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Biomedical subjects

R Dietz

Publications and source records attributed to R Dietz.

At least 163 records · Page 9Linked to original sources
PubMed1996

Improvement of vagal tone by ACE inhibition: a mechanism of cardioprotection in patients with mild-to-moderate heart failure.

A total of 35 patients in sinus rhythm and with mild-to-moderate congestive heart failure (CHF) (NYHA II-III) aged 53 (+/- 3) years were examined before therapy with angiotensin-converting enzyme (ACE) inhibitors. Of these patients, 16 were reexamined after therapy with ACE inhibitors for 17 +/- 3 days. The relation of hemodynamic alterations to vagal tone was assessed and the influence of parasympathetic (baroreflex activation) tone on survival was evaluated. Only hemodynamic responders to ACE inhibition showed a significant increase of vagal tone from 1.4 +/- 0.4 to 3.6 +/- 1.2 ms/mm Hg (p < 0.01). The magnitude of increase of vagal tone was dependent on the baseline level. All 35 patients were discharged on ACE inhibitors and were followed for 56 months or longer. We compared patients whose hearts survived (20 patients) with those whose hearts did not (15 patients). Twelve patients died and three underwent cardiac transplantation. The two groups differed (p < 0.05) in terms of mean arterial blood pressure (98 +/- 3 vs. 90 +/- 3 mm Hg), heart rate (82 +/- 2 vs. 93 +/- 4 beats/min), and mean pulmonary artery pressure (24 +/- 3 vs. 35 +/- 2 mm Hg). Cardiac index, stroke volume index, and right atrial pressures were not different. Heart survivors had lower (p < 0.05) renin values (3.6 +/- 0.8 vs. 9.0 +/- 3.6 Ang-I/ml/h) but norepinephrine values at baseline were not different. Baroreflex sensitivity was lower (p < 0.02) in survivors than in nonsurvivors (1.3 +/- 0.2 vs. 2.3 +/- 0.3 ms/mm Hg). We then calculated the mortality risk in relation to baroreflex sensitivity at the median BS of 1.6 ms/mm Hg. Survival was different (p < 0.004) between the resulting two groups: 2 of 15 subjects (13%) with high baroreflex sensitivity died, and 13 of 20 patients (65%) whose baroreflex sensitivity was less than 1.6 ms/mm Hg died. When systemic blood pressure, pulmonary artery pressure, stroke volume index, plasma norepinephrine concentrations, and baroreflex sensitivity were entered into a Cox proportional hazards regression, only systolic blood pressure and plasma norepinephrine values predicted survival (p < 0.001). We concluded that high vagal tone is correlated with a good prognosis in patients with CHF. ACE inhibitor therapy can increase the vagal tone significantly. This may alter the incidence of sudden cardiac death and thereby improve prognosis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Acute and chronic neutral endopeptidase inhibition in rats with aortocaval shunt.

In heart failure, sodium and water retention develop despite elevated plasma levels of atrial natriuretic peptide. Atrial natriuretic peptide is degraded in part by a neutral endopeptidase. Whether neutral endopeptidase inhibition improves sodium and water excretion in heart failure is unknown. We determined the effect of neutral endopeptidase inhibition on plasma levels of atrial natriuretic peptide and the renal response to acute volume expansion in rats with aortocaval shunts and in sham-operated controls. Acute endopeptidase inhibition with SQ 28,603 (30 mg/kg) elevated atrial natriuretic peptide plasma levels in both shunted rats (523 +/- 54 to 1258 +/- 330 pmol/L, P<.05) and controls (184 +/- 28 to 514 +/- 107 pmol/L, P<.05). Urinary cGMP excretion, which reflects renal action, increased in parallel. However, the diuretic and natriuretic responses to acute volume expansion were enhanced only in control rats and not in shunted rats. In contrast to the acute effects, chronic neutral endopeptidase inhibition with SCH 34826 (30 mg/kg twice daily) in shunted rats did not change atrial natriuretic peptide plasma levels or cGMP excretion. Nevertheless, the diuretic and natriuretic responses to acute volume load were increased by chronic endopeptidase inhibition in shunted rats (1789 +/- 154 to 2674 +/- 577 microL/80 min and 99 +/- 31 to 352 +/- 96 micromol/80 min, respectively; P<.05). Chronic endopeptidase inhibition attenuated the cardiac hypertrophic response to aortocaval shunt without changing arterial blood pressure. Our data show that the renal effects of neutral endopeptidase inhibition are not necessarily dependent on changes in atrial natriuretic peptide plasma levels but instead may be mediated by local inhibition of the neutral endopeptidase in the kidney. In addition, chronic endopeptidase inhibition may attenuate heart failure-induced cardiac hypertrophy independent of hemodynamic effects.

