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Objectives: The goals of this study were to examine the safety and feasibility of a routine (primary) stent strategy in acute myocardial infarction (AMI)., Background: Limitations of reperfusion by primary percutaneous transluminal coronary angioplasty (PTCA) in AMI include in-hospital recurrent ischemia or reinfarction in 10% to 15% of patients, restenosis in 37% to 49% and late infarct-related artery reocclusion in 9% to 14%. By lowering the residual stenosis and sealing dissection planes created by PTCA, primary stenting may further improve short- and long-term outcomes after mechanical reperfusion., Methods: Three hundred twelve consecutive patients treated with primary PTCA for AMI at nine international centers were prospectively enrolled. After PTCA, stenting was attempted in all eligible lesions (vessel size 3.0 to 4.0 mm; lesion length < or = 2 stents; and the absence of giant thrombus burden after PTCA, major side branch jeopardy or excessive proximal tortuosity or calcification). Patients with stents were treated with aspirin, ticlopidine and a 60-h tapering heparin regimen., Results: Stenting was attempted in 240 (77%) of 312 patients, successfully in 236 (98%), with Thrombolysis in Myocardial Infarction grade 3 flow restored in 230 patients (96%). Patients with stents had low rates of in-hospital death (0.8%), reinfarction (1.7%), recurrent ischemia (3.8%) and predischarge target vessel revascularization for ischemia (1.3%). At 30-day follow-up, no additional deaths or reinfarctions occurred among patients with stents, and target vessel revascularization was required in only one additional patient (0.4%)., Conclusions: Primary stenting is safe and feasible in the majority of patients with AMI and results in excellent short-term outcomes.

We reviewed the timing and mechanism of death in 1,184 consecutive patients with acute myocardial infarction (AMI) treated with primary angioplasty from 1984 to 1995. Of 98 deaths, 48 (49%) occurred early on day 0 or 1. The mechanisms of death were pump failure in 60 patients (61%), reinfarction in 7 patients (7.1%), left ventricular rupture in 5 patients (5.1%), arrhythmia in 3 patients (3.1%), other cardiac causes in 5 patients (5.1%), stroke in 6 patients (6.1%), anoxic encephalopathy in 7 patients (7.1%), and procedure-related deaths in 5 patients (5.1%). The strongest predictors of mortality were cardiogenic shock and unsuccessful reperfusion. Our data indicate that mortality after primary angioplasty, like thrombolytic therapy, is highest in the early hours and is usually due to pump failure. In contrast to thrombolytic therapy, the incidence of death from myocardial rupture and bleeding complications is low. Future treatment strategies will need to focus on the large number of patients with early death due to pump failure, especially patients with cardiogenic shock.

Objectives: A large, international, multicenter, prospective, randomized trial was performed to determine the role of prophylactic intraaortic balloon pump (IABP) counterpulsation after primary percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI)., Background: Previous studies have suggested that routine IABP use after primary PTCA reduces infarct-related artery reocclusion, augments myocardial recovery and improves clinical outcomes., Methods: Cardiac catheterization was performed in 1,100 patients within 12 h of onset of AMI at 34 clinical centers. Clinical and angiographic variables were used to stratify patients undergoing primary PTCA into high and low risk groups. High risk patients were then randomized to 36 to 48 h of IABP (n = 211) or traditional care (n = 226). The study had 80% power to detect a reduction in the primary end point from 30% to 20%., Results: There was no significant difference in the predefined primary combined end point of death, reinfarction, infarct-related artery reocclusion, stroke or new-onset heart failure or sustained hypotension in patients treated with an IABP versus those treated conservatively (28.9% vs. 29.2%, p = 0.95). The IABP strategy conferred modest benefits in reduction of recurrent ischemia (13.3% vs. 19.6%, p = 0.08) and subsequent unscheduled repeat catheterization (7.6% vs. 13.3%, p = 0.05) but did not reduce the rate of infarct-related artery reocclusion (6.7% vs. 5.5%, p = 0.64), reinfarction (6.2% vs. 8.0%, p = 0.46) or mortality (4.3% vs. 3.1%) and was associated with a higher incidence of stroke (2.4% vs. 0%, p = 0.03). IABP use did not result in enhanced myocardial recovery as assessed by paired admission to predischarge and 6-week rest and exercise left ventricular ejection fraction., Conclusions: In contrast to previous studies, a prophylactic IABP strategy after primary PTCA in hemodynamically stable high risk patients with AMI does not decrease the rates of infarct-related artery reocclusion or reinfarction, promote myocardial recovery or improve overall clinical outcome.

