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Nitroglycerin (NTG) and nifedipine (NIF) have the potential to augment coronary blood flow in addition to reducing peripheral determinants of myocardial oxygen demand as a synergistic protective mechanism during ischemia. To examine these effects, systemic and coronary hemodynamic responses were measured continuously before and during brief periods of myocardial ischemia induced by left anterior descending coronary balloon occlusion in 26 patients undergoing angioplasty (PTCA). Data were compared for two matched occlusion periods, one control and one "drug" occlusion. In 17 patients (NTG group), 200 micrograms of intracoronary NTG was given immediately before coronary occlusion. In nine patients (NIF group), 10 mg of sublingual NIF was given 15 minutes before the "drug" occlusion. NTG significantly but transiently reduced mean arterial pressure (91 +/- 11 to 82 +/- 15 mm Hg, p less than 0.05) and augmented basal coronary blood flow (95 +/- 38 to 127 +/- 54 ml/min, p less than 0.05) but did not alter great vein blood flow (59 +/- 29 vs 61 +/- 29 ml/min) or coronary occlusion pressure (25 +/- 7 to 24 +/- 7 mm Hg) during ischemia. NIF significantly reduced systolic, diastolic, and mean arterial pressure (119 +/- 21 to 95 +/- 8 mm Hg, p less than 0.001) and heart rate-pressure product from control. NIF maintained basal great vein blood flow (125 +/- 41 to 106 +/- 57 ml/min) during reduced myocardial oxygen demand, but did not affect great vein blood flow (73 +/- 29 to 79 +/- 37 ml/min) or coronary occlusion pressures during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

To assess whether pharmacologic coronary vasodilation could provoke new left ventricular wall motion abnormalities in patients with single vessel coronary artery disease, systemic hemodynamics, coronary blood flow velocity and left ventricular wall motion were measured by two-dimensional echocardiography during administration of 10 mg of intracoronary papaverine in 14 patients before and again immediately after left coronary angioplasty (group 1). As a comparison with an intravenous method, left ventricplar wall motion was analyzed after 0.56 mg/kg body weight of intravenous dipyridamole in a separate group of 13 patients with single vessel coronary disease (group 2). Heart rate-blood pressure product increased 3% to 6% in papaverine-treated patients and 14 ± 11% (p = NS) in dipyridamole-treated patients. No angiographic collateral vessels were present in either group. Although intracoronary mean flow velocity measured in the 14 group 1 patients and in 5 normal control subjects during papaverine treatment increased from 125% to 400% of basal flow velocity, papaverine induced new left ventricular wall motion abnormalities in only 5 of the 14 patients before coronary angioplasty. In three of five patients, left ventricular wall motion abnormalities persisted after successful coronary angioplasty. Four of the 14 patients demonstrated augmentation of left ventricular wall motion with papaverine. After intravenous dipyridamole, only 3 of the 13 group 2 patients developed new left ventricular regional asynergy. These data suggest that selective (papaverine) and, most likely, global (dipyridamole) augmentation of coronary flow alone does not reliably identify potential ischemic left ventricular regions affected by critical single vessel coronary artery disease.

An 81-year-old man with severe calcific aortic stenosis and coronary artery disease who refused surgical therapy was treated with sequential percutaneous balloon aortic valvuloplasty (PBAV) and percutaneous transluminal angioplasty. Before percutaneous balloon valvuloplasty, the mean aortic gradient was 76 mmHg, and the aortic valve area was .45 cm2. The aortic valve was dilated using 15-mm and 18-mm balloons. The mean gradient decreased to 40 mmHG, and the aortic valve area increased to .62 cm2. Percutaneous transluminal coronary angioplasty (PTCA) was performed 2 weeks later, and an 85% proximal left circumflex stenosis was successfully dilated to 20%. No complications were noted during either procedure. At 6-month follow-up, the patient had returned to normal activities and was asymptomatic. Thus, combined therapy with PBAV and PTCA is technically feasible in selected elderly patients with calcific aortic stenosis and anatomically suitable coronary artery disease. This nonsurgical therapeutic approach may be useful in the treatment of selected patients who refuse or who are deferred from cardiac surgery.

The acute hemodynamic effects of intravenous diltiazem were studied in 8 patients with coronary artery disease, left ventricular (LV) failure (New York Heart Association functional class III), a rest ejection fraction (EF) less than 40% or a cardiac index less than 2.4 liters/min/m2. Hemodynamic measurements and LV angiograms were performed at rest before and after the administration of diltiazem, 0.5 mg/kg, administered at a speed of 5 mg/min. Diltiazem treatment induced a decrease in heart rate from 68 +/- 12 to 55 +/- 9 beats/min (p less than 0.001). Mean aortic pressure decreased from 94 +/- 14 to 81 +/- 15 mmHg (p less than 0.05). Thus, the pressure-rate product significantly decreased under the influence of the drug, from 8,791 +/- 2,465 to 6,342 +/- 1,808 beats mm Hg/min, (p less than 0.001). Diltiazem induced no significant change of LV end-diastolic pressure, pulmonary wedge pressure, cardiac index and LV stroke work index. Systemic vascular resistance decreased (p less than 0.01), whereas pulmonary vascular resistance showed no change. End-systolic volume diminished (p less than 0.02), which accounts for the increase of stroke volume and ejection fraction (p less than 0.001). Disorders of regional contractility were not aggravated by diltiazem, and even improved in individual cases. Thus, intravenous diltiazem may be used safely in patients with heart failure. However, in view of the marked bradycardic effects seen in some cases, heart rate should be carefully monitored.

The LocalMed InfusaSleeve (IS) is a multi-lumen array with distal micro perforations designed to deliver agent at the site of angioplasty. Prior to the procedure, the IS is loaded onto a standard dilatation catheter (DC). Using standard technique, angioplasty is performed with the IS retracted. After lesion dilatation, the IS is tracked over the DC, aligning the micro perforation region of the IS with the balloon. The balloon is reinflated bringing the array into close proximity to the arterial wall. Agent(s) is delivered at specific pressures independent of balloon inflation. We have previously shown that agent delivery into the wall is dependent upon balloon inflation and drug delivery pressures. A pilot series was performed to evaluate the safety of heparin delivery via the IS. A total of 21 patients [emergent/urgent (2), elective cases (19)] with lesions at a variety of anatomic sites [LAD(10), LCx(3), ramus intermedius(1), RCA(6) and vein graft (1)] and complexity [ACC/AHA Lesion Type: A(8), B1(l0), B2(3)] were attempted. Following PTCA, heparin (1,000 U/ml) was delivered via the IS into the arterial lumen (balloon inflation pressure = 0.5 atm, drug delivery pressure = 40 psi). Failure to track the IS was noted in 2 cases. In 2 cases (RCA) a dissection was noted following agent infusion [NHLBI Type: A(1), B(1)]. The IS was used in conjunction with standard guide catheters [8 fr (15), 9 fr (6)], DC and guide wires. At discharge, no complications were noted. We Conclude 1) The IS can be used safely at a variety of anatomic sites, 2) The IS is compatible with standard PTCA equipment. 3) Local delivery of agent via LocalMed InfusaSleeve is a promising approach to reduce abrupt closure and restenosis.