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H R Figulla

Publications and source records attributed to H R Figulla.

At least 55 records · Page 3Linked to original sources

Recovery of the cardiac adrenergic nervous system after long-term beta-blocker therapy in idiopathic dilated cardiomyopathy: assessment by increase in myocardial 123I-metaiodobenzylguanidine uptake.

UNLABELLED: In chronic heart failure, elevated plasma norepinephrine (NE) levels and a disparity between the neuronal release and the effective reuptake of NE lead to an increased concentration of NE in the presynaptic cleft, causing a downregulation of the myocardial beta-adrenoceptors. The clinical and prognostic effectiveness of beta-blocker therapy has been shown in patients with chronic heart failure in several large trials. The purpose of this study was to investigate the effect of long-term beta-blocker therapy on the cardiac adrenergic nervous system as assessed by the myocardial uptake of 123I-metaiodobenzylguanidine (MIBG), an analog of NE, in idiopathic dilated cardiomyopathy (IDC). METHODS: In 10 patients with IDC and stable chronic heart failure the myocardial MIBG uptake was measured at baseline and at 1 y (median, 11.5 mo) after treatment with beta-blockers (metoprolol, n = 5; bisoprolol, n = 1; and carvedilol, n = 4) in addition to standard medication. In parallel with the changes in MIBG uptake, the New York Heart Association functional class, the left ventricular ejection fraction (LVEF), and the left ventricular end-diastolic diameter (LVEDD) were documented before and after 1 y of therapy with beta-blockers. RESULTS: During the 1-y follow-up, a significant increase in myocardial 123I-MIBG uptake (P = 0.005) in parallel with an improved LVEF (P = 0.005) and a reduced LVEDD (P = 0.019) was found. A trend toward an improvement of the New York Heart Association functional class under the beta-blocker therapy (P = 0.139) was also found. CONCLUSION: Assessment of the myocardial 123I-MIBG uptake is a useful noninvasive tool for evaluating changes in cardiac sympathetic nerve activity under medical therapy. Long-term treatment with beta-blockers in IDC causes a recovery of the cardiac adrenergic nervous system concomitantly with a clinical and hemodynamic improvement.

3-Iodobenzylguanidine↗

Cardiac troponins have no prognostic value for acute and chronic cardiac events in asymptomatic patients with end-stage renal failure.

BACKGROUND: Cardiovascular diseases determine overall mortality in patients with end-stage renal failure. Therefore, testing for myocardial ischemia is important. Elevation of cardio-specific troponins have been frequently measured in patients with end-stage renal failure. Thus, we studied systematically whether patients on chronic intermittent hemodialysis without overt coronary heart disease have increased serum levels of cardiac troponin T and cardiac troponin I. After 2 years, the patients were screened again for cardiac events. METHODS AND RESULTS: The patients had no history of angina during the previous 3 months or myocardial infarction (MI) within the previous 2 years. For analysis we used two cardio-specific assays for troponin T as well as for troponin I and compared the results with the CK-MB concentration. In a number of patients serum concentrations were elevated above the reference range as follows: troponin T rapid bedside assay: 41 of 100 patients, troponin I rapid bedside assay: 27 of 100 patients, quantitative measurement oftroponin T: 22 of 100 patients, quantitative measurement oftroponin I: 7 of 100 patients, CK-MB: 2 of 100 patients. The increased serum levels of cardiac troponins were neither the result of uremic perimyocarditis (pericardial effusion), changes in the hemodialysis regimen, pulmonary congestion nor were they consistent with the etiology of renal failure. None of the patients with an elevated troponin level in either of the test suffered from any acute cardiac event initially. Within 2 years 18 of 100 patients died, 13 out of them because of cardiac events. Fourteen patients had a myocardial infarction and 19 patients developed angina pectoris. Sensitivity and specificity (0.75 and 0.67) of troponin T rapid bedside assay for MACE (angina pectoris, MI, cardiac death) was lower compared to studies in patients with normal renal function. Correlation between troponin elevation and late outcome was low or absent. CONCLUSION: Patients on chronic intermittent hemodialysis frequently present with elevated TnT and TnI levels which cannot be used as predictors of acute and chronic cardiac events. Rapid bedside assays have a lower specificity than quantitative assays.

