Subendocardial and intramural temperature response during radiofrequency catheter ablation in chronic myocardial infarction and normal myocardium.

BACKGROUND: The ability of radiofrequency energy to extend across scar tissue is unknown. We investigated the effects of radiofrequency catheter ablation on intramural temperature in experimental chronic myocardial infarction. METHODS AND RESULTS: Myocardial infarction was induced in eight dogs by a transcatheter coronary artery occlusion-reperfusion technique. The dogs were reanesthetized after 15 to 24 days. Four additional dogs served as controls. The freshly excised preparations were cut and placed in a saline bath at 37 degrees C. Temperature-guided energy applications with a preselected catheter tip temperature of 80 degrees C were performed for 60 seconds with a 7F ablation catheter. Thermoelements were inserted into the ventricular muscle at depths of 2.5 to 3.0 mm ("subendocardial") and 5.5 to 6.0 mm ("intramural"). Surviving muscle fibers were interspersed among the transmural scar tissue. The maximal temperatures did not differ significantly between normal hearts and chronic infarctions at the subendocardial (64.5+/-6.4 degrees C versus 66.7+/-6.6 degrees C) or intramural thermo-element (51.9+/-5.7 degrees C versus 52.3+/-5.7 degrees C). The myocardial temperature rise was slow, and steady-state temperatures had not been reached after 60 seconds. The intramural temperatures in chronic infarctions measured 49.0+/-4.3 degrees C after 40 seconds of energy delivery and were still below the critical tissue temperature of 50 degrees C that is necessary to induce permanent myocardial damage. CONCLUSIONS: Temperature-guided radiofrequency ablation in a dog model of chronic myocardial infarction may induce tissue temperatures >50 degrees C at a depth of 5.5 to 6.0 mm. The intramural temperature rise was slow, indicating that long energy applications might be necessary if the arrhythmogenic substrate is subepicardial.

Antithrombin III and fibrinogen as predictors of cardiac events in patients with angina pectoris.

Because measurements of hemostatic factors might aid the prediction of cardiovascular clinical events, we investigated the long-term prognostic importance of selected hemostatic factors in patients with angina pectoris. At recruitment, 209 patients underwent clinical assessment and coronary angiography, and a range of hemostatic factors were measured. During the follow-up period of 9 years, 58 patients (28%) suffered a cardiac event (acute myocardial infarction or death from cardiac causes). The risk of cardiac events was positively related to baseline measurements of fibrinogen (risk ratio per SD [RR] increase 1.29, 95% confidence interval [CI] 0.99 to 1.68, P=.06) and negatively related to antithrombin III activity measurements (RR 0.75, 95% CI 0.59 to 0.95, P=.02). No other hemostatic factor measured was significantly related to the risk of having a cardiac event. Worsening of angina in the few weeks before and ejection fraction evaluation at the initial angiography were both strongly related to the risk of cardiac events. However, the relationships of fibrinogen and antithrombin III measurements to risk remained almost unchanged after adjusting for worsening of angina and ejection fraction. Fibrinogen and antithrombin III may have an important etiologic role in the prognosis of patients with angina pectoris.

Intracoronary stenting after unsuccessful PTCA. Early restenosis and explanation of stents during bypass surgery.

The case of a 63-year-old man is described, who received two intracoronary Palmaz-Schatz-Stents after dissection and occlusion following PTCA of two segments of the left anterior descending branch of the left coronary artery. Because of recurrent angina caused by early restenosis in the 'unprotected' segment between the stents, surgical revascularisation was performed and the stents were removed.

[Significance of intravascular ultrasound in arteriosclerotic calcified intima plaques: in vitro comparison of 20 and 12.5 MHz transducers]. / Wertigkeit des intravaskulären Ultraschalls bei arteriosklerotischen verkalkten Intimaplaques--in-vitro-Vergleich von 20- und 12,5-MHz-Transducern.

