Thrombolysis of tricuspid Björk-Shiley prosthesis with tissue-type plasminogen activator.
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Biomedical subjects
Publications and source records attributed to K Moritani.
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To assess the degree of collateral vessels after myocardial infarction, coronary angiograms, left ventriculograms, and exercise thallium-201 myocardial scintigrams of 36 patients with previous myocardial infarction were reviewed. All 36 patients had total occlusion of infarct-related coronary artery and no more than 70% stenosis in other coronary arteries. In 19 of 36 patients with transient reduction of thallium-201 uptake in the infarcted area during exercise (Group A), good collaterals were observed in 10 patients, intermediate collaterals in 7 patients, and poor collaterals in 2 patients. In 17 of 36 patients without transient reduction of thallium-201 uptake in the infarcted area during exercise (Group B), good collaterals were seen in 2 patients, intermediate collaterals in 7 patients, and poor collaterals in 8 patients (p less than 0.025). Left ventricular contractions in the infarcted area were normal or hypokinetic in 10 patients and akinetic or dyskinetic in 9 patients in Group A. In Group B, 1 patient had hypokinetic contraction and 16 patients had akinetic or dyskinetic contraction (p less than 0.005). Thus, patients with transient reduction of thallium-201 uptake in the infarcted area during exercise had well developed collaterals and preserved left ventricular contraction, compared to those in patients without transient reduction of thallium-201 uptake in the infarcted area during exercise. These results suggest that the presence of viable myocardium in the infarcted area might be related to the degree of collateral vessels.
Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.
Relations between left atrial contraction and left atrial early filling were studied in eight subjects with atypical chest pain from simultaneous left atrial pressure recordings and left atrial cineangiograms. The left atrial ejection phase was defined as the interval from the onset of the sharp systolic rise in left atrial pressure (a point) to the point of minimum left atrial volume (Vmin). The left atrial filling phase was divided into (a) the early filling phase, the period from Vmin to the nadir of left atrial pressure (x), and (b) the late filling phase, the period from x to the point of maximum left atrial volume (Vmax). During the early filling phase, when the left atrium filled as left atrial pressure diminished, approximately 37% of total atrial filling took place. There was a direct relation between left atrial volume measured at a and x points (r = 0.91, p less than 0.01). The extension fraction, measured as the ratio of filling volume during the early filling phase to minimum left atrial volume, was significantly correlated with ejection fraction, measured as the ratio of ejected volume (delta V) during ejection phase to left atrial volume at the a point (r = 0.97, r = 0.01). Both mean and peak filling rates of left atrial volume change during the early filling phase were directly proportional to the ejected volume, the ejection fraction, and the mean ejection rate of left atrial volume change during the ejection phase. Thus these results suggest that there is close interaction between left atrial contraction and left atrial early filling.
Our recent clinical studies on the negative dP/dt upstroke pattern suggested that the left ventricular pressure (LVP) deviated from the exponential curve during isovolumic relaxation period (IRP) in diseased hearts. To examine this further two types of monoexponential curve fitting were done in various heart diseases (normal (N): 8, angina pectoris (AP): 8, myocardial infarction (MI): 13, hypertrophic cardiomyopathy (HCM): 10, dilated cardiomyopathy (DCM): 8). LVP was measured by a Millar's catheter-tip transducer, and four types of time constant (T1-T4) were derived: T1 was calculated by an exponential curve fitting e-t/T1 + B (B is constant), T2 by the ratio Pm/peak (-) dP/dt (Pm is LVP at peak (-) dP/dt), T3 by the best exponential curve fit e-t/T3 + B + C (C is constant), and T4 by the ratio (Pm-C)/peak (-) dP/dt. If the exponential curve fitting was reasonable, the relation between T1 and T2, or T3 and T4, should be on the line of identity. The result was as follows: T2 = 1.4 T1 - 6.1 (r = 0.84) and T4 = 1.1 T3 - 10.7 (r = 0.94). Additionally, C (mmHg) in MI (-26 +/- 15), HCM (-36 +/- 19) and DCM (-32 +/- 20) were lower (p less than 0.05) than in N (-13 +/- 7). These findings suggest that the LVP during IRP could deviate from the monoexponential curve and that careful attention should be given to calculate the time constant in diseased hearts.