Adult↗

Immediate changes of collateral function after successful recanalization of chronic total coronary occlusions.

BACKGROUND: Coronary collaterals are essential to maintain myocardial function in chronic total coronary occlusions (TCOs). The aim of the present study was to assess the collateral circulation in TCOs before coronary angioplasty and to determine the recruitable collateral perfusion after recanalization by use of intracoronary Doppler flow velocimetry. METHODS AND RESULTS: In 21 patients with TCOs (duration >4 weeks), Doppler recordings of basal collateral flow were obtained before the first balloon inflation. Angioplasty was performed with stent implantation in all lesions. At the end of the procedure, recruitable collateral flow was measured during a repeat balloon inflation. The collateral flow index (CFI) was calculated from the velocity integral during the occlusion/velocity integral of antegrade flow. In 17 of 21 patients, angiography was repeated after 24 hours, and CFI was reassessed. Average peak velocity of collateral flow was 10.9+/-5.6 cm/s with a predominantly systolic flow (diastolic/systolic velocity ratio <0.5) compared with antegrade flow (diastolic/systolic velocity ratio >1.5). After recanalization, the average peak velocity of recruitable collateral flow dropped by >50% to 4.7+/-2.5 cm/s. CFI fell from 0.48+/-0.25 to 0.21+/-0.16 (P:<0.001). There was no further change of CFI during the following 24 hours. CFI was higher in patients with preserved regional ventricular function than in those with akinetic myocardium (0.57+/-0.23 versus 0.38+/-0.12, P:<0.05). CONCLUSIONS: Collateral circulation in TCO provided 50% of antegrade coronary flow. A considerable fraction of collateral flow was immediately lost after recanalization, indicating that TCO may not remain protected from future ischemic events by a well-developed collateral function.

Aged↗

Non-surgical extraction of right cardiac "thrombus in transit".

In two hemodynamically unstable patients, massive pulmonary embolism and free-floating right cardiac thrombi were diagnosed. Thrombolytic therapy was contraindicated and surgical treatment was rejected. In these two cases, we describe a successful non-surgical, percutaneous extraction of mobile right cardiac thrombi. Cathet. Cardiovasc. Intervent. 51:316-319, 2000.

Echocardiography, Transesophageal↗

Tumour necrosis factor-alpha expression in idiopathic dilated cardiomyopathy: correlation to myocardial inflammatory activity.

High numbers of inflammatory cells are found in a subgroup of patients with idiopathic dilated cardiomyopathy (IDCM). We hypothesized that the extent of inflammation is linked to myocardial TNF-alpha expression in human IDCM. Fourteen patients who consecutively underwent endomyocardial biopsy (EMB) were stratified into two groups-a group with low and a group with high myocardial inflammatory index (MII)-based on immunohistochemical analysis of cellular infiltration and HLA I and II expression. Myocardial TNF-alpha messenger RNA (mRNA) expression was determined by reverse transcriptase polymerase chain reaction, TNF-alpha protein was localized by immunohistochemistry and TNF-alpha serum levels were measured by EIA. IDCM patients with a high MII (n=6) showed a 1. 9-fold higher TNF-alpha mRNA expression when compared to IDCM patients with low MII (n=8, P=0.020). TNF-alpha protein was detected at perinuclear regions of cardiac myocytes and the endothelium. TNF-alpha serum levels were 3.0 (0.55) pg/ml in patients with high MII compared to 1.35 (0.20) pg/ml in patients with low MII (P=0.017). According to immunolocalization cardiac myocytes and the endothelium seem to be the major source of TNF-alpha production. Whether the elevated systemic level of TNF-alpha found in patients with high MII are elaborated by the myocardium or are produced by other tissues representing a general immune activation is not clear.

