Detection of a coronary arterial thrombus by indium-111-oxine-labeled platelet scintigraphy.

Coronary arteriography revealed significant left anterior descending coronary artery stenosis in a 72-year-old man with a history of myocardial infarction. Stenting of the stenotic vessel was performed. Twelve hours after stenting the patient complained of chest pain but emergent coronary arteriography did not show sign of any coronary arterial stenosis. Under suspicion of coronary thrombus formation, indium-111-oxine-labeled platelet scintigraphy was performed 5 days after stenting, and revealed accumulation of indium-111-oxine in the area corresponding to the stent implantation site.

Detection of inflammation in aortic aneurysms with indium 111-oxine--labeled leukocyte imaging.

BACKGROUND: The exact cause of aortic aneurysms is not completely understood. Histologically, the atherosclerotic lesions present in an aneurysm contain numerous inflammatory cells. This finding represents active atherosclerosis, which can cause lesion expansion. In this study we investigated the role of scintigraphy in the evaluation of inflammation in aortic aneurysms. METHODS AND RESULTS: We performed imaging using indium 111-oxine--labeled leukocytes in 14 patients with aortic aneurysms (10 thoracic and 4 abdominal) diagnosed by computed tomography. Peripheral blood evidence of inflammation was assessed on the same day. In 8 patients who subsequently underwent graft replacement of the aneurysm, the excised specimen was examined for evidence of inflammatory infiltration and correlated with the scintigraphic findings. Scintigraphic accumulation of labeled leukocytes was present in 10 of the 14 patients. Although all patients had a small increase in the erythrocyte sedimentation rate, there was no significant difference in the erythrocyte sedimentation rate between patients with positive and negative scintigram results. In 5 of the 8 surgical patients with positive scintigram results, the resected specimens demonstrated numerous inflammatory cells in the adventitia of the aortic wall and atherosclerotic changes in the media. There was no correlation between the presence of periaortic inflammatory adhesions at the time of surgery and the scintigraphic results. CONCLUSIONS: The accumulation of In-111-oxine--labeled leukocytes is a potentially useful scintigraphic marker of inflammatory infiltration in aortic aneurysms.

Acetylcholine-Induced response of coronary resistance arterioles in cholesterol-fed rabbits.

The extent to which reported abnormal responses of the human coronary circulation to acetylcholine in patients with hypercholesterolemia reflect endothelial injury is not clear. We used an in vitro rabbit model to determine whether these reactions involve endothelial or vascular smooth muscle dysfunction. Coronary resistance arterioles were isolated from hearts of rabbits fed 1% cholesterol to induce hypercholesterolemia or a control diet for 4 weeks. Arterioles were double cannulated with glass micropipettes and pressurized in a no-flow state. Acetylcholine contracted the arterioles in a concentration-dependent manner whether or not the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine was added. In control but not hypercholesterolemic preparations, contraction was significantly greater when endothelium was removed. In the hypercholesterolemic group, contraction significantly exceeded that in controls. In control but not high-cholesterol preparations, substance P dilated vessels with intact endothelium in a concentration-dependent manner. Addition of N(G)-monomethyl-L-arginine inhibited this response. With or without endothelium, norepinephrine contracted arterioles to a greater extent in the hypercholesterolemic group than in controls. We concluded that severe hypercholesterolemia decreased endothelially dependent factors by injuring endothelium and independently increased contractility of vascular smooth muscle.

Clinical course of patients with coronary ectasia.

OBJECTIVE: To compare the clinical prognosis between patients with diffuse coronary ectasia and those with localized coronary ectasia. DESIGN: Patients with coronary ectasia were divided into two groups based on the Markis classification (group D: types I-III and group L: type IV), and the clinical manifestations and prognosis were compared between the two groups. RESULTS: Group D patients (52.1 +/- 4 years) were significantly younger than group L patients (62.5 +/- 7 years). During the study, 4 patients in group D died suddenly. Three of the patients had type I coronary ectasia, and 1 had left main coronary ectasia. CONCLUSION: The results of the present study indicate that patients with diffuse coronary ectasia and left main coronary ectasia should be followed carefully.

The delayed recovery of impaired endothelium-dependent vasodilatory response after hemodynamic improvement in dogs with congestive heart failure.

