Biomedical subjects
Publications and source records attributed to H Nonogi.
A patient with acute right ventricular infarction who showed hyposecretion of atrial natriuretic peptide (ANP) in spite of abnormally high right atrial pressure and who died of a severe low cardiac output syndrome is reported. Right atrial infarction, which was proven at autopsy, may be responsible for this endocrine failure.
BACKGROUND: The heart has been demonstrated not only to be a pumping organ but also an endocrine organ secreting atrial natriuretic peptide (ANP). We hypothesized that myocardial ischemia may affect ANP secretion and that reperfusion therapy for acute myocardial infarction can preserve endocrine function of the heart. METHODS AND RESULTS: Twenty patients with acute right ventricular infarction were examined who underwent reperfusion therapy on admission. These patients had proximal occlusion of the dominant right coronary artery involving the right atrial branches: 9 patients with successful reperfusion (SRP group) and the remaining 11 patients with unsuccessful reperfusion (URP group). Within 24 hours after the onset of infarction, a volume loading test was performed after reperfusion therapy with measurements for plasma ANP levels and hemodynamics. Before the volume loading test, the plasma ANP level and mean right atrial pressure were similar between these two groups. However, in the URP group, percent increase in ANP in response to volume loading was strikingly smaller (URP, 45 +/- 18% versus SRP, 133 +/- 25%; P < .01) despite similar percent increase in mean right atrial pressure (URP, 100 +/- 46% versus SRP, 86 +/- 23%). The peak ANP level occurred significantly later in the URP group (69 +/- 16 hours) than in the SRP group (28 +/- 9 hours, P < .001) after the onset of infarction. CONCLUSIONS: The response of ANP release to volume loading is attenuated in patients with right ventricular infarction without coronary reperfusion. However, successful reperfusion induces a rapid recovery of cardiac endocrine function as well as its mechanical function. A sufficiently elevated plasma ANP level may be a useful predictor of hemodynamic improvement in patients with right ventricular infarction.
To evaluate prolonged diastolic dysfunction in acute coronary syndrome, mitral inflow velocities and left ventricular wall motion were examined with pulsed-wave Doppler and two-dimensional echocardiography in 14 patients with successful reperfusion, 8 patients without reperfusion after acute myocardial infarction, and in 10 patients with prolonged angina. Early peak flow velocity and the ratio of early to atrial peak flow velocity increased gradually both after the onset of acute myocardial infarction with reperfusion and cessation of angina pectoris. However, in acute myocardial infarction without reperfusion, early peak flow velocity and the ratio of early to atrial peak flow velocity decreased significantly. Atrial peak flow velocity remained unchanged in acute myocardial infarction with reperfusion, while it was decreased in angina pectoris on the seventh day. Regional systolic dysfunction abated gradually in acute myocardial infarction with successful reperfusion, and regional systolic dysfunction was not detected in angina pectoris on the third day. Thus, abnormalities in left ventricular early diastolic filling persisted for several days after reperfusion in acute myocardial infarction or cessation of angina. Left ventricular late filling remained unchanged in acute myocardial infarction, whereas, in angina pectoris, a compensatory increase in late filling diminished gradually with an increase in early filling. These results indicate that there are different types of recovery process after diastolic filling abnormalities in patients with acute coronary syndrome.
In this study, to determine whether preconditioning enhances the process of recovery from post-ischemic dysfunction, ultrasonic crystals were placed in 8 open-chest dogs to measure regional myocardial wall thickening in the ischemic area. A carotid-circumflex coronary artery bypass was created with an electromagnetic flow probe and a fixed stenosis was produced. Ventricular pacing was performed for 15 minutes at a rate of 190-220 bpm. After a 15 minutes rest period, a second pacing was performed in a similar manner. After cessation of the first pacing, circumflex wall thickening remained reduced significantly. Three minutes after cessation of the second pacing, circumflex thickening decreased further. After 15 minutes, wall thickening improved to the value recorded before the second pacing. The degree of improvement from 3 minutes to 15 minutes after the second pacing was greater than that after the first pacing. Thus, preceding demand ischemia modifies the rate of functional recovery from the next post-ischemic dysfunction, indicating that preconditioning of the ischemic myocardium enhances recovery from stunning.
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Myocardial washout of the new myocardial perfusion imaging agent, 99mTc-hexakis-2-methoxy isobutyl isonitrile (99mTc-MIBI) was studied in 23 patients with coronary artery disease. These patients were divided into three groups; 8 patients with effort angina pectoris (AP group), 6 with myocardial infarction who had reversible defect (MI-RD (+) group) and 9 with myocardial infarction who had not reversible defect (MI-RD (-) group). Regional radioactivities were determined with postexercise 1- and 3-hour myocardial planar images. In AP group, 99mTc-MIBI washout rate in ischemic area was smaller than in normal area (3.8 +/- 7.5% vs. 8.3 +/- 5.6%, p < 0.05), however, in the remaining two groups, there were no difference in washout between normal and infarct areas. Defect/normal ratios from postexercise 1 hour to 3 hours were slightly increased in AP and MI-RD (+) groups. Our results indicate that 99mTc-MIBI showed slight and incomplete myocardial redistribution in ischemic areas. These data showed to be considered in the interpretation of 99mTc-MIBI myocardial imaging.
