[Effect of left ventricular systolic function on left atrial filling--clinical study using radionuclide angiography].
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Biomedical subjects
Publications and source records attributed to R Kusukawa.
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A 62-year-old man had an acute myocardial infarction with successful thrombolysis. Coronary spasm was documented in the following angiographic study. This case demonstrated that coronary spasm is implicated in the pathogenesis of coronary thrombosis and subsequent myocardial infarction.
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.
Piperanometozine (OPC-8212) is a new, orally effective inotropic agent. To evaluate the efficacy of this agent on systemic hemodynamics and clinical symptoms in patients with congestive heart failure, a multicenter study was performed. Thirty four patients with New York Heart Association (NYHA) functional classes II to IV and initially treated with digitalis were enrolled from ten centers. After a washout period of one or two weeks (placebo period), digitalis was replaced by piperanometozine (30 or 60 mg/day) for four weeks, while other drugs were continued. Clinical symptoms, routine physical findings, electrocardiogram, chest roentgenogram, echocardiogram, exercise tolerance time, and routine laboratory data were obtained in 34 patients. Four patients were withdrawn from the study before completion. After the withdrawal of digitalis, heart rate was increased and ejection fraction was decreased. Exercise tolerance time was increased while other parameters were unchanged. At the end of the treatment period with piperanometozine, ejection fraction significantly (p less than 0.05) increased with a decrease in LV end-systolic volume (p less than 0.05), whereas heart rate and blood pressure remained unchanged. Systolic blood pressure/LV end-systolic volume (P/V index) tended to decrease after the withdrawal of digitalis and increase during piperanometozine therapy. Exercise tolerance time was further increased (p less than 0.01) and NYHA functional class was improved in 11 patients, whereas it worsened in only one patient. No major adverse effects were observed. These results indicate that a short-term therapy of oral piperanometozine restored the depressed cardiac performance of the heart and improved clinical symptoms in patients with congestive heart failure. Thus, this promising agent deserves further clinical study in long-term trials.
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.
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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.
To determine the immune disturbances involved in the pathogenesis of dilated cardiomyopathy (DCM), the conditions in humoral and cellular immunity of DCM patients were studied. To examine the status in humoral immunity in DCM patients, circulating anti-heart antibodies (AHAbs) were analyzed. Circulating-AHAbs were classified into 4 types "heterophile-like", "intracellular", "intercalated disc" and "nuclear" patterns by indirect immunofluorescence technique, and a high rate of heterophile-like antibody was found in DCM. The cytotoxicity of this antibody was examined in cultured myocardial cells using the two-step method of the complement dependent cytotoxic test. The mean cytotoxic index (CI) value of the heterophile-like antibody positive sera was 22.3, which showed an apparent cytotoxicity against the cultured cells and it may be complement dependent. In addition, the frequency of lymphocyte subsets using monoclonal antibodies (OKT4, OKT8, Leu7, Leu11) and natural killer (NK) activity were evaluated to determine whether DCM patients had an imbalance in cellular immune reactions, which support the hypothesis of an immune disturbance as the pathological mechanism of DCM. The peripheral lymphocyte counts were significantly lower in patients with DCM (1737 +/- 874/mm3) than in normal controls (NC, 2088 +/- 556/mm3) and in patients with ischemic heart diseases (IHD, 2395 +/- 469/mm3, both p less than 0.01). The percentage of T, B, OKT4 and OKT8 positive cells was not statistically different among DCM, IHD, and NC groups, whereas the percentage of T gamma cells was significantly reduced in DCM patients (6.5 +/- 5.0%, p less than 0.05). NK functional activity as tested in DCM patients was frequently deficient (24.1 +/- 16.7% in DCM, 36.7 +/- 12.2% in NC). After 4-hr incubation with recombinant interleukin2 (rIL2), rIL2 induced the enhancement of NK activity in 3 out of 4 DCM patients with low NK activity, although, there was a non-responder to rIL2 in this group. These results suggested that DCM patients have a low IL2 production and/or less numbers of mature cells with NK cell function. Therefore, an imbalance in humoral and cellular immune reactions may cause insidious myocardial damage and subsequently lead to development of DCM.
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Forty consecutive patients with small cell carcinoma of the lung were treated with chemotherapy, radiotherapy or both. Of 34 patients treated with chemotherapy, 24 were treated with combination chemotherapy, containing cyclophosphamide vincristine methotrexate and procarbazine, concurrent with small dose radiation therapy (500cGy/5 fraction) as a chemosensitizer (COMPrt). The response rate to this regimen was 81% (29% complete) and the 2 year survival rate was 28.6%. These results have been superior to other regimens and the toxicity was not see to be any higher. After completion of COMPrt regimen, 10 patients were treated with intrathoracic radiation therapy (average dose 3000cGy) and 3 received surgical treatment. Radiation therapy improved the 2-year survival rate (42.2%) when compared with those patients who received no radiation therapy (18.2%). Three patients received surgical treatment were considered to be disease-free for 23, 17, and 9 months respectively, after induction of chemotherapy.
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Dual echocardiogram was recorded simultaneously with phonocardiogram (PCG) to analyze the isovolumic relaxation time (IRT) of the left ventricle (LV) in 85 patients with various heart diseases and in 23 normal subjects. The measurements used were time intervals from the onset of the aortic component of the second heart sound (IIA) to the onset of the posterior deflection of the posterior aortic wall in the aortic root echocardiogram (X) (IIA-X interval), and to the onset of the most rapid opening motion of the anterior mitral leaflet (D') (IIA-D' interval) during early diastole. 1. The IIA-X interval was directly proportional to the IIA-D' interval in the entire study population. 2. The IIA-X interval was prolonged with advancing age in normal subjects. 3. The IIA-X interval was significantly increased in patients with hypertensive heart disease, old myocardial infarction, hypertrophic cardiomyopathy, and dilated cardiomyopathy, but significantly decreased in patients with mitral stenosis. Thus, the IIA-X interval, which was measured easily and noninvasively from the aortic root echocardiogram is a reliable indicator of the isovolumic relaxation time of the left ventricle, as well as of the IIA-D' interval.
To study the acute effects of isosorbide dinitrate (ISDN) on global and regional left ventricular (LV) diastolic filling, gated radionuclide ventriculographic studies were conducted in 21 normal persons before and after sublingual administration of ISDN. ISDN treatment caused significant increases in ejection fraction and peak LV ejection rate and it caused a delay in occurrence of peak LV filling, without statistically significant changes in peak LV filling rate globally and regionally. The ratios of peak LV filling rate to peak LV ejection rate decreased significantly both globally and regionally. These alterations induced by ISDN could be interpreted as indicating a failure of improvement of the early diastolic filling despite increased systolic function and heart rate in the global left ventricle and in regions of the left ventricle. Furthermore, ISDN caused early diastolic asynchronous filling. There was a negative correlation between this early diastolic asynchronous filling and the ratio of global peak LV filling to global peak LV ejection rate (r = -0.66, p less than 0.001), indicating that administration of ISDN to normal persons may produce early diastolic asynchronous filling associated with failure of improvement of diastolic filling despite increased systolic function and heart rate.
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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)