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We assessed the usefulness of myoglobin measured by latex agglutination methods as a parameter for successful reperfusion of the infarct-related artery. Plasma myoglobin levels were measured for 25 patients with acute myocardial infarction in whom thrombolysis and/or percutaneous transluminal coronary angioplasty (PTCA) were performed within 8 hours after the onset of symptoms. Blood samples were obtained before and 56 +/- 26 min (mean +/- SD) after commencing treatment. Plasma myoglobin levels were measured by quantitative and semi-quantitative latex agglutination methods, which required a procedure time of about 10 min. Coronary reperfusion was achieved by thrombolysis or PTCA in 22 cases (Group 1) but was not achieved by thrombolysis in 7 cases (Group 2). Before treatment (4.2 +/- 1.2 hours after the onset of symptoms), plasma myoglobin levels measured quantitatively and semi-quantitatively were 434 +/- 330 ng/ml and 4.6 +/- 4.2 fold, respectively. After treatment, the increased rate of myoglobin was significantly higher in Group 1 (8.4 +/- 7.5 and 9.2 +/- 7.1) than in Group 2 (1.8 +/- 0.5 and 1.7 +/- 0.5). Plasma myoglobin levels measured by quantitative and semi-quantitative latex agglutination methods showed a close correlation (r = 0.91, p < 0.01). In conclusion, measurement of plasma myoglobin levels by latex agglutination methods is a rapid and reliable way to confirm successful coronary reperfusion.

In this study the effects of exercise on peak aortic flow velocity (PFV), and the relationship between the maximum change in PFV and the extent of ischemia or infarction were examined. In 16 normal controls (NC) and 83 patients (pts) with documented coronary artery disease, continuous wave Doppler echocardiography and thallium-201 scintigraphy were performed simultaneously during supine bicycle exercise. The patients were grouped according to their results of thallium perfusion imaging: Group (G) 1 (10 pts) = normal; G-2 (30 pts) = ischemia without old infarction, G-3 (23 pts) = old infarction without angina, and G-4 (20 pts) = angina with old infarction. Three different PFV responses to exercise were observed. In NC, PFV increased progressively with exercise. In 28 pts (G-1 = 10, G-2 = 2, G-3 = 11, G-4 = 5), PFV increased as in NC (Type I). In 43 pts (G-2 = 24, G-3 = 9, G-4 = 10), PFV increased at the initial stage but was unchanged or decreased at the final stage (Type II). In 12 pts (G-2 = 4, G-3 = 3, G-4 = 5), PFV decreased progressively with exercise (Type III). The incidence of acute ischemia was 25% (7/28) in Type I, 79% (34/43) in Type II and 75% (9/12) in Type III. Furthermore, Doppler and scintigraphic studies were repeated during exercise in 16 pts (Type II = 14, Type III = 2) who underwent percutaneous transluminal coronary angioplasty (PTCA). After PTCA, in 11 of the 16 pts, the images of acute ischemia nearly resolved and profile of the PFV changed from Type II or III to Type I. In the remaining five patients, the results of both studies were unchanged. Finally, the maximum change of PFV showed good correlation with the extent of ischemia and/or prior infarction (in G-2, r = -0.50, p less than 0.01; in G-3 except for 11 pts of Type I, r = -0.76, p less than 0.01; in G-4, r = -0.80, p less than 0.001). The extents of ischemia and infarction in each group were considered to be far greater in Type III than those in the other Types. These results show that changing of PFV during exercise are related with the presence and extent of acute ischemia and/or infarction.

