A randomized trial comparing primary angioplasty with a strategy of short-acting thrombolysis and immediate planned rescue angioplasty in acute myocardial infarction: the PACT trial. PACT investigators. Plasminogen-activator Angioplasty Compatibility Trial.

OBJECTIVES: The study evaluated the efficacy and safety of a short-acting reduced-dose fibrinolytic regimen to promote early infarct-related artery (IRA) patency during the inherent delay experienced by infarct patients referred for angioplasty as the principal recanalization modality. BACKGROUND: Previous approaches using long-acting, full-dose thrombolytic infusions rarely showed benefit, but they did increase adverse event rates. METHODS: Following aspirin and heparin, 606 patients were randomized to a 50-mg bolus of recombinant tissue-type plasminogen activator (rt-PA) (alpha half-life 4.5 min) or to placebo followed by immediate angiography with angioplasty if needed. The end points included patency rates on catheterization laboratory (cath lab) arrival, technical results when PTCA (percutaneous transluminal coronary angioplasty) was performed, complication rates, and left ventricular (LV) function by treatment assignment and time to restored patency following angioplasty. RESULTS: Patency on cath lab arrival was 61% with rt-PA (28% Thrombolysis in Myocardial Infarction trial [TIMI]-2, 33% TIMI-3), and 34% with placebo (19% TIMI-2, 15% TIMI-3) (p = 0.001). Rescue and primary PTCA restored TIMI-3 in closed arteries equally (77%, 79%). No differences were observed in stroke or major bleeding. Left ventricular function was similar in both treatment groups, but convalescent ejection fraction (EF) was highest with a patent IRA (TIMI-3) on cath lab arrival (62.4%) or when produced by angioplasty within an hour of bolus (62.5%). However, in 88% of angioplasties, the delay exceeded 1 h: convalescent EF 57.3%. CONCLUSIONS: Tailored thrombolytic regimens compatible with subsequent interventions lead to more frequent early recanalization (before cath arrival), which facilitates greater LV function preservation with no augmentation of adverse events.

Effect of aerobic training on left ventricular diastolic filling.

The effects of aerobic training on left ventricular diastolic filling were determined and related to the effects on maximal oxygen uptake, left ventricular systolic function, and left ventricular mass. Nine untrained healthy males with a mean age of 32 years underwent a ten-week program of bicycle training. Echocardiographic left ventricular mass, maximal oxygen uptake, radionuclide-derived left ventricular ejection fraction, and average left ventricular filling rate were obtained before and after training. Training resulted in significant increases in maximal oxygen uptake (from 30 +/- 6 (mean +/- S.D.) to 40 +/- 7 ml/kg/min, p less than 0.001) and average left ventricular filling rate (from 2.04 +/- 0.36 to 2.22 +/- 0.31 end-diastolic volumes/sec, p less than 0.05), but no changes in heart rate, systolic blood pressure, left ventricular ejection fraction, or left ventricular mass. These data indicate that short-term high-intensity aerobic training enhances average left ventricular diastolic filling independent of any change in left ventricular geometry, systolic function, heart rate, or blood pressure.

Streptokinase dissolution of a right atrial thrombus associated with a temporary pacemaker.

Thrombosis of intravascular catheters is a well-recognized and potentially serious complication, which has been treated successfully with thrombolytic agents. A routine echocardiogram in a patient with a temporary transvenous pacemaker demonstrated a large thrombus attached to the pacing electrode. This was dissolved successfully and uneventfully with high-dose intravenous streptokinase therapy. To our knowledge, this is the first report of the successful lysis of a right atrial thrombus complicating a temporary transvenous pacemaker.

Rapid ventricular filling in left ventricular hypertrophy: I. Physiologic hypertrophy.

The effects of endurance training on the diastolic properties of the left ventricle were examined by comparing left ventricular filling rates in 11 male distance runners and 12 age-matched nonathletic control subjects selected to have nearly similar heart rates at rest. Maximal oxygen consumption was 69 +/- 11 ml/kg-min for the athletes and 48 +/- 8 ml/kg X min for the control subjects (p less than 0.001). Left ventricular end-diastolic dimension, posterior wall thickness and mass were determined by echocardiography, and average left ventricular filling rate was determined with a nonimaging scintillation probe. Electrocardiographic voltage was significantly greater in the athlete group than in the control group (sums of the voltages of the S wave in lead V1 and the R wave in lead V5 were 40 +/- 10 and 26 +/- 7 mV, respectively) (p less than 0.001), whereas ejection fraction was similar in the two groups. Despite a modest degree of left ventricular hypertrophy in the athlete group compared with the control group (left ventricular mass index 127 +/- 30 and 82 +/- 13 g/m2, respectively) (p less than 0.001), the average left ventricular filling rate was similar in the two groups (2.53 +/- 0.34 versus 2.38 +/- 0.29 end-diastolic counts/s, p = NS). There was no trend for the athletes with a higher left ventricular mass to exhibit a slower filling rate. These findings demonstrate that unlike pathologic hypertrophy associated with chronic hemodynamic over-loading, physiologic left ventricular hypertrophy is not accompanied by slowed left ventricular diastolic filling.

