Quantitative evaluation of regional myocardial blood flow by videodensitometric analysis of digital subtraction coronary arteriography in humans.

Videodensitometric analysis of digital subtraction coronary arteriography, a new approach for calculating contrast disappearance half-life (T1/2), was assessed in determining regional myocardial blood flow quantitatively. Forty-one patients with coronary artery disease and 12 with angiographically normal coronary arteries underwent digital subtraction coronary arteriography by manual injection of contrast medium into the left main coronary artery. The T1/2 was calculated from a time-density curve generated in the four sectors of the myocardium perfused by the left anterior descending coronary artery. The mean T1/2 value of the four sectors correlated inversely with the great cardiac vein flow measured by the thermodilution method (r = -0.89), and appeared to be a reliable index of myocardial blood flow. The relation of mean T1/2 with percent stenosis of the left anterior descending coronary artery was curvilinear (r = 0.88) and an abnormally high T1/2 occurred in patients with coronary stenosis greater than 75%. In patients with comparable stenosis of the left anterior descending artery, the apical T1/2 was significantly increased in those with impaired apical wall motion, while it was significantly decreased in those with coronary collateral vessels. These findings suggest that regional myocardial blood flow begins to decrease in vessels with greater than 75% stenosis, and that myocardial contraction and collateral flow are additional factors that modify regional myocardial blood flow. Thus, the contrast disappearance half-life (T1/2) derived by computerized washout analysis of digital subtraction coronary arteriograms proved useful as an index for quantitative evaluation of regional myocardial blood flow.

Termination of ventricular tachycardia by an implantable atrial pacemaker and external pacemaker activator.

An atrial pacemaker was implanted in a patient who had dilated cardiomyopathy, sinus node dysfunction, and drug-resistant ventricular tachycardia (VT). VT episodes were terminated by atrial overdrive pacing using an implanted pacemaker and a newly developed hand-held external programmer/transmitter. Although successful cases of termination of intractable VT by ventricular pacing have recently been reported, the ventricular method might increase the risk of accelerating VT. Atrial overdrive pacing is a safer method since it minimizes the possibility of tachycardia acceleration and, combined with antiarrhythmic drugs, it appeared to be a unique and useful approach for the treatment of drug-resistant VT.

Changes of left ventricular pressure-diameter-velocity relations by alterations of heart rate in conscious dogs.

Changes of left ventricular (LV) pressure-diameter-velocity relations by alterations in heart rate (HR) were investigated in 6 conscious dogs, instrumented with a pair of ultrasonic crystal probe, a micromanometer in LV and pacing electrodes on the left atrium. By atrial pacing the following four stages of HR were produced: stage (S)-I 112, S-II 134, S-III 158 and S-IV 179 bpm (mean HR). These alterations in HR were repeated before and during acute pressure loadings by methoxamine infusion. LV pressure-diameter and pressure-velocity relations were evaluated by the slope value of LV peak systolic pressure (LVSP)-end-systolic diameter, E (D) max, and by the ratio of changes in mV cf (mean velocity circumferential fiber shortening) and LVSP before and during pressure loading, delta mVcf/delta LVSP, respectively. The average of E(D) max at each stage of HR was 9.45, 12.63, 12.59, 11.22 mmHg/mm, and delta mVcf/delta LVSP was -0.009, -0.006, -0.007, -0.009 circ./sec.mmHg, respectively. E(D) max increased more at S-II and S-III than at S-I, and reversely, E(D) max decreased more at S-IV than at S-II. Similarly, delta mVcf/delta LVSP increased more at S-II than at S-I and decreased more at S-IV than at S-II, while delta LVSP and delta EDD (end-diastolic diameter) were not different between stages. These changes in E(D) max and delta mVcf/delta LVSP presented the mountainous pattern effected by alterations in HR, whose changes were almost similar to that of LV peak positive dp/dt and mVcf before pressure loading. Thus, E(D) max is augmented by an increase in HR, which suggests the Bowditch-effect. Reversely, a decrease in E(D) max at a higher rate indicates a depressed inotropic state. E(D) max is dependent on HR and is a sensitive indicator of the contractility of LV.

Reconsideration of heart rate-cardiac output relationships and resting cardiac function in patients with brady-arrhythmias.

