Intracoronary thrombosis treated with stent and abciximab in patient with membranous glomerulonephritis

The association of nephrotic syndrome with a hypercoagulable state and vascular thrombosis is well recognized. In all adult series of nephrotics, venous thrombosis are much more common than arterial thrombosis, which has been mainly reported in children. Intracoronary thrombus is among the rarest arterial thromboses. We present a case of acute myocardial infarction in a 39-year-old women with nephrotic syndrome secondary to membranous glomeluronephritis, in which subsequent coronary angiography showed no evidence of atherosclerotic change and thrombotic occlusion in the left main coronary artery which was successfully treated with intracoronary stent and intravenous abciximab.

The effects of antiproliferative drugs at stenotic area associated with primary atherosclerotic lesions in apoE knockout mouse - Change of vascular remodeling

Apolipoprotein (apo) E deficient mouse can produce reproducible fixed stenotic primary atherosclerotic lesion, which reveals failure to remodel of vascular lumen, in the ascending aorta, external carotid, common carotid, iliac, femoral and popliteal arteries. To evaluate the effect of drugs in regarding to both prevention of primary atherosclerotic lesion and vascular remodeling, a systematic analysis of distribution of atherosclerotic lesions was undertaken in chow-fed, 9-momth-old apo E deficient mice, which was administrated drugs including asprin, methotrexate, probucol, sulodexide, diltiazem, cilazapril, trimetazidine, molsidomine, pentoxiphylline and Ginexin (R) for 7 month from 3 month-old. On gross and microscopic examination, formation of primary atheroscleotic lesions could be delated and/or prevented patially by effets of these drugs. On morphometric examination, failure to remodel forming vascular stenosis could not be seen, though relatively mild atherosclerotic lesion occured at vascular tree. These data suggest that the stenotic process in advanced atherosclerotic vessels can be delayed and/or prevented by several drugs including methotrexate, probucol, sulodexide, diltiazem, cilazapril, trimetazidine, molsidomine, pentoxiphylline and Ginexin (R) in vivo state.

Feasibility of Low-Molecular-Weight-Heparin (Fraxiparine) for Primary Stenting in Acute Myocardial Infarction

BACKGROUND AND OBJECTIVES: The optimal anti-thrombotic strategy for primary stenting in acute myocardial infarction (AMI) is still controversial. We evaluated prospectively the efficacy and safety of low-molecular-weight-heparin (LMWH) for primary stenting in AMI. MATERIALS AND METHOD: From 1/1997 to 7/1998, 54 AMI pts underwent primary stenting with 96% of procedural success rate (52/54). Of these, five pts were excluded from the study for warfarinization or use of GP II b/ III a inhibitor despite of successful stenting (TIMI 3 flow and less than 30% of residual stenosis). In 47 pts included in the study, 5,000-10,000 U of unfractionated heparin was administered (IV/bolus) bofore primary stenting. After sheath removal, LMWH(Fraxiparine, 7500 U/S.C.BID) maintained for 10.6+/-5.7 days. Aspirin and ticlopidine (500mg/day for > or =4 weeks) were given before stenting. Pts were followed to determine early (0-30 days) and late (31-180 days) major adverse cardiac events (MACE). Subsequent revascularization involving other coronary arteries did not constitute an end point. RESULTS: In 47 Pts (M:F=32:15, age=57.7+/-11.3 yrs, range: 37-88), 50 stents (Nir:38, micro:7, Jo:5, LAD:LCX:RCA-=24:9:14) were implanted. Their immediate post-stenting MLD and diameter-stenosis (%) were 2.9+/-0.4 mm, 4.3+/-8.7%, respectively. No patient showed sub-acute stent thrombosis or major bleeding requiring blood transfusion or surgery. During 0-30 days, the primary combined end point occurred in 2 (4.2%):one repeated angioplasty for in-stent restenosis; one hospital death for pump failure (1 of 2 Killip IV pts at admission). 44 patients were followed for 180 days and additional three TVR (3/44(6.8%), one CABG, one repeated angioplasty and one recurrrent myocardial infarction)occurred between 30-180 days due to recurrent ischemia. CONCLUSION:Anti-thrombotic therapy with LMWH (Fraxiparine) is safe and feasible for primary stenting in AMI. But to illuminate the impact on the clinical outcomes such as major adverse cardiac events and restenosis, we need more large and controlled study.