Alanine↗
PubMed1996

The application of methods of non-linear dynamics for the improved and predictive recognition of patients threatened by sudden cardiac death.

OBJECTIVES: This study introduces new methods of non-linear dynamics (NLD) and compares these with traditional methods of heart rate variability (HRV) and high resolution ECG (HRECG) analysis in order to improve the reliability of high risk stratification. METHODS: Simultaneous 30 min high resolution ECG's and long-term ECG's were recorded from 26 cardiac patients after myocardial infarction (MI). They were divided into two groups depending upon the electrical risk, a low risk group (group 2, n = 10) and a high risk group (group 3, n = 16). The control group consisted of 35 healthy persons (group 1). From these electrocardiograms we extracted standard measures in time and frequency domain as well as measures from the new non-linear methods of symbolic dynamics and renormalized entropy. RESULTS: Applying discriminant function techniques on HRV analysis the parameters of non-linear dynamics led to an acceptable differentiation between healthy persons and high risk patients of 96%. The time domain and frequency domain parameters were successful in less than 90%. The combination of parameters from all domains and a stepwise discriminant function separated these groups completely (100%). Use of this discriminant function classified three patients with apparently low (no) risk into the same cluster as high risk patients. The combination of the HRECG and HRV analysis showed the same individual clustering but increased the positive value of separation. CONCLUSIONS: The methods of NLD describe complex rhythm fluctuations and separate structures of non-linear behavior in the heart rate time series more successfully than classical methods of time and frequency domains. This leads to an improved discrimination between a normal (healthy persons) and an abnormal (high risk patients) type of heart beat generation. Some patients with an unknown risk exhibit similar patterns to high risk patients and this suggests a hidden high risk. The methods of symbolic dynamics and renormalized entropy were particularly useful measures for classifying the dynamics of HRV.

Death, Sudden, Cardiac↗
PubMed1996

[New aspects of ACE inhibitor treatment of heart failure].

Coronary artery disease is the underlying cause in most of our patients with heart failure nowadays. The arguments put forward for treating these patients with ACE-inhibitors would be reinforced when convincing data are reported demonstrating 1) a reduction of malignant arrhythmias, 2) a reduction in reinfarction rate and 3) a reduction of progressive deterioration in left ventricular function. 1) ACE-inhibitors and malignant arrhythmias. The prolongation of life in heart failure patients treated with ACE-inhibitors might either derive from retarding the progression of heart failure (CONCENSUS I) or from reducing sudden cardiac death (VHeFT II-trial). However, it remains to be established whether the advantage for ACE-inhibitors in reducing sudden death only exists in comparison to a group of patients treated with the combination of hydralazine plus ISDN or whether this is true also in comparison to a placebo group. 2) ACE-inhibitors and reinfarction. Retrospective analysis of data from studies of left ventricular dysfunction (SOLVD) and from the survival and ventricular enlargement (SAVE) study suggested that ACE-inhibitors may reduce the reinfarction rate by about 20%. The underlying mechanisms are not well understood but could in part be mediated by improving endothelial function and/or attenuating the inhibition of PAI-1 through the administration of ACE-inhibitors. 3) ACE-inhibitors and progressive left ventricular dysfunction. ACE-inhibitors are effective means in retarding the remodeling process after myocardial infarction. This is not only true for the progressive increase in left ventricular dimension, but also for the progressive loss of contractile function in the primarily unaffected myocardium. Both, clinical and experimental studies suggest that the observed reduction in mortality is particularly related to the attenuation of the remodeling process by ACE-inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Cyclic GMP-mediated phospholamban phosphorylation in intact cardiomyocytes.

