Improved outcome using IVUS-guided stent implantation: premise or promise?
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
R Erbel
Publications and source records attributed to R Erbel.
Role of intravascular ultrasound imaging in identifying vulnerable plaques.
UNLABELLED: A plaque that has a large lipid core and a thin fibrous cap may undergo rupture. Once it ruptures, it may lead to thrombus formation and subsequent vessel occlusion. To identify unstable plaques before they rupture is essential for clinical management and patient's prognosis. Intravascular ultrasound (IVUS) opens a new window for the assessment of plaque morphology to identify vulnerable plaques and plaque rupture. We examined 144 patients with angina and ischemic ECG changes using IVUS. Ruptured plaques, characterized by a plaque cavity and a tear on the thin fibrous cap, were identified in 31 patients (group A) of which 23/31 (74%) clinically presented as unstable angina. Plaque rupture was confirmed by injecting contrast medium filling the plaque cavity during IVUS examination. Of the patients without plaque rupture (group B, n = 108), only 19 (18%) had unstable angina. No significant differences between the 2 groups were found concerning the vessel and plaque areas (p > 0.05). The percent stenosis in group A (56.2 +/- 16.5%) was significantly lower than in group B (67.9 +/- 13.4%) (p < 0.001). Area of the plaque cavity in group A (4.1 +/- 3.2 mm2) was significantly larger than the echolucent zone in group B (1.32 +/- 0.79 mm2) (p < 0.001). The plaque cavity/plaque ratio in group A (38.5 +/- 17.1%) was larger than the echolucent area/plaque ratio in group B (11.2 +/- 8.9%) (p < 0.001). The thickness of the fibrous cap in group A (0.47 +/- 0.20 mm) was significantly thinner than that (0.96 +/- 0.94 mm) in group B (p < 0.001). CONCLUSIONS: Plaques seem to be prone to rupture when the echolucent area is larger than 1 mm2, the echolucent area/plaque ratio greater than 20% and the fibrous cap thinner than 0.7 mm. IVUS has the capacity of identifying plaque rupture and vulnerable plaques. This may have potential influence on patients management and therapy.
Adult↗
[Current aspects on differentiating thoracic pain symptoms].
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Angina Pectoris↗
Chest pain after coronary interventional procedures. Incidence and pathophysiology.
Chest pain following successful percutaneous coronary interventions is a common problem. Although the development of chest pain after coronary interventions may be of benign character, it is disturbing to patients, relatives and hospital staff. Such pain may be indicative of acute coronary artery closure, coronary artery spasm or myocardial infarction, but may also simply reflect local coronary artery trauma. The distinction between these causes of chest pain is crucial in selecting optimal care. Management of these patients may involve repeat coronary angiography and additional intervention. Commonly, repeat coronary angiography following percutaneous transluminal coronary angioplasty (PTCA) in patients with chest pain demonstrates widely patent lesion sites suggesting that the pain was due to coronary artery spasm, coronary arterial wall stretching or was of non-cardiac origin. As reported by the National Heart, Lung and Blood Institute PTCA Registry, 4.6% of patients after angioplasty have coronary occlusions, 4.8% suffer a myocardial infarction, and 4.2% have coronary spasm. The frequency of chest pain after new device coronary interventions (atherectomy and stenting) seems to be even higher. However, only the minority of patients with post-procedural chest pain have indeed an ischemic event. Therefore, the vast majority of patients have recurrent chest pain without any signs of ischemia. There is some evidence that non-ischemic chest pain after coronary interventions is more common after stent implantation as compared to PTCA (41% vs. 12%). This may be due to the continuous stretching of the arterial wall by the stent as the elastic recoil occurring after PTCA is minimized. In conclusion, chest pain after coronary interventional procedures may potentially be hazardous when due to myocardial ischemia. However, especially after coronary stent placement, cardiologists must consider "stretch pain" due to the overdilation and stretching of the artery caused by the stent in the differential diagnosis. Clinically, it is, therefore, important to recognize that in addition to ischemia-related chest pain other types of chest pain do exist with cardiac origin.
Angina Pectoris↗
Spontaneous and iatrogenic microembolization. A new concept for the pathogenesis of coronary artery disease.
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Animals↗
Non-invasive characterization of cardiac microvascular disease by nuclear medicine using single-photon emission tomography.
