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A 28-year-old man was admitted to our hospital in a hypotensive state 2 hours after taking 8,400 mg disopyramide. Infusion of catecholamine and gastric lavage restored normal blood pressure. However, 8 hours after taking the disopyramide he became hypotensive again and electrocardiographic findings revealed bizarre ventricular complexes resulting in ventricular flutter. Although standard cardiopulmonary resuscitation was not effective, his circulatory status was maintained by percutaneous cardiopulmonary support (PCPS). After 36 hours electrocardiography showed sinus rhythm, and his cardiac function became normal. Patients with severe cardiac dysfunction or cardiac arrest caused by disopyramide intoxication can be supported by PCPS until cardiac function is restored.

Rapid and complete reperfusion is important for the reduction of infarct size and mortality in acute myocardial infarction. The optimum reperfusion therapy with regard to the recanalization rate and the time elapsing between onset and complete reperfusion was evaluated. One hundred fifty-four patients with total occlusion of the infarct-related artery within 6 hours of the onset were classified into four therapy groups: PTCA group (n = 58) undergoing primary percutaneous transluminal coronary angioplasty (PTCA), t-PA-IC group (n = 44) receiving tissue plasminogen activator (t-PA) intracoronary infusion, t-PA-IV group (n = 14) receiving intravenous t-PA infusion, and mt-PA-IV group (n = 38) receiving intravenous mutant t-PA infusion. Although the recanalization rate was high in the PTCA group, there were no differences between the four groups as a supplement to immediate or rescue PTCA. The time elapsing between initiation of thrombolysis and complete reperfusion was shorter in the mt-PA-IV group than in the t-PA-IV group. Assuming the time from hospital arrival to initiation of intravenous thrombolysis was 20 min, the recanalization rate at 60 min after arrival in hospital was higher in the mt-PA-IV group than the PTCA and t-PA-IC groups. Although additional coronary angiography and PTCA may be required to improve the low recanalization rate compared with primary PTCA, intravenous infusion of mutant t-PA was the most promising therapy to achieve early reperfusion.

The effects of right ventricular outflow pacing were studied in 13 patients (mean [+/-SD] 69.8 +/- 8.2 years old). All patients received DDD pacemakers except two patients with implanted VVI pacemakers who had chronic atrial fibrillation. Cardiac output and pulmonary capillary wedge pressure were measured by Swan-Ganz catheter. Pacing rate was fixed at 70-80/min and atrioventricular delay was fixed at 165 msec. When the pacing site was changed from the right ventricular apex to the right ventricular outflow during right ventricular pacing in 11 patients, cardiac output increased from 3.3 +/- 0.6 to 3.4 +/- 0.5 l/min (p < 0.001), and wedge pressure decreased from 9.3 +/- 1.9 to 8.8 +/- 2.0 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow during atrioventricular pacing in eight patients, cardiac output increased from 3.9 +/- 0.4 to 4.0 +/- 0.4 l/min (p < 0.05), and wedge pressure decreased from 7.1 +/- 2.3 to 6.6 +/- 2.1 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow in seven patients with ejection fraction (EF) greater than 55%, cardiac output increased from 3.6 +/- 0.5 to 3.7 +/- 0.4 l/min (p < 0.05), and in four patients with EF less than 55%, it increased from 2.9 +/- 0.4 to 3.0 +/- 0.4 l/min (p < 0.01). Cardiac function was improved by right ventricular outflow pacing compared to right ventricular apex pacing regardless of the pacing mode or cardiac function.

The clinical significance of additional ST segment elevation immediately after reperfusion in acute myocardial infarction (AMI) is still unclear. The influence of additional ST elevation on myocardial damage was examined in 62 patients with first anterior AMI. All patients had coronary reflow (thrombolysis in myocardial infarction: TIMI grade III) within 6 hours after the onset of infarction and no subsequent reocclusion for at least 14 days. The patients were classified into two groups: group ST (+), 26 patients with additional ST elevation (> or = 5 mm increase in sigma ST in lead V1-V6) immediately after reperfusion, and group ST(-), 36 patients without additional ST elevation. Myocardial damage was estimated by the number of abnormal Q wave before and 1 hour after reperfusion (nQpre and nQpost. There were no significant differences in the elapsed time, ECG indexes before reperfusion and regional wall motion (RWM: SD/chord; SD = standard deviation) in the acute phase and 14 days after the onset between the two groups. Moreover, within each group the patients were classified into two groups on the basis of RWM 14 days after the onset: group A = RWM < -2.5 in group ST (+) (n = 17); group B = RWM > or = -2.5 in group ST(+) (n = 9); group C = RWM < -2.5 in group ST (-) (n = 14); group D = RWM > or = -2.5 in group ST(-) (n = 22). There were no significant differences in the elapsed time between the four groups. nQpre was highest in group C and was lowest in group D (group A: 2.1, group B: 1.9, group C: 4.1, group D: 1.4), and nQpost was highest in group C and group A, and was lowest in group D (group A: 4.1, group B: 2.7, group C: 4.4, group D: 2.0). There was a significant increase in nQ after reperfusion (nQpost-nQpre) in group A and group B, which was greater in group A than in group B. The increase in sigma ST after reperfusion was greater in group A than in group B. There was no significant increase in nQ after reperfusion in group C and in group D, and both nQpre and nQpost were highest in group C, and lowest in group D. Infarct size was larger in group A and in group C than group B and group D, and there was no significant improvement in RWM in group A and in group C. In conclusion, additional ST elevation immediately after reperfusion seems to occur in patients with not so severe myocardial damage before reperfusion, and may reflect reperfusion injury. Additional ST elevation is not observed in patients with preceding extensive myocardial damage which may be irreversible or not still advanced at the time of reperfusion.