Cardiomyopathy, Dilated↗

[Cardiorespiratory desynchronization after acute myocardial infarct].

The prognosis of cardiac diseases can be estimated from the variability of regulation parameters of the cardiovascular system. Changes in the variability of a regulation parameter causes disturbances in the synchronisation of interacting control loops. Conclusions about the severity of the underlying functional impairment can be drawn from these disturbances. This study investigates the synchronisation of the control loops of the heart rate and respiration (cardiorespiratory synchronisation, CRS) after acute myocardial infarction. We investigated 43 patients after myocardial infarction and 27 healthy controls. To quantify the CRS the synchronisation in phase of respiration and heart rate was assessed. The heart rate variability (HRV) was also assessed. Patients after myocardial infarction have a significantly reduced HRV and CRS. There is a non-linear relationship between HRV and CRS. Patients with left ventricular enlargement and reduced left ventricular ejection fraction (< or = 45%) significantly differed from the other infarct patients and controls in CRS but not in HRV. They had a marked degree of cardiorespiratory desynchronisation and were identified by a threshold value. CRS is a measure of the interaction of respiration control and heart rate control. After myocardial infarction, a reduction of the HRV can be observed. The desynchronisation of the control loops of respiration and heart rate especially appears in large infarcts. This can be quantitatively assessed by the method presented.

Adult↗

[Acute acral ischemia in all fingers possibly due to a Borrelia infection].

Acute interruption of circulation in the distal fingers can be both expression of an embolic event as well as the first manifestation of a vasculitis or collagenosis. The search for its cause is frequently difficult. In many cases a specialized analysis of the coagulation system as well as diagnostics such as ultrasound scan of the heart or a systematic antibody scanning do not reveal the origin of an embolus or the underlying disorder. On the basis of a case-report we would like to focus on a possible context between an infection of Borrelias stage III and consecutive deterioration of peripheral arterial perfusion in the fingers. Besides Jo-1- and positive sceleton-muscle-antibodies there were no serological and clinical indications for an autoimmune disease. It was possible to avoid acral necrosis by means of an antibiotic, immunosuppressive and rheological therapeutic concept. We recommend to control the borellia-antibody-level in cases of obscure threatening peripheral necrosis caused by arterial perfusion stop.

Acute Disease↗

Systemic and splanchnic endothelin-1 plasma levels in liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS).

AIMS/BACKGROUND: Endothelin-1 (ET-1) may be a mediator for portal hypertension in liver cirrhosis. The aim of the present study was to determine the concentrations of ET-1 in the systemic and splanchnic circulation before and after reduction of portal hypertension by transjugular intrahepatic portosystemic shunt implantation (TIPS). METHODS: Plasma concentrations of immunoreactive ET-1 were measured in peripheral venous blood samples from 25 patients with liver cirrhosis before and at 1, 3, 9 and 15 months after TIPS. Furthermore, acute effects of TIPS on ET-1 were studied in plasma samples from the hepatic vein, the portal vein 30 minutes before and after TIPS and in the femoral artery (only after TIPS) in a subgroup of 15 patients. In addition, the portocaval pressure gradient was determined before and after TIPS. RESULTS: Before TIPS peripheral venous plasma ET-1 concentrations (n=25; median 4.2 pg/ml; range 1.9-14.7) were significantly increased in patients with refractory ascites (n=7; median 7.8, range 3.5 14.7) compared to patients with repetitive bleeding (n=18; median 3.4; range 1.9-7.1) (p=0.003). Furthermore, peripheral ET-1 concentrations correlated with the degree of liver dysfunction according to the Child-Pugh classification (Spearman's r=0.46; p=0.02). Following TIPS, peripheral ET-1 concentrations remained unchanged during a follow-up of 15 months. Before TIPS, a positive gradient of ET-1 concentrations from portalvenous to hepatovenous and peripheral venous levels was found (p<0.03). Immediately after TIPS, arterial ET-1 concentrations reached markedly increased levels in individual patients (88, 92 and 103 pg/ml). Severe systemic reactions to these high levels were not observed. Peripheral venous, hepatovenous and portalvenous ET-1 concentrations did not correlate with portocaval pressure gradients. CONCLUSION: Cirrhotic patients demonstrated unchanged peripheral venous ET-1 concentrations up to 15 months after TIPS. Portal congestion was associated with increased ET-1 levels in the prehepatic splanchnic area. The effect of portal decompression on splanchnic and systemic ET-1 levels deserves further investigation.