Different types of heart rate (HR)-cardiac output (COP) relationships were compared with their clinical features and hemodynamic findings in 56 patients with brady-arrhythmias (BA). HR was raised by increments of 10 beats per minute (bpm) at 3 min intervals, from spontaneous rates to 100 or 110 bpm by right ventricular pacing. Cardiac and left ventricular (LV) functions at BA were evaluated by intra-cardiac pressures, COP measured by the thermo-dilution method and echocardiographic data. HR-COP relationships were divided into the following 3 types: 24 patients of flat (F), 18 of peaked (P) and 14 of increased (I) type. There were more patients with complete atrio-ventricular block, particularly His-ventricular block, and cardiomyopathic patients with the "P" type than with the other types. Cardiac index, stroke index, stroke work index and systemic vascular resistance were greater in "I", but these differences were not significant. LV peak systolic pressure (LVSP) and end-diastolic pressure (EDP) in "I" increased more than in "F". EDP, LV end-diastolic and end-systolic dimension (ESD) in "P" increased more than in "F". Systolic excursion and LVSP/ESD ratio in "I" increased more than in the other types. Heart failure prior to implantation of pacemaker (PM) and post-PM occurred more frequently in "P". "F" and "I" patients showed comparatively good clinical courses after PM. Thus, cardiac and LV function during BA are maintained in "F" and are impaired in "P", as reported previously. On the other hand, cardiac functions are maintained in "I" as they are in "F", mainly due to contributions of the Frank-Starling mechanism and partly due to maintenance or slight augmentation of contractility.

[Cross-sectional echocardiographic visualization of the infarcted site in myocardial infarction: correlation with electrocardiographic and coronary angiographic findings].

Three dimensional assessment of the site of myocardial infarct was performed using cross-sectional echocardiography in 68 patients with old myocardial infarction. Patients with a history or electrocardiographic findings suggestive of double or multiple infarctions were excluded from the study. In patients with abnormal Q waves in V1 to V3, a regional wall motion abnormality (asynergy) was observed in the anterior portion of the interventricular septum (IVS) and the anterior free wall of the left ventricle (LV) which was extended from the base to apex. Most of them had a significant stenosis in the left anterior descending artery (LAD) distal to the first diagonal branch. Patients with Q waves in V1 to V5 or V6 showed extensive asynergy in the anterior IVS, anterior and lateral free walls of the LV extended from the base to apex. LAD stenosis proximal to the first diagonal branch seemed to be the corresponding coronary lesion. In patients with Q waves in V3 to V5 or V6, asynergy was limited to the apical half of the anterior wall of the LV. In patients with Q waves in II, III and a VF, asynergy was observed in the basal half of the posterior wall and the posterior portion of the IVS.

[Left ventricular function in hypertrophic cardiomyopathy: a Tc-99m radionuclide angiographic study during exercise].

Hypertrophic cardiomyopathy (HCM) generally shows increased systolic function of the left ventricle at rest, although patients with HCM often have decreased exercise tolerance and develop dyspnea or chest pain. The present study was to investigate of left ventricular (LV) function during exercise in 26 patients with HCM using Tc-99m equilibrium angiocardiography, and to elucidate the mechanism of impaired functional reserve during exercise. Controls consisted of 11 normal volunteers and 12 patients with chest pain syndrome who had no abnormality on coronary arteriography or left ventriculography. In patients with HCM, LV ejection fraction decreased from 65 +/- 8 (mean +/- SD)% at rest to 59 +/- 18% at peak exercise, in contrast to an increase among controls (from 56 +/- 9% to 64 +/- 9%). As compared with resting values, cardiac output increased to 168 +/- 24% at peak exercise in HCM, but the increase was significantly less than that in controls (215 +/- 47%). Stroke volume decreased gradually to 83 +/- 16% during exercise in HCM, while it increased to 114 +/- 10% at an exercise level of half intensity, and it decreased slightly to 106 +/- 16% at peak exercise. LV end-systolic volume decreased among controls to 78 +/- 27% at peak exercise, but remained unchanged in HCM (118 +/- 58%). An increase in peak ejection rate at peak exercise was less in HCM than in controls (143 +/- 26% vs 170 +/- 42%). No significant differences were observed between the two groups concerning changes in indices of LV diastolic function including LV end-diastolic volume, peak filling rate or 1/3 filling rate during exercise. In the analysis of LV function curves, pulmonary arterial diastolic pressure increased to a greater extent in HCM than in controls (19 +/- 6 mmHg vs 11 +/- 6 mmHg); whereas, an increase in the stroke work index was less in HCM (80 +/- 26 g.m/m2/beat vs 121 +/- 21 g.m/m2/beat) at peak exercise. Thus, the LV function curve shifted downward and to the right in patients with HCM. The above findings indicate that LV functional reserve during exercise is impaired, especially as to systolic function in patients with HCM, while deterioration of diastolic function may be partly compromised by elevated filling pressure.

