spontaneous increase in the electrocardiographic (ECG) R-wave voltage after acute myocardial infarction (MI) is a unique phenomenon, and regeneration of R-waves or disappearance of Q-waves after acute ischemic events has been reported. [1][2][3][4][5][6][7] With the prevalence of interventional therapy, it is thought that this phenomenon is increasing, but little is known regarding the physiological mechanism involved.Patients with acute MI always undergo echocardiography in order to evaluate changes in wall motion, left ventricular (LV) cavity, and LV function over time. Myocardial scintigraphy provides important information about myocardial perfusion and/or metabolism. Specifically, a combined study of myocardial metabolic tracer with perfusion tracer provides clues about the myocardial status in the healing stage of MI. [8][9][10] Perfusion -metabolism mismatch of the Circulation Journal Vol. 70, November 2006 perfusion/metabolic dual-tracers represents impaired but viable myocardium in the risk area, which is involved in functional recovery after revascularization in patients with acute MI. 11-13 Therefore, both examinations are cardinal diagnostic modalities for patients after acute MI.In this study, we performed dual-isotope scintigraphy and echocardiography, and compared the findings with ECG results to determine the physiological mechanism of the increase in ECG R-wave voltage during the acute to the subacute phase after revascularization in patients with acute MI. Methods PopulationOne hundred and seventy-one consecutive patients with first onset of acute MI who underwent emergency coronary revascularization, dual-isotope scintigraphy, and echocardiography between January 1998 and March 2004 were retrospectively examined. Acute MI was diagnosed by typical chest pain for >30 min, ECG ST-elevation of ≥0.1 mV (1 mm) in at least 2 contiguous leads, and a characteristic rise in plasma creatine kinase-MB activity. All patients underwent emergency coronary angiography (CAG) immediately after the ECG diagnosis and subsequent coronary revascularization. In the emergency CAG, antegrade flow was characterized using the Thrombolysis In Myocardial Background The physiological mechanism of the increase in the electrocardiographic (ECG) R-wave voltage after revascularization in patients with acute myocardial infarction (MI) needs to be elucidated. Methods and ResultsOne hundred and thirty-eight MI patients (83: anterior MI, 45: inferior MI, 10: lateral MI) underwent ECG and echocardiography in both the acute and subacute phases after emergency revascularization, as well as a resting thallium-201/iodine-123 15-p-iodophenyl-3-(R,S)-methyl pentadecanoic acid myocardial scintigraphy in the acute phase. The total sum of the R-wave voltage (∑R) was calculated over multiple leads on ECG for each infarcted lesion. Scintigraphic defect on each tracer was expressed as the percentage (%) defect of the total left ventricular (LV) myocardium. The % defect-discordance on both images in the acute phase and the % increase in ∑R an...

An age-related change in cardiac performance is apparent at an approximately 1 year follow-up in postmenopausal women. In particular, the increase in LV systolic function tends to show the greatest value in the 50s subjects among the 3 generations.

We compared resting beta-methyl-iodophenyl pentadecanoic acid (BMIPP) tomography with resting thallium-201 tomography in 28 patients with unstable angina. Tracer distribution was displayed on a polar map and compared with a normal standard deviation map obtained from a group of 12 normal subjects. The extent scores and severity scores obtained by BMIPP were significantly greater than those obtained by thallium-201. Confirmation by coronary angiography revealed the sensitivity of the methods in identifying patients to be 89% for BMIPP and 54% for thallium-201. There were significant differences between BMIPP and thallium-201 in the sensitivities of detecting postischemic jeopardized myocardium in the area supplied by the right coronary artery (RCA; 53% vs 18%, p < 0.05), left circumflex artery (LCX; 78% vs 39%, p < 0.025) and all 3 vessels combined (71% vs 35%, p < 0.001) but no significant differences in specificity (RCA: 82% vs 64%; LCX: 70% vs 90%; and total 3 vessels combined: 75% vs 79%). In conclusion, resting BMIPP tomography is more sensitive than resting thallium-201 tomography in detecting postischemic myocardial damage in patients with unstable angina.

This study was designed to determine the effects of antiarrhythmic agents on global left ventricular (LV) function during exercise in patients with chronic LV dysfunction. Thirty-five patients with LV dysfunction [LV ejection fraction (LVEF) < 45%] and ventricular arrhythmias were studied. They were randomly classified into 3 groups: patients who received a single oral dose of 6 mg/kg disopyramide phosphate (n = 12), those who received a single oral dose of 4 mg/kg mexiletine hydrochloride (n = 12), and those who received a single oral dose of 4 mg/kg pilsicainide hydrochloride (n = 11). First, all patients were subjected to baseline rest and peak exercise, equilibrium-gated cardiac-pool scintigraphy with 99mTc-human serous albumin of 740 MBq (baseline data). Second, on a separate day, they were given drugs once, and were subsequently subjected to rest and peak exercise equilibrium-gated cardiac-pool scintigraphy. Exercise LVEF and peak ejection rate (PER) after administration were significantly lower in the disopyramide and pilsicainide groups than in the mexiletine group (p < 0.05, respectively). The changes in LVEF and PER from rest to peak exercise after administration were significantly less than the baseline changes in those in the disopyramide and pilsicainide groups (p < 0.05, respectively). However, no significant changes in functional parameters were recognized in the mexiletine group. Due care should be taken when disopyramide and pilsicainide are administered to patients with chronic LV dysfunction since they reduce systolic LV function during exercise.

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