Adult↗

Comparison of biochemical markers for the detection of minimal myocardial injury: superior sensitivity of cardiac troponin--T ELISA.

OBJECTIVES: Patients with minimal myocardial injuries who present clinically with unstable angina, early stages of myocardial infarction or myocarditis require different therapy strategies to those without. The newer diagnostic assays for detecting myocardial lesions (cardiac Troponin T and cardiac Troponin I [cTnT, cTnI], glycogenphosphorylase - BB [GPBB]) are reported to be more sensitive and specific than common biochemical markers such as CK and myoglobin. Our study tested whether the recently developed four assays cTnT-ELISA (in vitro), cTnT rapid bedside assay, cTnI rapid bedside assay, and GPBB (Immunoenzymetric assay) are effective in detecting minimal myocardial injuries caused by endomyocardial biopsy. We compared them with CK activity (CK-cat), CK-MB activity (CK-MBcat), CK-MB-concentration (CK-MB-mass) and Myoglobin concentration (Myo-conc.). PATIENTS AND METHODS: Twenty-four patients [six female, 18 male, age (mean): 47 years (20-65)] underwent diagnostic endomyocardial biopsy. Between four and six biopsies were taken from the mid-right ventricular aspect of the interventricular septum of the heart. Blood was drawn before catheterization (baseline), 10 min after the biopsy, in the next morning, and in the morning of the second day after (days 1 and 2). RESULTS AND CONCLUSION: Because of very low CKcat it was not possible to analyse CK-MBcat with reliable precision. The assay for GPBB and cTnI rapid bedside assay did not indicate this minimal myocardial injury. The CK cat, CK-MB mass, and myoglobin assays indicated significant increase at 10 min after biopsy but remained within reference range. cTnT rapid bedside assay indicated this minimal myocardial injury in 50% (P < 0.05). cTnT-ELISA (in vitro) was increased above the reference limit in 54%. This increase was 3. 6-fold the upper reference limit (P < 0.01). In our study, due to superior discriminating power, cTnT-ELISA (in vitro) was the most sensitive assay for minimal myocardial injuries.

Adult↗

Lack of association between 27-bp repeat polymorphism in intron 4 of the endothelial nitric oxide synthase gene and the risk of coronary artery disease.

The gene encoding endothelial nitric oxide synthase (ecNOS) is a candidate gene for the mediation of initial endothelial cell damage seen in arteriosclerosis. Although the association of ecNOS polymorphisms with hypertension has been studied extensively, there is little information regarding its association with coronary artery disease (CAD). We decided to study a 27 base-pair tandem repeat polymorphism in intron 4 of the ecNOS gene in 1043 individuals (413 controls, 630 patients with CAD) who consecutively underwent coronary angiography at our institution. The frequencies of the genotypes drawn from 1038 individuals were 0.69, 0.28 and 0.03 in the controls and 0.73, 0.25 and 0.02 in individulas with CAD for the ecNOS4b/b, ecNOS4b/a and ecNOS4a/a genotypes, respectively (p = n.s). There was no shift of the genotype frequencies from the expected distribution based on the Hardy-Weinberg equilibrium. Neither the rare ecNOS4a allele nor the ecNOS4a/a genotype conferred an independent risk factor for CAD in subgroups, e.g. smokers, diabetic individuals, hypertensive individuals and individuals with a low conventional risk for CAD. In five individuals we identified an additional 27-bp repeat in the ecNOS gene (ecNOS4c), which occurred heterozygous with the ecNOS4b allele (ecNOS4b/c genotype). In conclusion, the ecNOS4a allele as well as the ecNOS4a/a genotype did not show a general association with CAD in the studied European population. Even in high-risk subgroups the ecNOS4a/4a genotype did not represent an independent risk factor for CAD. In addition, the severity of CAD was not associated with the ecNOS4a allele/ecNOS4a/a genotype.