In about 10 to 30% of patients with typical angina undergoing coronary angiography for suspicion of stenotic coronary artery disease angiographically normal coronary arteries are found. Kemp et al. in 1973 coined the term syndrome X to describe this entity. In a substantial portion of these patients pathologic findings in myocardial scintigraphy are present. Sensitivity and specificity of thallium-201 exercise imaging by visual analysis of images in the presence of significant coronary stenosis is 84 and 88%, respectively. Several investigators have reported abnormal results in radionuclide exercise tests in patients with angiographically normal coronary arteries. Some of these results can be explained by myocardial bridging, vasospasm, left or right bundle branch block, hypertrophic cardiomyopathy, or absorption artifacts. In the majority of cases, however, these abnormalities are not sufficient to explain the scintigraphic findings. Formerly often claimed "false positive", recent studies suggest that endothelial dysfunction might be the reason for the observed perfusion defects. When comparing patients with angiographically unobstructed coronary arteries with and without perfusion defects in stress myocardial perfusion imaging, patients with pathological results show a significantly lower increase of coronary flow after intracoronary injection of the endothelial-dependent vasodilator acetylcholine. Endothelial-independent vasodilation, however, is not impaired in these patients. In addition, intracoronary Doppler measurements reveal that perfusion defects in myocardial scintigraphy only occur if coronary blood flow in this perfusion area is significantly reduced. These results suggest that regional endothelial dysfunction may cause hypoperfusion in myocardial perfusion imaging and underline the important role of the microcirculation in the distribution of radiotracers. Another striking scintigraphic pattern in patients with microvascular angina is the high incidence of reverse redistribution. These perfusion defects, apparent in images obtained 4 hours after exercise stress testing, often cannot be assigned to the perfusion territory of one of the major epicardial vessels. This results in a marked inhomogeneous radionuclide distribution pattern in resting images. The inhomogeneity is associated with a significant reduced resting coronary flow velocity in these patients. As histologically confirmed microvessel disease is often accompanied by slow-flow phenomenon reflecting decreased resting flow velocity, the results suggest that the inhomogeneous perfusion pattern is caused by microvascular dysfunction. Furthermore, the heterogeneity of nuclide distribution supports the hypothesis that endothelial function is not homogeneous in the entire myocardial microcirculation, but varies considerably. In conclusion, microvascular dysfunction by itself seems to cause regional myocardial hypoperfusion, as documented by myocardial scintigraphy. When interpreting pathological scintigraphic results in patients without significant epicardial stenosis, true blood flow and myocardial perfusion abnormalities must be assumed.
Animals↗
Prevalence of microvascular disease in patients with significant coronary artery disease.
Coronary flow velocity reserve (CFVR) measurement using intracoronary Doppler techniques has been increasing accepted for the assessment of physiological significance of epicardial stenosis and the functional changes after coronary interventions. However, large discrepancy exists concerning the acute changes of CFVR immediately after intervention. The purpose of this study was to investigate the prevalence of microvascular dysfunction in patients with significant coronary artery disease. Intracoronary Doppler flow measurements were performed in a total of 212 patients who underwent coronary interventions because of significant epicardial stenosis using 0.014" Doppler flow wire (Cardiometrics, Inc, Mountain View, CA). Intracoronary bolus injection of adenosine (12 micrograms for the right coronary and 18 micrograms for the left coronary arteries) was used to induce hyperemic reaction. CFVR was registered as the ratio of average peak velocity during hyperemia (hAPV) to at baseline (bAPV). Successful coronary interventions either by percutaneous transluminal coronary balloon angioplasty (PTCA) or by stenting could significantly improve the CFVR. In 80 patients with PTCA, the bAPV elevated from 16.6 +/- 2.1 cm/s to 20.6 +/- 13.4 cm/s and hAPV from 30.1 +/- 15.9 cm/s to 45.2 +/- 17.7 cm/s (both p < 0.001) with PTCA and the CFVR increased from 1.94 +/- 0.78 to 2.58 +/- 0.87 correspondingly (p < 0.001). Significant elevation of coronary flow parameters were also found in 132 patients with subsequent stent implantation (bAPV from 15.3 +/- 6.7 cm/s to 18.7 +/- 9.1 cm/s, hAPV from 28.7 +/- 14.4 cm/s to 44.3 +/- 17.7 cm/s and CFVR from 1.90 +/- 0.70 to 2.59 +/- 0.87, all p < 0.001). Reduction of CFVR (< 3.0) after intervention still existed in 46 (61.3%) of 80 patients after PTCA and 88 (66.7%) of 132 patients after stenting. Moreover, CFVR < 3.0 were found in 50 (45.9%) of 109 reference vessels in patients with single vessel disease. Significant improvement of coronary flow velocity and coronary flow velocity reserve could be obtained after successful angioplasty. However, microvascualr dysfunction existed in a large proportion of patients either in normal reference vessels or in target vessels after interventions.
