Journal of cardiography最新文献

To assess the left ventricular (LV) diastolic properties, the influence of heart rate change induced by atrial pacing on LV pressure-mitral valve (MV) flow velocity curves was studied. Simultaneous recording of MV flow velocity using pulsed Doppler echocardiography and LV pressure via a catheter-tip micromanometer was performed in 12 cases with past history of Kawasaki disease. Heart rates were increased in gradations of 10 beats from rest to 180 beat/min, or to the time when A-V block occurred. Diastolic LV pressures and MV flow velocities were plotted manually every 10 msec to establish pressure-velocity relationships at each heart rate. The relationship of LV pressure and MV flow velocity was non-linear, and formed a loop. At rest, this loop showed counterclockwise rotation (CCR) in all cases. By increasing heart rate, rotation changed from CCR to clockwise rotation (CR), except in two cases. With much greater increase in heart rate, CCR reappeared in five cases (second CCR). CCR may indicate that the increment of MV flow is smaller than the fall in LV pressure in the early diastolic filling period, suggesting the existence of inflow resistance. This is thought to be physiologic, and it is suspected that it is produced mainly by the MV and subvalvular structures. CR indicates that the MV flow velocity increases more rapidly than the fall in LV pressure, demonstrating that the resistance to inflow is reduced by increasing heart rate, and the increment of left atrial (LA) driving pressure plays a main role. In a case with simultaneous recording of LA and LV pressures, LA pressure became elevated and the LA-LV pressure gradient increased with an increasing heart rate. This suggests that the increment of LA pressure relates to a decrease of inflow resistance. The second CCR suggests that a resistance is produced beyond a capacity to compensate for elevated LA pressure. It can be speculated that this resistance is related to visco-elasticity of the LV, in addition to the MV and subvalvular structures.

Coronary artery aneurysms are the most frequent and important complication of Kawasaki disease, but valvular disease is less frequently observed. During the last three years, we have observed mitral regurgitation (MR) in nine (7.3%), aortic regurgitation (AR) in six (4.6%) and tricuspid regurgitation (TR) in five (4.2%) patients with Kawasaki disease. The diagnosis of valvular disease was confirmed by Doppler echocardiography in all patients. Cardiac murmurs typical of regurgitation were audible in approximately half the patients with MR and AR, and in only one with TR. By chest radiography, cardiomegaly was observed in five of nine patients with MR and in three of six with AR, but in none with TR. Similarly, the ECG finding of cardiac overload was observed in four patients with MR and in three with AR, but in none with TR. Thus, Doppler echocardiography proved very valuable for diagnosing valvular regurgitation in patients with Kawasaki disease. Other cardiovascular complications included coronary artery aneurysms in all except for only one patient with TR. Subsequent myocardial infarction was observed in three patients with MR and in two with AR. Valvular lesions complicating Kawasaki disease generally carry a good prognosis, without progression to stenotic valvular lesions. Although the exact mechanism of this complication is obscure, it is postulated that the valvular lesion results from myocardial infarction or from inflammation of the valvular leaflets or apparatus of the valve following carditis.

To evaluate cardiac function, ventricular power during ejection (power) and the rate of change of power (dPower/dt) were assessed noninvasively. Power was determined from the product of aortic flow (Fa(t] and brachial arterial pressure (Pa(t]. Fa(t) was measured at the suprasternal notch using an ultrasonic pulsed Doppler flowmeter with a 2 MHz carrier frequency and 10 KHz repetition frequency. The maximum detectable blood velocity was 380 cm/sec. Pa(t) was measured using a newly-developed method based on indirect unloading techniques and an air pressure system. There were 21 normal subjects and seven patients with coronary artery disease in this study. The following results were obtained. There was no significant difference between power patterns calculated by Pa(t) and Pao(t) (aortic pressure measured by catheter). The average peak dPower/dt was 160.2 J/sec2 in normal subjects, 145.2 L/sec2 in patients with ejection fractions greater than 50%, and 93.5 J/sec2 in patients with ejection fraction less than 50%. Peak dPower/dt was significantly decreased in patients with the lower ejection fraction (p less than 0.005). The results indicated that this index is clinically useful in evaluating cardiac contractility.