To clarify the usefulness of the combined assessment of exercise (EX)-induced abnormalities in myocardial perfusion and regional wall motion for detecting coronary artery disease (CAD), we carried out first-pass radionuclide angiography and myocardial perfusion imaging during EX and at rest by 99mTc-tetrofosmin. Twenty-four patients with angiographically proven CAD, 9 (Gp A) with single and 15 (Gp B) with multivessel disease, were studied. The sensitivity for the detection of CAD was 78% of Gp A, 73% of Gp B in planar image and 78%, 87% in SPECT image, respectively. When left ventricular ejection fraction and regional ejection fraction (rEF) were combined with the result of myocardial perfusion, sensitivity increased up to 89% of Gp A, 100% of Gp B. Diagnostic accuracy of LAD, LCX and RCA was 79%, 88% and 83%, respectively. Regional EF in ischemic areas decreased during EX in both Gps, particularly in Gp B. Regional EF in relatively normal perfusion areas did not significantly change in Gp A, but decreased in Gp B. These results suggest that 99mTc-tetrofosmin contributes to the improvement of sensitivity for CAD by combined assessment of EX-induced wall motion and myocardial perfusion abnormalities.
To evaluate the effects of aspirin on thrombin generation in patients with unstable angina, plasma levels of thrombin-antithrombin III complex (TAT) as a new marker of thrombin generation and of 11-dehydro-thromboxane B2 (11-dehydro-TXB2) as an indicator of platelet activation were measured in 18 patients with unstable angina, including 8 patients with prolonged rest angina (> 15 minutes). Aspirin DL-lysine (900 mg) was administered intravenously to 9 of the 18 patients (aspirin group); the other 9 were not given aspirin during the first 24 hours of hospitalization (non-aspirin group). Clinical characteristics, angiographic features and medications other than aspirin were similar between the 2 groups. Levels of plasma TAT and 11-dehydro-TXB2 were significantly higher (p < 0.05) in patients with prolonged rest angina than in those without the condition (n = 10). In 5 patients with prolonged rest angina who received aspirin, plasma TAT levels (ng/ml) were significantly decreased (4.52 +/- 1.18 at baseline, 2.50 +/- 0.65 at 1 hour and 2.16 +/- 0.42 at 24 hours after aspirin administration, p < 0.01) with a significant decrease in plasma 11-dehydro-TXB2 levels. However, the reduction in TAT after aspirin administration was slight in patients without prolonged rest angina (n = 4). In contrast, levels of plasma TAT and 11-dehydro-TXB2 in the non-aspirin group remained unchanged during the study period. These results suggest that aspirin rapidly reduces thrombin generation through inhibition of platelet activity in patients with unstable angina with prolonged rest angina.
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Noninvasive first-pass radionuclide ventriculography may permit the assessment of global and regional left ventricular function during dipyridamole infusion. Twenty patients with > or = 75% stenosis of at least one coronary artery were studied to assess the sensitivity of the technique in detecting coronary artery disease. Seven (35%) had regional dysfunction after dipyridamole infusion, and 16 (80%) developed lower than normal response in left ventricular ejection fraction (an increase of less than 5%) after dipyridamole infusion. When both regional dysfunction and subnormal rejection fraction were considered together, the sensitivity was 80%. Eight normal subjects were studied to assess specificity. None developed regional dysfunction, and left ventricular ejection fraction invariably increased after dipyridamole infusion in all normal subjects, with an increase of less than 5% in only one subject; therefore, the specificity was 88%. It is concluded that the assessment of regional dysfunction with dipyridamole infusion itself is not sensitive, whereas the assessment of changes in left ventricular ejection fraction is sensitive and specific in detecting coronary artery disease.
Changes in left ventricular diastolic properties of pacing-induced stunned myocardium were examined in 10 anesthetized dogs instrumented with a micromanometer for left ventricular pressure and sonomicrometers for left ventricular short axis, anterior and posterior segment lengths, and posterior wall thickness. After the creation of a critical stenosis on a carotid-circumflex coronary artery bypass, left ventricular pressure and dimensions were recorded simultaneously during temporary superior and inferior vena caval occlusion to allow for the construction of end-diastolic pressure-segment length curves. After 15 min of high-frequency pacing (190-220 beats/min), measurements were repeated and compared with those before pacing. The mean lengthening rate of each dimension during the first half of diastole was calculated as an index of early diastolic function. Three minutes after the end of pacing, coronary blood flow and perfusion pressure were unchanged, whereas systolic function of the posterior wall was depressed, indicating stunning of the posterior myocardium. The time constant of left ventricular pressure decay was prolonged by 14%. The mean lengthening rate during the first half of diastole decreased by 50% in the left ventricular internal short axis and by 119% in the posterior segment. Despite the significant impairment of early diastolic function, the regional end-diastolic pressure-segment length relation of the posterior wall was unchanged. Thus, in contrast to the results reported for pacing-induced ischemia that were measured immediately after pacing, the distensibility of the left ventricular wall in stunned myocardium induced by pacing was unchanged despite depressed early diastolic function.
