[Thrombolysis in acute myocardial infarct].
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Biomedical subjects
Publications and source records attributed to R Erbel.
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This study used intravascular ultrasound (IU) to assess the incidence and extent of left main coronary artery (LMCA) disease and the effects of arterial remodeling. Sixty-nine patients undergoing cardiac catheterization were imaged with a 20 MHz rotational-tip IU device. Nine of the 69 studies (13%) could not be analyzed because of technical (n = 2) or anatomic (n = 7) reasons. Of the remaining 60 patients, 38 (63%) had at least 1 lesion in the left coronary artery perfusion territory by angiography; significant LMCA stenosis was present in 2 patients (3%). Intravascular ultrasonography demonstrated plaques in 27 of 60 LMCAs (45%), 6 of them in patients with normal angiograms. Twenty-four plaques (89%) were eccentric and calcium was present in 4 (15%). The mean minimal lumen diameter was 4.9 +/- 0.8 mm, the maximal lumen diameter was 5.6 +/- 0.8 mm, the planimetered lumen area was 22.6 +/- 6.0 mm2, the plaque area was 3.9 +/- 5.8 mm2, the vessel area was 26.5 +/- 5.9 mm2, and the area stenosis was 13 +/- 19%. In the 27 patients with plaque, plaque area was 8.7 +/- 5.7 mm2 and the area stenosis was 30 +/- 17%. The vessel area was significantly larger in diseased LMCAs (p < 0.001) and correlated with plaque area (r = 0.46). IU examination of the LMCA was feasible in 87% of patients and was more reliable for delineating plaques than angiography.
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OBJECTIVES: This study describes the transesophageal echocardiographic and follow-up findings in patients with aortic intramural hemorrhage. BACKGROUND: Localized aortic intramural hemorrhage resulting in layered thickening of the aortic wall seems to represent a variant of acute aortic dissection without communication or a typical moving intimal flap. In autopsy studies this variant, attributed to a rupture of the vasa vasorum, has been described in 5% to 10% of patients with dissection. METHODS: In a prospective transesophageal echocardiographic study in patients with aortic dissection performed between 1986 and 1991, the diagnosis of intramural hemorrhage was established in 15 of 114 patients and either confirmed anatomically (7 patients) with an additional diagnostic imaging technique or on the basis of clear follow-up changes (8 patients). RESULTS: Elderly patients (mean age 70 years) with a history of hypertension were affected by this variant of dissection. The ascending aorta was involved in 3 patients and the descending aorta in 12. The longitudinal extent varied between 3 and 20 cm, and wall thickness varied between 0.7 and 3 cm. Classic aortic dissection developed in five patients (33%) and rupture in four (27%). Regression of aortic wall thickening was noted in two patients, whereas three patients became asymptomatic without apparent wall changes (33%). Surgery was performed in 5 patients, whereas medical therapy was continued in 10. During a mean follow-up period of 11 months, eight patients (53%) died because of complications of the aortic disease. CONCLUSIONS: Intramural hemorrhage represents a variant of aortic dissection and may be an early finding in patients who develop classic aortic dissection or rupture. Transesophageal echocardiography is an excellent method for the detection of intramural hemorrhage and for monitoring these patients.
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Percutaneous transluminal coronary angioplasty (PTCA) failed in 29 of 1,150 patients (2.5%) after successful passage of the guide wire. The reasons for failure were inability to pass the lesion with a balloon in 28 patients and inability to dilate the lesion in 1 patient. In these patients (15 stenoses and 14 chronic occlusions) rotational ablation was performed. We were able to pass the burr through the lesion in all of them, resulting in a reduction of diameter stenosis from 87 +/- 15 to 51 +/- 18%. Rotational ablation alone was initially successful (stenoses reduction > 20% and residual stenoses < 50%) in 15 of 29 (52%) patients. Additional PTCA was performed in 21 of 29 (72%) patients, in 8 to optimize the initially successful result and in 13 because the outcome was unsatisfactory. After dilatation the diameter stenosis was reduced to 41 +/- 14% immediately after the procedure and to 36 +/- 13% at 24 hr control. Overall success was achieved in 21 of 29 (72%) patients immediately after the procedure and in 26 of 29 (90%) patients at 24 hr control. No acute major complications occurred. We conclude that rotational ablation can be used as a safe and effective alternative when PTCA is not successful.
