Complete Vessel Occlusion Research Articles

Immunohistopathologic evaluation of choroidal neovascular membranes following Verteporfin-photodynamic therapy

Purpose To evaluate the vascularization and proliferative activity in choroidal neovascular membranes due to age-related macular degeneration after verteporfin photodynamic therapy and submacular removal. Design Interventional case series. Methods In a retrospective review of seven patients who underwent removal of subfoveal classic choroidal neovascular membranes after treatment with photodynamic therapy 3 to 146 days earlier, membranes were stained for CD 34, CD 105, and Ki-67 and correlated with clinical pictures and fluorescein angiography. Results Fluorescein angiography performed on the day of surgery disclosed nonperfusion of the treated area 3 days after photodynamic therapy, but perfusion and leakage were seen at greater post–photodynamic therapy intervals. Membranes excised 3 days after photodynamic therapy showed CD34 and CD105 positive, mostly occluded vessels. The endothelial cells appeared damaged. Ki-67 activity was low. In membranes excised 34 to 146 days after photodynamic therapy, all vessels appeared patent and were lined by healthy endothelial cells with strong expression of CD34 and CD105. Ki-67 expression was elevated after 34 days but decreased thereafter. Conclusion Photodynamic therapy did not cause a general or complete occlusion of vessels within the choroidal neovascular membranes, as suggested by fluorescein angiography 3 days postintervention, but the endothelial cells appeared to be severely damaged. Proliferative activity within these specimens was reduced. At longer intervals after photodynamic therapy, the fibrovascular tissue seemed to recover; perfusion, hyperfluorescence, and leakage of the choroidal neovascular membranes could be detected by fluorescein angiography. The clinical appearance showed a correlation with the immunohistologic characteristics of an increased proliferative activity and patent vascularization.

Pressure-controlled Vascular Clamp: A Novel Device for Atraumatic Vessel Occlusion

Morphological vessel injury after clamping has been an important problem in vascular surgery. Although various techniques have been employed to occlude a vessel during a surgical procedure, a complete, atraumatic occlusion method has not yet been developed. In the present study, we describe use of a novel pressure-controlled and balloon-jawed vessel clamp to provide atraumatic vessel occlusion. We compared its traumatic effect on femoral arteries with that resulting from use of a conventional De Bakey vascular clamp in a canine model. During surgical application, our clamp provided complete vessel occlusion with no oozing in distal arteriotomy. On histological examination of the clamped vessel segments, we observed no destruction of the vessel wall, compared to widespread injury of the De Bakey vascular clamp. Despite some difficulties in application, we think this technique could be a promising method for vascular procedures.

Renal trauma: a practical guide to evaluation and management.

1. Blunt trauma and gross hematuria. Gross hematuria is the most reliable indicator for serious urological injury. The degree of hematuria, however, does not correlate with the degree of injury. In fact, renal pedicle avulsion or acute thrombosis of segmental renal arteries can occur in the absence of hematuria while renal contusions can present with gross hematuria. 2. Blunt trauma, microscopic hematuria and shock. Significant microscopic hematuria is >5 RBC/HPF in the first voided or catheterized specimen. Shock is any presence of systolic blood pressure <90 during transport or upon arrival in the emergency room. Blunt trauma patients with microhematuria and no shock have minor renal injuries in nearly all cases. Miller and McAninch, based on findings in over 2000 blunt renal trauma injuries determined that in <0.2% of cases will a grade 2 or more severe renal injury be missed. These patients are the victims of multiple trauma and thus during the evaluation of other intra-abdominal injuries, most of the missed major renal injuries will be detected. When patients who were imaged for associated intra-abdominal injuries are included only 0.03% of significant renal injuries were not identified. 3-5 3. Major deceleration injury. The kidney primarily floats free in a bed of fat contained within the envelope of Gerota's fascia. The kidney is fixed at only two points, the ureter and the vascular pedicle. Because of poor fixation, the kidney can be easily dislocated by sudden acceleration or deceleration. Kidney dislocation can result in tearing of the collecting system at the ureteropelvic junction (UPJ) or tearing of renal artery intima, resulting in partial to complete vessel occlusion. Such injuries can occur with major deceleration, as in head-on motor vehicle accidents (MVA) or