Aged↗

[Effect of choice of baseline correction interval on localization of electrical heart activity].

The electric heart activity can be localised from body surface mapping data with computer algorithms. At higher heart rates the T and P waves merge. Thus, the offset can not be subtracted in the TP segment. We investigated 28 healthy volunteers with signal averaged 31-lead magnetocardiography. The offset of the baseline was determined in the TP-segment and in the PR-segment, respectively. The electrical heart activity was localised in the initial 30 ms of the QRS complex (Q), at the QRS maximum (R), and at the T wave maximum (T). The volume currents were considered by using a boundary element model with the compartments lungs and torso. The 3D positions of the dipoles, the dipole orientations, and the dipole strengths were calculated using the data preprocessed with two different offset correction intervals. The offsets of the TP and PR segments significantly differed one from another. The average deviations of the dipole localisation were within a few centimetres (Q: 20 +/- 31 mm, R: 6 +/- 13 mm, T: 14 +/- 30 mm). However, in a small number of subjects (Q: n = 5, R: n = 2, T: n = 5) we observed a deviation of more than 30 mm. These deviations were not linearly correlated to the differences in the baseline offsets. High resolution recordings continuously detect heart activity in the PR segment. The correction of the baseline in the PR segment instead of the TP segment may introduce artefacts in the source localisation and therefore should be avoided.

Adolescent↗

Temporal properties of high frequency intra-QRS signals in myocardial infarction and healthy hearts.

The prevalence of late potentials after myocardial infarction depends on the site of the infarction. This may be caused by the different activation onsets of the anterior and inferior myocardial segments. Therefore, in anterior infarcts the high frequency signals may be concealed within the QRS whereas in the inferior infarcts they last beyond the end of the QRS. We compared the timing and the spatial patterns of high frequency intra-QRS signals (IQSs) in the different infarction sites. We investigated 14 patients with anterior infarcts, 17 patients with inferior infarcts, and 10 healthy subjects. 31-lead magnetocardiograms were recorded in left precordial position and averaged. The QRS signals were smoothed with a Savitzky-Golay filter. The smoothed QRS signals were subtracted from the measured ones. The difference of the signals (frequency band of about 60-200 Hz) representing the high frequency components was quantified. The percentage of the high frequency signals was calculated for the entire QRS, for the first and for the second half, respectively. We found that in patients with anterior infarcts the high frequency components predominantly appeared in the first half of the QRS whereas in inferior infarcts these components predominantly appeared in the second half of the QRS. The different infarction sites were associated with different spatial patterns of the high frequency signals on the body surface. In healthy subjects there was not such a preferential association of time intervals and high frequency signals. Late potentials are the special case of high frequency signals appearing in the terminal QRS. It is the general property of the myocardium to generate high frequency signals associated with the depolarization of infarcted tissue. The timing of such signals and the spatial distribution patterns on the body surface may help to identify the location of the sources.

Aged↗

Three-year follow-up of patients with silent ischemia in the subacute phase of myocardial infarction after thrombolysis and early coronary intervention.