BACKGROUND: Nonuniformity is a determinant of diastolic function. In patients with hypertrophic cardiomyopathy, hypertrophy, abnormal calcium handling, and regional ischemia can also play a role. This study was designed to assess regional mechanics, asynchrony, and asynergy in patients with hypertrophic cardiomyopathy. METHODS AND RESULTS: Nine control subjects and 22 patients with hypertrophic cardiomyopathy were studied by biplane left ventriculography and high-fidelity pressure tracings for the assessment of diastolic function by computing the time constant of isovolumic relaxation, peak filling rate, and the constant of passive chamber stiffness. Regional mechanics were evaluated by dividing the left ventricle into six sectors in the right and left anterior oblique projections. Systolic and diastolic asynchrony were assessed from the coefficient of variation of the regional time intervals from end diastole to end systole and to peak filling rate, respectively. Asynergy was evaluated from the coefficient of variation of the regional area reduction. Regional passive elastic properties were estimated by computing the regional constant of chamber stiffness. In patients with hypertrophic cardiomyopathy, isovolumic relaxation was prolonged (time constant of isovolumic relaxation 101 +/- 41 versus 51 +/- 16 milliseconds in control subjects; P < .001) and the constant of chamber stiffness was increased (0.056 +/- 0.038 versus 0.025 +/- 0.010 mL-1; P < .001). Both systolic and diastolic asynchrony as well as asynergy were found. Regional mechanics showed hyperkinesia in the free wall, whereas the septum exhibited normal wall motion and increased constant of chamber stiffness. CONCLUSIONS: Diastolic function is impaired in hypertrophic cardiomyopathy, and such an impairment is the consequence of nonuniformity and hypertrophy. The regions where the myopathic process is more pronounced show normal wall motion but increased stiffness. The inhomogeneity of regional wall motion with regional hyperkinesia and normokinesia of neighboring regions results in left ventricular asynergy.
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The theoretical and clinical validity of immunochemiluminometric assay of creatine kinase (CK)-MB protein mass was assessed in patients with acute myocardial infarction and the results were compared with those of immunoinhibition assay of CK activity. Serial changes of both CK-MB protein mass and CK-MB activity were analyzed in 20 consecutive patients. In all 312 samples from 20 patients, protein mass and activity of CK-MB showed good correlation. The exponential fitting of the time-value curve of CK-MB protein mass showed a better correlation coefficient than that of CK-MB activity (0.97 +/- 0.02 vs 0.93 +/- 0.07, p < 0.05), indicating that the CK-MB level measured by the immunochemiluminometric assay was less scattered than that measured by the immunoinhibition method. This finding was most evident at lower CK-MB values (< 500 IU/l). The rate of disappearance from serum of CK-MB protein mass was faster than that of CK-MB activity (0.54 +/- 0.23 hr-1 vs 0.28 +/- 0.13 hr-1, p < 0.001). This may indicate that some amount of the CK-MB activity may be inactivated in the early phase of the release into the serum from the necrotic myocardium. Thus, the immunochemiluminometric assay of CK-MB protein mass has superiority in the diagnosis of acute myocardial infarction compared with the immunoinhibition method, especially when the measured CK-MB level is low. This feature may be useful to distinguish a small myocardial infarction from severe ischemia without myocardial necrosis.
To evaluate the changes in the left ventricular diastolic filling dynamics after severe myocardial ischemia, serial pulsed Doppler examinations of mitral flow were performed in 10 patients with unstable angina. Peak early and late filling velocities (E and A), the ratio (E/A), the area E (Ei) and A (Ai) and the ratio (Ei/Ai) were measured one, 3, and 7 days and one month after the last ischemic episode. Seven of 10 patients were treated with percutaneous transluminal coronary angioplasty (PTCA), and the same indexes were obtained one, 3, and 7 days and one month after PTCA. E/A and Ei/Ai increased significantly on the 3rd and 7th days, however, no further increase was observed one month after the last ischemic episode and after PTCA. Left ventricular diastolic dysfunction induced by severe myocardial ischemia persisted for several days after the stabilization of myocardial ischemia. After the ischemic episodes were stabilized by administering pharmacological therapy, left ventricular diastolic dynamics were unchanged before and after PTCA. These results indicate that there may be diastolic myocardial stunning in patients with unstable angina.