Occlusion of infusion vessels on γ-linolenic acid infusion

γ-linolenic acid (GLA) is known to have selective tumoricidal action. In this study, the effect of lithium salt of GLA conjugated to iodized lymphographic oil (LGIOC) was injected intra-arterially close to the origin of tumor-feeding vessel(s) was studied. Four patients with stage 4 cancer disease (2 with hepatocellular carcinoma, 1 with giant cell tumor of the bone, and one with renal cell carcinoma), were selected for the study. Angiography, radiography and computed axial tomography were performed prior to and immediately after the injection of LGIOC and at periodic intervals. All four patients tolerated the treatment well. The most significant observation was the complete occlusion of the tumor-feeding vessels after LGIOC injection. Follow-up angiograms performed in all the patients showed occlusion of the tumor-feeding vessels is more or less permanent. A significant reduction in the size of the tumor was also observed in these patients. LGIOC showed occlusion of tumor-feeding vessels after infusion, and further studies are needed to confirm these preliminary results.

Embolization of Collateral Vessels Using Mechanically Detachable Coils in Young Children with Congenital Heart Disease

Our objective was to evaluate the usefulness of embolizing collateral vessels using mechanically detachable coils (MDCs) in children aged 3 years or younger with congenital heart disease. The subjects were 8 children with congenital heart disease featuring collateral vessels (age 18 days-3 years): 3 with a single ventricle, 2 with the tetralogy of Fallot, 2 with pulmonary atresia, and 1 with a ventricular septal defect. The embolized vessels were the major aortopulmonary collateral artery (MAPCA) in 5 patients, the persistent left superior vena cava in 2, and the coronary arteriovenous fistula in 1. A 4 or a 5 F catheter was used as the guiding device, and embolization was performed using MDCs and other conventional coils introduced through the microcatheter. One patient had growth of new MAPCAs after embolization, and these MAPCAs were also embolized with MDCs. Thus, a total of 9 embolization procedures were performed in 8 patients. Complete occlusion of the collateral vessels was achieved in 8 of 9 procedures (89%). Seven of 8 patients (88%) had uneventful courses after embolization, and MDC procedures appeared to play important roles in avoiding coil migration and achievement of safe coil embolization. One patient who underwent MAPCA embolization showed no improvement in heart function and died 2 months and 19 days later. Embolization of collateral vessels using MDCs in young children with congenital heart disease can be an effective procedure and a valuable adjunct to surgical management.

RETRACTED: Abrupt and complete occlusion of tumor-feeding vessels by γ-linolenic acid

This article has been retracted by the Publisher. Reason: This article was previously published in Nutrition, Volume 18, Issue 7–8, pages 662–664 and inadvertently published again in Nutrition, Volume 18, Issue 9, pages 767–769.

Cardiac and cerebral manifestations of antiphospholipid syndrome

We describe cardiac and cerebral manifestations in 27 patients with the antiphospholipid syndrome and give a review of the literature. We studied 27 patients with either cardiac, cerebral or both manifestations, who also were diagnosed with the antiphospholipid syndrome (APS). All patients fulfilled the proposed classification criteria for the APS according to the Scientific Standardisation Committee of the International Society of Thrombosis and Haemostasis (1). Three patients died. Eighteen of the 27 patients had coronary artery disease with either thrombotic coronary occlusions, high grade stenosis or complete vessel occlusion. In three patients the left main artery was involved. Ten patients had involvement of the left anterior descending artery (LAD), 6 patients of the circumflex artery (RCX) and 5 patients had involvement of the right coronary artery (RCA). As valvular lesions have been described in association with the APS it should be noted that in 16 cases there was mitral- and/or aortic valve disease and in 3 cases tricuspid valve disease. Four patients underwent mitral- and/or aortic- and/or tricuspid valve replacement. 7 patients presented with a history of cerebrovascular involvement; 5 of these patients had cerebral infarction, one patient recurrent cerebral bleeding under oral anticoagulation and another patient presented with cognitive disorders. Three of the 7 patients had a prior history of myocardial infarction, whereas 3 patients underwent mitral or aortic valve replacement. The frequent occurrence of coronary disease, cardiac valvular disease and cerebral disease in patients diagnosed with APS may suggest a causative relationship between the presence of PL antibodies and vascular disease.