To clarify the mechanism of recanalization and reocclusion in thrombolysis and percutaneous transluminal coronary angioplasty (PTCA), the plasma concentrations of beta-thromboglobulin (beta-TG), thromboxane B2 (TXB2) and platelet aggregation adenosine diphosphate (ADP) (2 microM/ml, collagen 2 micrograms/ml) were assessed in 11 normal subjects and in 19 patients with acute myocardial infarction whose infarct-related vessels were recanalized by thrombolysis and/or PTCA. In patients with acute myocardial infarction, the plasma concentrations of beta-TG and TXB2 were significantly higher than those in normal subjects (beta-TG: 128 +/- 132 ng/ml vs 38 +/- 17 ng/ml, TXB2: 131 +/- 154 pg/ml vs 36 +/- 18 pg/ml). Collagen-induced platelet aggregation decreased significantly in patients with acute myocardial infarction; whereas, ADP-induced platelet aggregation showed no significant difference. Infarct-related vessels recanalized by thrombolysis (seven patients: group 1) and PTCA (seven patients: group 2) were patent on the follow-up angiograms. Infarct-related vessels were reoccluded in five patients immediately after PTCA or during the follow-up angiography (group 3). Beta-TG and TXB2 did not change before and after recanalization in groups 1 and 2, but increased significantly after recanalization in group 3 (beta-TG: 155 +/- 185 ng/ml----269 +/- 233 ng/ml, TXB2: 104 +/- 87 pg/ml----169 +/- 91 pg/ml). Platelet aggregation did not differ significantly among the three groups. We concluded that platelets are not activated during thrombolysis and/or PTCA in cases without reocclusion, while platelets are markedly activated during PTCA in cases with reocclusion. Thus, it is suggested that platelet activation plays an important role in the mechanism of reocclusion.

To ascertain the usefulness of continuous wave Doppler echocardiography in evaluating the severity of mitral regurgitation (MR), 29 patients with MR and 10 normal subjects were examined. The patients were categorized in three groups according to the angiographic evidence of severity of MR. To analyze the flow velocity patterns of MR, the time to peak velocity index (time from onset of MR signal to peak flow velocity/duration of MR signal), the A/B ratio (the ratio of the first and second half of the systolic MR signal area), systolic peak velocity, and diastolic peak velocity were measured using continuous wave Doppler echocardiograms. The velocity patterns of MR differed significantly among the three groups. With severer MR, the flow velocity pattern showed an earlier appearance of the peak in systole, a steeper decrease in systole and a greater increase in early diastole. The time to peak velocity index was 55 +/- 7% (mean +/- SD) in mild MR, 42 +/- 6% in moderate MR and 35 +/- 5% in severe MR. This index shortened significantly in accord with the severity of MR (mild vs moderate MR: p less than 0.001, moderate vs severe MR: p less than 0.05). The A/B ratio was 1.06 +/- 0.12 in mild MR, 1.23 +/- 0.10 in moderate MR and 1.41 +/- 0.07 in severe MR. This ratio increased significantly with the severity of MR (mild vs moderate MR: p less than 0.01, moderate vs severe MR: p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

To demonstrate diastolic pulmonary forward flow, pulsed and continuous wave Doppler echocardiograms were recorded in four patients with postoperative residual pulmonary stenosis and regurgitation (Group I). To clarify the mechanism, we further examined 24 patients with pulmonary regurgitation without diastolic pulmonary forward flow, including three patients with surgical correction of tetralogy of Fallot (Group IIa) and 21 patients with functional pulmonary regurgitation (Group IIb), and compared the peak velocity and pressure half time of pulmonary regurgitation among the three groups. Diastolic pulmonary forward flow was characterized as a flow signal which began after the abrupt cessation of pulmonary regurgitation and continued until the beginning of ejection flow. The onset of the flow coincided with that of premature opening of the pulmonary valve, and was following atrial contraction in one, before atrial contraction in two, and mid-diastolic in one. The velocity of diastolic pulmonary forward flow was increased during inspiration and its maximum velocity was 1.3 m/sec. Simultaneous recording of pressures and continuous wave Doppler echo performed in two patients in Group I showed the equalization of right ventricular and pulmonary artery pressures during the flow. There was no significant difference in the peak velocity of pulmonary regurgitation among the three groups of patients. The mean pressure half time was significantly shortened in patients in Group I (90 +/- 11 msec) compared with those in patients in Group IIa (143 +/- 40 msec, p less than 0.05) and Group IIb (310 +/- 71 msec, p less than 0.001). In conclusion, a diastolic pulmonary forward flow seems to be produced by the rapid equalization of right ventricular and pulmonary artery pressures due to severe pulmonary regurgitation in the face of decreased right ventricular compliance.