We investigated whether impaired endothelium-dependent vasodilatory response recovers as heart failure improves. The femoral blood flow responses to intra-arterial administration of nitroglycerin (NTG) and acetylcholine (ACh) were examined in dogs with 2-week pacing-induced chronic congestive heart failure (congestive heart failure group; CHF, n = 12). Thereafter, pacing was stopped and hemodynamic changes and femoral blood flow responses were re-examined either 1 week (recover 1 week group; Re 1W, n = 6) or 4 weeks (recover 4 weeks group; Re 4W, n = 6) after the cessation of pacing. Another group in which a pacemaker was implanted without pacing served as the control group (n = 8). In CHF, heart rate and pulmonary artery pressure increased, and echocardiography revealed increased left ventricular diastolic dimension and reduced percent fractional shortening compared with those in the control group. In Re 1W, all hemodynamic parameters returned to the basal levels and did not differ from those in the control group. Although there was no significant difference in the blood flow responses to NTG among the 4 groups, the responses to ACh in CHF were significantly reduced compared with those in the control group. Despite the recovered hemodynamics, femoral blood flow responses to ACh were still reduced in Re 1W, but they returned to the levels of the control group in Re 4W. Thus, vascular endothelial dysfunction recovers along with improvement in CHF, however, the recovery of endothelial function is delayed in comparison with improvement in cardiac function.

Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats.

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.

ANG II reverses selective inhibition of alpha 2-adrenoceptor sensitivity after in vitro isolation of arterioles.

To determine whether in vitro isolation attenuates alpha 2-reactivity, we examined postjunctional alpha-adrenoceptor sensitivity of isolated rat skeletal muscle first-order arterioles that we have previously characterized in vivo. Microdissected, pressurized arterioles (mean lumen diam +/- SE, 115 +/- 7 microns) were studied after cannulation with micropipettes. As expected, the alpha 1-antagonist, prazosin (10(-8) M), produced a parallel, 10-fold dextral displacement of the phenylephrine (alpha 1-agonist) concentration-response curve, whereas the alpha 2-antagonist, rauwolscine (10(-7) M) had no effect. However, prazosin inhibited UK-14,304 (full alpha 2- but partial alpha 1-agonist), which was opposite to our previous in vivo studies of these vessels; namely, prazosin shifted the UK-14,304 response curve by 21-fold, whereas rauwolscine induced only a twofold shift. These data suggest a loss of alpha 2-adrenoceptor responsiveness after in vitro isolation. In a second experiment, the presence of 10 pM angiotensin II, which was subthreshold for constriction, increased phenylephrine sensitivity 10-fold, UK-14,304 sensitivity 16-fold, and the UK-14,304 maximal response by 63%; the half maximum effective concentration response to UK-14,304 was now abolished by rauwolscine at a concentration that did not inhibit phenylephrine constriction. These data suggest that in vitro conditions selectively attenuate alpha 2-adrenoceptor sensitivity, and that subthreshold angiotensin II restores alpha 2-sensitivity to in vivo values.

In vitro analysis of alpha-adrenoceptor interactions with the myogenic response in resistance vessels.

The interaction of alpha 1- and alpha 2-adrenoceptor constriction of isolated rat cremaster small arteries (mean diameter +/- SEM, 114 +/- 5 microns) with the myogenic mechanism was examined with in vitro videomicroscopy. Microdissected vessels were double-cannulated with glass micropipets in a tissue bath, and intraluminal pressure was set at 65 mm Hg baseline pressure. Norepinephrine (NE) concentration-response curves were obtained alone and in the presence of prazosin or rauwolscine to establish the concentration of NE required to selectively stimulate alpha 1- or alpha 2-adrenoceptors. A bimodal response was produced by NE alone, indicating interaction with more than one receptor population. Rauwolscine and prazosin each produced dextral displacement at low (< 0.1 microM) NE concentrations. However, while prazosin exhibited competitive antagonism, rauwolscine did not antagonize NE at concentrations > or = EC50 value. Thus, both alpha 1- and alpha 2-adrenoceptors mediate constriction at low NE concentrations, but only alpha 1-receptors contributed to constriction at intermediate and high concentrations. These data are in contrast to previous findings for the same vessels studied in vivo. Diameter responses to increases and decreases in transmural pressure from baseline were examined in the relaxed (passive) state with nitroprusside present, during spontaneous intrinsic tone, and during induced alpha 1- or alpha 2-tone (EC20 concentration of NE plus rauwolscine or prazosin). Myogenic constriction during increases in lumen pressure and myogenic inhibition of tone during decreases in pressure were greatest during alpha 2-tone, less during intrinsic tone and least during alpha 1-tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary pressure-flow, pressure-function, and function-myocardial oxygen consumption relations in postischaemic myocardium.