In order to assess the prognostic value of silent myocardial ischemia in acute myocardial infarction after thrombolysis and early coronary angiography (14-48 h after start of thrombolysis) including percutaneous transluminal coronary angioplasty, if indicated, 126 patients underwent 24 h-Holter-monitoring in the early postinfarction period. The 24 h-Holter-recording was initiated directly after early coronary intervention (40+/-11 h after onset of symptoms). Of the 126 patients initially eligible for the study 29 had to be excluded from further analysis for clinical or methodical reasons. Of the remaining 97 patients, 10 (10%) had silent ischemia (group A) and 87/97 (90%) patients showed no significant ST-segment alterations. Both groups did not significantly differ from each other with regard to baseline clinical characteristics, severity of coronary artery disease and frequency of successful percutaneous transluminal coronary angioplasty. The left ventricular ejection fraction showed a trend towards lower values in patients with than in those without silent ischemia (47+/-15% vs. 55+/-13%, p=0.07). When both silent ischemia and left ventricular ejection fraction <40% were present, a subset of patients at high risk for cardiac death could be identified (specificity: 98%, positive predictive accuracy: 75%). By Kaplan-Meier analysis, significantly more cardiac deaths occurred in group A than in group B (30% vs. 6%, p<0.01) during the three-year follow-up (950+/-392 days) after acute myocardial infarction. Regarding the cardiac events during long-term follow-up (emergency percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, non-fatal reinfarction, and cardiac death) there was no significant difference between both groups (30% vs. 18%, NS). In conclusion, Holter monitor-detected silent ischemia in the subacute phase of myocardial infarction after thrombolysis followed by early delayed coronary intervention occurs in 10% of the patients indicating either a residual ischemia in the infarcted zone despite a combined reperfusion strategy or a remote ischemic potential in case of multivessel disease. In this small selected group of infarct patients too, silent ischemia is to be considered as an important non-invasive parameter to predict cardiac death during long-term follow-up and provides valuable complementary information to left ventricular dysfunction, a well established prognostic marker in the postinfarction period.

Adult↗

Cardiac sympathetic activity as measured by myocardial 123-I-metaiodobenzylguanidine uptake and heart rate variability in idiopathic dilated cardiomyopathy.

In patients with idiopathic dilated cardiomyopathy (IDC) the increased sympathetic activity owing to chronic congestive heart failure leads to an imbalance of cardiac autonomic tone, as reflected by decreased heart rate variability (HRV). Iodine-123-metaiodobenzylguanidine (123-I-MIBG), which has the same affinity for sympathetic nerve endings as norepinephrine, can be used to assess the integrity and function of the cardiac sympathetic nervous system. The aim of the present study was to measure cardiac sympathetic activity by assessing 123-I-MIBG uptake compared with HRV in patients with IDC. In 12 patients with IDC and mild to moderate heart failure, myocardial MIBG uptake was calculated from the myocardial (M) to left ventricular cavity (C) voxel values density ratio and the 123-I activity in a blood sample as a reference (= M/C ratio) using a double radionuclide study with 123-I-MIBG and technetium-99m-MIBI. To investigate the relation between myocardial MIBG uptake and HRV in time domain, the linear regression between the M/C ratio, a new scintigraphic parameter, and the mean RR interval or the HRV triangular index, respectively, was determined. A significant correlation between the M/C ratio and mean RR interval (r = 0.52; p = 0.016) or M/C ratio and HRV triangular index (r = 0.76; p = 0.003), respectively, was found. Thus, the significant correlation between the M/C ratio and HRV indicate that they are both suitable noninvasive methods for evaluating cardiac sympathetic activity in patients with IDC and, furthermore, favor the view that there is evidence of a relation between HRV and the disorder of the cardiac presynaptic sympathetic nerve endings as demonstrated by a reduced M/C ratio.

3-Iodobenzylguanidine↗

Determinants of stent restenosis in chronic coronary occlusions assessed by intracoronary ultrasound.