Abrupt and complete occlusion of tumor-feeding vessels by γ-linolenic acid

Abrupt and complete occlusion of tumor-feeding vessels by γ-linolenic acid

Prevalence and significance of coronary collateral circulation in patients with acute myocardial infarct

Angiograms from consecutive and unselected patients with acute myocardial infarction were studied with respect to the prevalence as well as the significance of coronary collateral circulation to myocardium distal to the acute coronary occlusion. Coronary angiograms were obtained from 700 consecutive and unselected patients with an acute transmural infarction within 3.7 +/- 3 hours (0.5-12) of symptom onset. No patient had undergone i.v. thrombolysis prior to angiography. Complete and acute vessel occlusion was found in 626/700 patients (89%). Coronary collaterals were detected and graded using Rentrop's classification. The grade of collateral circulation was related to the clinical course after 30 days and to the global and regional left ventricular wall motion. Collaterals were found in 334 patients (69%); 242 patients (38%) had collateral flow grade 2 or 3. Collaterals were demonstrated more frequently in women vs men and in patients with multivessel disease. The prevalence of collaterals was unrelated to age and the presence of diabetes mellitus. Patients who had angiography within 3 hours of symptom onset had collaterals detected less frequently than patients who had angiography beyond 6 hours (66% vs 75%, p < 0.05). No collaterals were found in 17/37 patients (47%) in cardiogenic shock and inferior MI but in only 30/164 patients (18%, p < 0.01) without shock. Global and regional left ventricular wall motion after 2 weeks was unrelated to the degree of coronary collateral circulation during acute myocardial infarction. Collateral circulation to myocardium distal to an acutely occluded coronary artery is detected in 2/3 patients during the acute infarct phase. The absence of collaterals is related to the early occurrence of cardiogenic shock in patients with inferior MI but not to the presence of diabetes mellitus. After direct angioplasty of the infarct vessel, the protective effects of coronary collaterals on chronic LV function remain uncertain.

Endovascular Administration after Intravenous Infusion of Thrombolytic Agents for the Treatment of Patients with Acute Ischemic Strokes

OBJECTIVE To determine the feasibility of combined intravenous and intra-arterial thrombolytic therapy for acute ischemic strokes and to evaluate its associated risks, using magnetic resonance imaging as a triage tool. Intravenous treatment followed by intra-arterial infusion may increase the rate of recanalization and lead to better clinical results, with reduced frequency of intracranial hemorrhage. METHODS Our Brain Attack Team evaluated patients who presented within 3 hours after symptom onset. Patients who did not demonstrate improvement and exhibited no evidence of intracranial hemorrhage on head computed tomographic scans were treated with intravenously administered recombinant tissue plasminogen activator (0.6 mg/kg) and underwent emergency magnetic resonance imaging of the head. T2-weighted turbo-gradient and spin echo and echo-planar diffusion- and perfusion-weighted imaging scans were obtained. Patients with evidence of imaging abnormalities indicating acute cortical infarction underwent cerebral angiography. After determination of vessel occlusion, intra-arterially administered urokinase (up to 750,000 units) or intra-arterially administered recombinant tissue plasminogen activator (maximal dose, 0.3 mg/kg) was used to achieve recanalization. RESULTS We treated 45 patients with this protocol. The mean age was 67 ± 13 years, and 58% of the patients were women. There was a significant improvement in National Institutes of Health Stroke Scale scores after treatment. There was good correlation between abnormal perfusion-weighted imaging findings and cerebral angiographic findings (complete vessel occlusion). The incidence of symptomatic intracranial hemorrhage was 4.4% in this cohort. Seven patients died in the hospital, and the majority of survivors (77%) experienced good outcomes (Barthel index of ≥95) 3 months after treatment. CONCLUSION Our data demonstrate that this protocol is feasible and that combined intravenous and intra-arterial thrombolysis to treat acute ischemic strokes is sufficiently safe to warrant further evaluation.