Generally, the time from the onset of acute myocardial infarction (MI) to peak serum creatine kinase (CK) activity is short in patients with acute MI after successful reperfusion. However, in some patients peak CK is observed more than 16 hours after the onset of acute MI despite successful reperfusion. To elucidate the clinical characteristics of patients with late peak CK, CK activity was examined in 55 patients (mean age: 57.5 +/- 10.2 years) with initial acute anterior MI after successful reperfusion. All patients had coronary reflow (TIMI grade 3) within 6 hours after onset of acute MI and no subsequent reocclusion for at least 14 days. The patients were classified into two groups: group E, 41 patients with peak CK observed within 16 hours of onset of acute MI (mean 8.7 hours), and group L, 14 patients with peak CK observed after more than 16 hours (mean 18.7 hours). Although there were no significant differences in the time elapsed between the two groups, the mean peak CK was significantly lower in group L than in group E (2,179 +/- 861 vs 5,379 +/- 2,569 mU/ml, p < 0.01). Well-developed collateral supplies to the infarcted area before reperfusion were observed more frequently in group L (79% vs 24%, p < 0.01). The sum of ST elevation in all leads before reperfusion was lower in group L (12 +/- 7 vs 20 +/- 12 mm, p < 0.01) and additional ST elevation during reperfusion was not observed in group L (0% vs 56%, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship between the time course of inverted T-waves during the acute phase and infarct size and left ventricular (LV) function was studied in 46 patients (mean age: 57.3 +/- 9.7 years) with reperfused first anterior wall acute myocardial infarction (MI). All patients had coronary reflow within 6 hrs after the onset of MI and were without subsequent reocclusion for at least 14 days. The T-wave inverted progressively and rapidly with maximum depth between 26 and 60 hrs (mean time: 37.1 +/- 12.4 hrs). A significant correlation was found between the maximum T-wave depth (T-peak) in all patients and peak CPK, left ventricular ejection fraction (LVEF), regional wall motion, % abnormally contracting segment (%ACS), end-diastolic and end-systolic volume indices (EDVI,ESVI) at day 14 after the onset of MI (p < 0.05). T-wave inversion within 24 hrs after onset of MI was observed in 43 patients (93%). There were significant correlations between the depth of T-wave inversion occurring in patients 24 hrs after onset of MI (T24) and peak CPK, LVEF, regional wall motion, % ACS, EDVI, and ESVI at day 14 (p < 0.05). The sensitivity and specificity for patients with EDVI > 87.0 ml/m2 at day 14 increased by more than 20% over normal values, predicted by a T24 of 3.0 mm or less, were 94% and 93%, respectively. The sensitivity and specificity for patients with EF < 40% at day 14 predicted by a T24 of 3.0 mm or less, were 90% and 75%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Non-invasive evaluation of systemic hemodynamics during exercise in ischemic heart disease (IHD) was attempted by simultaneous measurement of cardiac output by the CO2 rebreathing method and indirect blood pressure in 44 males and 7 females with suspected IHD who underwent left ventriculography and coronary angiography. Thirty-nine of the 51 patients had abnormalities in the regional left ventricular systolic function (asynergy) and/or 75% or more stenosis of the major coronary arteries (IHD group). The other 12 patients were free of these findings, and injection of acetylcholine into the coronary arteries did not induce spasm. These patients were used as the control group. There were no differences in cardiac index (CI), mean blood pressure (MBP), or total peripheral resistance index (TPRI) at rest between the 2 groups. The IHD group had significantly lower CI (p < 0.01) and significantly higher TPRI (p < 0.05) during 25 and 50W exercise than the control group. There were no differences in MBP. A discriminant function using the change in CI (delta CI: l/min/m2) and the percent change in TPRI (% delta TPRI: %) during 25W exercise could predict IHD or control patients with probabilities of 82 and 83%, respectively. D = 3.66-1.39 x (delta CI)-6.67 x 10(-3) x (% delta TPRI), where D > or = 0.3 indicates IHD, and D < 0.3 indicates control. These results suggest that IHD patients have abnormal systemic hemodynamics during mild upright ergometer exercise, even though the resting hemodynamics are nearly normal.(ABSTRACT TRUNCATED AT 250 WORDS)