Objectives: The purpose of this study was to evaluate the importance of late infarct-related artery patency for recovery of left ventricular function and late survival after primary angio-plasty for acute myocardial infarction., Background: Infarct-related artery patency is thought to improve late survival by its effect on preservation of left ventricular function. Patency may also enhance late survival by preventing left ventricular dilation and reducing arrhythmias, independent of myocardial salvage. However, most studies have not shown patency to be an independent predictor of survival when late left ventricular function is taken into account., Methods: We followed up 576 hospital survivors of acute myocardial infarction treated with primary angioplasty for 5.3 years. Ejection fraction and infarct-related artery patency were determined at follow-up catheterization at 6 months. Predictors of late cardiac survival were determined using Cox regression models., Results: Patients with patent arteries had more improvement and a better late ejection fraction than patients with occluded arteries (56.3% vs. 47.9%, p = 0.001). In patients with acute ejection fraction < 45%, late survival was better in those with patent versus occluded arteries (89% vs. 44%, p = 0.003), but patency was not a significant predictor after improvement in ejection fraction was taken into account. In patients with a large anterior infarction, patency was a significant independent predictor of late survival., Conclusions: Infarct-related artery patency is important for recovery of left ventricular function, and in patients with acute ejection fraction < 45%, patency is important for late survival. Our data are consistent with the hypothesis that the survival benefit is due primarily to the effect of patency on recovery of left ventricular function. In patients with a large anterior infarction, patency appears to provide an additional late survival benefit independent of myocardial salvage. These observations support the need for additional clinical trials of late reperfusion in patients with a large anterior infarction.

The benefit of thrombolytic therapy given late after the onset of acute myocardial infarction (AMI) has been controversial because of low reperfusion rates and limited myocardial salvage. Persistent chest pain has been used as a criteria for late intervention, but there is little documentation to validate this practice. Clinical outcomes and myocardial salvage were evaluated in 74 patients with AMI and persistent chest pain who underwent late reperfusion (> 6 hours) with direct coronary angioplasty, and these were compared with outcomes in 460 patients with early reperfusion (< or = 6 hours). Patients with late reperfusion had a high infarct artery patency rate (96%), a low hospital mortality rate (5.4%), and a low incidence of reinfarction (1.4%) and recurrent ischemia that were similar to patients with early reperfusion. Patients with late reperfusion had surprisingly good recovery of left ventricular function with improvement in ejection fraction from 50% to 60% at follow-up angiography. Patients with late reperfusion had a greater incidence of collateral flow (45% vs 22%, p < 0.001) and a lower value of peak creatine kinase (1,357 vs 2,057 U/liter, p < 0.001) than patients with early reperfusion. This study emphasizes the importance of persistent chest pain as a marker of continued myocardial viability in patients who present late after AMI. These data suggest that the probable mechanism of continued viability is preserved flow to the infarct zone. Patients with AMI and persistent chest pain may benefit from reperfusion therapy beyond 6 to 12 hours.