Endovascular Administration after Intravenous Infusion of Thrombolytic Agents for the Treatment of Patients with Acute Ischemic Strokes

To determine the feasibility of combined intravenous and intra-arterial thrombolytic therapy for acute ischemic strokes and to evaluate its associated risks, using magnetic resonance imaging as a triage tool. Intravenous treatment followed by intra-arterial infusion may increase the rate of recanalization and lead to better clinical results, with reduced frequency of intracranial hemorrhage. Our Brain Attack Team evaluated patients who presented within 3 hours after symptom onset. Patients who did not demonstrate improvement and exhibited no evidence of intracranial hemorrhage on head computed tomographic scans were treated with intravenously administered recombinant tissue plasminogen activator (0.6 mg/kg) and underwent emergency magnetic resonance imaging of the head. T2-weighted turbo-gradient and spin echo and echo-planar diffusion- and perfusion-weighted imaging scans were obtained. Patients with evidence of imaging abnormalities indicating acute cortical infarction underwent cerebral angiography. After determination of vessel occlusion, intra-arterially administered urokinase (up to 750,000 units) or intra-arterially administered recombinant tissue plasminogen activator (maximal dose, 0.3 mg/kg) was used to achieve recanalization. We treated 45 patients with this protocol. The mean age was 67 +/- 13 years, and 58% of the patients were women. There was a significant improvement in National Institutes of Health Stroke Scale scores after treatment. There was good correlation between abnormal perfusion-weighted imaging findings and cerebral angiographic findings (complete vessel occlusion). The incidence of symptomatic intracranial hemorrhage was 4.4% in this cohort. Seven patients died in the hospital, and the majority of survivors (77%) experienced good outcomes (Barthel index of >or=95) 3 months after treatment. Our data demonstrate that this protocol is feasible and that combined intravenous and intra-arterial thrombolysis to treat acute ischemic strokes is sufficiently safe to warrant further evaluation.

Alcoholism, hypercortisonism, fat embolism and osseous avascular necrosis. 1971.

Alcoholism, hypercortisonism, fat embolism and osseous avascular necrosis. 1971.

Diaspirin Cross-Linked Hemoglobin Fails to Improve Left Ventricular Diastolic Function after Fluid Resuscitation from Hemorrhagic Shock

In severe hemorrhagic shock, left ventricular (LV) diastolic dysfunction is an early sign of cardiac failure due to compromised myocardial oxygenation. Immediate fluid replacement or, in particular, administration of a hemoglobin-based oxygen carrier (diaspirin cross-linked hemoglobin; DCLHb) improves myocardial oxygenation; therefore, positive effects on LV diastolic function could be expected. The effects of fluid resuscitation from severe hemorrhagic shock with DCLHb were investigated in 20 anesthetized domestic pigs. After generation of a critical left anterior descending coronary artery stenosis (narrowing of the artery until disappearance of reactive hyperemia after a 10-second complete vessel occlusion), hemorrhagic shock (mean arterial blood pressure 45 mm Hg) was induced within 15 min by controlled blood withdrawal and maintained for 60 min. Fluid resuscitation consisted of replacement of the plasma volume withdrawn during hemorrhage by infusion of either 10% DCLHb (DCLHb group, n = 10) or 8% human serum albumin (HSA) oncotically matched to DCLHb (HSA group, n = 10). After completion of resuscitation, an observation period of 60 min elapsed. Measurements of central hemodynamics, myocardial oxygenation, and LV diastolic function were performed at baseline, after induction of critical coronary artery stenosis, after 60 min of hemorrhagic shock, immediately after resuscitation, and 60 min later. While 5 out of 10 animals treated with HSA died within the first 20 min after fluid resuscitation from acute LV pump failure, all DCLHb-treated animals survived until the end of the protocol (p < 0.05). Despite superior myocardial oxygenation due to augmentation of the arterial O₂ content as well as of coronary perfusion pressure, no beneficial effects on LV diastolic function were observed after infusion of DCLHb. Peak velocity of LV pressure decrease (dp/dt_min) did not reveal significant differences between the two groups. Immediately after completion of fluid resuscitation with DCLHb, the time constant of LV diastolic relaxation (τ) was prolonged when compared with HSA-treated animals (p < 0.05), indicating retardation of early LV diastolic relaxation. Our data suggest that DCLHb fails to improve LV diastolic function after fluid resuscitation from severe hemorrhagic shock. However, positive effects on myocardial perfusion and oxygenation result in a significant reduction of the mortality of severe hemorrhagic shock.