STUDY OBJECTIVE: The aim was to study coronary pressure-flow, pressure-myocardial wall motion and myocardial wall motion-myocardial oxygen consumption relations in postischaemic myocardium with prolonged myocardial dysfunction (stunned myocardium) in comparison with normal myocardium. DESIGN: Regional myocardial wall thickening was measured with ultrasonic crystals, and postischaemic myocardial dysfunction was achieved by occlusion of a carotid-left anterior descending coronary artery bypass (15 min) and reperfusion (30 min). Coronary perfusion pressure was decreased in 10 mm Hg steps by constricting the bypass before and after producing postischaemic myocardial dysfunction. At each constriction step, coronary flow, regional wall thickening, and regional myocardial oxygen consumption in the area perfused by the left anterior descending artery were measured. EXPERIMENTAL MATERIAL: 12 anaesthetised open chest mongrel dogs, weighing 12-16 kg, were studied. MEASUREMENTS AND MAIN RESULTS: At the basal level, myocardial wall thickening of postischaemic myocardium was depressed compared to normal myocardium, at 18.5(SD 8.9)% v 1.3(7.1)%, p less than 0.01. With coronary stenosis, wall thickening gradually decreased at a coronary pressure below 60 mm Hg in normal myocardium, but remained unchanged until mean coronary pressure was reduced to 50 mm Hg in postischaemic myocardium. Myocardial wall thickening of postischaemic myocardium was always more depressed than normal myocardium. At any level of coronary pressure, coronary flow in postischaemic myocardium was not different from normal myocardium. There was no difference in regional myocardial oxygen consumption between normal and postischaemic myocardium at any level of coronary pressure. However, regional myocardial oxygen consumption in postischaemic myocardium was higher than in normal myocardium performing similar levels of myocardial wall thickening. CONCLUSION: The coronary pressure-function relation but not the pressure-flow relation changed in postischaemic myocardium after a 15 min coronary occlusion. Regional myocardial oxygen consumption was relatively increased in postischaemic myocardium.

Post transplanted infective endocarditis.

The patient, a 51-year-old man, was receiving immunosuppressants for 2 yr after renal allotransplantation. He had heart failure with aortic regurgitation, fever, anemia and a history of odontectomy on admission. He was resistant to medical treatments and died from cerebral emboli. On autopsy, vegetation of the aortic valve was identified. Progression of atherosclerosis, which may have been due to steroids and chronic rejection, was prominent. This report is the first case of infective endocarditis following organ transplantation in Japan. Such complications as infective endocarditis and atherosclerosis will be on the rise with the increase of numbers or organ transplantations.

Effects of intermittent coronary sinus occlusion on experimental myocardial infarction and reperfusion hemorrhage.

The effects of intermittent coronary sinus occlusion (ICSO) on the size of myocardial infarction and reperfusion hemorrhage was evaluated. In Protocol 1, 8 dogs with ICSO and 8 controls underwent 4h of occlusion of the left anterior descending coronary artery. The same number of dogs underwent 4h of occlusion followed by 1h reperfusion in Protocal 2. The ICSO was started 1h after the ligation and continued through the occlusion period. There was no difference between the ICSO and the control group in hemodynamics and regional myocardial blood flow using hydrogen clearance method. However, ICSO did accelerate the rate of decline in intramyocardial CO2 tension. The half life of CO2 tension was 256 +/- 106 min in the control group but 139 +/- 34 min in the ICSO group (p less than 0.01). Lactate extraction rate showed the improving tendency during ICSO period. The ICSO resulted in a 50% and 80% reduction on an average in the size of infarct and reperfusion hemorrhage, respectively. We conclude that ICSO has prospective effects on myocardial ischemia with promise for clinical application.

Positive indium-111 leukocyte imaging in post myocardial infarction syndrome.

