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Early coronary artery intervention is emerging as the treatment of choice for patients with high risk acute coronary syndromes (ACS). However, most patients with ACS are admitted to hospitals which do not have ready access to interventional therapy. Extending the benefits of early intervention to this population is problematic at such community hospitals, since this approach would require either emergency transfer to a tertiary center or the performance of angioplasty on-site at hospitals without cardiac surgical capability. A third solution, pre-hospital ambulance triage to interventional centers, is not currently practised in most countries. A growing body of evidence indicates that hospitals without cardiac surgical capability can establish safe and effective primary angioplasty programs. Patients with acute myocardial infarction (AMI) who are randomized to transfer for primary angioplasty without fibrinolytic treatment have fewer major adverse cardiac events than those treated with fibrinolytics alone or fibrinolytics and transfer. In patients with unstable angina (UA) or non-ST-elevation AMI, an early aggressive approach led to a significant reduction in the composite end-point of death, AMI, or rehospitalization for recurrent UA at 6 months with no increase in cost, compared with conservative management. Ongoing trials in Europe indicate that pre-hospital ambulance triage of patients with large AMI to interventional centers can be remarkably rapid, safe, and effective. In order to improve the access of such patients to early intervention, 3 interdependent solutions are proposed:The development of more interventional programs at those hospitals without cardiac surgical facilities that can meet rigorous standards. The development of protocols to insure the early and more frequent transfer of patients with high-risk ACS to interventional centers for coronary angiography and revascularization. The pre-hospital triage of patients with AMI to established heart attack centers with 24-hour, 365-day emergency interventional capability for immediate primary angioplasty (after the model of trauma centers). Universal triage/transfer of all such patients to interventional centers could, however, quickly flood the capability of all tertiary surgical hospitals. With the aging of the 'baby boomers' in the near future, the need for interventional facilities will increase even further. Thus the second and third solutions above will ultimately depend on the first solution. Improving the delivery of interventional therapy to patients with ACS can provide a substantial healthcare benefit to society.

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Advanced age is associated with increased mortality in acute myocardial infarction (AMI) but the mechanism remains unclear. We performed a pooled analysis of 3,032 patients from the Primary Angioplasty in Myocardial Infarction (PAMI)-2, Stent-PAMI, and PAMI-No Surgery On Site trials to determine which clinical, hemodynamic, and angiographic characteristics in the elderly were associated with in-hospital death. There were 452 patients aged >/=75 years and 2,580 patients aged <75 years. Older patients had a lower number of risk factors for coronary artery disease but more comorbidities. Acute catheterization demonstrated more 3-vessel disease, higher left ventricular (LV) end-diastolic pressure, lower LV ejection fraction, and higher initial rates of Thrombolysis In Myocardial Infarction (TIMI) trial 2 or 3 flow. Elderly patients were equally likely to undergo percutaneous intervention but had a lower procedural success rate and lower rates of final TIMI 3 flow, and older patients were more likely to have post-AMI complications. In-hospital mortality was 10.2% and 1.8%, respectively (p = 0.001). Cardiac and noncardiac mortality was higher in elderly patients, and no significant differences in causes of death were identified. Multivariate analysis revealed that the strongest predictors of death were age >/=75 years, lower LV ejection fraction, lower final TIMI flow, higher Killip class, need for an intra-aortic balloon pump (IABP), and post-AMI stroke/transient ischemic attack, or significant arrhythmia. Despite avoiding thrombolysis, elderly patients remain at increased risk of bleeding, stroke, and other post-AMI complications, and death. Cardiac risk factor analysis and acute catheterization offer prognostic information but do not completely explain the mechanism of increased in-hospital mortality in the elderly.

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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.

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Recognition that myocardial infarction is caused by coronary thrombosis has stimulated a search for a safe, rapidly acting, and effective thrombolytic regimen. Tissue plasminogen activator (t-PA) can provide relatively clot-selective thrombolysis, but one quarter of patients fail to achieve reperfusion, lysis speed is not optimal, and higher doses have been associated with an increased incidence of hemorrhagic stroke. We report the results of a multicenter study of pro-urokinase, a second naturally occurring plasminogen activator that has structural similarities to t-PA but has a different mechanism of action. Pro-urokinase was administered 3.9 +/- 1.1 hours after the onset of chest pain to 40 patients with acute myocardial infarction with angiographically confirmed complete coronary occlusion (TIMI grade 0). After a 90-minute intravenous infusion of pro-urokinase (4.7-9 million units, 36-69 mg) 51% (20 of 39) of the patients demonstrated reperfusion (TIMI grade 2 or 3) occurring 64.8 +/- 22.3 minutes after initiation of therapy. Fibrinogen levels fell only 10 +/- 17% from baseline, confirming the fibrin specificity of pro-urokinase. As with t-PA, however, this specificity was only relative. alpha 2-Antiplasmin decreased to 39% and plasminogen decreased to 64% of initial values. Fibrinogen degradation products increased 63% and the fibrin-specific D-dimer increased 8.7-fold. Thus, pro-urokinase produces relatively clot-selective coronary thrombolysis similar to that produced by t-PA, but the use of either pro-urokinase or t-PA alone in higher doses would be likely to produce more nonspecific effects.