We describe a case of spontaneous coronary artery dissection that gave rise to post infarction unstable angina. An ambiguous angiographic appearance was shown by intracoronary ultrasound to arise from an extensive coronary dissection. The dissection membrane separating true and false lumina and features to suggest sluggish flow and early thrombosis in the false lumen were observed. No increase in lumen calibre was evident on ultrasound after PTCA (probably a consequence of the relatively large ultrasound catheter blank), but coronary flow reserve measured with intracoronary Doppler did improve and the patient remained stable and free of angina following the procedure.
To investigate risk factors for embolization in patients with echocardiographically detected left atrial thrombi and to evaluate thrombus development, we examined 29 patients with transesophageal and transthoracic echocardiography at two points during a follow-up of 18 months. We compared patients with a history of possible arterial embolization (n = 13) with those without (n = 16) in regard to age, gender, left atrial dilatation, localization of the thrombus in the left atrial cavity, spontaneous echo contrast, and atrial fibrillation. Eight patients were treated with aspirin, 20 with phenprocoumon. Only left atrial spontaneous contrast was associated with thromboembolism (10/15 patients with spontaneous contrast experienced arterial embolism; p = 0.038). In six patients arterial embolism occurred after thrombus detection (14% per patient per year). Four of these patients were treated with phenprocoumon, two with aspirin. At reexamination, one thrombus was detected in the patient without anticoagulant treatment and one thrombus was detected in the 8 patients treated with aspirin (13%), compared with ten thrombi detected in the 20 patients (50%) treated with phenprocoumon (p = NS). In 17 patients no thrombus was seen at reexamination. Since only 2 patients had undergone thrombectomy and 3 experienced arterial embolism during follow-up, thrombi disappeared under medical therapy in 12 patients. Patients with left atrial thrombi have a high risk of arterial embolization despite proper anticoagulative or antiplatelet treatment. Embolization occurs significantly more often if spontaneous echo contrast can be visualized. Left atrial thrombi can be reduced in size by the administration of antiplatelet and anticoagulative agents.(ABSTRACT TRUNCATED AT 250 WORDS)
To test the hypothesis that left heart opacification is dependent on pulmonary artery pressure, we analyzed consecutively 12 patients with normal and 8 patients with abnormal pulmonary artery pressure with a new lung capillary stable echo contrast agent. Patients underwent contrast echocardiographic examination within 6 hours before right and left heart catheterization with 200 mg/ml and 400 mg/ml SHU 508A intravenously. The mean pulmonary artery pressure was 15.4 mmHg in the patients with normal pulmonary artery pressures and 46.4 mmHg in the patients with pulmonary hypertension (p < 0.000). Echocardiograms were video-intensitometrically analyzed for intensity maximum (MAX), half-time of video-intensity decay (T1/2), area under the intensity curve (AUC) in the right and left ventricle and transit time from left to right heart (TT). Patients with normal pulmonary artery pressure showed sufficient left heart opacification, in the left ventricle MAX was 37 +/- 15 IU, AUC measured 653 +/- 463 IUxs and T1/2 was 4.4 +/- 2.6 s, while patients with elevated pulmonary artery pressure showed no significant left heart opacification. In the left ventricle MAX was 8 +/- 10 IU (p = 0.006), AUC measured 66 +/- 108 (p = 0.003) and T1/2 was 2.0 +/- 2.0 s (p = 0.041). TT was significantly increased in patients with elevated pulmonary artery pressure (11.8 +/- 4.6 s versus 6.5 +/- 2.8 s in patients with normal pulmonary artery pressure, p = 0.005). Thus, elevated pulmonary pressure has a significant impact on left heart opacification, which may be used for diagnostic purposes.
OBJECTIVES: This study was performed to determine the potential of intravascular ultrasound in the detection and delineation of aortic dissection. BACKGROUND: Intravascular ultrasound is a new technique capable of displaying real-time cross-sectional images of arterial vasculature. Its clinical use has been explored mostly in coronary and peripheral arterial circulation. METHODS: Intravascular ultrasound imaging of the aorta was performed using a 20-MHz ultrasound catheter in 28 patients with suspected aortic dissection. All patients underwent contrast angiography; 7 had computed tomography; and 22 had transesophageal echocardiography. RESULTS: Imaging of the aorta from the root level to its bifurcation was performed in all patients in an average of 10 min. No complications occurred. Dissection was present in 23 patients and absent in 5. In the patients without dissection, intravascular ultrasound revealed normal aortic anatomy. In all 23 patients with dissection, intravascular ultrasound demonstrated the intimal flap and true and false lumena. The longitudinal and circumferential extent of aortic dissection, contents of the false lumen, involvement of branch vessels and the presence of intramural hematoma in the aortic wall could also be identified. In cases where aortography could not define the distal extent of the dissection, intravascular ultrasound did. CONCLUSIONS: Our experience in this series of patients with aortic dissection indicates that intravascular ultrasound could be valuable in the identification and categorization of aortic dissection and in the description of associated pathologic changes that may be clinically important. It can be performed rapidly and safely and could serve as an alternative or adjunct diagnostic procedure in patients with aortic dissection.