Background: After direct angioplasty in the setting of acute myocardial infarction, patients were followed clinically and angiographically for 6 months at six experienced centers to evaluate outcomes., Methods and Results: Of 258 patients with 6-month follow-up after surviving initial hospitalization, 5 (2%) died, 8 (3%) had nonfatal infarctions, 56 (22%) had chest pain, of whom 25 (10%) required hospitalization, and 42 (16%) patients needed repeat angioplasty. Of 203 eligible patients, 154 (76%) had angiographic follow-up. The infarct-related artery remained patent (defined as TIMI 2 or 3 flow) in 87%, while 13% developed reocclusion (TIMI 0 or 1 flow) by 6 months after discharge. Patients with reocclusion were more likely to have adverse events, including 35% with clinically evident reinfarction and 59% requiring repeat angioplasty. The median ejection fraction improvement from acute to follow-up study was 6%, with no improvement in patients with a reoccluded infarct-related artery and an 8% improvement in patients with a patent infarct-related artery., Conclusions: The positive clinical outcomes recorded immediately after direct angioplasty persisted through 6 months of follow-up. Although the incidence of clinical end points was equivalent to or lower than thrombolytic therapy trials, restenosis is a substantial problem. These findings provide evidence beyond the initial hospitalization that direct angioplasty is a reasonable choice for the treatment of acute myocardial infarction.

During a 14-month period, 6 experienced centers prospectively enrolled 271 patients into a registry in which percutaneous transluminal coronary angioplasty was the primary treatment for acute myocardial infarction. Patients age > 18 years who presented with ST-segment elevation on the 12-lead electrocardiogram were enrolled if symptom duration was < 12 hours and there was no proclivity for bleeding. An independent core angiographic laboratory processed the angiographic data. Of 271 patients giving informed consent, 245 (90%) were deemed anatomically suitable and underwent angioplasty therapy. Upon leaving the catheterization laboratory 98% of patients had achieved reperfusion; 92% had a residual visual stenosis < or = 50%. Emergency bypass surgery was required in 14 patients (5%) for either failed angioplasty (n = 3) or presumed life-threatening anatomy (n = 11). The in-hospital mortality rate was 4%, whereas the reinfarction rate was 3% and the stroke rate was 1%, with 1 intracranial hemorrhage and 2 embolic events. Bleeding requiring > or = 2 units of blood occurred in 46 patients (18%); 14 of these transfusions were related to coronary artery bypass surgery. Primary angioplasty is associated with a high reperfusion rate, low in-hospital mortality and few recurrent myocardial ischemic events. These results point to the need for a large-scale trial comparing angioplasty with thrombolytic therapy in the setting of acute myocardial infarction.

Background: The value of routine administration of intravenous thrombolytic agents during percutaneous transluminal coronary angioplasty (PTCA) therapy of acute myocardial infarction (MI) has not been determined. Therefore, we prospectively randomized 122 patients with evolving MI to PTCA therapy with or without adjunctive intravenous streptokinase therapy., Methods and Results: Patients with ECG ST segment elevation who presented within 4 hours of symptom onset, had no contraindication to thrombolytic therapy, and were not in cardiogenic shock were enrolled. They were treated immediately with intravenous heparin (10,000 units) and oral aspirin (325 mg) and randomized to treatment with placebo or streptokinase (1.5 M units) administered intravenously over 30 minutes. Patients then were taken immediately to the catheterization laboratory, and those with suitable coronary anatomy underwent immediate PTCA. Subsequent clinical course, serial radionuclide ventriculography, and 6-month repeat angiography were analyzed. A total of 106 patients were treated with PTCA. Use of PTCA was similar for placebo (92%) and streptokinase (83%) groups. Angioplasty was successful in 95% of patients, with no difference in placebo (93%) and streptokinase (98%) groups. Serial radionuclide ventriculography demonstrated no difference in 24-hour (52 +/- 12% versus 50 +/- 12%) or 6-week (51 +/- 12% versus 51 +/- 13%) ejection fraction values for placebo and streptokinase groups, respectively. Contrast ventriculography demonstrated improvement in immediate (54 +/- 12%) versus 6-month (60 +/- 15%, p < 0.05) values for the overall group. No differences in 6-month values were present (58 +/- 15% versus 62 +/- 15%, p = NS) for placebo and streptokinase groups, respectively. Coronary angiography was performed in 75% of the 90 patients eligible for restudy. Arterial patency was 87% at 6 months, and coronary restenosis was present in 38% of patients. No differences in chronic patency or restenosis were detected for the two treatment groups. Although adjunctive intravenous streptokinase therapy did not improve outcome, it did complicate the hospital course. Hospitalization was longer (9.3 +/- 5.0 versus 7.7 +/- 4.4 days, p = 0.046) and more costly ($25,191 +/- 15,368 versus $19,643 +/- 7,250, p < 0.02). Transfusion rate was higher (39% versus 8%, p = 0.0001) and need for emergency coronary bypass surgery was greater (10.3% versus 1.6%, p = 0.03) for the streptokinase-treated patients., Conclusions: Adjunctive intravenous streptokinase therapy does not enhance early preservation of ventricular function, improve arterial patency rates, or lower restenosis rates after PTCA therapy of acute MI. Hospital course is longer, more expensive, and more complicated. For these reasons, PTCA therapy of acute MI should not be routinely performed with adjunctive intravenous streptokinase therapy.