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A 53-year-old man with Fabry's disease was studied by echocardiography. Both M-mode and two dimensional echocardiographic examinations produced findings indistinguishable from those previously described as virtually diagnostic of cardiac amyloidosis. Possible causes for the "granular sparkling" appearance and clinical implications of the similarities were discussed.

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The acute effects of intravenous nadolol (0.01 and 0.02 mg/kg) on cardiac electrophysiologic parameters were assessed with His bundle recording and programmed atrial stimulation. The higher dose of nadolol reduced resting heart rate (71 vs. 65 beats/min, P less than 0.02), and the degree of slowing was related to the initial heart rate (r = -0.68, P less than 0.05). Atrioventricular conduction time as defined by the paced A-H interval, rose by 12 msec (P less than 0.001) after nadolol (0.02 mg/kg) administration. Atrial refractoriness increased (by 10 msec, P less than 0.02) only at the higher dose level with nadolol. At both dose levels, atrioventricular nodal effective and functional refractory periods were increased (P less than 0.02) by a mean of 45 and 21 msec, respectively, suggesting greater sensitivity of atrioventricular nodal refractoriness to beta-adrenergic blockade. Nadolol's effects were generally similar to those of previously reported studies with other beta-adrenergic blockers. These data suggest that nadolol slows conduction through the atrioventricular node and increases atrial and atrioventricular nodal refractoriness.

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M-mode and two-dimensional echocardiograms were obtained in a patient with acute dissecting aneurysm of the ascending aorta. The M-mode echocardiogram disclosed apparent "duplication" of the non-coronary aortic cusp. Two-dimensional echocardiograms showed this finding to be the result of the motion of a flap of torn aortic intima. This new M-mode finding appears to be a highly specific echocardiographic sign for aortic dissection.

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Thallium-201 and microspheres were injected into the blood simultaneously during left circumflex (LC) occlusion in open chest dogs. The dogs were sacrificed 6-8 minutes later and regional myocardial (201)TI and microsphere concentrations determined. In dogs with permanent LC occlusion the myocardial (201)TI distribution approximated blood flow distribution as judged by the microsphere concentrations. Release of LC occlusion 45 seconds after (201)TI injection almost obliterated the myocardial (201)TI deficit in the area of the LC without changing the microsphere results, presumably a result of deposition of (201)TI during reactive hyperemia. Either delaying the onset of reflow until 3 minutes of attenuating the magnitude of reactive hyperemia by LC stenosis markedly decreased the change in (201)TI distribution due to reflow. We conclude that for a given degree of reversible regional myocardial ischemia at the time of (201)TI injection, the perfusion deficit observed on the initial scintigram will be influenced by the subsequent duration of ischemia and by the magnitude of postischemic reactive hyperemia.

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We used angiography in a prospective study of the coronary circulation in patients with acute coronary insufficiency. Reversible ST-T changes during the acute illness corresponded anatomically with severely narrowed coronary arteries (80 to 95 per cent stenosis). Angiograms repeated four months later showed new complete occlusions in nine of 30 severely stenotic arteries. Eight of the new occlusions occurred in severely narrowed arteries previously correlated with regional ST-T changes. Six patients had myocardial infarctions, five of which corresponded with the site of a new occlusion. These results provide indirect evidence that the acute coronary-insufficiency syndrome commonly represents intermittent transient coronary-artery occlusion and a threat of new permanent occlusion of the same artery. Myocardial infarction in these patients appeared to occur as a complication of the new occlusion.

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The use of a simple technique for multiplane echocardiographic analysis and study of the effect of arrhythmia enabled us to investigate the mechanism of premature opening of the aortic valve in two patients with subacute aortic insufficiency. In one patient, premature opening evolved with the development of left ventricular dilatation and failure. In this case the prematurity of opening in each beat was related to diastolic filling time and was accompanied by septal recoil and by premature closure of the mitral valve. We classified this as the diastolic duration-dependent subgroup. In the second patient, who had a hypertrophied, non-dilated left ventricle, premature opening depended on atrial contraction and was independent of diastolic filling time. This case defined an atrial contraction-dependent subgroup. In the light of these findings we analyzed previously reported cases in patients with acute severe aortic insufficiency. These patients appear to fall into the diastolic duration-dependent subgroup.

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