Radionuclide angiographic exercise left ventricular performance in chronic aortic regurgitation: relationship to resting echographic ventricular dimensions and systolic wall stress index.

Forty-five patients with chronic aortic regurgitation (AR) underwent first-pass radionuclide angiocardiography (RNA) at rest and during upright bicycle exercise, as well as M-mode echocardiography at rest. Abnormal left ventricular (LV) exercise reserve, defined by the absolute change in ejection fraction (EF), was present in 16 of 45 patients (36%). Seven of ten patients with abnormal resting EF (less than 50%) and three of seven symptomatic patients had normal LV exercise responses. Patients with normal LV exercise reserve by RNA had LV dimensions by echo at end diastole (5.9 +/- 0.2 vs 6.5 +/- 0.3 cm, p = NS) and end systole (3.9 +/- 0.2 vs 4.4 +/- 0.3 cm, p = NS) comparable to those in patients wht abnormal LV exercise reserve. However, the mean corrected LV end-diastolic (LVED) radius/wall thickness ratio was significantly greater in AR patients with abnormal LV exercise reserve than in those with normal LV exercise reserve (395 +/- 15 vs 315 +/- 16, p less than 0.01). There data suggest that resting echocardiographic LV dimensions as well as the corrected echo LVED radius/wall thickness ratio have a variable relationship to RNA LV exercise performance in patients with chronic AR.

Imaging experimental infective endocarditis with indium-111-labeled blood cellular components.

The capability of radionuclide imaging to detect experimental aortic valve infective endocarditis was assessed with indium-111 (111In)-labeled blood cells. Sequential cardiac imaging and tissue distribution studies were obtained in 17 rabbits with infective endocarditis after administration of 111In-platelets and in five after 111In-polymorphonuclear leukocytes. Forty-eight to 72 hours after platelet administration, in vivo imaging demonstrated abnormal 111In uptake in all animals in the region of the aortic valve in an anatomically distinct pattern. Images of the excised heart showed discrete cardiac uptake conforming to the in vivo image and gross pathological examination. 111In platelet uptake in vegetations from the 17 animals averaged 240 +/- 41 times greater than that in normal myocardium and 99 +/- 15 times greater uptake in blood. In contrast, 111In-leukocyte cardiac imaging showed no abnormal aortic valve uptake 24 hours after tracer administration and the lesion myocardium activity ratio was only 5 +/- 2 (3 +/- 1 for lesion/blood activity). Four normal rabbits demonstrated neither positive 111In platelet scintigraphs nor abnormal cardiac tissue uptake. Likewise, noncellular 111In was not concentrated to any significant extent in three animals with infective endocarditis. This study demonstrates that 111In platelet, but not leukocyte cardiac imaging, is a sensitive technique for detecting experimental infective endocarditis. The imaging data conform to the cellular pathology of the infective endocarditis vegetation.

Technetium-99m stannous pyrophosphate imaging of experimental infective endocarditis.

Technetium-99m stannous pyrophosphate (99mTc-PYP) cardiac scintigraphy was performed in 15 rabbits with experimental Streptococcus sanguis aortic valve infective endocarditis. The animals were imaged five to seven days after the administration of bacteria, and in each case abnormal accumulation of the tracer was visualized in the region of the aortic valve. Three types of cardiac scintigraphic patterns were demonstrated: focal, multifocal and extensive, each correlating well with the anatomical extent of the lesion as defined by gross pathology. Tissue distribution studies demonstrated a 30 +/- 5.3 (mean +/- SEM) fold excess of radionuclide uptake in the infective endocarditis lesion compared with that of normal myocardium. Imaging of excised hearts from four animals showed an excellent correlation with in vivo imaging as well as gross pathology. Five animals with nonbacterial thrombotic aortic valve endocarditis demonstrated similar scintigraphic and tissue distribution results. In contrast, four normal animals failed to demonstrate abnormal 99mTc-PYP cardiac scintigrams or tissue uptake. This study demonstrates that 99mTc-PYP cardiac scintigraphy is a sensitive technique to detect experimental aortic valve endocarditis.

Unsuspected substantial pericardial effusions detected by echocardiography.

In a consecutive series of 1,225 routine echocardiograms, a pericardial effusion (PE) was present in 15% and was considered substantial in 10%. Sixty-one percent (68/111) of the latter were clinically unsuspected. A retrospective analysis of these patients showed that 60% (41/68) had underlying heart disease such as congestive heart failure, left ventricular hypertrophy, or asymmetric septal hypertrophy without other discernible causes for PE. In patients referred specifically for suspected pericardial effusion, 67% (29/43) had diseases recognized as causes of pericardial effusion. Unsuspected substantial PE are commonly detected by echocardiography, especially in patients with underlying heart disease.