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The time from admission to reperfusion in patients with acute myocardial infarction (AMI) was compared according to the type of hospital and treatment strategy. A total of 164 patients with a first AMI within 12h of onset were enrolled at one tertiary emergency center (TEC) and 6 community hospitals (CHs). The subjects were randomly assigned to receive either primary percutaneous transluminal coronary angioplasty (PTCA) (TEC-primary PTCA and CHs-primary PTCA groups) or 800,000 units of intravenous monteplase, half the standard dose of a mutant tissue plasminogen activator (t-PA), followed by rescue PTCA if the Thrombolysis in Myocardial Infarction (TIMI) flow grade was 2 or less (TEC-monteplase and CHs-monteplase groups) on the first coronary angiogram. Sixty minutes after admission, TIMI flow grade 3 rates of the study groups were as follows, in descending order: TEC-monteplase group, CHs-monteplase group, TEC-primary PTCA group, and CHs-primary PTCA group (56%, 41%, 36%, and 8%, respectively; p

It has been reported that cardiac function can be improved by implanting a DDD pacemaker (PM) and setting a short atrioventricular (AV) delay in patients with impaired cardiac function. A previous report found that the critical AV delay that induces diastolic mitral regurgitation (MR) may represent the upper limit of the optimal AV delay. The optimal AV delay can be predicted by a simple method: slightly prolonged AV delay minus the interval between the end of the atrial kick and complete closure of the mitral valve (duration of diastolic MR) at the AV delay setting. The patient was a 84-year-old man with an old myocardial infarction. He had repeated admissions to hospital for congestive heart failure. ECG showed prolongation of the PQ interval (0.28 s) and complete left bundle branch block. Cardiac function was improved by AV sequential pacing when the AV delay was set at 120 ms. After DDD-PM implantation, the cardiothoracic ratio decreased from 57 to 45% and cardiac function was improved from New York Heart Association class III to I. The AV delay was optimized during follow-up. Four years after PM implantation, the patient was in good condition without further hospital admission. (Jpn Circ J 2001; 65: 46 - 49)

It is unknown whether the pathogenetic mechanisms underlying acute myocardial infarction (AMI) differ according to the clinical presentation of preinfarction angina, so the present study measured plasma levels of C-reactive protein (CRP) in 280 patients with AMI in whom serum creatine kinase levels were normal on admission and increased subsequently. Patients were classified into 3 groups according to the type of preinfarction angina: no angina (n=95), stable angina (n=48), and unstable angina (n= 137). Patients with unstable angina were subdivided according to the Braunwald classification: class IB (n=39), class IIB (n=22), and class RIB (n=76). There were no differences among the 5 groups in baseline characteristics. CRP on admission was significantly higher and the level of physical activity at symptom onset was significantly lower in the Braunwald class RIB group than in the other groups, but no differences were observed among the other groups. Patients with preinfarction Braunwald class IIB unstable angina had higher CRP levels on admission and symptom onset at a lower level of physical activity. In such patients, the pathogenetic mechanisms may differ from those in other subsets of patients with AMI and active inflammation may play a more important role in AMI onset.

The present study investigated the relationship between myocardial damage and C-reactive protein (CRP) levels, with no increase in creatine kinase (CK) activity, immediately after the onset of acute myocardial infarction (AMI) in 85 patients with their first reperfused anterior AMI without CK elevation on admission and no ischemic events during hospitalization. Patients were classified into those with low levels (0.3 mg/dl) of CRP (Group L; n=67) and those with high levels (or =0.3 mg/dl) of CRP (Group H; n=18). Group H had a higher proportion of patients with a history of preinfarction angina (89 vs 55%, p0.01), especially unstable angina. SigmaST in leads V1-6 on admission ECG was lower in Group H than in Group L (14+/-7 vs 21+/-13 mm, p0.05). Predischarge left ventriculography showed that the left ventricular global ejection fraction (55+/-11 vs 48+/-10%, p0.01) and SD/chord at the left anterior descending artery lesion (-1.7+/-0.9 vs -2.3+/-0.9, p0.01) were better in Group H. Multivariate analysis demonstrated that both CRP on admission (p=0.011) and preinfarction angina (p=0.002) were independently associated with better regional wall motion (SD/chord-2.0) before discharge. These results suggest that the clinical situation of elevated CRP immediately after onset is associated with less myocardial damage and better left ventricular function in reperfused anterior AMI.

Atrial flutter (AF) is a troublesome arrhythmia for patients with an implanted pacemaker. Although it has recently become possible to eliminate AF by radiofrequency catheter ablation (RF-CA), the incidence of AF before and after pacemaker implantation has not been clarified. The present study was conducted with 123 consecutive patients (69.3+/-11.6 (SD) years old) implanted with pacemakers, excluding patients who had chronic atrial fibrillation (AFib) when the pacemaker was implanted; 69 patients with atrioventricular (AV) block and 54 patients with sick sinus syndrome (including 29 patients with bradycardia-tachycardia syndrome). All patients were implanted with physiological pacemakers. The follow-up period was 4.7+/-1.9 years. In 11 of the 123 patients (8.9%), AF was observed before pacemaker implantation and the incidence was significantly higher in patients with sick sinus syndrome than in those with AV block (16.7 vs 2.9%, p

We report a case of successful transaortic closure of a postinfarction ventricular septal rupture using a Swan-Ganz catheter. The method markedly reduced a left-to-right shunt and the improved hemodynamic condition of the patient, an 81-year-old woman, was maintained for about a week before surgical treatment. Inflation of the balloon with water made the balloon visible via echocardiography and was effective in maintaining inflation and echocardiographic follow-up.

The efficacy of a short atrioventricular (AV) delay in patients with dilated cardiomyopathy has been reported, but there are deleterious effects of right ventricular pacing. Diastolic mitral regurgitation (MR) is observed in patients with elevated left ventricular end-diastolic pressure and can be induced by prolonging the AV delay in patients with DDD pacemakers. The critical PQ interval that induces diastolic MR may represent the upper limit of the optimal PQ interval. The efficacy of AV sequential pacing and diastolic MR were studied in 11 patients (68.3+/-13.7 (SD) years old) with intrinsic AV conduction and with implanted DDD pacemakers. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan-Ganz catheter and transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 ms starting from 65 ms. Pacing rate was fixed at 70-80 beats/min. In 6 of the 11 patients, diastolic MR was observed under atrial pacing and the critical PQ interval for the appearance of diastolic MR was 0.22+/-0.04 s. CO was increased from 3.8+/-0.8 to 4.3+/-0.9 L/min (p0.05) and PCWP was decreased from 7.5+/-2.8 to 5.5+/-1.6 mmHg (p0.05) by shortening the AV delay till the diastolic MR disappeared. On the other hand, in 5 of the 11 patients, diastolic MR was not observed, and CO (4.2+/-0.5 to 4.3+/-0.5L/min, ns) and PCWP (5.8+/-4.6 to 5.4+/-3.9 mmHg, ns) were not improved by AV sequential pacing. In conclusion, cardiac function may be improved by AV sequential pacing and setting the AV delay under the critical PQ interval for the appearance of diastolic MR when the diastolic MR is observed. However, AV sequential pacing may be either ineffective or even deleterious for patients in whom diastolic MR is not observed.