The cGMP-mediated phospholamban phosphorylation was investigated in cardiomyocytes in response to receptor-dependent (atrial natriuretic peptide, ANP) and -independent (sodium nitroprusside; SNP) cGMP generation. ANP (1 nM-1 microM) induced phospholamban phosphorylation in a concentration-dependent fashion (EC50: 5.0 +/- 0.09 nM). Concomitantly, an elevation in cGMP levels was observed. Phospholamban was also dose-dependently phosphorylated in response to SNP, but it required about three orders of magnitude higher concentrations (EC50: 2.9 +/- 0.03 microM) than ANP. Treatment of the cells with 8Br-cGMP (10 microM) or with the specific activator of cGMP-protein kinase 8-pCPT-cGMP (1-100 microM) mimicked these effects. The results demonstrate for the first time that a ANP/cGMP signaling pathway exists in neonatal cardiomyocytes which may contribute to modulation of heart contractility.

Animals↗
PubMed1995

Vectorcardiographic monitoring to assess early vessel patency after reperfusion therapy for acute myocardial infarction.

Reperfusion therapy has lowered mortality in patients suffering from acute myocardial infarction. Failure to reperfuse is associated with an increased short- and long-term mortality. In a prospective study we used dynamic vectorcardiography to monitor 96 patients with acute myocardial infarction treated with reperfusion therapy to non-invasively assess coronary patency. The results from continuous monitoring were compared to those obtained from angiography. By using trend-analysis of QRS vector difference and ST vector magnitude, we were able to correctly identify 58 of the 70 patients (83%) with a reperfused infarct-related artery, and 19 of the 26 patients (73%) with a persistently occluded artery demonstrated at an early angiogram (diagnostic accuracy 80%). In patients with high-grade collateral flow to the infarct-related area, the results of the vectorcardiographic monitoring and of angiography showed the largest disagreement, whereas the accuracy of vectorcardiographic monitoring was high: 88% among patients without collaterals. The present results suggest that QRS complex and ST segment vectorcardiographic monitoring is a useful tool for assessing early coronary artery patency, and that dynamic vectorcardiography may help in identifying candidates for emergency coronary angiography.

Acute Disease↗
PubMed1995

Baroreflex sensitivity and cardiovascular mortality in patients with mild to moderate heart failure.

OBJECTIVE: To assess the influence of both sympathetic (plasma noradrenaline concentrations) and parasympathetic (baroreflex activation) tone on survival in patients with congestive heart failure. DESIGN: Invasive study with determination of parasympathetic activity and follow up for at least 4.5 years. SUBJECTS: 35 patients with sinus rhythm and mild to moderate heart failure (New York Heart Association grades II-III) (mean age 53 (SD 3)). RESULTS: 20 patients whose hearts survived were compared with 15 patients whose hearts did not (12 died and three received transplants). The two groups differed significantly in terms of mean arterial blood pressure (98 (3) v 90 (3) mm Hg), heart rate (82 (2) v 93 (4) beats/min), and mean pulmonary artery pressure (24 (3) v 35 (2) mm Hg) (all P < 0.05), while cardiac index, stroke volume index, and right atrial pressures were not different. The survivors had significantly lower plasma renin activities (3.6 (0.8) v 9.0 (3.6) angiotensin I/ml/h; P < 0.05) and tended to have lower noradrenaline values than non-survivors (170 (23) v 286 (74) pg/ml) at baseline. Baroreflex sensitivity was significantly lower in non- survivors than in survivors (1.3 (0.2) v 2.3 (0.3) ms/mm/Hg); P < 0.02). As the time of cardiac transplantation is dependent on complex logistical factors the three patients who received a transplant were excluded from the analysis of survival time. The risk of death in relation to baroreflex sensitivity at the median sensitivity of 1.48 ms/mm Hg was calculated. Survival was significantly different (P < 0.04) between the resulting two groups; three of the 16 subjects with high baroreflex sensitivity died compared with nine of the 16 with a baroreflex sensitivity < 1.48 ms/mm Hg. When systemic blood pressure, pulmonary artery pressure, stroke volume index, plasma noradrenaline concentrations, and baroreflex sensitivity were entered into a Cox proportional hazards regression, only systolic blood pressure and plasma noradrenaline values predicted survival (P < 0.001). CONCLUSIONS: Low vagal tone is correlated with a poor prognosis in patients with heart failure. Sympathetic tone measured as plasma noradrenaline concentration also contributed to survival. An additional contribution of vagal tone to survival could not be shown when sympathetic tone was considered simultaneously. This may be due to the inverse relation of sympathetic and parasympathetic tone and to the insensitivity of the multiple regression method to identify additional risk factors in small numbers of patients.