Aneurysm of the left aortic sinus causing acute myocardial infarction.

A 30-year-old female had an acute myocardial infarction complicated by congestive heart failure. Angiography demonstrated an aneurysm in the area of the left aortic sinus. The aneurysm compressed and displaced the main trunk of the left coronary artery and the proximal portion of the left anterior descending artery. This aneurysm was considered to be the cause of the infarction. Aortic valve replacement and removal of the aneurysm were performed. Postoperative studies revealed good function of the replaced valve, good antegrade filling of the left coronary artery, and improved left ventricular function.

[Mechanism of exercise-induced ST segment deviation in myocardial infarction: a 201T1-myocardial scintigraphic study].

Exercise-induced ST segment deviation was investigated using thallium-201 myocardial scintigraphy and correlated with coronary artery lesions in 25 patients with old myocardial infarction. Seven of eight patients without ST deviation showed no reversible perfusion defect by near maximal exercise, and six had no significant stenosis in the coronary arteries perfusing the non-infarcted area. During exercise, ST segment depression was induced in 12 patients and six of them developed a reversible perfusion defect in the non-infarcted area, associated with significant stenosis of the corresponding coronary arteries. Remaining six patients, however, did not show a reversible perfusion defect and four of them had no significant stenosis of the coronary arteries perfusing the non-infarcted area. In nine patients with exercise-induced ST segment elevation in leads with Q waves, a reversible perfusion defect was not detected in seven (78%) and five (71%) of them had no significant coronary artery stenosis as well. Four patients developed both ST segment elevation in leads with Q waves and ST segment depression in other leads. One patient who had significant coronary artery stenosis in the non-infarcted area and showed a reversible perfusion defect developed 1.5 mm ST elevation in II, III, a VF leads and 4 mm ST depression in precordial leads. In the remaining three patients who did not show a reversible perfusion defect and significant coronary artery stenosis in the non-infarcted area, ST depressions were less than 2 mm.(ABSTRACT TRUNCATED AT 250 WORDS)

[Exercise two-dimensional echocardiography: correlation between exercise induced asynergy and coronary artery lesions].

Exercise two-dimensional (2-D) echocardiography was performed in patients with suspected coronary artery disease, and exercise induced left ventricular asynergy was evaluated qualitatively and was compared with the coronary artery stenosis and electrocardiographic ST changes. Subjects were 12 patients with angina of effort, 8 patients with spontaneous angina, 8 patients with chest pain syndrome with the normal coronary artery, and 7 patients with hypertrophic cardiomyopathy (HCM). Cases with myocardial infarction were excluded from this study. 1) Left ventricular asynergy during exercise was observed in 10 and ST depression in 11 of 12 patients with angina of effort. In patients with spontaneous angina, left ventricular asynergy and ST depression during exercise were observed in 2 of 8 patients without anginal pain, and both patients had coronary artery stenosis of 90% or more. 2) Exercise induced asynergy was also observed in 4 of 7 patients with HCM without coronary artery stenosis. It seemed likely that the markedly hypertrophied myocardium and impairment of left ventricular compliance and relaxation may induce relative myocardial ischemia.

[Detection of exercise induced left ventricular asynergy by two-dimensional echocardiography (author's transl)].

In order to detect an exercise induced asynergy, cross-sectional echocardiography was performed during multistage maximal bicycle ergometer stress test in the supine position. 1) Left ventricular (LV) asynergy occurred earlier than or simultaneously with the appreciable ST segment change. 2) In patients with angina, LV asynergy appeared in the area of dominant coronary stenosis, while ST depression was seen in V3-6 as well as II, III and aVF, despite of the localized area of asynergy. 3) In patients with myocardial infarction, LV asynergy increased or extended over or around the infarcted area except one case, ST segment elevated in the leads over the infarction with abnormal Q waves and depressed in the reciprocal leads. These observations revealed that ST depression does not necessarily mean an occurrence of new ischemia over the corresponding area in myocardial infarction. Thus exercise cross-sectional echocardiography was demonstrated to be a good method to detect an exercise induced ischemia and would be particularly valuable in view of the coronary artery bypass.