Adult↗
Coronary microembolization--its role in acute coronary syndromes and interventions.
The diagnosis coronary artery disease is classically based on patient's symptoms and morphology, as analyzed by angiography. The importance of risk factors for the development of coronary atherosclerosis and disturbance of coronary vasomotion is clearly established. However, microembolization of the coronary circulation has also to be taken into account. Microembolization may occur as a single or as multiple, repetitive events, and it may induce inflammatory responses. Spontaneous microembolization may occur, when the fibrous cap of an atheroma or fibroatheroma (Stary i.v. and Va) ruptures and the lipid pool with or without additional thrombus formation is washed out of the atheroma into the microcirculation. Such events with progressive thrombus formation are known as cyclic flow variations. Plaque rupture occurs more frequently than previously assumed, i.e. in 9% of patients without known heart disease suffering a traffic accident and in 22% of patients with hypertension and diabetes. Also, in patients dying from sudden death microembolization is frequently found. Patients with stable and unstable angina show not only signs of coronary plaque rupture and thrombus formation, but also microemboli and microinfarcts, the only difference between those with stable and unstable angina being the number of events. Appreciation of microembolization may help to better understand the pathogenesis of ischemic cardiomyopathy, diabetic cardiomyopathy and acute coronary syndromes, in particular in patients with normal coronary angiograms, but plaque rupture detected by intravascular ultrasound. Also, the benefit from glycoprotein IIb/IIIa receptor antagonist is better understood, when not only the prevention of thrombus formation in the epicardial atherosclerotic plaque, but also that of microemboli is taken into account. Microembolization also occurs during PTCA, inducing elevations of troponin T and I and elevations of the ST segment in the EKG. Elevated baseline coronary blood flow velocity, as a potential consequence of reactive hyperemia in myocardium surrounding areas of microembolization, is more frequent in patients with high frequency rotablation than in patients with stenting and in patients with PTCA. The hypothesis of iafrogenic microembolization during coronary interventions is now supported by the use of aspiration and filtration devices, where particles with a size of up to 700 microns have been retrieved. In the experiment, microembolization is characterized by perfusion-contraction mismatch, as the proportionate reduction of flow and function seen with an epicardial stenosis is lost and replaced by contractile dysfunction in the absence of reduced flow. The analysis of the coronary microcirculation, in addition to that of the morphology and function of epicardial coronary arteries, and in particular appreciation of the concept of microembolization will further improve the understanding of the pathophysiology and clinical symptoms of coronary artery disease.
Angioplasty, Balloon, Coronary↗
Skin microcirculation in healthy subjects and patients with arteriosclerosis.
The concept to use the human skin microcirculation as a pharmacological in-vivo test system is old; however, methods developed in the 50s have been abandoned because of side effects and/or use of radioactive substances. We describe a newly developed minimally invasive method that allows in-vivo pharmacology in the human skin microcirculation injecting very low doses of a substance of drug without any systemic effects. The double injection technique (DIT) bears the potential to predict the effects of a drug and/or the vascular reactivity or dysfunction of other less accessible areas of the circulation (e.g. the myocardium). The DIT has been applied for studies in healthy volunteers and patients with atherosclerosis; the focus of interest was endothelial (dys-)function and the effect of exogenous vasoactive drugs. Using endothelin antagonists, we investigated the role of endogenous endothelin under physiological conditions and in atherosclerosis. The NO-synthase inhibitor L-NMMA has been applied to study the L-arginine-NO-pathway and the role of endothelial adrenoceptors. Ongoing studies with the DIT comparing coronary and skin microcirculation may help to develop minimally invasive methods to predict the effects of drugs and vascular function in the heart.
Arteriosclerosis↗
[Anti-ischemic effect of verapamil within the scope of interventional recanalization].