The importance of a patent infarct-related artery (IRA) for hospital and late survival was examined in 383 patients with acute myocardial infarction treated with direct coronary angioplasty. At hospital discharge, 317 of 348 patients (91%) had a patent IRA and mean follow-up left ventricular (LV) ejection fraction (EF) was 58%. Cardiac survival after hospital discharge at 1, 3 and 6 years was 99, 95 and 90%. Patency of the IRA was the most important determinant of hospital mortality: patent versus occluded IRA, 5 vs 39% mortality, p less than 0.001. Follow-up LVEF was the most important determinant of late cardiac mortality: follow-up LVEF greater than or equal to 45 versus less than 45%, 2 versus 24% mortality, p less than 0.001. Patency of the IRA was not a significant predictor of late cardiac mortality in the group as a whole: patent versus occluded IRA, 4.7 versus 6.5% mortality, p = 0.67. In the subgroup of patients with depressed initial LVEF less than 45%, patency was a significant predictor of late cardiac mortality: patent versus occluded IRA, 9.2 versus 40% mortality, p = 0.03. Patients with a patent IRA had better recovery of LV function than patients with an occluded IRA (follow-up LVEF 58.5 versus 47.6%, p less than 0.001). When late cardiac mortality was adjusted for differences in follow-up LVEF, patency was no longer a significant predictor of late mortality. Our results indicate patency of the IRA is the most important determinant of hospital survival, and LV function (measured after recovery) is the most important determinant of late cardiac survival.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary angioplasty without prior thrombolytic therapy was performed in 383 patients with acute myocardial infarction (AMI). Patients were divided into 2 groups depending on whether they were candidates or non-candidates for thrombolytic therapy. Patients were not considered thrombolytic candidates if they: (1) presented in cardiogenic shock, (2) were greater than or equal to 75 years of age, (3) had had coronary artery bypass surgery or, (4) had a reperfusion time of greater than 6 hours. Thrombolytic and nonthrombolytic candidates had similar rates of reperfusion (92 vs 88%), nonfatal reinfarction (6.0 vs 5.9%) and recurrent myocardial ischemia (1.8 vs 0%). Thrombolytic candidates had a lower mortality rate (3.9 vs 24%, p less than 0.0001) and a lower incidence of bleeding (4.6 vs 10.9%, p less than 0.05). Improvement in left ventricular ejection fraction at follow-up angiography was 4.4% in thrombolytic and 10.5% in nonthrombolytic candidates (p less than 0.002). Ejection fraction improved most in patients with anterior wall AMI (7.7% in thrombolytic candidates, 15.1% in nonthrombolytic candidates) and in patients with reperfusion times greater than 6 hours (14.2%). These outcomes suggest that direct coronary angioplasty is a viable alternative method of reperfusion in patients with AMI who are candidates for thrombolytic therapy. Nonthrombolytic candidates are a high-risk group of patients. Direct coronary angioplasty may be beneficial in certain subgroups, especially for patients in cardiogenic shock and for patients presenting greater than 6 hours after the onset of chest pain with evidence of ongoing ischemia.