The response of the coronary artery to a small dose (0.01 mg) of ergonovine was observed in nine patients without variant angina and in 10 patients with variant angina. Coronary angiograms were obtained before and after small and larger (routinely used) doses of ergonovine. With the larger dose, all 10 patients with variant angina had total or subtotal spastic occlusion accompanied by angina and ECG changes. Excluding the site of spastic occlusion produced by the larger dose of ergonovine, diameters of proximal, middle, and distal segments in each major coronary artery were measured before and after a small dose of ergonovine. The mean percentage of change in diameter (diameter before - diameter after a small dose of ergonovine)/diameter before a small dose of ergonovine X 100% in patients without variant angina was not significantly different from that in patients with variant angina (5.2 +/- 9.5% vs 7.0 +/- 11.9%, respectively). However, in patients with variant angina, a small dose of ergonovine produced a percentage of change in diameter of 39.8 +/- 15.3% at the site of spastic occlusion included by a larger dose of ergonovine, compared with that of 7.0 +/- 11.9% in the remaining non-spastic coronary arteries (p less than 0.05). These results indicate that patients with variant angina have local segments which respond differently to ergonovine from the remaining segments of coronary arteries. Clinically, this observation might be helpful in determining the angiographic positivity to ergonovine.
Left atrial function in patients with hypertensive heart disease was compared with that in control subjects. In patients with hypertensive heart disease, the time constant of left ventricular relaxation was significantly greater than that in controls (54 +/- 18 vs 31 +/- 16 msec; p less than 0.01). The ratio of left ventricular filling volume before atrial contraction (left atrial reservoir volume/left atrial emptying volume before atrial contraction, and conduit volume/flow volume from the pulmonary vein into the left ventricle) to left ventricular stroke volume was significantly smaller than that in controls (65 +/- 13 vs 76 +/- 7%; p less than 0.05). In patients with hypertensive heart disease, the ratio of reservoir volume to stroke volume was not significantly different from that in controls, while the ratio of conduit volume to stroke volume was significantly smaller than that in controls (43 +/- 13 vs 57 +/- 9%; p less than 0.05). The latter ratio was inversely correlated with the time constant of left ventricular relaxation (r = -0.05, p less than 0.05). In patients with hypertensive heart disease, the ratio of left ventricular filling volume during atrial contraction to stroke volume was significantly larger than that in controls (35 +/- 13 vs 24 +/- 7%; p less than 0.05). The ratio of left ventricular filling volume during atrial contraction to stroke volume had a significant inverse correlation with the ratio of conduit volume to stroke volume (r = -0.84, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise tests with sublingual nitroglycerin were performed on 7 patients with true positive and 8 patients with false positive exercise test results. Four of 7 patients with true positive changes and 8 patients with false positive changes underwent exercise cardiac scintigraphy. Scintigrams showed perfusion defects in 4 patients with true positive outcomes, and no perfusion defect in 8 patients with false positive outcomes. Exercise tests with sublingual nitroglycerin were performed with the same load as that without nitroglycerin. In all 7 patients with true positive exercise test results, ST segment depression observed in the control exercise test was not observed in the nitroglycerin exercise test. In the false positive patients, ST segment depression observed in the control exercise test remained unchanged in 7 of 8 patients receiving nitroglycerin. Exercise tests with sublingual nitroglycerin as well as exercise cardiac scintigraphy are valuable tods in differentiating false positive from true positive patients. Furthermore, these data suggest that ST segment depression in the false positive patients may not be related to myocardial ischemia.
One hundred ninety-seven patients with a history of acute myocardial infarction (AMI) were interviewed to evaluate the character of angina pectoris relative to physical activity before AMI and at the onset of AMI. Ninety-two patients had no angina before AMI and 105 had angina. Among the 105 patients with angina, 58 had chronic stable angina that did not change before AMI, 22 noted worsening of symptoms within 2 weeks before AMI, and 25 had onset of angina within 2 weeks before AMI. In the 92 patients without angina before AMI, AMI occurred during heavy exertion in 10 (11%), mild exertion in 43 (47%), at rest in 28 (30%), and during sleep in 11 (12%). In the 58 patients with chronic stable angina, 47 had angina during exertion, 7 during rest and 4 during both. However, subsequent AMI occurred during heavy exertion in 9 (15%), during mild exertion in 16 (28%), at rest in 25 (43%), and during sleep in 8 (14%). In the patients without angina, or with chronic stable angina without worsening of symptoms, AMI occurred unpredictably or differently from the mode of physical activity precipitating angina before AMI.