Mechanisms of atherosclerotic plaque stabilization for a lipophilic calcium antagonist amlodipine

Coronary artery disease (CAD) is the result of atherosclerosis, a vascular disorder characterized by abnormalities in vasoconstriction and endothelial function, ultimately leading to partial or complete vessel occlusion. Because the atherosclerotic plaque is marked by changes in calcium regulation, there has been interest in a potential antiatherosclerotic role for calcium antagonists. In support of this hypothesis, a recent clinical study demonstrated in patients with CAD that treatment with the lipophilic dihydropyridine-type calcium antagonist amlodipine resulted in significantly fewer cardiovascular procedures and events. The Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) evaluated the effects of amlodipine on the development and progression of atherosclerotic lesions in coronary and carotid arteries in 825 patients with documented CAD. The results of PREVENT showed that patients receiving amlodipine had marked reductions in hospitalization for revascularization and unstable angina compared with placebo in a population consisting of either normotensive or controlled hypertensive patients. Ultrasound approaches determined that amlodipine therapy was also associated with significant slowing in carotid atherosclerosis—an important surrogate marker for CAD—over the 3-year period. This vascular-wall benefit associated with amlodipine treatment was not related to changes in blood pressure. The findings from PREVENT were consistent with a second reported study known as the Coronary Angioplasty Amlodipine Restenosis Study (CAPARES). These clinical results have led to an interest in potential plaque-stabilization properties of this lipophilic calcium antagonist. In this article, cellular and molecular mechanisms of action that may contribute to a beneficial role for a calcium antagonist in the treatment of atherosclerosis will be reviewed.

MR angiographic investigation of transient focal cerebral ischemia in rat

Contrast agent free time-of-flight magnetic resonance angiography (TOF-MRA) was applied to the intraluminal thread occlusion model of experimental stroke in rat. It was combined with perfusion- and diffusion-weighted imaging (PWI and DWI) sequences to correlate occlusion and reopening of the middle cerebral artery with alterations in these well-established magnetic resonance sequences. Since TOF-MRA can be repeated without limitations, the time course of vascular patency is demonstrated during an experimental period of up to 8 h (2 h control, 1 h ischemia, 3-6 h reperfusion). With an acquisition time of 10 min, TOF-MRA proved to be suitable to analyze the vascular state of occlusion and reperfusion repetitively in longitudinal studies. Spatial resolution was sufficient to observe neurovascular structural details. In eight out of 10 animals complete vessel occlusion by the intraluminal thread could be validated by an entirely extinguished signal of the ipsilateral middle cerebral artery (MCA) in the angiograms. This was in accordance with a perfusion deficit in the MCA vascular territory detected by PWI (reduction to 30.4 +/- 7.4% relative to contralateral side) and a disturbance of water ion homeostasis monitored by DWI in this area. One animal showed a delayed occlusion after 30 min of MCA occlusion, in another animal vessel occlusion failed. In seven out of the eight successful occlusion experiments there was immediate reperfusion after withdrawal of the thread. One animal showed a delayed reperfusion after suture retraction. Remarkable hemispheric differences in vascular branching of the MCA could be recognized in three out of 10 animals. In conclusion, TOF-MRA is considered a helpful method to survey even in small laboratory animals the correct time course of vascular occlusion and reopening in experimental ischemia, and provides complementary information to the tissue perfusion status monitored by PWI and the ischemic lesion territory detected by DWI.

Theoretical investigation of the role of choriocapillaris blood flow in treatment of subfoveal choroidal neovascularization associated with age-related macular degeneration