We report on a 46-year-old male with unstable angina pectoris due to a total proximal occlusion of the left circumflex artery. At the side of a plaque rupture there was a thrombotic occlusion. With PTCA recanalization was possible, but a dissection occurred, therefore coronary stents were implanted. Besides an optimal morphological result and recurrent applications of nitroglycerin, the baseline blood flow velocity declined from initial 16 cm/s to 11 cm/s after PTCA down to 8.4 cm/s after stent implantation. Because peak flow velocity remained almost unchanged, the low baseline velocity ("slow flow phenomenon") did not lead to an impaired coronary flow velocity reserve (CFVR). Only after application of 1 mg verapamil, a sustained flow velocity on a higher baseline level was reached (17 cm/s), at the same time typical signs of ischemia in the ECG (ST-segment depressions) improved. Additionally, in the non-treated LAD there was an increase in coronary blood flow velocity from 10 cm/s up to 25 cm/s. The reduction in coronary blood flow velocity with increasing manipulations might be due to an impairment of the coronary microcirculations with increasing alpha-adrenergic vasoconstriction, a distribution of vasoactive agents and peripheral microembolizations. Only after administration of verapamil, a calcium channel blocker with non-specific anti-adrenergic effects, the slow flow was removed and ECG signs of ischemia improved. The blood flow velocity in the non-treated LAD was low at baseline and improved after verapamil. This phenomenon leads to the conclusion that mechanisms with vasoconstrictive effect are present in the whole coronary system, but these mechanisms are less pronounced in non-treated vessels.
Angina, Unstable↗
[Hemostatic closure of arterial puncture site using Angio-Seal after diagnostic heart catheterization or coronary intervention].
Conventional manual compression and subsequent application of pressure bandages is associated with prolonged immobility and significant patient discomfort. Routine anticoagulation as well as the use of new interventional devices and platelet inhibiting strategies lead to a higher incidence of local bleeding complications after diagnostic cardiac catheterization or coronary angioplasty. Immediate sheath removal increases patient comfort. The Angio-Seal system uses a biodegradable anchor and collagen plug for sealing of arterial puncture sites. Several studies showed the safety and efficacy of this device. Technical deployment success ranges between 88 and 100%. Significant reduction in time to hemostasis allows for earlier patient ambulation and shorter in-hospital stay compared to manual compression with peripheral complications not being increased.
Angioplasty, Balloon, Coronary↗
[Analysis of mitral annulus excursion with tissue Doppler echocardiography (tissue Doppler echocardiography = TDE). Noninvasive assessment of left ventricular, diastolic dysfunction].
BACKGROUND: Mitral inflow velocity, deceleration time, and isovolumic relaxation time recorded by Doppler echocardiography have been widely used to evaluate left ventricular diastolic function but are affected by age, heart rate, loading conditions, and other factors. The diastolic mitral anulus velocity assessed by tissue Doppler echocardiography (TDE) was suggested to provide additional information about LV relaxation less affected by filling pressures. AIM OF THE STUDY: This study was designed to assess the clinical utility of mitral anulus velocity in the evaluation of left ventricular diastolic function. PATIENTS AND METHODS: Three groups of patients with a systolic ejection fraction > 45% were separated: 10 normal volunteers (60 +/- 10 y, CON group), 15 asymptomatic patients with known coronary artery disease (60 +/- 11 y, CAD group) and 15 patients with long-term arterial hypertension and heart failure symptoms (58 +/- 9 y, HYP group). The mitral inflow profile (E, A, E/A) was measured by pulsed Doppler, and the deceleration time (DT) and the isovolumic relaxation period (IVRT) were calculated. Systolic, early, and late diastolic velocities of the septal mitral anulus (ST, ET, AT, ET/AT) were assessed by pulsed TDE. All study subjects had invasive measurements of left ventricular end diastolic filling pressures during left heart catheterization. RESULTS: In the AH group, ET (6.9 +/- 4.8 cm/s) and ET/AT (0.71 +/- 0.28) were reduced compared to the CON group (11.7 +/- 4.7 cm/s and 1.11 +/- 0.36, p < 0.05, respectively) and the CAD group (8.9 +/- 5.4 cm/s and 0.85 +/- 0.26, respectively, p = ns). The groups did not differ with respect to the mitral E/A ratio, the deceleration time and the isovolumic relaxation time. LVED in the HYP group (16 +/- 8 mm Hg) was elevated compared to the CON group (8 +/- 3, p < 0.05) and the CAD group (12 +/- 6 mm Hg, p = ns). No correlation was found between ET and LVED (r = 0.26). When the combination of mitral E/A ratio > 1 with LVED > or = 15 mm Hg was classified as pseudonormalization, the pseudonormalization could be identified by a peak early diastolic mitral anulus velocity (ET) < 7 cm/s and an ET/AT ratio < 1 with a sensitivity of 77% and a specificity of 88%. CONCLUSIONS: The early diastolic mitral anulus velocity assessed by TDE (ET) is a preload-independent index of LV relaxation. TDE permits the detection of diastolic dysfunction in patients with a pseudonormal mitral inflow and elevated filling pressures.