Baroreflex↗
PubMed1994

Medical compared with surgical treatment for massive pulmonary embolism.

We compared embolectomy (when available) with thrombolysis in patients with shock and massive pulmonary embolism. 13 patients were operated on, 10 (77%) of whom survived. The inferior vena cava was routinely clipped. The 24 medically treated patients were given alteplase until systemic and pulmonary artery pressures stabilised and heparin thereafter; 16 (67%) survived. Major haemorrhage occurred in 28% of medically treated patients, but was not fatal. 1 patient had a small cerebral haemorrhage that resolved without drainage. One-fifth of the medical group had a re-embolism, which suggests that temporary caval umbrellas are indicated in medically treated patients. Thrombolysis may provide a life-saving option and a randomised trial is warranted.

Adult↗
PubMed1994

Emergency coronary stenting for dissection during percutaneous transluminal coronary angioplasty: angiographic follow-up after stenting and after repeat angioplasty of the stented segment.

OBJECTIVES: The purpose of this study was to assess the angiographic results after emergency coronary stenting and after repeat angioplasty for restenosis within the stent. BACKGROUND: There is still little angiographic information about lumen renarrowing and its correlates after emergency stenting, and data with regard to the angiographic outcome of repeat angioplasty within the stent are almost nonexistent. METHODS: This study was based on the quantitative evaluation of angiograms performed before and immediately after intervention and at 6-month follow-up. The study included 164 of the 183 eligible patients with emergency Palmaz-Schatz stent implantation and 31 of those with restenosis within the stent who had repeat angioplasty. RESULTS: Stenting produced an improvement in minimal lumen diameter from 0.82 +/- 0.41 to 2.76 +/- 0.47 mm (mean +/- SD) and in diameter stenosis from 74.9 +/- 11.5% to 18.3 +/- 8.1%. Elastic recoil was 0.51 +/- 0.34 mm, or 16%. At 6-month follow-up, 32.3% of the patients had restenosis (> or = 50% stenosis). Minimal lumen diameter decreased to 1.84 +/- 0.78 mm, and diameter stenosis increased to 41.7 +/- 21.0%. The degree of lumen loss correlated significantly with the length of the original stenosis and the initial lumen gain achieved by stenting. Thirty-one patients with in-stent restenosis underwent repeat angioplasty. The primary success rate was 100%, and no abrupt vessel closure was verified. Minimal lumen diameter increased from 0.85 +/- 0.35 to 2.18 +/- 0.39 mm, and diameter stenosis decreased from 69.7 +/- 12.9% to 28.6 +/- 9.4%. Elastic recoil was 0.82 +/- 0.38 mm, or 27%. At follow-up, 38.5% of the patients had restenosis. Minimal lumen diameter was reduced to 1.72 +/- 0.67 mm, and diameter stenosis increased to 42.4 +/- 18.1%. CONCLUSIONS: Angiographic results of emergency coronary stenting compare favorably with those of conventional angioplasty. In-stent balloon redilation in patients with restenosis is associated with excellent short-term results and a restenosis rate not different from that reported for nonstented vessels.

Aged↗
PubMed1994

Verapamil treatment after coronary angioplasty in patients at high risk of recurrent stenosis.