A wide spectrum of cardiac hypertrophy has been observed in hypertensive patients. In this study, the responses of hemodynamics and sympathetic drives to exercise among hypertensive patients with various types of left ventricular hypertrophy were investigated. Twenty-five patients with untreated essential hypertension (WHO I and II) were classified as those with and without asymmetric hypertrophy (with AH, n = 7; without AH, n = 18) by their echocardiographic patterns. Ten normotensives served as controls. Exercise was performed on a braked bicycle ergometer; the initial work load was 50 watt. The work load increased progressively by 25 watt at three minute-intervals to the target heart rate, exhaustion, or positive ST.T changes. Blood pressure, heart rate, plasma norepinephrine and hemodynamic parameters by echocardiography were estimated at rest and during exercise. Systolic blood pressure and increased heart rate by exercise in all groups. In patients with AH, a rapid increase was observed, and the increase in systolic blood pressure at submaximum exercise was significantly greater than those in normotensives or patients without AH (p less than 0.05). During exercise, endsystolic dimension decreased in normotensives and in patients without AH (p less than 0.01), but the change was not significant in patients with AH. Percent fractional shortening and percent systolic wall thickening of the interventricular septum and left ventricular posterior wall increased significantly in normotensives and in patients without AH (p less than 0.05), but they were unaltered in patients with AH. Although plasma norepinephrine significantly increased in all groups by exercise, the increase in patients with ASH was greater than those in the other groups (p less than 0.05). These results suggest that hyperresponsiveness of systolic blood pressure and heart rate to exercise may play a role in the pathogenesis of AH, and that this type of hypertrophy could be associated with abnormalities of the sympathetic nervous system.

The effects of nitroglycerin (NTG) on relaxation characteristics of the infarcted and non-infarcted myocardium were investigated by calculating a segment length on the epicardium of the left ventricle for 16 patients with old myocardial infarction. The spatial segment length was measured between two points which were identified as a junction of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Regional myocardial stiffness was expressed as delta P/delta L, where delta P was an increment of left ventricular (LV) diastolic pressure from the lowest LV diastolic pressure to the pressure at the maximal segment length, and delta L was the difference of two segment lengths corresponding to those pressures. Myocardial stiffness decreased from 0.0402 +/- 0.0293 mmHg/mm to 0.0212 +/- 0.0157 with intracoronary NTG (p less than 0.01) and from 0.0220 +/- 0.0090 to 0.0136 +/- 0.0124 with sublingual NTG (p less than 0.001) in the non-infarcted portions. However, it was unchanged with both intracoronary and sublingual NTG in the infarcted portions. NTG may cause venous pooling and may decrease diastolic wall tension of the left ventricle as its indirect effect on the non-infarcted myocardium. Also, the non-infarcted myocardium may be influenced by dilatation of the epicardial coronary artery. Muscle stiffness of the infarcted myocardium was unchanged, probably due to the rigidity of myocardial fibrosis. It was concluded that in myocardial infarction diastolic distensibility of the non-infarcted portion can be improved by NTG both through indirect and direct effects.

Relationship between left axis deviation and left anterior fascicular block (LAFB) was investigated by estimating the ventricular excitation and contraction sequence using body surface potential mapping and phase image analysis by radionuclide ventriculography. This study included seven normal persons, eight patients with complete right bundle branch block (RBBB) without left axis deviation (LAD), twelve with RBBB and unblocked axis (determined by the first half of the QRS complex) of 0 degrees or farther deviated to the left (RBBB with LAD), and three with isolated LAD. The isochrone ventricular activation maps (VAT maps) were obtained by body surface mapping technique. Planar phase images in the left anterior oblique projection and short-axis ventricular tomographic phase images using a seven-pinhole collimator were constructed by ECG-gated equilibrium blood pool scintigrams. On the VAT maps of RBBB, there was a markedly delayed conduction to the right ventricle, however, in the left ventricle, the excitation was initiated in the anterior paraseptal region, and it proceeded rapidly toward the lateral and posterior walls, and in the same direction as normal. The VAT maps of RBBB with LAD were categorized in three types according to the activation sequence in the left ventricle. Type I, the same as maps of RBBB, consisted of three cases. Type II, four cases, showed excitation starting from the apex and ascending in the anterior wall. There were five cases of type III, which showed the earliest excitation in the basal posteroparaseptal region, proceeding toward the apex and ascending in the anterior wall. Type II was considered compatible with block of the left anterosuperior fascicle, and type III was that of left anterosuperior and midseptal fascicles. In types II and III, the phase delay in the left anterior wall was recognized in tomographic phase images, and the difference between right and left ventricular mean phase angles in planar phase images was significantly smaller than in cases of isolated RBBB, These were thought to support the existence of LAFB. The range of the unblocked axis of RBBB with LAD was -3 degrees approximately 13 degrees (-7.7 +/- 5.0 degrees) in type I, -8 degrees approximately -30 degrees (-19.8 +/- 9.1 degrees) in type II, and -33 degrees approximately -60 degrees (-51.0 +/- 10.9 degrees) in type III. All cases with left axis deviation beyond -30 degrees were of type III, and suspected to have extensive damage, including the midseptal fascicle.(ABSTRACT TRUNCATED AT 400 WORDS)