Adult↗
[Quantitative detection of changes in the thoracic aorta in patients with chronic aortic dissection using transesophageal echocardiography].
The aim of this serial 3 year follow-up study in 42 clinically stable patients with chronic aortic dissection was to assess quantitatively morphologic changes of the descending thoracic aorta (AD) using transesophageal echocardiography (TEE). Communicating dissections (ca) were present in 16/19 patients with operated type I and in 11/23 patients with type III AD whereas 12/23 type III AD according to De Bakey were non-communicating (nc). Diametral enlargement of the disc. thoracic aorta was 4 mm (mean value) at 1 year in all patients, 5.9 mm in type I ca, 7.2 mm in type III ca but only 3.1 mm in type III nc at 3 years. The ratio between true lumen and false lumen (FL) changed in ca AD from 1:2 to 1:3 over the period of 3 years but remained constant at 1:1 in ncAD. Progressive thrombosis of the false lumen (FL) occurred in 76% of patients but complete thrombosis of the FL occurred in only 6% of type I ca, 18% type III ca but in 84% of type III nc patients. Our results confirm observations that non-communicating dissections seem to have a more favorable outcome and less aneurysmal dilatation compared to ca dissection.
Adult↗
Potential and pitfalls of electron-beam computed tomography in detecting coronary atherosclerosis.
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Coronary Angiography↗
The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events.
OBJECTIVES: The impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events. BACKGROUND: An embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined. METHODS: The relationship among the occurrence of major embolic events, echocardiographic vegetation size, endothelial cell activation, thrombin generation, fibrinolysis and APA was examined in 91 patients with definite infective endocarditis, including 26 patients with embolic events and 65 control subjects without embolic events. RESULTS: Overall, 14.3% of patients exhibited elevated APA levels. Embolic events occurred more frequently in patients with elevated levels of APA than in patients without (61.5% vs. 23.1%; p = 0.008). Patients with elevated levels of APA showed higher levels of prothrombin-fragment F1 +2 (p = 0.005), plasminogen-activator inhibitor 1 (p = 0.0002), von Willebrand factor (p = 0.002) and lower levels of activated protein C (p = 0.001) than patients with normal levels of APA. Thrombin generation and endothelial cell activation were both positively correlated with levels of APA. The occurrence of elevated APA levels was frequently associated with structural valve abnormalities (p = 0.01) and vegetations >1.3 cm (p = 0.002). CONCLUSIONS: Infection-associated elevated APA levels in patients with infective endocarditis are related to endothelial cell activation, thrombin generation and impairment of fibrinolysis. This may contribute to the increased risk for major embolic events in these patients.
Adult↗
Improved high-frequency transthoracic flow velocity measurement in the left anterior descending coronary artery after intravenous peripheral injection of levovist.