Relation between Coronary Flow Reserve and Myocardial Perfusion State and Change of Coronary Flow Reserve in Acute Myocardial Infarction

BACKGROUND AND OBJECTIVES: The state of the coronary microcirculation is one of the major determinants of the prognosis of patients who have had successful reperfusion for acute myocardial infarction (AMI). We investigated whether the vasodilatory reserve in the infarcted myocardium correlated with the perfusion state at early recovery phase in 12 anterior wall AMI patients. MATERIALS AND METHOD: We measured coronary flow variables with Doppler wire, after successful revascularizaiton by PTCA within 2 weeks following AMI and 13+/-0.5 months later, in the infarct related artery of AMI pts who received successful thrombolytic therapy. Myocardial perfuison state was evaluated by semiquantitative method (opacification score and opacification index) with myocardial contrast echocardiography (MCE) at the same time. Patients were divided into two groups according to initial perfusion status (perfusion defect group (PD (+), n=7), no-perfusion defect group (PD (-), n=5)). RESULTS: 10 minutes after completion of the intervention, the coronary flow reserve (CFR) was 2.0+/-0.4 (mean+/-SD): it increased to 2.7+/-0.7 (p=0.002) at follow up. The difference of initial CFR was not significant between PD (+) and PD(-) group. However, it significantly improved in the PD (-) group compared to PD (+) group at follow up (3.19+/-0.39 vs. 2.39+/-0.7, p=0.046). Opacification index and initial CFR were significantly correlated (r=0.79, p<0.05). CONCLUSION: The perfusion state of infarcted myocardium was significantly correlated with coronary flow reserve in anterior wall AMI and CFR was significantly improved in patients with relatively preserved myocardial perfusion.

Response of the Rat Heart to Bilateral Ovariectomy and Estrogen

BACKGROUND AND OBJECTIVES: Although ovarian estrogen is believed to decrease coronary heart disease by improving plasma lipoprotein and enhancing vasodilation, estrogen effect on heart tissue has not been shown yet. So we investigated the effect of the ovariectomy and estrogen on rat heart tissue. MATERIALS AND METHODS: Female Sprague Dawley rats, about 3 months of age, were subjected to sham surgery (n=9) or bilateral ovariectomy (n=20) and maintained untreated for 8 weeks after surgery. We administered estrogen (20 mg/Kg subcutaneously, 3 times/week) to 10 ovariectomized rats for 4weeks; the remaining ovariectmized rats received only saline. Animals were divided in 3 group:group 1 (control); sham op, group 2; ovariectomized only, group 3; ovariectomy+estrogen. We measured left ventricular thickness [IVS+LVPW)/2] and number of cardiomyocytes and interstitial fibrosis on light microscope (H & E and Masson's trochrome stain) and electron microscope. RESULTS: 1) LV wall thicknesses were significantly increased in group 2 and group 3 as compared with group 1 (2.45+/-0.1 and 2.46+/-0.11 vs 2.31+/-0.15 mm). 2) There were no significant change in the number of cardiomyocyte between group 1, group 2 and group 3 (54.3+/-5.7, 60.2+/-19.4, 52.5+/-14.1). 3) Group 2 and group 3 show more interstitial edema (44% and 62.5% vs 0%) on LM and more interstitial edema and the increase of number of mitochondria on EM than group 1. CONCLUSION: Bilateral ovariectomized rats show the increase of LV wall thickness, which was caused by interstitial edema without cardomyocyte hypertrophy and these changes were not reversed by the short-term administration of estrogen for 4 weeks.

Effects of Ischemic preconditioning on the Post-ischemic Myocardial Dysfunction and Coronary Flow in the Isolated Rat Hearts

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.

Effects of Ischemic preconditioning on the Post-ischemic Myocardial Dysfunction and Coronary Flow in the Isolated Rat Hearts

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.