Coronary angiography of both right and left coronary arteries, using the Sones technique, was performed during the attack of total spastic obstruction in 11 patients with clinically documented history of variant angina. None of the patients had more than 70% stenosis of organic atherosclerosis in any coronary artery and none had a history of myocardial infarction. Total spastic obstruction occurred spontaneously in 3 of 11 patients, and was provoked by ergonovine maleate in eight patients. Six patients had total spastic obstruction in the left anterior descending coronary artery, four patients had total obstruction in the right coronary artery, and one patient had total obstruction in the left anterior descending and right coronary arteries. In 7 of 11 patients, the coronary artery distal to the total spastic obstruction received collaterals from the nonspastic artery. The collaterals disappeared promptly when the spastic coronary artery was patent. These patients had ST segment elevation in the ECG during the attacks. In the remaining four patients, the spastic artery did not receive any collaterals from the nonspastic artery, associated with ST segment elevation during the attacks. These findings suggest that the brief, repetitive total occlusion of the coronary artery may stimulate the enlargement of collaterals. These collaterals may not always function to prevent the ischemia of the myocardium on the ECG.
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To compare two expressions of the time constant for ventricular relaxation, 39 patients with various heart diseases (six normal, six angina pectoris [AP], 13 myocardial infarction [MI], eight hypertrophic cardiomyopathy [HCM], and six congestive cardiomyopathy [CCM]) were studied. One time constant was obtained by the method of Weiss et al. (T1) and the other was the ratio of left ventricular pressure at peak (-) dP/dt (Pm) to peak (-) dP/dt (T2). The deviation of T2 from T1 was expressed as 100 X (T2 - T1)/T1 (delta %). In normal subjects, T1 was nearly equal to T2 (32 +/- 3 and 32 +/- 6 msec, respectively), resulting in a low value of delta (-1 +/- 9). However, delta values in AP (20 +/- 23, p less than 0.05), MI (24 +/- 26, p less than 0.05), HCM (37 +/- 21, p less than 0.001), and CCM (46 +/- 24, p less than 0.001) were significantly higher than in normal subjects. Thus T1, T2, or delta separated the patient groups from the control subjects, and there were significant differences between T1 and T2 among the types of heart disease.
Left ventricular (LV) function was evaluated in 31 patients, who had total occlusion of the left anterior descending coronary artery and less than 70% stenosis of the other two major coronary arteries or any branch. Fifteen of 31 patients had a history of angina pectoris before acute myocardial infarction (AMI) and 16 of 31 patients had no history of angina pectoris before AMI. The patients with angina pectoris before AMI had a significantly better ejection fraction, percentage of abnormally contracting segment, and regional wall motion than those without angina pectoris before AMI. These data suggest that the symptom of angina pectoris before AMI could be a favorable sign in preserving LV function when the patients subsequently had AMI.
Coronary angiography was performed at rest and during bicycle exercise immediately after the onset of angina and significant ST segment elevation or depression in the ECG. Of 11 patients, six showed significant reduction of coronary lumen diameter at the site of organic stenosis; mean values of stenosis (range) before and during exercise were 55% (25% to 88%) and 98% (89% to 100%), respectively. Five patients did not have any diameter change of the organic lesion; mean values of stenosis (range) before and during exercise were 84% (74% to 89%) and 84% (73% to 92%), respectively. Excluding the areas of these stenoses, diameters of left main coronary artery, proximal, middle, and distal left anterior descending, circumflex, and right coronary artery segments were measured before and during exercise. Diameter in each coronary artery segment during exercise was not significantly changed from that before exercise, both in the groups with and without diameter reduction. Exercise provoked a localized worsening of coronary artery stenosis without changing the diameter in the remaining artery. These findings suggest that the worsening of stenosis might be caused by a regional abnormality of the coronary artery that is not necessarily related to the degree of organic stenosis.