The aim of this in vitro study was to analyze the diagnostic performance of intravascular ultrasound (IVUS) in vessel wall calcifications and to compare the accuracy of mechanical 12.5 and 20 MHz transducers. Fourty-three sections of 10 vessels with signs of arteriosclerotic disease on pathologic examination were examined. Slices 500 microns thick were obtained and examined radiographically at 9 fold magnification. In each section, identical segments were defined, amounting to a total of 344 segments. The IVUS sections were analyzed by 3 experienced readers. For statistical evaluation ROC analysis was performed using magnification radiography as a reference. An area under the curve (AUC) of 0.79 was obtained for the 12.5 transducer and of 0.83 for the 20 MHz transducer. Additionally, sensitivity, specificity, and accuracy were determined. Sensitivity depended on the morphology, size, and density of the calcified lesions. We therefore conclude that the sensitivity of intravascular ultrasound concerning calcified arteriosclerotic plaques is limited and that there is no significant (p < 0.01) difference between mechanical 20 and 12.5 MHz transducers in examining iliac arteries.

Plasma Lp(a) levels correlate with number, severity, and length-extension of coronary lesions in male patients undergoing coronary arteriography for clinically suspected coronary atherosclerosis.

The relation between lipoprotein(a) [Lp(a)] as an independent risk factor for coronary atherosclerosis and the severity and extension of angiographically detectable coronary atherosclerotic lesions has not been systematically evaluated. In 118 male patients (54.3 +/- 7.4 years) with suspected coronary artery disease and without a history of myocardial infarction undergoing coronary angiography, the relation between plasma Lp(a) levels and other lipoproteins and the severity and extension of coronary lesions was studied. The coronary angiograms were evaluated in a blinded manner according to three scores: vessel score (0 to 3 points for 0 to 3 vessels with stenoses > or = 70%), stenosis score (0 to 32 points; number and severity of coronary stenoses or lesions), and extent score (0 to 100 points; length-extension of all coronary lesions in relation to the total coronary vessel length). The score values obtained were analyzed for correlations with age and levels of total cholesterol (6.08 +/- 1.26 mmol/L; mean +/- SD), high-density lipoprotein cholesterol (1.04 +/- 0.33 mmol/L), low-density lipoprotein cholesterol (4.18 +/- 1.15 mmol/L), triglycerides (1.88 +/- 1.37 mmol/L), and Lp(a) in plasma (19.5 +/- 22.6 mg/dL). Bivariate correlation analysis resulted in positive correlations between Lp(a) and vessel score (P < .01), stenosis score (P < .01), and extent score (P < .05). With multivariate analyses, besides Lp(a) plasma level (nl), only patient age showed a significant correlation to all three scores used, whereas none of the lipid parameters correlated significantly with all three scores.

Characterization of atherosclerosis in a patient with familial high-density lipoprotein deficiency.

We describe the cardiovascular state of a 60-year-old homozygous patient with familial HDL deficiency (Tangier disease). The patient was examined by coronary angiography and intravascular ultrasound because of chest pain at rest and on exertion. We found a normal left ventricular function, moderately diffuse coronary sclerosis without stenosis and no critical stenosis of peripheral arteries. Intravascular ultrasound revealed the three layer appearance of arterial intima, media and adventitia with normal thickness. No calcified plaques or intimal hyperplasia could be detected apart from a single, discrete atherosclerotic lesion in one iliac artery segment. Concentric non-occlusive atherosclerotic lesions which are readily detectable with intravascular ultrasound were not found. The lack of severe atherosclerosis was remarkable insofar as massive foam cell formation and the virtually complete absence of circulating HDL is characteristic of Tangier disease and has been previously demonstrated in this patient. Our findings suggest that HDL deficiency and foam cell formation in Tangier disease are not necessarily associated with accelerated development of atherosclerosis.

[Coronary angiography and intravascular ultrasound examination of a 60-year-old patient with familial HDL deficiency (Tangier disease)]. / Koronarangiographie und intravaskuläre Ultraschalluntersuchung bei einem 60jährigen Patienten mit familiärer HDL-Defizienz (Tangier-Krankheit).

A 60-year-old homozygous patient with familial high density lipoprotein deficiency (Tangier disease) was examined by coronary angiography and intravascular ultrasound because of typical angina pectoris. We found a normal left ventricular function, moderately diffuse coronary sclerosis without stenosis, and no critical stenosis of peripheral arteries. Intravascular ultrasound revealed normal thickness and the three-layer appearance of the arterial intima, media, and adventitia within the peripheral arteries, and showed a single, discrete arteriosclerotic lesion in one iliac artery segment. The lack of severe atherosclerosis was remarkable insofar as massive foam cell formation in reticuloendothelial tissues and the virtually complete absence of circulating HDL is characteristic of Tangier disease and had been previously demonstrated in this patient.

