safety of the combination of heparin and ridogrel therapy and its antiplatelet efficacy was examined in the setting of percutaneous transluminal coronary angioplasty (PTCA). In 32 patients without known aspirin intake for 10 days before PTCA, therapy with ridogrel (300-mg intravenous bolus) was begun just before PTCA and continued orally at a dose of 300 mg twice daily until discharge. Heparin was administered as a 10,000 IU bolus dose before PTCA and followed by an intravenous infusion at a rate of 1,000 IU/hour for 24 hours. Bleeding problems at the arterialentry site occurred in 13 patients, which required a blood transfusion in only 2 patients. One patient underwent emergency bypass surgery without specific problems of hemostasis. Ridogrel virtually eliminated thromboxane [B.sub.2] from the serum (29,2900 [+ or -] 6,555 pg/0.1 ml before vs 63 [+ or -] pg/0.1 ml at 2 hours after ridogrel), with a concomitant increase in serum 6-keto-prostaglandin [F.sub.1[alpha]] (511 [+ or -] 34 pg/0.1 ml before vs 1,190 [+ or -] 146 pg/0.1 ml at 24 hours after ridogrel). There were no acute reocclusions in the ridogrel-treated patients, whereas acute reocclusions occurred in 5.6% of the patients taking the standard aspirin + heparin regimen during the same period. Furthermore, at 6-month clinical follow-up patients treated with ridogrel compared favorably with those receiving standard treatment. (Am J Cardiol 1991;68:463-466), Percutaneous transluminal coronary angioplasty (PTCA) is a technique used to dilate (widen) the coronary arteries, which supply blood to the heart. PTCA is used in the treatment of conditions such as atherosclerosis, in which cholesterol-rich deposits narrow the coronary arteries, diminishing the cardiac blood supply. While this therapy is quite effective, 2 to 11 percent of patients undergoing PTCA suffer reocclusion shortly after the procedure. One strategy for preventing reocclusion after PTCA has been the administration of drugs that prevent adhesion of blood platelets to the arterial wall (the precipitating factor in initiating reocclusion); however, the drugs currently available are not completely effective. A newly available drug, ridogrel, has been proposed as a more effective antiplatelet drug for use in this setting. This agent acts by inhibiting key enzymes involved in the platelet-initiated clotting process. To evaluate the utility and safety of ridogrel, a study involving 32 eligible patients (of 352 potential enrollees) referred for PTCA were administered either ridogrel and heparin or aspirin and heparin immediately after PTCA. (Aspirin and heparin are anticlotting medications.) Biochemical measurements indicated that ridogrel virtually eliminated blood levels of the enzymes on which it works. None of the patients treated with ridogrel suffered reocclusion after PTCA; 5.6 percent of the aspirin and heparin-treated patients did. At six-month follow-up, both groups of patients showed similar (low) levels of disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

To investigate the antiischemic efficacy of intravenously administered diltiazem, 42 patients were randomlY allocated to receive placebo or active treatment before 1-vessel percutaneous transluminal coronary angioplasty (PTCA). The development of myocardial ischemia was studied using subjective (pain) and objective electrocardiography) parameters. Pretreatment with intravenous diltiazem resulted in a significantly delayed onset of ischemic pain and ST-segment elevation; these variables also returned to baseline earlier after balloon deflation. Thus, intravenous diltiazem prevents or delays the onset of myocardial ischemia during repetitive transient coronary occlusions; improvement of the myocardial blood flow distal to the coronary occlusion or impedance of calcium entry into the ischemic cell are considered as possible mechanisms. Because PTCA is increasingly used in patients with poor left ventricular function and more extensive disease, and because recent evidence suggests that better PTCA results could be obtained by the use of longer inflation times, the addition of diltiazem to the classic armamentarium could be beneficial. (Am J Cardiol 1989;64:1103-1107), Percutaneous transluminal coronary angioplasty (PTCA) is a procedure for treating narrowed coronary arteries, which are the major blood vessels that bring blood to the heart. A catheter or tube-like structure with a small inflatable balloon is inserted into the narrowed portion of the artery, and the balloon is inflated, thereby mechanically dilating the narrowed coronary artery. In PTCA, inflation of the balloon causes transient occlusion, or blockage, of the coronary artery. This leads to regional ischemia, or insufficient blood flow to specific portions of the heart. Medications can be given before PTCA to reduce or prevent regional ischemia. The anti-ischemic effect of the drug diltiazem was assessed in 42 patients who were scheduled to undergo PTCA; half the patients received pretreatment with diltiazem while the other half received an inert placebo. During the PTCA procedure, chest pain and changes in the electrocardiogram, a recording of the electrical activity of the heart, were used as indicators of ischemia. Pretreatment with diltiazem delayed the onset of pain and ECG changes associated with ischemia, and both of these indicators returned to normal after deflation of the balloon more quickly with diltiazem than without. The results show that intravenous diltiazem delays the onset of myocardial ischemia during repetitive and brief blockage of the coronary arteries. Diltiazem may exert its effects by improving blood flow beyond the blocked portion of the coronary artery, or by blocking the entry of calcium into the ischemic cell; diltiazem is a calcium blocking agent. Thus, diltiazem may be a useful medication for delaying the onset of ischemia in patients undergoing PTCA; it may be particularly helpful if longer balloon inflation periods (which may prove to be more effective than briefer periods) are utilized in the future. (Consumer Summary produced by Reliance Medical Information, Inc.)