Primary angioplasty for the treatment of acute myocardial infarction: experience at two community hospitals without cardiac surgery.

OBJECTIVES: We sought to establish the safety and efficacy of primary percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction (AMI) at two community hospitals without on-site cardiac surgery. BACKGROUND: Though randomized studies indicate that primary angioplasty in AMI may result in superior outcomes compared with fibrinolytic therapy, the performance of primary angioplasty at hospitals without cardiac surgery is debated. METHODS: Three experienced operators performed 506 consecutive immediate coronary angiograms with primary angioplasty when appropriate in patients with suspected AMI at two community hospitals without cardiac surgery, following established rigorous program criteria. RESULTS: Clinical high risk predictors (Killip class 3 or 4, age > or = 75 years, anterior AMI, out-of-hospital ventricular fibrillation) and/or angiographic high risk predictors (left main or three-vessel disease or ejection fraction <45%) were present in 69.6%. Angioplasty was performed in 66.2%, with a median time from emergency department presentation to first angiogram of 94 min and a procedural success rate of 94.3%. The in-hospital mortality for the entire study population was 5.3%. Of those without initial cardiogenic shock, the in-hospital mortality was 3.0%. Of 300 patients who were discharged after primary angioplasty, only four died within the first 6 months, with 97.7% follow-up. No patient died or needed emergent aortocoronary bypass surgery because of new myocardial jeopardy caused by a complication of the cardiac catheterization or angioplasty procedure. CONCLUSIONS: Immediate coronary angiography with primary angioplasty when appropriate in patients with AMI can be performed safely and effectively in community hospitals without on-site cardiac surgery when rigorous program criteria are established.

Details of coronary stenosis morphology influence its hemodynamic severity and distal flow reserve.

Differences in coronary flow reserve with anatomically similar coronary artery stenoses have been attributed to 1) nonstandard physiologic conditions, 2) inadequacies of measurements of coronary artery stenosis dimension and/or coronary blood flow, and 3) inadequate hyperemic stimulus. Our study tested the hypothesis that details of coronary artery stenosis geometry, which may or may not be apparent on coronary angiograms, also may contribute importantly to such differences. A simple and complex coronary artery stenosis, each of which reduced vessel cross-sectional area by 84%, was introduced in random order into the left anterior descending coronary artery of nine closed-chest, sedated swine. The simple stenosis had a single lumen while the complex stenosis had five small lumena whose combined area equaled that of the single lumen stenosis. Measurements of hemodynamics and regional myocardial blood flow (microspheres) were made at control and after 10 minutes of adenosine infused at 400 micrograms/min and then at 800 micrograms/min distal to each stenosis. Both heart rate and aortic mean pressure were controlled and thus did not change versus initial baseline (129 +/- 4 minutes and 120 +/- 10 mm Hg, mean +/- SD, respectively) during the study. Baseline total flow (ml/sec) distal to the stenosis was similar at each control (1.05 +/- 0.35 vs. 0.92 +/- 0.34, simple versus complex, respectively; p = NS). At maximal adenosine, total flow with the simple stenosis was 3.44 +/- 0.92 versus 2.77 +/- 0.51 for complex (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic response to prolonged reduction of myocardial blood flow distal to a severe coronary artery stenosis.

Limited data are available concerning the effects of mild-to-moderate, sustained reductions of coronary blood flow on myocardial aerobic metabolism. This study tested the hypothesis that a sustained flow reduction distal to a severe coronary artery stenosis may be well tolerated (after the initial insult is passed) because of gradual improvement in the balance between myocardial oxygen supply and demand. Studies were performed in eight sedated, closed-chest domestic swine that were instrumented with an artificial coronary arterial stenosis (80% diameter reduction). Hemodynamics, regional myocardial blood flow and oxygen, lactate, acid, and base metabolism were measured before stenosis and at 5, 20, 60, 120, and 180 minutes after stenosis insertion. Regional myocardial function (ultrasonic length sensors) was measured serially during 2 hours in three additional swine. After stenosis placement, endocardial and transmural flows declined (p less than 0.05) compared with flows before stenosis (from 1.54 +/- 0.37 to 0.73 +/- 0.24 ml/min/g [mean +/- SD] and from 1.44 +/- 0.31 to 1.19 +/- 0.25 ml/min/g, respectively). Thereafter, flows remained unchanged for the duration of the study. Similarly, prestenosis heart rate (135 +/- 7 beats/min), aortic mean pressure (113 +/- 17 mm Hg), and tension time index (27.1 +/- 3.6 mm Hg.sec) remained constant for the duration of the study. In contrast, regional coronary venous pH declined (p less than 0.05) compared with prestenosis levels (7.35 +/- 0.02) 5 minutes after stenosis (7.28 +/- 0.04), but it returned to prestenosis levels during the next hour. Regional coronary venous PCO2 exhibited a similar pattern (i.e., acute increase during poststenosis with gradual return to prestenosis levels).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of pressure-controlled intermittent coronary sinus occlusion on pacing-induced myocardial ischemia in domestic swine.

This study tested the hypothesis that pressure-controlled intermittent coronary sinus occlusion (PICSO) would be useful in ameliorating myocardial ischemia under conditions characterized by preserved, but reduced (relative to demand), myocardial blood flow. Studies were conducted in closed-chest, sedated domestic swine prepared with an artificial stenosis that reduced luminal diameter of the animal's left anterior descending coronary artery by 80%. Measurements of hemodynamics, regional myocardial blood flow, and oxygen, lactate, and nucleoside metabolism were obtained in 10 animals (1) before placement of stenosis, (2) 30 min after insertion of stenosis, (3) after 30 and 60 min of PICSO, and (4) 30 min after discontinuation of PICSO. Two groups of control animals were studied to observe the natural history of metabolic markers of ischemia. Control group I consisted of four animals studied concurrently and subjected to the same protocol except for the fact that PICSO was not applied. Control group II consisted of eight additional animals studied as a group. A specially designed balloon-tipped catheter positioned in the proximal portion of the animal's great cardiac vein was used to provide PICSO. Heart rate was controlled by atrial pacing (rate, 145 beats/min) through the study. After placement of the stenosis, flow in endocardial and transmural layers distal to the stenosis declined significantly (p less than .01) vs control. Application of PICSO failed to increase arterial inflow distal to the stenosis in any myocardial layer. Myocardial aerobic metabolism was adversely affected by stenosis and changed from consumption of lactate, inosine, and hypoxanthine before stenosis to production at 30 min after stenosis. Although PICSO was associated with reduced production and a return toward consumption of lactate, inosine, and hypoxanthine, a similar pattern of changes in lactate, inosine, and hypoxanthine metabolism was observed in control animals over a comparable period of time. In addition, regional myocardial oxygen extraction and consumption were not changed vs poststenosis levels by PICSO. However, in comparison with controls, PICSO did accelerate the rate of resolution of myocardial ischemia as assessed by lactate metabolism. At 30 min of PICSO (or sham) the change vs poststenosis was +33.6 +/- 25.0 mumol/min/100 g in the PICSO but only +6.7 +/- 29.7 in the control group (p = .05). We conclude, therefore, that even though PICSO did not alter the final level of myocardial ischemia under conditions modeled in this study it did accelerate its rate of resolution, an effect that may be beneficial clinically.