[Allograft vasculopathy in the early phase of orthotopic heart transplantation: angiography, intravascular ultrasound and functional in vivo findings]. / Allograft-Vaskulopathie in der Frühphase nach orthotoper Herztransplantation: angiographische, intravaskulär-sonographische und funktionelle In-vivo-Befunde.

Accelerated graft coronary atherosclerosis disease is the main reason for long-term mortality and morbidity of heart transplant recipients. The aim of this in vivo study was to evaluate coronary atherosclerotic vessel abnormalities and endothelial function using angiography, intravascular ultrasound, and intracoronary acetylcholine infusion. Fourteen patients (11 male, 3 female; mean age 49.3 years) were examined early after heart transplantation (mean interval after transplantation: 11 weeks) because of coronary artery disease (n = 8), idiopathic dilatative cardiomyopathy (n = 7), mitral valve replacement (n: 1) or left atrial filiae of a leiomyosarcoma (n = 1). Mean age of the donor hearts (female n = 8) was 29 years; 3 patients received double- and 14 patients triple-immunosuppression. All patients underwent biplane ventriculography and coronary angiography; a total of 120 coronary segments (main stem 21, left anterior descending artery 85, circumflex artery 14) was examined by intravascular ultrasound (20 MHz, 3.5 F catheters). In 13 patients, acetylcholine was infused into the proximal left anterior descending artery (0.15 microgram/min to 150.0 micrograms/min) to evaluate vasomotion within this segment. Ventriculography demonstrated regional wall abnormalities in 2 patients, angiography revealed 9 noncritical stenotic segments in 5 patients. Intravascular ultrasound detected 52 cross-sectional areas with a three-layer appearance indicating intimal thickening. Mean circumferential expansion of intimal proliferation was 192 degrees and mean intimal thickness was 0.35 mm. Only 5 segments of the sonographically pathological cross-sectional areas showed angiographic evidence of atherosclerotic lesions. After intracoronary infusion at a lower dose (0.15 and 1.5 micrograms/min) of acetylcholine, vasoconstriction was observed in 2 patients, at a dose of 15.0 and 150.0 micrograms/min in 10 patients. This response to acetylcholine did not depend on the intravascular or angiographical extent of atherosclerotic vessel abnormalities. In heart transplant recipients, coronary artery abnormalities can already be depicted at an early stage using intravascular ultrasound. The majority of patients show coronary vasoconstriction following infusion of acetylcholine at a higher dose. Further investigation is necessary to clarify whether the depicted vessel wall abnormalities can already be interpreted as newly developed graft atherosclerosis and whether abnormal vasomotion after acetylcholine is indicative of endothelial dysfunction.

Validation of intravascular ultrasound in arteriosclerotic peripheral vessels.

In this in vitro-study, we validated intravascular ultrasound for the detection of irregular luminal contours, intraarterial structures, intimal thickening in peripheral arteriosclerotic human vessel segments and we compared sonographic criteria to the composition of arteriosclerotic lesions. Sixty-nine post-mortem segments of human peripheral arteries (6 patients) were fixed in formalin, examined with intravascular ultrasound and morphologically evaluated. Specificity, sensitivity, both positive and negative predictive value and accuracy of intravascular ultrasound for the detection of irregular luminal contours, intra-arterial structures and intimal thickening were determined for each of four quadrants. Ultrasonic features (echogeneity, homogeneity, shadowing of echoes) were also compared to the composition of lesions. Intravascular ultrasound detected regular (normal) luminal contours with a high specificity of 96.5%, a sensitivity of 65.0% and an accuracy of 88.4%. Intra-arterial structures were detected with a sensitivity of 88.6%, a specificity of 97.8% and an accuracy of 96.4%. Arteriosclerotic lesions could be localized with a sensitivity of 86.1%, a specificity of 99.1% and an accuracy of 86.9%. Intimal thickening was detectable with a sensitivity of 85.9%, a specificity of 87.8% and an accuracy of 86.2%. Meanwhile, fibrous, atheromatous and combined lesions without calcification did not show shadowing of echoes. The majority of fibrous or atheromatous lesions presented with homogeneous echoes showing hypo-, hyper- and normal density echoes. Using a 20-MHz transducer, homogeneity and echogeneity of echo patterns cannot accurately predict the different components of combined arteriosclerotic lesions.