New ultrasonic technology allows noninvasive measurement of the flow in the distal left anterior descending coronary artery. The goal of this study was to validate transthoracic determination of coronary flow velocity with the intracoronary Doppler flow wire technique. In 20 patients with normal coronary arteries, 2 intracoronary and 2 comparative transthoracic Doppler measurements (TTDMs) of the average peak velocity (APV) and the mean systolic and diastolic velocities were performed. The diastolic/systolic ratio was calculated. Blood flow velocity was determined in the distal left anterior descending coronary artery with a Doppler guide wire. Color Doppler and subsequent pulsed wave Doppler readings in an optimal left lateral position were available within 1 hour after completion of the invasive examinations. TTDM were performed during continuous administration of 2.0 g of contrast agent. A modified apical view was obtained from the fourth or fifth intercostal space, and a high-frequency transducer was used (7 MHz for 2-dimensional and 6 MHz for color Doppler imaging; 3.5 MHz for pulsed wave Doppler readings). The Doppler flow signal quality was graded from I to III (I = no flow mapping obtainable, II = poor quality, III = Doppler signals with a well-defined outline). In 13 (65%) patients, 26 TTDMs revealed signal quality of grade III. APV was calculated to be within normal limits (APVecho = 19.96 +/- 7.62 cm/s vs APVinvasive = 20.77 +/- 7.87 cm/s). APVecho correlated well with APVinvasive (r = 0.85, y = 0.82x + 2.85, P <.001). The mean difference between APVecho and APVinvasive (Bias) was -0.81 +/- 4.23 cm/s. No correlation was found between invasive and noninvasive measurements of diastolic/systolic velocity ratios (P >.05). High-frequency TTDM provides reliable data on APV in the majority of patients. It has the potential to be introduced as a relevant screening test for follow-up of patients after interventional treatment.
Blood Flow Velocity↗
Does remodeling occur in the diseased human saphenous vein bypass grafts? An intravascular ultrasound study.
BACKGROUND: Coronary artery remodeling is a common phenomenon in human atherosclerotic arteries. Controversies exist concerning the presence of absence of the remodeling process in diseased human coronary saphenous vein bypass grafts. The purpose of the study was to observe the vessel and lumen dimensions in patients who had undergone saphenous vein grafting with intravascular ultrasound to find out whether the remodeling process exists in the diseased human saphenous vein bypass grafts. METHODS: A total of 43 saphenous vein bypass grafts from 43 patients (39 males, 4 females, mean age 63+/-8 years); 1-16 years (mean 9.3+/-4.0 years) after grafting, who had not undergone previous catheter intervention, were studied using intravascular ultrasound. The vessel, lumen and plaque area were measured at the lesion segment as well as in the proximal and distal reference segments. The percent stenosis was calculated. RESULTS: In 43 bypass grafts having severe stenosis before intervention, plaque was eccentric in 69.4% and concentric in 30.6%. No calcification was detected in 75% cases and 25% cases has mild-moderate intimal calcification. The vessel area in the lesion segment was 19.0+/-9.7 mm2, significantly larger than the proximal reference segment 12.8+/-4.0 min2 as well as the distal reference segment 12.9+/-3.6 mm2 (p < 0.001). It was also larger than that of the average area of the proximal and distal reference segments (p < 0.001). The vessel area increased in accordance with plaque area (p < 0.001). A weak relationship existed between vessel area and percent stenosis (r = 0.37, p = 0.04). CONCLUSION: In contrary to previous findings, diseased human saphenous vein bypass grafts undergo focal compensatory enlargement (remodeling) in the presence of plaque formation. The underlying mechanism is probably similar to that in de novo atherosclerosis.
Adaptation, Physiological↗
Comparison of normal and diseased pulmonary artery morphology by intravascular ultrasound and histological examination.
The study was performed to determine the morphological characteristics of normal and diseased pulmonary arteries by ultrasound (intravascular ultrasound, IVUS) and histology. Forty-nine cadaver segments of pulmonary arteries from 16 postmortem patients were imaged in vitro by IVUS and compared to matched histological sections. The pulmonary vasculature of 11 patients with pulmonary hypertension was investigated in vivo by IVUS. In the in vitro study, 34 of a total of 143 histological sections of the segmental pulmonary arteries showed fibrotic wall components; the remaining 109 sections had regular components. Imaged by IVUS, the wall of the regular and fibrotic arteries revealed a single layer histologically, representing the intima, media, adventitia and connective tissue. Adjacent lung tissue could be detected by IVUS and was confirmed by the histological section. In three patients with a history of chronic embolic pulmonary hypertension, IVUS revealed thrombi or a double vessel wall layer. Histologically, the material extracted after pulmonary thromboendarterectomy in two patients showed wall-adherent thrombus features of early organization. In all other patients only a single wall layer was seen. The vessel walls (intima, media, adventitia and connective tissue) of regular and slightly fibrosed pulmonary arteries show only a single layer. Wall-adherent organized thrombi in chronic embolic pulmonary hypertension can be detected by IVUS as a second inner vessel layer. Thus IVUS may represent an additional tool for detecting chronic embolic pulmonary hypertension when the results of pulmonary angiography or computed tomography are not definite.
Adult↗