Kaname Iida

Mechanisms of stress-induced ST elevation and negative T-wave normalization studied by serial cardiokymogram in patients with a previous myocardial infarction

Seventeen patients with a previous myocardial infarction were studied during pacing to characterize the clinical correlates of ST elevation, to analyze the relation between ST elevation and negative T-wave normalization and to investigate the mechanism of these electrocardiographic changes. Myocardial ischemia was evaluated by measurement of blood lactate, and wall motion was analyzed using cardiokymographs concurrently and serially. Results show that ST elevation and negative T-wave normalization were most marked in leads containing abnormal Q waves, that ST elevation greater than or equal to 1 mm during pacing was associated with a significant increase in left ventricular end-diastolic pressure and deterioration of left ventricular wall motion and that the magnitude of ST elevation and negative T-wave normalization was significantly correlated, but the latter appeared earlier and more markedly. In addition, there was no significant correlation between the extent of either ST elevation or negative T-wave normalization and myocardial lactate production. Thus, ST elevation and negative T-wave normalization are caused by abnormal left ventricular wall motion rather than myocardial ischemia. Negative T-wave normalization is a more sensitive marker of abnormal wall motion than ST elevation in patients with a previous myocardial infarction.

Daily variations of ECG and left ventricular parameters at exercise in patients with anginal attacks but normal coronary arteriograms

In 21 patients with typical exercise-induced anginal pain but normal coronary arteriograms (group N) and in 14 patients with angiographically proved coronary stenosis (group C), symptom-limited ergometer exercise ECG and radionuclide angiocardiography were performed twice on two different days. Exercise-induced ST changes showed larger variations between the two exercise tests in group N than in group C ([delta ST1-delta ST2]: 0.07 +/- 0.06 mV in group N, 0.03 +/- 0.03 mV in group C, p less than 0.05). Rate pressure product and left ventricular ejection fraction at exercise also showed larger variations between the two tests in group N than in group C (p less than 0.001, p less than 0.05, respectively). However, substantial overlaps existed in some cases in the two groups. In conclusion, some of the patients with exercise-induced anginal pain but normal coronary arteriograms may have a variable threshold of exertional chest pain probably caused by variation in coronary vascular tone, and the other patients may have a fixed threshold of chest pain caused by other mechanisms.

A study of ventricular contraction sequence in complete right bundle branch block by phase analysis

Twenty-four patients with complete right bundle branch block (CRBBB) combined with and without left axis deviation (LAD) on ECG, were compared with 17 normal subjects to evaluate the right ventricular contraction sequence and pattern in detail. Blood pool scintigrams were obtained in the left anterior oblique projection, and these images were analyzed by first component Fourier harmonics.In the normal subjects, the phase value distribution representing the pattern of ventricular contraction was almost homogeneous in both the right and left ventricles (RV & LV). In the CRBBB patients without LAD, the phase images showed apparent phase delay in the right ventricle. In the CRBBB patients with LAD, the phase images showed many different contraction patterns varying from normal to RV phase delay, owing to the effects of the hemiblock. Quantitative analysis of the absolute values, showed that the mean (RV-LV) value was 6.6±8.4 msec in the normal subjects. In the CRBBB patients without LAD, the duration of the QRS complex correlated with the mean (RV-LV) value, whereas no difference was observed between the duration of the QRS complex and the standard deviation of the right ventricle. Using phase analysis the degree of the RBBB can be determined from the phase images, and can be quantitatively analyzed as in electrical studies.

Perfusion and mechanical analysis with technetium-99m 2-methoxy-isobutyl-isonitrile in a case of dilated cardiomyopathy

With technetium-99m 2-methoxy-isobutyl-isonitrile (99mTc-MIBI), regional wall thickening in a patient with dilated cardiomyopathy was analyzed by the first component Fourier method. The regional wall thickening was compared with thallium-201 and99mTc-MIBI SPECT imaging. Thallium-201 SPECT images showed mildly reduced perfusion in the posterior wall and redistribution in the septum, whereas99mTc-MIBI images showed heterogeneous accumulation around the left ventricular circumference. By means of phase analysis, diffusely decreased wall thickening and discontinuity of percent wall thickening in neighboring segments were observed throughout the left ventricle. Regional wall motion and wall thickening correlated roughly. However, discrepancies between the mechanical function and myocardial perfusion, and discrepancies in regional myocardial perfusion between thallium-201 and99mTc-MIBI were observed.

The Human Sinus Node Electrogram on the Overdrive Suppression Test and Estimated Sinoatrial Conduction Time Measurements

Sinus node electrograms (SNEs) on atrial overdrive suppression test (AOD) and estimated sinoatrial conduction time (SACT) measurements were recorded. Typical SNE (TSNE), characterized by low-frequency, anatomically localized pre-P wave potentials (Reiffel et al.) were obtained in 12 of 18 patients (pts) with normal sinus node function (group I) and 15 of 26 pts with sick sinus syndrome (SSS) (group II). In 9 of 15 SSS pts but only 2 or 12 in group I “atypical” SNEs (ASNE) with inverted waves at the beginning of P wave were recorded on SNE recordings of the first sinus recovery beat by overdrive atrial pacing (OAP) for either AOD or SACT measurements, or both. On the basis of ASNE following OAP, the 26 SSS pts fell into 3 subgroups: TSNE with the same configuration as recorded before OAP was observed without ASNE throughout the study in 6 pts (IIA). ASNE was observed without TSNE throughout the study in 11 pts (IIB). TSNE before OAP and ASNE following OAP were recorded in 9 pts (IIC). Corrected sinus node recovery time in IIB was significantly longer than in either IIA or IIC (P < 0.0005). Estimated SACT (Narula’s method) for either A, B or C was significantly (P < 0.0005) longer than in group I. There was no significant difference in either estimated SACT or directly measured SACT between IIA and IIC. A significant correlation existed between estimated SACT and directly measured SACT in group I (r = 0.88) and IIA (r = 0.75) (P < 0.01) but not in IIC (r = 0.48). ASNE may result from a pacemaker shift.