[Intravascular ultrasound in peripheral calcified vascular lesions: comparison with direct magnification radiography]. / Intravaskulärer Ultraschall bei peripheren verkalkten Gefässläsionen: Vergleich zur direktradiographischen Vergrösserung.

Intravascular ultrasound can detect calcified peripheral arteriosclerotic lesions by hyperdense echo patterns and shadowing of subintimal layers. Nevertheless, 20 MHz ultrasound systems have not been validated for the detection of peripheral calcifications; besides, it is unknown whether the depiction of calcified lesions by intravascular ultrasound depends on the morphology of the calcification. Histological evaluation of severely calcified arteries is difficult because the preparation of those specimens often causes artefacts, e.g., fracture of calcified structures. Direct magnification radiography, currently used in forensic medicine or skeleton examination, is based on a minimized focus and enables the edge-enhanced views of calcifications with high discrimination. In this in-vitro-study direct radiological magnification was used to validate intravascular ultrasound. Forty-nine segments of human peripheral arteries were fixed in formalin, examined with intravascular ultrasound and, as a reference, radiographically magnified using a newly developed microfocus x-ray tube. Sensitivity, specificity, positive and negative predictive value, and accuracy of intravascular ultrasound for the detection of calcified wall areas were determined and compared to the appearance (configuration, circumferential and areal expansion, density, number of fragments) of these calcifications. Thicknesses of 110 single calcified structures were estimated on sonograms and radiograms. The overall sensitivity of the 20 MHz intravascular ultrasound system for the detection of calcification in 913 sectors was 70%, specificity 53%, positive predictive value 66%, negative value 58% and accuracy 62%. The depiction of calcified regions by direct magnification radiography showed that the sensitivity strongly depended on the density of the calcification. Sensitivity was 81% with calcified lesions of high density, but only 51% with lesions of low density.(ABSTRACT TRUNCATED AT 250 WORDS)

Prothrombin activation fragment 1 + 2 and thrombin antithrombin III complexes in patients with angina pectoris: relation to the presence and severity of coronary atherosclerosis.

Plasma levels of the prothrombin activation fragment 1 + 2 (F 1 + 2) and of thrombin antithrombin III complexes (TAT) were determined in 225 patients with angina pectoris undergoing coronary angiography. Oral anticoagulant therapy was associated with a marked reduction in mean F1 + 2 (0.63 vs 1.62 nmol/l, p < 0.0001) and TAT levels (1.65 vs 2.23 micrograms/l, p < 0.0001). Omitting patients on oral anticoagulants, TAT values showed a positive association with patients' age (r = 0.18; p = 0.01) and were slightly higher in patients with a history of myocardial infarction than in those without (2.47 vs 2.11 micrograms/l; p = 0.06). Both F1 + 2 and TAT levels were increased in patients with angiographically verified coronary atherosclerosis as compared to patients with angina and angiographically normal coronaries (F1 + 2: 1.76 vs 1.36 nmol/l, TAT: 2.35 vs 2.00 micrograms/l; p-values after adjusting for age, sex and past history of myocardial infarction 0.06 and 0.11 respectively). However, no graded relationship between F1 + 2 or TAT values and severity of atherosclerosis was observed. This study provides suggestive evidence that a procoagulant state exists in patients with angina pectoris and coronary atherosclerosis. Its relevance in predicting coronary ischaemic events needs to be studied prospectively.

Value of intravascular ultrasound in the diagnosis and characterization of patent ductus arteriosus in an adult patient.

We report the case of a 47-year-old patient with a patent ductus arteriosus who underwent angiography and percutaneous intravascular ultrasound examination. The case illustrates that intravascular ultrasound contributes to the characterization of patent ductus arteriosus when a surgical or trans-catheter closure is planned, as calcifications of the wall as well as aneurysmal dilatations can be ruled out. Furthermore, measurements of the diameter of the ductus can be made.

Relation of fibrinogen to presence and severity of coronary artery disease is independent of other coexisting heart disease. The ECAT Angina Pectoris Study Group.