Calculation of left ventricular wall stress in man has traditionally required angiographic and left ventricular pressure measurement, making study of interventions difficult. We have developed a combined hemodynamic-ultrasonic technique for measuring left ventricular meridional wass stress (sigma m) throughout the cardiac cycle. Simultaneous measurements of left ventricular pressure, ultrasonically determined wall thickness (h[echo]), and minor axis (D[echol]) were made during cardiac catheterization in nine subjects, three with chronic left ventricular pressure overload, four with left ventricular volume overload and two with normal left ventricular function. Within 30 minutes, left ventricular cineangiography was performed in each subject and angiographic wall thickness (h[angio]) and minor axis (D[angio]) were measured. Comparison of values for each subject throughout the cardiac cycle (average 18 data points/cycle) yielded close correlation: For D(echo) versus D(angio), r values ranged from 0.82 to 0.98 whereas for h(echo) versus h(angio), r values ranged from 0.56 to 0.98 for the nine subjects. Meridional wall stress was calculated after the method of Sandler and Dodge as PRi2/h(2Ri + h), where Ri equals the inner wall radius, calculated as D/2 for both ultrasonic and angiographic methods. Agreement between ultrasonic and angiographic methods was excellent in each subject, with close superimposition of the stress-time plots constructed by the different techniques. In summary, a new method for measurement of left ventricular wall stress has been developed and validated by comparison with an angiographic reference standard. This method has potential advantages, including the ability to study meridional wall stress continuously and to assess its response to serial interventions.

We report the presence of an unusual systolic murmur associated with a traumatic left ventricular pseudoaneurysm. Echophonocardiographic studies showed the murmur to begin at the first heart sound, but end well before the second heart sound. It seems likely that the murmur is caused by the systolic flow of blood from the left ventricle into the relatively noncompliant pseudoaneurysm. The echocardiographic scan of the left ventricle demonstrated a relatively echo-free space posterior to the left ventricular wall, supporting the diagnosis of pseudoaneurysm, which has confirmed with angiographic studies and at surgery. These findings indicate that a combination of noninvasive techniques is useful in establishing this diagnosis.

Emergency coronary angioplasty was performed in 127 patients presenting to a community hospital with acute myocardial infarction. Reperfusion and successful dilatation were performed in 117 patients (92%) at 3.3 +/- 1.8 hours from the onset of pain. Eleven patients (8.6%) died, ten patients (7.9%) developed reocclusion, and ten patients (7.9%) required coronary bypass surgery during the initial hospitalization. Late restenosis occurred in 36% (27/76) of patients restudied or 27% (27/100) of patients at risk for restenosis. Ejection fraction improved in patients with patent vs occluded vessels (8.4% +/- 8.2% vs -4.1% +/- 6.0%) and improved most in anterior vs inferior vs posterolateral infarcts (11.0% +/- 8.4% vs 6.8% +/- 6.4% vs 2.6% +/- 7.5%). Posthospitalization follow-up in all patients (mean, 13.4 months) revealed only one late death. Of the patients followed up, 83% had no angina, and 17% of patients had mild angina. Our experience demonstrates that coronary angioplasty for acute myocardial infarction can be performed in the community hospital by an experienced cardiovascular laboratory team with a high success rate, a low reocclusion rate, an improvement in ejection fraction, and an excellent long-term prognosis. The community hospital setting allows early access to patients and creates the potential for early reperfusion and myocardial salvage.