PURPOSE: To investigate the relationship between choriocapillaris blood flow and blood flow through an overlying choroidal neovascularization, as it relates to photocoagulation-induced changes in the choriocapillaris circulation. METHODS: A theoretical model that simulates the blood flow in the choriocapillaris and choroidal neovascularization of the human eye was developed, based on histologically determined vascular geometry and experimentally measured blood pressure gradients. The choriocapillaris blood pressure and blood flow were examined before and after simulated photocoagulation of various Sattler layer vessels entering the choriocapillaris in the vicinity of the choroidal neovascularization. (The Sattler layer is the inner layer of medium-sized choroidal vessels that includes both arterioles and venules that supply the choriocapillaris.) RESULTS: The theoretical model showed that both partial and complete occlusion of either Sattler arteriole or venous vessels in the vicinity of the capillary-like vessels connecting a choroidal neovascularization to the underlying choriocapillaris results in significant choroidal neovascularization blood flow reduction. These theoretical results are similar to clinically observed changes induced by laser photocoagulation of feeder vessels. (In this discussion, the term “feeder vessels” refers to those vessels in an indocyanine green angiogram image that appear to supply blood to a choroidal neovascularization; these vessels appear to be Sattler layer vessels, rather than the histologically demonstrated short, capillary-like vessels that form choriocapillaris-choroidal neovascularization communications.) CONCLUSIONS: Reduction of choriocapillaris blood flow underlying a choroidal neovascularization may be sufficient to reduce the blood flow rate in the choroidal neovascularization and thereby reduce the associated retinal edema. The results also suggest that reduction of choriocapillaris blood flow may be the common hemodynamic event associated with the successful application of several currently practiced methods of choroidal neovascularization treatment, including feeder vessel photocoagulation, photodynamic therapy, transpupillary thermotherapy, and prophylactic drusen photocoagulation. Ultimately, this model may be useful in determining optimal placement of laser photocoagulation burns to achieve a desirable perturbation in choroidal blood flow distribution and thereby reduce choroidal neovascularization blood flow to the extent necessary to obliterate associated retinal edema.

Lack of In Vivo Function of CD31 in Vascular Thrombosis

A murine model of endothelial cell injury-based vascular thrombosis was used to test the role of platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) in blood cell aggregate formation and vessel occlusion in vivo. Photochemically-induced thrombus formation was analyzed in detail using intravital fluorescence microscopy of individual microvessels in cremaster muscle preparations of CD31-deficient and wildtype mice. In venules, epi-illumination induced rapid thrombus formation with first platelet deposition after 0.56 +/- 0.11 min and complete vessel occlusion within 5.05 +/- 0.45 min. In arterioles, thrombus formation was markedly delayed with first platelet deposition after 3.03 +/- 0.47 min and complete vessel occlusion within 10.04 +/- 1.26 min. Kinetics of thrombus formation in both venules (first platelet deposition: 0.52 +/- 0.1 min; vessel occlusion: 5.03 +/- 0.52 min) and arterioles (first platelet deposition: 3.06 +/- 0.68 min; vessel occlusion: 10.02 +/- 1.38 min) of CD31-deficient mice was found almost identical compared with that in wildtype animals. Tail bleeding time was 233 +/- 24 s in wildtype and 243 +/- 32 s in CD31-deficient mice. Moreover, CD31-deficient and wildtype mice revealed comparable interaction of leukocytes to endothelium. This study shows for the first time in vivo that CD31 is not critically involved in blood cell thrombus formation upon endothelial cell injury.

Diaspirin-crosslinked hemoglobin reduces mortality of severe hemorrhagic shock in pigs with critical coronary stenosis

To evaluate the effects of resuscitation with a 10% diaspirin-crosslinked hemoglobin (DCLHb) solution on global hemodynamic variables, systemic and myocardial oxygen transport and tissue oxygenation, and contractile function of the left ventricle in an experimental model of severe hemorrhagic shock and critical stenosis of the left anterior descending coronary artery (LAD). Prospective, placebo-controlled, randomized study. Experimental animal laboratory. A total of 20 anesthetized pigs. After implementation of a permanent critical LAD stenosis (ie, maintenance of basal blood flow but absence of reactive hyperemia after a 10-sec complete vessel occlusion), hemorrhagic shock (target mean aortic pressure, 45 mm Hg) was induced within 15 mins by programmed withdrawal of blood and maintained for 60 mins. Subsequently, the volume of plasma lost during hemorrhage was replaced by either a balanced electrolyte solution containing 10 g/dL DCLHb (DCLHb group; n = 10) or an 8 g/dL human albumin solution (HSA) oncotically matched to DCLHb (HSA group; n = 10). Data were collected immediately after the infusion of the different solutions and again after 60 mins had elapsed. Although five of ten HSA-treated animals died of acute left ventricular failure within the first 20 mins after complete fluid resuscitation, all of the DCLHb-treated animals survived the 60-min observation period after resuscitation (p < .05). This significant difference in mortality is explained by higher coronary perfusion pressure in DCLHb-treated animals (75 +/- 17 vs. 27 +/- 17 torr DCLHb vs. HSA group; p < .05) and persistence of subendocardial ischemia and hypoxia (radioactive microspheres method) in HSA-treated animals on resuscitation particularly affecting the LAD-supported myocardium (subendocardial oxygen delivery: 20 +/- 11 vs. 3 +/- 1 mL oxygen x g(-1) x min(-1), DCLHb vs. HSA group; p < .05). Except for enhanced myocardial contractility immediately on infusion of DCLHb (maximal left ventricular pressure increase: 2373 +/- 782 vs. 1730 +/- 543 torr x sec(-1) DCLHb vs. HSA group; p < .05), no differences were detected between groups concerning the variables of systemic oxygen transport, tissue oxygenation, and regional contractile function of the myocardium (determined with microsonometry). Fluid resuscitation with 10% DCLHb solution completely reverses hemorrhagic shock-induced subendocardial ischemia and hypoxia in the presence of compromised coronary circulation and thereby prevents early death after resuscitation.