Six hundred fifty seven patients with angina pectoris underwent coronary angiography after measurement of plasma fibrinogen levels. Coronary artery disease (CAD) was angiographically confirmed in 75% of the patients. Other cardiac disease, either alone or in combination with CAD, was diagnosed in 8% and 11% of cases, respectively; 17% of the patients had no evidence of overt heart disease. Fibrinogen concentrations showed a graded increase according to the severity of coronary stenosis (p = 0.02) but were not significantly associated with any other cardiac heart disease. However, patients with valvular heart diseases had on average a 5.9% elevation of fibrinogen levels as compared to patients without proven cardiac disease (p = 0.08), similar to the observed 6.9% increase for CAD (p = 0.005). On average, patients with cardiomyopathies or pulmonary hypertension had only a 1.6% or 1.2% increase, respectively. The increase in fibrinogen levels associated with CAD was similar in patients with and without coexisting heart diseases. The results demonstrate a significant positive relation of fibrinogen to the presence and severity of CAD irrespective of a possible confounding influence from other cardiac diseases. The results therefore lend support to the hypothesis of a pathogenetic role for fibrinogen as a cardiovascular risk factor.

[Diagnostic value of intravascular ultrasound diagnosis in peripheral arteriosclerotic blood vessel changes]. / Aussagekraft der intravaskulären Ultraschalldiagnostik bei peripheren arteriosklerotischen Gefässveränderungen.

Intravascular ultrasound is an adjunct for the diagnosis of atherosclerotic peripheral vessels. In this in-vitro study, 69 segments of human peripheral arteries were fixed in formalin, examined with intravascular ultrasound and pathomorphologically evaluated. Sensitivity, specificity, both positive and negative predictive value and accuracy of intravascular ultrasound for the detection of irregular lumen contours, intraarterial structures and intimal thickening were determined for each of four quadrants. Sonographic features (echogeneity, homogeneity, shadowing of echoes) were compared to the architecture of lesions. Intravascular ultrasound detected regular (normal) lumen contours with high specificity (96.5%), a sensitivity of 65.0%, and an accuracy of 88.4%; intraluminal structures were detected with a sensitivity of 88.6%, a specificity of 97.8%, and an accuracy of 96.4%. Most atherosclerotic lesions could be localized with a sensitivity of 86.1%, a specificity of 99.1%, and an accuracy of 86.9%. Slight intimal thickening was detectable with a sensitivity of 85.9%, a specificity of 87.8%, and an accuracy of 86.2%. Comparison of sonographic features and the pathomorphological architecture of atherosclerotic lesions revealed that fibrous, atheromatous, and complex lesions without calcification did not show shadowing of echoes. The majority of fibrous or atheromatous lesions presented with homogeneous echoes; these lesions showed hypo-, hyper- and normodense echoes. The homogeneity of echoes did not help to identify the different components of combined atherosclerotic lesions. Thus, intravascular ultrasound is able to detect irregular lumen contours, intraluminal structures, and intimal thickening, but further sonographic criteria are needed to identify the architectural structure of combined lesions.

[Detection of pacemaker electrode infection using intravascular ultrasound]. / Nachweis einer Schrittmacherelektroden-Infektion mittels intravaskulärem Ultraschall.

The case of a 60-year-old man who developed fever 14 months after last implantation of a DDD pacemaker system is reported. Though staphylococcus epidermidis could be identified in several blood cultures, transthoracic and transesophageal echocardiograms and scintigraphy with antibodies to human leucocytes could not identify any focus of infection. The percutaneous intravascular and intracavitary ultrasound examination clearly demonstrated a vegetation within the subclavian vein, being attached to the ventricular lead; within that segment of the vein the atrial lead showed a small hyperdense structure. Further vegetations along the leads within the right atrium and ventricle could be ruled out. Subsequent removal of the pacemaker system caused resolution of the signs of inflammation.

Sodium channel blockers in the treatment of ventricular arrhythmias: different effects in the normal, ischaemic or failing heart?

In past decades, numerous experimental and clinical studies have improved our knowledge of the electrophysiological effects of sodium channel blockers, as well as of the mechanisms of arrhythmogenesis. However, the mechanisms of antiarrhythmic as well as potentially proarrhythmic drug action have been less well clarified. Sodium channel blocker agents have different effects on the normal, ischaemic, and failing heart since their antiarrhythmic actions depend on the substrate and the mechanisms of arrhythmogenesis, as well as other mostly interrelated cardiac and non-cardiac factors. Strict criteria of efficacy and safety have to be applied when sodium channel blockers are used for the treatment of ventricular arrhythmias.

Lack of association between haemostatic variables and the presence or the extent of coronary atherosclerosis.

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.