The diagnosis of post myocardial infarction syndrome (PMIS) is sometimes difficult because of the absence of a specific test. We report a 68-year-old man with PMIS who had a persistent accumulation of indium-111 oxine labeled leukocytes in the infarcted myocardium for 1 month. The uptake of leukocytes preceded the appearance of the main symptoms and disappeared with the clinical improvement after the therapy with steroids. Leukocyte imaging has a potential as a useful tool for early diagnosis, evaluation of therapy and assessing the mechanism of PMIS.

[Blood flow patterns in the left ventricle in patients with myocardial infarction and ventricular aneurysm: evaluation using real-time two-dimensional Doppler echocardiography].

To evaluate how the intraventricular blood flow is affected by the size of a left ventricular aneurysm and ventricular dysfunction, systolic left ventricular blood flow patterns were evaluated using two-dimensional Doppler flow images (real-time 2-D Doppler echo). The subjects consisted of 10 normal controls, 35 patients with anteroseptal infarction, two patients with inferior infarction and five patients with anteroseptal-inferior infarctions. The systolic period was divided into three subsets; early, mid- and end-systole. Forty-two patients with myocardial infarction were classified into three groups according to the left ventricular inflow patterns on real-time 2-D Doppler echo using the apical left ventricular long-axis approach; i.e., inflow signals confined to early systole (Group I), visualized up to mid-systole (Group II) and end-systole (Group III). Left ventricular end-diastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), and % non-contractile circumference (delta L) were calculated by the same echocardiographic approach. Ejection fraction (EF) was calculated by left ventricular cineangiography using the Simpson's method. The left ventricular inflow Doppler signals in the normal controls and Group I turned in the apex and then directed toward the left ventricular outflow tract during late diastole and early systole. Significant differences in EF were observed among the three groups. EF in Group I, II and III was 53 +/- 9%, 41 +/- 8% and 29 +/- 7%, respectively. However, LVDd, LVDs and delta L had the largest values in Group III and the smallest values in Group I. LVDd, LVDs and delta L were smallest in Group I and largest in Group III. In the normal controls, the left ventricular inflow signals proceeded to the apex and directed toward the left ventricular outflow tract in the early systolic period. Various changes in the inflow pattern were observed in patients with myocardial infarction and severe wall motion abnormalities, including delayed timing in proceeding from the apex to the left ventricular outflow tract, stagnant blood at the apex and further inflow of blood toward the apex even during end-systole. The patients with sustained inflow during late systole had hypofunction of the left ventricle as demonstrated by smaller EF and larger LVDd, LVDs, and delta L. In conclusion, the observation of intracardiac blood flows by real-time 2-D Doppler echo is of help in evaluating the severity of myocardial infarction.

[Interventricular septal wall motion abnormality in left bundle branch block].

An experimental study was performed to clarify the mechanism of perfusion defects in the interventricular septum on T1-201 scintigraphy, as seen in patients with left bundle branch block (LBBB) having normal coronary arteries. In anesthetized open-chest dogs, the following parameters were assessed during right atrial pacing as a control, left ventricular pacing to produce right bundle branch block (RBBB), and right ventricular pacing for LBBB; 1. intramuscular pressure in the interventricular septum, 2. blood flow of the left anterior descending coronary artery (LAD) measured by an electromagnetic flowmeter; 3. regional myocardial blood flow (MBF) determined at three sites, including the interventricular septum, LAD area, and left circumflex coronary artery (LCx) area using the H2-washout method. Aortic pressure, left ventricular pressure, and M-mode echocardiograms were recorded during the procedures. During right ventricular pacing, LAD flow remained unchanged; whereas MBF at the interventricular septum decreased from 99.6 +/- 23.4 to 79.2 +/- 17.6 ml/min/100 g, but MBF at the LCx area increased from 103.2 +/- 19.8 to 122 +/- 18.4 ml/min/100 g. In contrast, there were no significant changes in regional flow in any sites during left ventricular pacing. During right ventricular pacing, an early systolic dip was observed in the septal wall concomitantly with the onset of rise in intramuscular pressure in the interventricular septum. However, the beginning of the rise in left ventricular pressure was delayed 33 +/- 4 msec after that of the septal intramuscular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

[Infarct size determined by emission computed tomography using 99mTc-PYP: effect of coronary thrombolysis].