Fifty-three patients were studied with combined echo-phonocardiography or phonocardiography alone following prosthetic valve replacement. In sixteen of these patients, clinical deterioration developed, and all subsequently underwent cardiac catheterization and/or surgery. Two patients came to autopsy. Included in this group of sixteen patients were five with obstructed prosthesis, six with paravalvular regurgitation, and five with left ventricular dysfunction. Measurements were made of the time interval from the aortic valve closure sound to the peak opening of the mitral prosthesis determined echocardiographically or to the mitral prosthetic opening click (A2-MVO). Echocardiographic studies of left ventricular wall motion were also performed. The A2-MVO interval was significantly shortened (P less than 0.01) with prosthetic valve obstruction (.05 +/- .02 sec) and paravalvular regurgitation (.05 +/- .01 sec) compared with normally functioning prostheses (Starr-Edwards ball valves .10 +/- .02 sec, Lillehei-Kaster tilting disc prostheses .09 +/- .01 sec). Shortening of this interval was not specific for these conditions because it was sometimes shortened with left ventricular dysfunction. Echocardiographic studies of left ventricular wall motion were helpful in distinguishing among prosthetic valve obstruction, paravalvular regurgitation and left ventricular dysfunction. The combined echo-phonocardiographic technique was especially helpful in detecting malfunction of tilting disc prostheses, because the technique enables measurement of the A2-MVO interval in the absence of an audible opening click.

The effect of sodium nitroprusside on the relationship between left ventricular pressure and volume during diastole was studied in 11 patients with congestive heart failure. Nitroprusside was infused to lower mean arterial pressure approximately 20-30 mm Hg. High fidelity left ventricular pressures were recorded in all patients simultaneously with left ventricular cineangiography (biplane in eight and single plane in three patients), allowing precise measurement of pressure and volume throughout the cardiac cycle. Left ventricular diastolic pressure-volume curves were constructed in each patient from data obtained before and during nitroprusside infusion. In 9 of 11 patients there was a substantial downward displacement of the diastolic pressure-volume curve during nitroprusside infusion, with left ventricular pressure being lower for any given volume with nitroprusside. Serial left ventricular cineangiograms performed 15 min apart in six additional subjects who did not receive sodium nitroprusside showed no shift in the diastolic pressure-volume relation, indicating that the shift seen with nitroprusside was not due to the angiographic procedure itself. A possible explanation for the altered diastolic pressure-volume relationships with nitroprusside might be a direct relaxant effect of nitroprusside on ventricular muscle, similar to its known relaxant effect on vascular smooth muscle. Alternatively, nitroprusside may affect the diastolic pressure-volume curve by affecting viscous properties or by altering one or more of the extrinsic constraints acting upon the left ventricle.

Because of recent studies suggesting that vasodilators affect ventricular compliance, we studied the effect of sodium nitroprusside and nitroglycerin on the mechanical performance of 21 isolated cat papillary muscles. The muscles were stimulated isometrically at 36 beats/min. Sixteen of the muscles were made hypoxic (95% N2, 5% CO2) for 50 minutes and then reoxygenated. Sodium nitroprusside (10(-5) M) added to four of these muscles prior to hypoxia substantially diminished the tension prolongation (both the time to peak tension, TTP, and time for tension to fall to 1/2 its peak value, RT 1/2) that characterizes recovery from hypoxia. TTP and RT 1/2 measured 2 minutes after reoxygenation were 300 +/- 20 msec and 528 +/- 26 msec for the control muscles compared to 208 +/- 13 msec and 248 +/- 22 msec for the muscles pretreated with nitroprusside. Nitroprusside had no effect on the fall and recovery of peak developed force or on the rise and fall of resting force. Furthermore, nitroprusside had no effect on the above parameters in nonhypoxic muscles. We also found that nitroprusside in concentrations of 10(-7) M and nitroglycerin in concentrations of 10(-5) M had little or no effect on tension prolongation. The results of the study indicate that nitroprusside is capable of blocking the tension prolongation that occurs during recovery from hypoxia and may prevent the incomplete myocardial relaxation thought to characterize this phenomenon. Since nitroglycerin had no effect on tension prolongation, it is possible that other factors also may be important in the apparent increase in left ventricular compliance associated with administration of vasodilators to patients.