Comparison of electrocardiographic findings in patients with AL (primary) amyloidosis and in familial amyloid polyneuropathy and anginal pain and their relation to histopathologic findings

To assess the prevalence of chest pain and ischemic electrocardiographic (ECG) changes and relate them to histopathologic findings of coronary arteries in cardiac amyloidosis, 33 patients with AL (primary) amyloidosis and 60 patients with familial amyloid polyneuropathy (FAP) were examined. Five patients (15%) with AL amyloidosis had recurrent anginal pain with exertion and 2 of them also experienced anginal pain after orthostatic hypotension. The chest pain was associated with transient downsloping or horizontal ST-segment depression with or without T-wave inversion in right precordial leads, whereas the remaining patients with AL amyloidosis and all patients with FAP did not show anginal pain or ischemic ST-T changes. Histologic sections of coronary arteries were obtained in 12 patients with AL amyloidosis, including 4 of the 5 patients who had angina pectoris and in 25 patients with FAP. Three patients with anginal pain had variable degrees of stenoses of the intramural coronary arteries by amyloid deposition predominantly in the media with normal or nearly normal epicardial arteries. One patient with AL amyloidosis who had effort angina showed marked stenosis and complete occlusion of the small coronary vessels by transmural amyloid deposition. The remaining 8 patients with AL amyloidosis and 25 with FAP without chest pain did not exhibit any stenosis or occlusion of both the epicardial and intramural vessels. These findings suggest that ischemic ST-T changes with chest pain are not so rare in patients with AL amyloidosis, and that markedly decreased myocardial oxygen supply due to diffuse stenotic or occlusive disease of the small coronary vessels by amyloid deposition contributes to the development of clinically significant ischemic heart disease in these patients.

Dilated cardiomyopathy associated with simian AIDS in nonhuman primates.

Cardiomyopathy is being recognized with increasing frequency in patients with AIDS, yet the relationship between HIV infection and cardiac contractile dysfunction remains obscure. The purpose of the present study was to determine if infection with simian immunodeficiency virus (SIV) in nonhuman primates is associated with cardiac dysfunction and myocardial injury. Left ventricular size and function were determined by 2D echocardiography in 16 rhesus macaques before and at weekly intervals following infection with cloned pathogenic SIV(mac) 239 or the highly attenuated SIV(mac) 239 nef deletion mutant. A second group of 15 rhesus macaques chronically infected with pathogenic (n=6) or nonpathogenic (n=9) virus were studied at >2 years following infection. Cardiac tissues from 24 rhesus macaques chronically infected (>2 years) with pathogenic SIV were reviewed for evidence of cardiac pathology. Acute infection (<6 weeks) with either pathogenic or nonpathogenic SIV caused neither contractile dysfunction nor cardiac pathology. However, LV ejection fraction was significantly (P<0.05) depressed (43+/-7%) in rhesus macaques chronically infected with pathogenic SIV compared with rhesus macaques chronically infected with nonpathogenic SIV (61+/-3%). Furthermore, two thirds of rhesus macaques that succumbed to simian AIDS had myocardial pathology including lymphocytic myocarditis (n=9) and coronary arteriopathy (n=6), with complete vessel occlusion (n=4) and associated myocardial infarction and necrosis. This unique model is valuable in understanding the pathogenesis of cardiac injury associated with retroviral infection in a relevant nonhuman primate model of AIDS.