Emission computed tomography with 99mTc-PYP was used to estimate infarct size in 38 patients with documented acute myocardial infarction. In the present study, the effect of thrombolysis with Urokinase on infarct size and on left ventricular function was assessed. Fourteen patients with acute myocardial infarction who underwent intracoronary thrombolysis within six hours after the onset of symptoms, and 24 patients who underwent conventional therapy were the subjects of this study. Infarct size was measured by drawing a region of interest around the myocardial pyrophosphate uptake for each tomographic slice. The boundary was then defined as 65% of the maximal count within the region of interest as determined by phantom volume studies. The total number of voxels was obtained by adding those in all slices and multiplying the sum by the voxel volume (0.205 ml per one voxel) to determine the infarct volume. Measurement of the 99mTc-PYP uptake on the tomographic image revealed an average infarct size of 100.1 +/- 36.0 ml (ranged 45 to 198). The calculated infarct volume correlated significantly with sigma CPK (p less than 0.01) and with left ventricular ejection fraction (p less than 0.01), but not with the peak CPK. In patients with acute inferior myocardial infarction, the mean infarct volume was 78.4 +/- 29.1 ml in the coronary thrombolysis group, and 105.1 +/- 33.7 ml in the conventional bypass graft treatment group (p less than 0.05). We concluded that successful intracoronary thrombolysis may reduce infarct size. ECT imaging with 99mTc-PYP to determine infarct size may be clinically applicable in patients with acute myocardial infarction.

[Scintigraphic detection of thrombi using indium-111-labeled autologous platelets].

Intracardiac and arterial thrombi were examined by scintigraphy using In-111-oxine labeled autologous platelets. In 22 cases of myocardial infarction including six with ventricular aneurysms, four had positive findings of thrombi on imaging and detected also by echocardiography. All four had ventricular aneurysms. The so-called "moya-moya" echoes (fuzzy echoes) were demonstrated in two of these four cases. We encountered two cases with positive findings on imaging in 13 with mitral valve disease. These two had systemic embolic episodes after scintigraphic examination. "Moya-moya" echoes were detected in the left atrial cavity in four with negative findings on imaging. Positive images were obtained in two of three with acute arterial occlusive disease, and in both cases platelet deposition was observed in the proximal site of obstruction. Though thrombectomy was performed for one of these two cases, no thrombus was detected at the site of platelet deposition. After one month, re-examination revealed only negative findings in all sites in both these patients. In the six cases of aortic aneurysm, three had platelet deposition within their aneurysms, and surgery was performed for these positive cases, but one of them had no thrombus. Positive images were obtained in only one of seven patients with chronic arterial occlusive disease. Coagulation tests and platelet studies were investigated for patients with positive or negative platelet scans. Only the data of the thrombo-test showed a significant difference (97 +/- 9% vs 23 +/- 7%, p less than 0.001). Three cases of positive imaging became negative after anticoagulant therapy. We tried ECT for eight cases 24 hours after injection of In-111-oxine labeled platelets. Three cases showed clear images of thrombi, while the planar images could not detect them at an early stage. Therefore, we propose that ECT can be a useful technique for diagnosing intracardiac thrombi in early stage.

[Echocardiography in superacute phase of myocardial infarction: an experimental study].

The significance and usefulness of two-dimensional echocardiography (2DE) in the evaluation of superacute phase of myocardial infarction were studied in 13 dogs with coronary occlusion, and 2DE findings were compared with the hemodynamic indices. Myocardial infarction was produced by the occlusion of anterior descending branch of the left coronary artery in 13 anesthetized adult mongrel dogs. In 6 dogs, the end-diastolic area and percent fractional shortening (%FS) in each short-axis view of the left ventricle at the level of the mitral valve, chordae tendineae, papillary muscles, low papillary muscles and apex were measured during 60 minutes, and end-diastolic wall thickness of infarct area situated in the transitional zone between the septum and the anterior wall were compared with that of non-infarct area immediately and subsequent 60 minutes after occlusion. Positive dP/dt/P, time constant T and cardiac output were measured simultaneously with an echocardiographic study. Severe enlargement and expansion of the left ventricular cavity (ballooning) and a decrease of %FS and thinning of the left ventricular wall perfused by the occluded artery occurred immediately after occlusion and persisted during subsequent 60 minutes. Time constant T was significantly prolonged, while positive dP/dt/P and cardiac output were decreased immediately and continued up to 60 minutes after occlusion. 2DE findings corresponded well with the changes of cardiac function and hemodynamics determined simultaneously. We concluded that the detection of the left ventricular ballooning is important in the diagnosis of superacute phase of myocardial infarction in dogs.