Chronic coronary occlusions have a high recurrence rate that can be reduced by stenting, but this rate remains higher than in nonocclusive lesions. To analyze possible determinants of restenosis in these lesions, intracoronary ultrasound was performed during the recanalization procedure. A chronic coronary occlusion of > or = 1 month duration (range 1 to 33 months; median 3.3) was successfully recanalized in 41 patients. Quantitative ultrasound analysis was performed before and after stent placement, with measurement of the luminal area, the extent of the plaque burden at the site proximal and distal to the occlusion, and within the occlusion and the subsequent stent. The degree of compensatory enlargement of the coronary artery within the occlusion was determined by comparing the average of the total vessel area of the proximal and distal reference with the lesion site. Early reocclusion (subacute stent thrombosis) was observed in 1 patient (2.4%). The angiographic control after 6 months showed restenosis in 9 patients with 1 late reocclusion. The overall recurrence rate was 24%. There was no difference in clinical and procedural characteristics between lesions with restenosis and without restenosis. The latter had a larger minimum stent area (7.59 +/- 1.96 mm2 vs 5.71 +/- 0.90 mm2; p <0.01), and there was evidence for more compensatory vessel enlargement in lesions without restenosis. Thus, intracoronary ultrasound showed that a smaller minimum stent area was a major predictor of angiographic restenosis, and it occurred more often in occlusions without compensatory vessel enlargement.

Angioplasty, Balloon, Coronary↗

Unexpanded, irretrievable stent in the proximal right coronary artery: successful management with stent graft implantation.

Stent loss and failure of retrieval are rare; nevertheless, complications have to be taken into account during percutaneous coronary intervention. Here we report a case of an unexpanded, irretrievable Palmaz-Schatz stent in the proximal right coronary artery near to the ostium and the successful management by implanting a synthetic stent graft.

Angioplasty, Balloon, Coronary↗

[Direct coronary stent implantation without predilatation--a new therapeutic approach with a special balloon catheter design].

Stent implantation serves as the gold standard for proximal lesions of the coronary arteries with a diameter between 2.75-3.5 mm. Our new concept aims at a reduced procedure duration and fluoro-time as well as a decreased ischemic period during stent implantation. A new therapeutic concept of a direct stent implantation without predilatation was tested using a specially developed balloon catheter on which various 14-16 mm long "slotted-tube" stents are mounted between two conical, radiopaque markers. In 105 consecutive patients, who were scheduled for angioplasty, this method of direct stent implantation was performed. Six of the procedures were performed for acute myocardial infarction and 8 in so-called high-risk procedures. The direct stent implantation was successful in 88%. In 6%, predilatation of the lesion site was necessary before stent placement. In the remaining 6%, a stent could not be successfully implanted despite the availability of various other systems. Comparison of the direct stent implantation with conventional stent placement with predilatation revealed that 1) The fluoro-time for direct stent implantation, compared to the conventional method, was 8.4 +/- 4.9 min vs. 13.7 +/- 8.0 min; p < 0.05, respectively. Furthermore, there were less balloons used per lesion for direct stent implantation (1.4 +/- 0.4) compared to the conventional method (1.7 +/- 0.7), but there was not a significant difference. 2) If we compare those patients with successful direct stent implantation with those with the unsuccessful procedures, the latter group had a higher percent of angiographically visible calcification at the site of the lesion (80% vs. 18%; p < 0.01). In addition, these patients had an increased average age (72 +/- 7 vs. 61 +/- 11 yrs; p < 0.01). The success rate of direct stent implantation did not depend on lesion diameter stenosis before PTCA. Stent dislocation was observed in 3.8% of the procedures, and a single case of stent embolism was seen. In conclusion, the direct stent implantation offers the advantages of a shortened fluoro-time, the use of fewer balloons, and has the potential of less ischemic stress compared to the conventional method of stent implantation with predilatation, if old patients with calcified lesions are excluded. This should be proved on a large scale in future studies also considering a learning curve with regard to the new method. Whether this new approach also reduces the restenosis rate, warrants further studies.

Adult↗