OBJECTIVE: To evaluate the efficacy of high-dose verapamil treatment (240 mg twice daily) in the prevention of angiographic restenosis after primary successful coronary angioplasty in patients at high risk of recurrent obstruction. DESIGN: A placebo controlled, double blind trial in which patients with stable angina pectoris and patients with unstable angina or non-Q wave infarction treated with 330 mg aspirin and 75 mg dipyridamole twice daily were randomised to a verapamil group or a control group. Follow up angiography was performed 6 months after angioplasty or sooner if signs of recurrent ischaemia developed. SETTING: University department of cardiology. PATIENTS: 196 consecutive patients undergoing coronary angioplasty from the beginning of April 1987 to the end of March 1989 and meeting the selection criteria that included the presence of at least one of six predefined risk factors for restenosis. At the time of coronary angioplasty 113 patients had unstable angina or non-Q wave infarction and 83 had stable angina pectoris. RESULTS: In 89 (91%) patients in the verapamil group and in 83 (85%) control patients follow up angiograms were available. The restenosis rate was lower in the verapamil group (48.3%) than in the placebo group (62.7%) (odds ratio 0.56, 95% confidence interval (CI) 0.303 to 1.025 p = 0.059). Of the 172 patients in whom follow up angiograms were available, 24 (13 taking verapamil and 11 taking placebo) did not comply with the trial for more than 40 (34) days (mean (1 SD)). For the remaining 148 patients the restenosis rate was 47.4% in the verapamil group and 63.9% in the placebo group (odds ratio 0.52, 95% CI 0.271 to 0.993, p = 0.046). In the 97 patients with unstable angina or non-Q wave infarction the restenosis rate was not significantly influenced by verapamil (55.8% with verapamil v 62.2% with placebo, odds ratio 0.77, 95% CI 0.339 to 1.728, p = 0.520). In the 75 patients with stable angina pectoris the restenosis rate dropped from 63.2% with placebo to 37.8% with verapamil (odds ratio 0.36, 95% CI 0.137 to 0.917, p = 0.038). CONCLUSION: The observed beneficial effect of high-dose verapamil treatment on the angiographic restenosis rate in patients with stable angina pectoris and at increased risk of recurrent obstruction requires confirmation in further prospective studies.

Aged↗
PubMed1994

[New methods for the detection of high risk patients in cardiology].

Common non-invasive diagnostic methods like Holter monitoring or the analysis of high-resolution ECG and heart rate variability are unable to accurately assess the individual risk for sudden cardiac death, since they describe only statistical, linear or strictly periodic parameters. Using new methods of non-linear dynamics one can now calculate parameters which much better describe the dynamic behaviour of complex systems. The application of these new methods should therefore lead to an improved identification of high-risk patients. The results of this first pilot investigation show on the one hand that ventricular arrhythmias are quick detectable using phase space plots, and on the other hand that the new methods of non-linear dynamics could lead to a new classification of high-risk patients.

Adult↗
PubMed1994

[Therapy with ACE inhibitors in chronic heart failure and limited kidney function].

UNLABELLED: Renal function in 31 patients with mild to moderate heart failure (NYHA Classes II-III) was studied before and during treatment with ACE-inhibitors. Maximal treatment doses were based on randomization: captopril 3 x 12.5 mg or lisinopril or enalapril, both 1 x 10 mg. Before therapy and at the end of titration phase (after 6 days) glomerular filtration rate and renal blood flow were determined from inulin and PAH clearance (steady-state method). In the total study group the median arterial pressure significantly decreased from 94 mmHg to 84 mmHg (p < 0.01), whereas glomerular filtration rate was only moderately, however, significantly reduced from 103 ml/min to 97 ml/min (median values, p < 0.01). Renal blood flow, however, increased from 372 ml/min to 403 ml/min (p < 0.01). Changes in glomerular filtration rate (GFRd) were significantly dependent on those of renal blood flow (GFRd = 0.07 RPFd - 9.2; p < 0.05). All three ACE-inhibitors showed similar changes in glomerular filtration rate and renal blood flow. Ten of the patients had additionally received cyclooxygenase inhibitors. With respect to severity of heart failure and renal function these patients did not differ from the remaining 21 patients of the group. In both groups, a decrease of glomerular filtration rate was found, however, in those patients who had received acetylsalicylic acid there was no increase of renal blood flow. CONCLUSION: A small, however significant decrease of glomerular filtration rate is already seen in patients with mild to moderate heart failure treated with ACE-inhibitors. Increase of renal blood flow counteracts the decrease of glomerular filtration rate. During concomitant application of acetylsalicylic acid the increase of renal blood flow remains absent.

Aged↗
PubMed1994

Interactions between the renin-angiotensin system and the parasympathetic nervous system in heart failure.