Significance of ST Segment, R Wave, Q Wave and QRS Score for Assessing Myocardial Perfusion in Acute Myocardial Infarction

BACKGROUND AND OBJECTIVES: The restoration of infarct-related coronary artery (IRA) patency in acute myocardial infarction (AMI) linked to a significant improvement in survival. Because of microvascular and cellular injury, patent IRA does not always represent successful reperfusion. With progress of myocardial ischemia, standard 12 lead ECG shows evolutional changes of ST-segment, R wave and Q wave. But their relations to myocardial perfusion were uncertain. METHODS: Total 41 patients of the first anterior wall AMI were enrolled and serial ECGs were taken to measure sum of ST-segment elevation (sigma ST), sum of Q wave (sigma Q), sum of R wave (sigma R), and QRS score (QRSs) proposed by Selvester in each patients before thrombolytic therapy (i), after coronary angiography at 90 minutes of thrombolytic therapy (a), and before discharge (d). Myocardial contrast echocardiography was performed within 10 days of AMI to estimate opacification score (OS) and opacification index (OI) in segments of LAD territory. We investigate the relation between evolution of ECG changes and perfusion status of infarcted myocardium. RESULTS: 1) There was no relation between OI and sigma ST, but sigma R and QRSs showed significant relation with OI before discharge (r=0.59, - 0.33, p<0.05, respectively), post thrombolytic therapy (r=0.51, - 0.61, p<0.05), and baseline ECG (r=0.53, - 0.51, p<0.05). 2) The number of segments with OS (0.5) showed no singificant relation to the degree of sigma ST and sigma Q, but number of segments with OS (0) showed singinficant relation to that of sigma R and QRSs (r of sigma Ri, sigma Ra, sigma Rd vs number of segments with OS (0)= - 0.59, - 0.66, - 0.43, p<0.05, QRSi, QRSa, QRSd vs number of segments with OS (0)=0.58, 0.58, 0.57, p<0.05). CONCLUSION: These findings suggest that the ECG changes of R wave and QRS scores could be useful markers of perfusion state in thrombolytic era.

Changes of Mitral Inflow According to Position in Patients with Dilated Cardiomyopathy

BACKGROUND AND OBJECTIVES: Dilated cardiomyopathy(DCMP) probably is the end result of myocardial damage produced by various causes and shows various clinical manifestations. Some patients with DCMP experience more shortness of breath when change their position especially in left lateral decubitus position. We investigated whether the symptomatic changes according to position in DCMP patients were related to the changes of mitral inflow pattern. MATERIALS AND METHOD: DCMP patients with New York Heart Association functional class III or IV, who felt more shortness of breath when changed their position, were studied. The patients with atrial fibrillation or with moderate and severe valvular heart disease were excluded. Early and late atrial left ventricular filling velocities and time velocity integrals(TVI) and it's ratios of mitral inflow, heart rates, isovolumic relaxation time(IVRT), decelaration time(DT) of early mitral inflow were analysed in each decubitus position. RESULTS: 4 men and 3 women were included and their mean age was 60.3 years. 6 patients had mild mitral regurgitation and 4 patients had mild aortic regurgition. All patients felt more shortness of breath in left lateral decubitus position. Peak velocity and TVI of early mitral inflow were not changed significantly according to position. Peak velocity of late mitral inflow was increased significantly with right lateral decubitus position(Lt; 39.0+/- 14.1cm/sec, Rt; 49. 4+/-23.6cm/sec, p<0.05). TVI of late mitral inflow was increased significantly with right lateral decubitus position(Lt; 2.8+/-1.1cm, Rt; 3.8+/-1.9cm, p<0.05). Ratio of early and late mitral inflow peak velocity was decreased significantly with right lateral decubitus position(Lt; 2.13+ 0.34, Rt: 1.62+/-0.57, p<0.05). Ratio of early and late mitral inflow TVI was decreased significantly with right lateral decubitus position(Lt; 3.13+/-1.49, Rt; 2.13+/-1.32, p<0.01). Heart rate, IVRT, DT were not changed significantly according to position. CONCLUSION: In DCMP patients with symptomatic relief in right lateral position, mitral inflow patterns were changed. And this finding suggests that symptomatic relief may be related to decreased left ventricular filling pressure.