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Objectives. The present study investigated the long-term changes in the electrocardiographic (ECG) hallmarks of the Japanese form of apical hypertrophy. Background. Giant negative T waves and tall R waves in the left precordial leads are the ECG hallmarks of the Japanese form of apical hypertrophy. However, the long-term course is largely unknown. Methods. Twenty-nine patients with apical hypertrophy (26 men, 3 women, mean age ± SD 50.4 ± 8.2 years) who showed left precordial giant negative T waves (≤−10 mm) and tall R waves (≥26 mm) and spade configuration in the left ventriculogram were followed up for 10.9 ± 3.7 years. Results. The intermediate follow-up ECGs (5 to 9 years) showed disappearance of giant negative T waves in 31% and of tall R waves in lead V5in 6%. At the long-term follow-up study (≥10 years), loss of giant negative T waves increased to 71%, with average T wave negativity in lead V4or V5decreasing from −16.5 ± 5.1 to −6.9 ± 4.2 mm. These T wave changes were associated with decreases in R wave amplitude in lead V5from 40.7 ± 9.6 to 26.1 ± 13.8 mm, with loss of tall R waves in lead V5in 38% of patients and development of abnormal Q waves in two patients. Conclusions. During the long-term follow-up of the Japanese form of apical hypertrophy, giant negative T waves disappeared in association with decreases in R wave amplitude in lead V5, indicating that these ECG hallmarks are clinical features that evolve progressively during the natural course of the disease.

We investigated whether percutaneous transluminal coronary angioplasty (PTCA) would induce neutrophil activation in patients with coronary artery disease. Blood samples were taken from the coronary sinus in 14 patients who underwent PTCA and in 9 control subjects who underwent coronary arteriography (CAG). Flow cytometry was used to measure membrane surface expression of beta 2 integrin (CD11b) and the generation of hydrogen peroxide in neutrophils after ex vivo phorbol myristate acetate stimulation by 2,'7'-dichlorofluorescein. Neutrophil elastase was measured by an immunoenzymatic method. Surface expression of CD11b increased significantly, approximately twofold, after PTCA but not after CAG. Mean fluorescence intensity of 2',7'-dichlorofluorescein in stimulated neutrophils decreased significantly after PTCA, suggesting a previous in vivo activation, but not after CAG. Neutrophil elastase increased significantly after PTCA but not after CAG. These data indicate that PTCA induces neutrophil activation and suggest that neutrophils may contribute to the ischemic injury.

Severe coronary artery stenosis with endothelial injury in the canine model induces cyclic coronary flow variations (CFVs), which are partially due to spontaneous platelet aggregation and dislodgement at the stenotic site. In the present study, we used anesthetized open-chest and unsedated closed-chest dogs with CFVs to investigate whether oxidative metabolic burst (hydrogen peroxide generation) occurred in neutrophils during CFVs and whether CFVs were attenuated by superoxide dismutase (SOD) and catalase. CFVs were produced by placing a cylindrical constrictor on the left anterior descending coronary artery (LAD). LAD blood flow was monitored by means of a Doppler flow probe placed proximally to the constrictor, and the severity of CFVs was expressed by both the frequency of CFVs and mean LAD blood flow. Hydrogen peroxide generation in neutrophils was measured by flow cytometry, using single cell analysis, and was expressed as the mean fluorescence intensity of 2’, 7’-dichlorofluorescein. Dogs received an intravenous infusion of saline (n = 8), SOD (5 mg/kg, n = 7), catalase (5mg/kg, n = 7), or a combination of SOD and catalase (same doses, n = 7). Although the mean fluorescence intensity did not change in sham-operated dogs without CFVs (61.7 ± 15.8 to 60.4 ± 11.8; NS), the intensity in the dogs with CFVs was significantly increased during CFVs (62.2 ± 13.7 to 79.8 ± 9.8; P < 0.005). These results indicate that hydrogen peroxide is generated in neutrophils.

To elucidate the mechanism of ST segment depression in patients with syndrome X, myocardial blood flow and myocardial O2 and lactate uptake were evaluated in 25 patients who had exhibited chest pain but had normal coronary arteriograms. Fourteen of the patients had chest pain and ST segment depression in an exercise stress test (SX), while the remaining 11 did not exhibit either of these symptoms (control). Atrial pacing induced significant ST segment depression in all patients with SX and did not do so in controls. There was no evidence of coronary artery spasm produced by intravenous administration of ergometrine maleate in any patients. Myocardial blood flow was measured with a Webster’s thermodilution catheter. Coronary flow reserve was defined as the increase occurring in coronary flow after the administration of intravenous dipyridamole (0.56 mg/kg), divided by coronary flow at rest. After the administration of dipyridamole, the coronary flow reserve was 2.70 in the SX group and 2.90 in the controls; this difference was not significant. During atrial pacing, there was a reduction of myocardial lactate uptake and a rise in left ventricular end-diastolic pressure in the SX group, but not in the controls. Oxygen saturation in coronary sinus blood did not change significantly in the controls, while it rose significantly in SX patients.