An intravascular ultrasound examination was performed in order to evaluate an angiographically complicated lesion. Intravascular ultrasound was able to demonstrate spontaneous plaque rupture in a patient with recent acute subendocardial infarction. The inconclusive angiographic appearance was clarified by the intravascular examination and led us to conclude that the myocardial infarction was due to plaque rupture with subsequent thrombotic occlusion, which had spontaneously resolved by the time of the study.
Intimal disruption is known to induce prolonged intimal functional disturbance and is thought to be one of the mechanisms contributing to restenosis after PTCA. Although such damage can be induced by minimal trauma, the inevitable far greater disruption caused by passage of the PTCA apparatus through the stenosis does not appear to induce significant angiographically documented intimal proliferation. Pathological studies, however, have suggested that such a process might occur. Intravascular ultrasound allows in vivo study of vessel wall shape and constitution and is a far more sensitive detector of coronary atheroma than angiography. In this study we sought to determine the frequency of such functional disturbances and to assess their significance with respect to restenosis. The study group comprised 18 patients who underwent IVUS examination immediately after PTCA and at 6-months follow-up. They were analysed for luminal dimensions and vessel wall changes at the site of PTCA and at the level of the proximal non-treated segment. Seven patients (38%) had restenosed at follow-up IVUS examination; two patients had angiographically demonstrated luminal narrowing proximal to the PTCA site whereas seven had new intimal thickening in the proximal non-treated segment demonstrated by IVUS. Six patients had no intimal changes in either PTCA treated or untreated segments. Proximal intimal thickening was seen more frequently in those in whom increased intimal thickening at the PTCA site was noted. A trend (P < 0.1) was found towards an increased rate of new proximal vessel disease in those patients who had angiographically restenosed. IVUS demonstrates new intimal thickening in proximal non-treated segments in a considerable number of or patients undergoing PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)
Predisposing factors for aortic dissection are well known from necropsy series. To evaluate the frequency of aortic and aortic valve disease in aortic dissection in vivo, 139 patients with acute aortic dissection (96 men, 43 women, mean age 60.5 +/- 15.7 years) were studied by transoesophageal echocardiography (TEE) using 3.5 and 5.0 MHz transducers. Left ventricular hypertrophy by TEE, defined as an end-diastolic wall thickness of the left ventricular septal wall over 1.5 cm, was found in 42 (67.7%) of 62 patients with type I, in 10 (58.8%) of 17 patients with type II and in 46 (76.7%) of 60 patients with type III dissection. The mean value for the aortic root diameter was 3.2 +/- 1.3 cm.m-2 in type I dissection and 2.8 +/- 0.9 cm.m-2(ns) in type II dissection. In the patient group with type III dissection this diameter was significantly smaller (1.8 +/- 0.9 cm.m-2; P < 0.001). Thickening of aortic valve leaflets was demonstrated in six (9.7%) of 62 patients with aortic dissection type I (two of them with mild aortic stenosis), in two (11.8%) of 17 patients with aortic dissection type II and in 15 (25.0%) of 60 patients with aortic dissection type III. A bicuspid aortic valve was diagnosed in five (6.3%) of 79 patients with aortic dissection types I and II and in one (1.7%) of 60 patients with type III dissection. By colour coded Doppler echocardiography, aortic regurgitation was found in 46 (74.2%) of 62 patients with type I, 13 (76.5%) of 17 patients with type II and 23 (38.3%) of 60 patients with type III dissection.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute occlusion of the left main coronary artery (LMCA) is a rare angiographic finding. We report five patients with acute myocardial infarction (AMI) and one patient with unstable angina, in whom reperfusion was achieved or attempted with percutaneous transluminal coronary angioplasty (PTCA). All patients had a long history of stable angina pectoris. The indication for emergency PTCA was cardiogenic shock in the five patients with MI. PTCA was successful in five of six patients. Three patients with reperfusion survived, three died. All survivors underwent coronary artery bypass grafting (CABG) and were still alive at 23 months, 3 and 8 years respectively in NYHA functional class II or III. All patients had a dominant right coronary artery, but only the survivors had moderate or extensive collateralization. Our experience and the literature review indicate that the clinical outcome of patients with acute LMCA occlusion is strongly dependent on the presence or absence of intercoronary collaterals.