The effects of nitroprusside (NP) on hemodynamics, especially on venous flow velocity of the inferior vena cava (IVC) were evaluated in 20 remote myocardial infarction patients. NP was given beginning at 10 micrograms/min, with subsequent increments of 10 micrograms/min every 5 minutes until the systolic blood pressure was reduced to about 30 mmHg. Pressure was measured by a catheter-tip micromanometer. Flow velocity of IVC was measured by a catheter-tip flow velocity probe. NP significantly decreased left ventricular systolic pressure, left ventricular end-diastolic pressure, mean aortic pressure, right ventricular systolic pressure, right ventricular end-diastolic pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure, systemic vascular resistance index (SVRI) and left ventricular volume. Cardiac index (CI) was unchanged and stroke volume index was decreased. IVC pressure was unchanged, while right atrial (RA) pressure decreased. Subsequently, the pressure difference between IVC and RA increased significantly. The amplitude of IVC flow velocity decreased significantly. Twenty patients were classified into two groups according to whether or not the CI increased by NP. CI increased in 9 patients (group I) and decreased in 11 patients (group D). Compared to group D, control CI and the slope of end-systolic pressure-volume relation were less and the difference between IVC pressure and RA pressure was greater in group I. The patients with higher control SVRI had greater increase in CI during NP. In our study, the greater the depression of cardiac performance and the higher the SVRI, the greater the improvement of left ventricular pumping function during NP.
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We investigated the influence of the miscellaneous structures surrounding the left atrium on left atrial shape and examined the feasibility and problems in evaluating its size using the anteroposterior dimension of the M-mode echocardiogram. Using two-dimensional echocardiography, left atrial anteroposterior short-axis dimension (S), long-axis dimension (L), transverse-axis dimension (T) which cross perpendicularly one another, and area in the long-axis section (AREA) were measured in 84 subjects. The left atrial size was defined as AREA X T. The population of this study consisted of 24 subjects without heart disease, 24 with mitral valve disease and 34 with miscellaneous heart diseases other than mitral valve disease. Some of them were associated with the thin chest, chest deformity by thoracoplasty or the markedly dilatated right atrium. In subjects with the thin chest the left atrium was compressed in the anterior and posterior directions, in patients who underwent thoracoplasty it was elongated in the cranial and caudal directions, and in those with the markedly dilatated right atrium it was compressed in the right and left directions. It can be speculated that surrounding structures have some direct effects on left atrial dynamics. As left atrial size increased, these three dimensions (S, L and T) increased disproportionally. Because the contribution of each dimension to the left atrial volume change is proportional to the ratio of dimensional change and S has the largest ratio, S contributed to left atrial volume change more than the others. That is the reason that left atrial volume was not proportional to S or S3. The relationship between S and AREA during one cardiac systole was almost linear in individual studies. The slope in the S-AREA relation, however, was greater in the cases with a larger value of S. Therefore, when the extent of the change in S is used as an index of atrial volume change, it should be normalized by S. Because the left atrium expanded in any directions, either S or other dimensions reflected its size. In cases with the distorted left atrium, however, evaluation of left atrial size by the use of a single dimension alone was inadequate.(ABSTRACT TRUNCATED AT 400 WORDS)
The sizes of both left atrial (LA) and right atrial (RA) cavities were assessed in 16 patients by esophageal echocardiography and biplane cineangiography. The changes in echocardiographic dimension and cineangiographic volume during 1 cardiac cycle showed excellent correlations in both atria. In the left atrium, the relation between the echocardiographic dimension and the cineangiographic volume was significant (r = 0.83) and was fitted by the following power function: LA volume (ml) = 0.94 X LA dimension (mm) 1.24. In the right atrium, the relation between the dimension and the volume was significant; RA volume (ml) = 0.015 X RA dimension (mm) 2.34 (r = 0.95). Thus, esophageal echocardiography is a useful method for evaluating LA and RA size and simultaneously observing of both atria.