We have developed a new noninvasive method to evaluate regional left ventricular (LV) function by digital subtraction angiography (DSA) without the use of contrast medium. DSA images of the left ventricle with and without contrast medium were obtained from 35 patients with anterior myocardial infarction (MI) and from 35 control subjects. Using an image-processing computer, regional LV time-density curves were constructed for one cardiac cycle. Regional LV time-density curves obtained from DSA without the use of contrast medium presented a pattern similar to those from intravenous DSA. The amplitude of regional LV time-density curves in patients with MI decreased along with increasing severity of regional wall motion abnormality assessed by conventional left ventriculography. In attempting semi-quantitative evaluation by DSA without the use of contrast medium, the regional wall motion index (RWI) in the 6 segments of the left ventricle was calculated by normalizing segmental density changes to the maximal segmental density changes. When compared with control subjects, patients with MI have significantly lower RWIs in the anterolateral and apical regions. RWI showed a good correlation with the regional ejection fraction (REF) obtained from intravenous contrast DSA (r = 0.83). RWI decreased with increasing severity of regional wall motion abnormality by qualitative analysis in conventional left ventriculography, being consistent with REF. The diagnostic accuracy of RWI therefore seemed to be comparable to that of REF derived from intravenous contrast DSA. These results indicate that computerized analysis of DSA without the use of contrast medium is a valuable noninvasive method for semi-quantitative assessment of regional LV function.

To assess the effects of pacing-induced left bundle branch block on left ventricular (LV) systolic and diastolic performance, we performed digital subtraction ventriculography while simultaneously measuring LV pressure with a catheter tip micromanometer. The subjects included 10 patients with a sinus rhythm, a normal QRS duration and PR interval within 0.22 sec. LV performance was assessed during both right atrial pacing (AP) and atrioventricular sequential pacing (AVP) at the same pacing rate. The atrioventricular pacing interval during AVP was adjusted to be the maximal interval that showed the QRS configuration seen during complete right ventricular pacing. LV end-diastolic pressure and volume during AVP did not differ from those during AP. Peak positive and negative dp/dt during AVP were significantly lower than those during AP. Time constants were also significantly longer during AVP. The QRS duration during AVP significantly correlated with end-systolic volume and time constants, and inversely correlated with ejection fraction and +dp/dt. These observations indicated that conduction disturbance per se, induced by AVP, could not only impair LV systolic performance but also diastolic performance, possibly due to asynchronous contraction and relaxation of the left ventricle.

To clarify the mechanism of stress-induced ST segment elevation in patients with previous anterior myocardial infarction, we examined myocardial lactate metabolism during atrial pacing in 32 patients with previous anterior myocardial infarction (MI group) and 11 control subjects (control group). In the MI group, atrial pacing resulted in new or additional ST segment elevation in leads with Q waves in 15 patients (ST elevation group), ST segment depression in 7 (ST depression group), but induced no appreciable ST segment changes in the remaining 10 patients (ST unchanged group). In all patients, the ST segment changes were identical to the results of exercise stress testing which was carried out prior to the atrial pacing. Lactate extraction ratio increased moderately during the atrial pacing in the control group (p

Right ventricular ejection fractions were determined by videodensitometric computer analysis of digital subtraction angiography in 50 patients with various cardiac diseases. Using intravenous injection of 35 ml sodium meglumin diatrizoate at a constant rate of 12 ml/min, serial right ventriculograms were obtained in the right anterior oblique projection. Right ventricular enddiastolic and end-systolic counts and ejection fractions were obtained by integrating densitometric counts within the, right ventricular region of interest, in addition to application of the conventional pyramidal method. The obtained right ventricular densitometric counts correlated closely (r=0.91) with the single-plane right ventricular volumes. The right ventricular ejection fraction determined by video-densitometry also exhibited satisfactory correlation (r=0.74) with that by single-plane ventriculography. Thus, videodensitometric analysis of digital subtraction right ventriculograms are an acceptable method for the determination of the right ventricular ejection fraction, and therefore videodensitometric analysis is recommended as a convenient method for clinical practice.