Isolated pig hearts (German farm pigs) were characterized after global in-vivo ischaemia as a potential alternative to in-vivo animal studies. Hearts were harvested from adult farm swine at the abattoir 10.3 +/- 2.1 min after incision of the carotid artery. They were immediately perfused and thereafter stored in ice-cold cardioplegic (St Thomas's) solution. After 38 +/- 3 min, retrograde perfusion was started with oxygenated pig blood (37 degrees C; 5000 U Heparin.l-1; pH 7.38 +/- 0.1; 11 mmol glucose.l-1) at a flow rate of 85 ml.min-1 100 g-1 wet weight (gww-1) for 30 min (n = 10). Additionally, shortly after obtaining the hearts, ATP and CP content were measured by enzymatic tests in 10 pigs at the beginning and after 15 and 30 min of reperfusion. Heart rate was 90 +/- 14 min-1 with little variation during 30 min. Perfusion pressure increased from 89 +/- 17 mmHg to 100 +/- 17 mmHg (NS). Wet weight rose from 488 +/- 33 to 548 +/- 45 g (P < 0.002). CK increased from 2180 +/- 558 to 5900 +/- 1018 U.l-1 (P < 0.001). Calcium in the perfusate decreased from 2.45 +/- 0.15 to 2.2 +/- 0.25 mmol.l-1 and magnesium increased from 0.85 +/- 0.2 to 1.79 +/- 0.35 mmol.l-1 (both P < 0.001). The transmural ATP and CP content was 2.8 +/- 0.48 and 5.08 +/- 0.88 mumol.gww-1.ATP fell moderately during reperfusion to 2.6 +/- 0.35 mumol (NS) and CP rose to 6.0 +/- 1.2 mumol (P < 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of the study was to evaluate prospectively the effect of a continuous perfusion balloon catheter ('High Flow CPC Mainz', Schneider/Pfizer Europe AG, CH-8052 Zurich, Switzerland) on tolerated inflation time during elective PTCA (n = 31), and its usefulness in cases of unsatisfactory morphological or functional results after PTCA (n = 42). Sixty-five patients were male, eight female; their mean age was 57.6 +/- 8.85 years. The target vessel was the LAD in 39 patients, the RCA in 29, the LCX in three, and bypass grafts in two. Seven patients had type A lesions, 44 type B and 22 type C, respectively. The target lesion was in the proximal third of the coronary artery in 41 patients, in the mid-third in 30, and in the distal third in two. Side branches were involved in 24 patients. The median size of the standard PTCA balloon was 3.00 mm and 3.5 mm for the CPC. Tolerated inflation time rose from 36 +/- 21 s to 213 +/- 108 s (P < 0.01). Additionally, the CPC catheter was used in 42 patients with symptomatic dissections (ST segment elevation, chest pain, or impaired contrast run-off) after PTCA. Wall wrapping by CPC was successful in 24 (57%) and unsuccessful in 18 (43%) patients. A significant difference was found for the inflation times tolerated between patients with successful (265 +/- 99 s) and unsuccessful wall wrapping (161 +/- 108 s; P < 0.01). Of the 18 patients with unsuccessful wall wrapping, 11 (61%) required an intracoronary stent, and six patients (30%) could be managed by medical treatment alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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The classical triad of sudden devastating chest pain, electrocardiographic absence of acute myocardial infarction, and identification of an upstream flap in the ascending aorta by transesophageal echocardiography (TEE) indicates aortic type A dissection requiring emergent surgery. Among 34 patients presenting with clinical signs and symptoms of an aortic dissection, three did not show the mandatory flap in the upstream aorta. The only echocardiographic finding was aortic wall thickening indicating an intramural hematoma. Two of these patients showed early aortic ectasia and one showed a pericardial effusion. Despite the missing flap echocardiographically, surgery was performed in all three patients. The surgical approach was the same as that for patients with a type A dissection. Two patients are doing well after the procedure, and one patient died after reoperation. The postoperative histologic work-up confirmed that there was no intimal tear or dissection of the intimal layer. We conclude that the echocardiographic finding of an intramural hematoma combined with typical clinical signs of chest pain, with myocardial infarction ruled out, requires emergent surgical intervention.