The increase of sympathetic activity in heart failure is accompanied by reduced parasympathetic tone. The renin-angiotensin system (RAS) is often activated in heart failure. It not only has multiple interactions with the sympathetic nervous system but also may influence vagal tone directly via angiotensin II. Animal studies show a reduction of parasympathetic tone by a direct action of angiotensin II in the area postrema, where the blood-brain barrier is absent. It is possible that in addition to the sympathetic and renin-angiotensin systems the parasympathetic nervous system may also influence prognosis in heart failure. Therefore, baroreflex sensitivity (BS) as an index of vagal tone was examined in 35 patients with moderate-to-severe heart failure (NYHA II-III). Independent of the severity of heart failure, BS was lower the higher the plasma renin activity. At 56 months after initial examination, a comparison of the surviving patients (group 1, n = 20) with the patients who died or underwent heart transplantation (group 2, n = 15) did not reveal significant differences in the initial hemodynamic data. However, group 2 patients showed a tendency to higher initial plasma renin activity and a significantly lower BS (1.3 +/- 0.2 versus 2.2 +/- 0.3 ms/mm Hg; p < 0.05). It is concluded that in patients with heart failure a relation between the RAS and the parasympathetic nervous system is likely, as there is a significant negative relationship between BS and plasma renin activity. Among patients with similar degrees of heart failure, low vagal tone identifies patients with a poor prognosis.

Age Factors↗
PubMed1993

Dosing of ACE inhibitors in postinfarct protection.

ACE inhibitors improve not only symptoms and signs of heart failure in patients with symptomatic left ventricular dysfunction but also lead to a slower progression of heart failure. In asymptomatic patients with left ventricular dysfunction, the progression to symptomatic heart failure is retarded by ACE inhibitors. As heart failure is preceded in about 80% by myocardial infarctions, trials were designed to influence the development of heart failure after myocardial infarction. It could be shown that therapy with ACE inhibitors ameliorates the progressive left ventricular dilatation and that this effect is translated into a significant increase of life expectancy. Mainly based on the CONSENSUS I study, large doses of ACE inhibitors were used in most subsequent trials. The mean daily doses of enalapril were 18.4 mg in the CONSENSUS I trial and 16.6 and 16.7 mg in both arms of the SOLVD trial. There is a trend towards lower doses of ACE inhibitors, as in the SAVE trial only 79% of the patients taking captopril received the target dose of 150 mg daily. Smaller studies used similar target doses, but a beneficial effect on left ventricular enlargement has been shown with a daily dose of only 75 mg captopril. Based on the hypothesis that the left ventricular enlargement is mainly determined by the activation of the local cardiac renin angiotensin system, even lower, and therefore better tolerated, doses of ACE inhibitors may prove effective. However, studies comparing the effect of different doses of ACE inhibitors on left ventricular remodeling are missing. Consequently, the above-mentioned target doses of ACE inhibitors should be aimed at when treating patients after myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Time course of restenosis during the first year after emergency coronary stenting.

BACKGROUND: Prevention of abrupt vessel closure after percutaneous transluminal coronary angioplasty (PTCA) represents one of the current indications for intracoronary stent implantation. After the procedure, the stented segment undergoes luminal changes that may lead to late restenosis. This study was undertaken to assess the time course of luminal changes during the first year after emergency placement of coronary stents. METHODS AND RESULTS: Coronary stenting was indicated in patients with present or threatened vessel closure secondary to large dissections after PTCA. From June 1989 to May 1991, 82 patients who received Palmaz-Schatz stents and did not have early vessel occlusion after stenting were enrolled into a serial angiographic follow-up study. Coronary normal reference diameter and minimal luminal diameter were measured with an automated edge detection technique. Patients who underwent repeat PTCA for restenosis were excluded from further serial angiography. The restudy rate at 3, 6, and 12 months was 96%, 81%, and 90% of the eligible patients, respectively. The incidence of restenosis (defined as a diameter stenosis > or = 50%) was 22.0% at 3 months, 31.9% at 6 months, and 33.2% at 12 months. Minimal luminal diameter was increased from 0.66 +/- 0.32 mm before to 2.85 +/- 0.43 mm immediately after stenting. It was 0.46 +/- 0.31 mm smaller than the diameter of the maximally inflated balloon during the procedure. The reduction in minimal luminal diameter was 0.80 +/- 0.69 mm (p = 0.0001) for the first 3 months, 0.29 +/- 0.52 mm (p = 0.0001) between 3 and 6 months, and 0.13 +/- 0.32 mm (p = 0.01) for the last 6 months. The percentage of patients who presented a significant change in minimal luminal diameter (defined as > 0.60 mm) declined from 50.6% during the first 3 months and 18.9% between 3 and 6 months to 6.5% for the period between 6 and 12 months. CONCLUSIONS: The incidence and the time course of restenosis after emergency coronary stenting are similar to that reported for conventional PTCA. Coronary lumen dimensions demonstrated a peak change at 3 months and remained mostly stable after the first 6 months.

Aged↗