This is a report of two brothers, six and five years of age, with systemic carnitine deficiency and cardiomyopathy, whose symptoms were improved after oral administrations of DL-carnitine. They had had progressive muscle weakness since three years of age. The elder brother's radiograph on admission showed cardiomegaly with a cardiothoracic ratio of 60%, and his electrocardiogram showed left ventricular hypertrophy and tall, peaked T waves in the precordial leads. The echocardiogram showed slight thickening of the cardiac muscle and decreased ejection fraction. Skeletal muscle biopsy specimens and sera were assessed for carnitine content. The skeletal muscle specimens revealed lipid storage myopathy, and the carnitine contents of the skeletal muscle and sera were both decreased. Myocardial biopsy for the elder brother revealed mitochondrial accumulation. Cardiomyopathy caused by carnitine deficiency is often fatal, but may be cured. Carnitine deficiency should be considered whenever a patient with cardiomegaly and progressive skeletal muscle weakness is encountered.

A personal computer-based system for automatically evaluating external systolic time intervals (STI) suitable for practical clinical use is presented. In 56 consecutive unselected subjects, ranging in age from 16 to 77 years (mean = 51 years), the STI recorded with standard technique were computed manually and automatically. Manual and automatic techniques correlated closely in all indices studied (Q-Q interval: r = 0.995; electromechanical systole: r = 0.975; pre-ejection period (PEP): r = 0.985; left ventricular ejection time (LVET): r = 0.973, PEP/LVET: r = 0.981, p less than 0.001). These results demonstrate that automatic evaluation of STI can be effectively made with good reliability using inexpensive hardware.

Several methods of digital subtraction angiography (DSA) were compared to determine which could better visualize regional myocardial perfusion using coronary angiography in seven patients with myocardial infarction, two with angina pectoris and five with normal coronary arteries. Satisfactory DSA was judged to be achieved if the shape of the heart on the mask film was identical to that on the live film and if both films were exactly superimposed. To obtain an identical mask film in the shape of each live film, both films were selected from the following three phases of the cardiac cycle; at the R wave of the electrocardiogram, 100 msec before the R wave, and 200 msec before the R wave. The last two were superior for obtaining mask and live films which were similar in shape, because the cardiac motion in these phases was relatively small. Using these mask and live films, DSA was performed either with the continuous image mode (CI mode) or the time interval difference mode (TID mode). The overall perfusion of contrast medium through the artery to the vein was adequately visualized using the CI mode. Passage of contrast medium through the artery, capillary and vein was visualized at each phase using TID mode. Subtracted images were displayed and photographed, and the density of the contrast medium was adequate to display contour lines as in a relief map. Using this DSA, it was found that regional perfusion of the contrast medium was not always uniform in normal subjects, depending on the typography of the coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)

An aenurysm of a diverticulum of the ductus arteriosus in a 33-year-old man was presented. The chest radiography revealed a mass obscurring the aortic window above the hilus of the left lung. His blood pressure was 130/70 mmHg, and there was no difference in pressures between the upper and lower or between the right and left extremities. A CT scan of the chest showed 30 X 34 mm angioma adjacent to the descending aorta and pulmonary artery. Aortography and contrast radiography of the right ventricle revealed a cystic pedunculated aneurysm at the superior portion of the descending aorta. The base of the left pulmonary artery was slightly displaced. There was no communication between the aorta and pulmonary artery, nor was any significant difference in pressure between the ascending and descending aorta. This case was diagnosed as an aneurysm of the diverticulum of the ductus arteriosus, and then it was resected. The abnormality was confirmed by the localization of the aneurysm and histopathologic findings, but the presence of the ligamentum arteriosum was not confirmed. This is the 23rd case of the aneurysm of the diverticulum of the ductus arteriosus in adults, and the first case in Japan in which the diagnosis was made in a living patient, followed by successful surgery.