The increased left ventricular end-diastolic pressure associated with myocardial ischemia was studied in 19 patients at cardiac catheterization. Single plane left ventriculograms were performed using high fedelity micromanometer tipped catheters before and immediately following rapid atrial pacing. Left ventricular diastolic properties were evaluated by constructing diastolic pressure-volume curves from the simultaneous pressure and volume data. In seven control patients, there was no significant change in left ventricular hemodynamics or the diastolic pressure-volume curve after atrial pacing. Twelve patients with significant coronary artery disease developed angina during pacing and had an increased left ventricular end-diastolic pressure (18 +/- 2 mm Hg, control, vs 30 +/- 2 mm Hg, angina, P less than .01) in the immediate post-pacing period. In these patients, the post-pacing ejection fraction was modestly decreased (0.63 +/- 0.03, control, vs 0.57 +/- 0.03, angina P less than 0.01), and left ventricular volumes at end systole (59 +/- 8 cc, control, vs 74 +/- 9 cc, angina, P less than 0.0125) were increased. The post-pacing diastolic pressure-volume curves in all 12 patients were shifted upward as compared with control so that for any given diastolic volume, pressure was higher during angina. The data indicate that the increased left ventricular diastolic pressure during myocardial ischemia is the result of both impaired left ventricular systolic performance and altered left ventricular diastolic properties.

Eight patients with metastatic malignancy of the pericardium who demonstrated the hemodynamics of subacute effusive-constrictive pericarditis were studied. All patients had clinical evidence of cardiac tamponade due to malignant pericardial effusion and were referred for therapeutic pericardiocentesis. In six in whom pericardiocentesis was successfully performed, right atrial pressure remained elevated after pericardiocentesis and return of the intrapericardial pressure to zero; in these patients, hemodynamic data were initially compatible with tamponade but suggested constriction after removal of the pericardial fluid. In the remaining two patients, echocardiography revealed pericardial fluid, but attempted pericardiocentesis was unsuccessful. In these two patients, the hemodynamic data suggested pericardial constriction; subsequent pathologic examination revealed neoplastic involvement of the visceral pericardium. Thus, subacute effusive-constrictive pericarditis, previously recognized as a complication of tuberculosis or mediastinal radiation, may also be due to metastatic malignancy. The syndrome can readily be demonstrated when right heart catheterization is performed in conjunction with pericardiocentesis.

Acute and follow-up angiograms were analyzed in 75 patients with acute myocardial infarction treated with emergency coronary angioplasty to determine factors that might predict improvement in left ventricular ejection fraction. Ejection fraction improved 8.4 +/- 8.2% in 60 patients who maintained patent infarct vessels at follow-up angiography, compared with -4.1 +/- 6.0% in 15 patients who developed reocclusion (p less than .001). In patients with patent infarct vessels, univariate analysis revealed the following significant predictors of improvement in ejection fraction: initial ejection fraction (r = -.38, p less than .003) subtotal vs total stenosis (12.9 +/- 9.3% vs 6.9 +/- 7.3%, p less than .02), infarct vessel (left anterior descending 11.0 +/- 8.4%, right 6.8 +/- 6.4%, circumflex 2.6 +/- 7.5%, p less than .02), and time to follow-up study (less than or equal to 15 days vs greater than 15 days) (4.8 +/- 5.8% vs 9.8 +/- 8.6%, p less than .03). Reperfusion time (less than or equal to 2 hr vs greater than 2 hr) predicted improvement when subtotal stenoses and stuttering infarctions were excluded (10.6 +/- 7.0% vs 4.9 +/- 6.9, p less than .03). Multivariate analysis showed initial ejection fraction and subtotal vs total stenosis to be independent predictors. Patients with anterior infarctions, low initial ejection fractions, and subtotal stenoses or reperfusion times less than or equal to 2 hr are likely to benefit most from coronary angioplasty for acute myocardial infarction.