Polymorphism in the chemokine receptor 7 gene (CCR7) is associated with previous myocardial infarction in patients undergoing elective coronary angiography.

Coronary artery disease (CAD) remains a major cause of death in developed countries. Both environmental and, less known, genetic factors contribute to progression of CAD to myocardial infarction (MI). Immune system is activated in patients with CAD through dendritic cells (DCs), which present plaque antigens to T lymphocytes. Production of proinflammatory cytokines by activated T cells contributes to plaque rupture in MI. Chemokine receptor 7 (CCR7) on DCs is required for their chemotaxis from plaque to lymph nodes. This makes possible an interaction of DCs with T lymphocytes and initiation of specific immune response. We hypothesized that single nucleotide polymorphisms (SNPs) in CCR7 gene locus are associated with previous MI in patients with CAD. To test this hypothesis, we genotyped six SNPs from the CCR7 gene locus in 300 consecutive patients, admitted for elective coronary angiography. We performed univariate-, multivariate- (including potential confounders) and haplotype-based tests of association of SNPs with previous MI and results of angiography. Allele A of rs17708087 SNP was associated with previous MI. This association remained significant after adjustment for age, sex, smoking, hypercholesterolaemia and drugs used by patients (odds ratio 2.13, 95% confidence interval: 1.13-3.86). Therefore, we conclude that CCR7 gene locus harbours a polymorphism that modifies risk of MI in patients with CAD. Replication of this association could be sought in a prospective cohort of initially healthy individuals.

Evaluation of profilin 1 as a biomarker in myocardial infarction.

OBJECTIVE: Profilin 1 (Pfn1) is likely to be involved in atherogenesis and myocardial infarction (MI). Clinical data on this subject are very limited. The aim of this study was to search for associations between serum Pfn1 and a number of parameters in MI patients: symptom onset to PCI time (OPT), myocardial necrosis markers, thrombolysis in myocardial infarction (TIMI) flow, antiplatelet drugs, heparin administration and typical atherosclerosis risk factors. PATIENTS AND METHODS: We included patients with type 1 MI (according to the Third Universal Definition of Myocardial Infarction) who were able to precisely determine the time of symptom onset. Exclusion criteria involved conditions potentially altering platelet function. We screened 114 patients and included 65. We assessed serum Pfn1 in three time points: on admission (Pfn1_0), 24 hours post PCI (Pfn1_24) and 48 hours post PCI (Pfn1_48) and correlated it with OPT, cardiac necrosis markers (troponin T, CK, CKMB), TIMI flow in the infarct-related artery, pre-hospital P2Y12-antagonist and heparin administration and known atherosclerosis risk factors. RESULTS: Patients with a shorter OPT had higher Pfn1_0 (838.5 vs. 687.1 pg/ml, p=0.007). Patients with impaired coronary flow post PCI had lower Pfn1_24 (748.2 vs. 925.2 pg/ml, p=0.017) and Pfn1_48 (744.5 vs. 879.8, p=0.031. Pfn1_24 and Pfn1_48 were lower in patients who received a P2Y12 antagonist prior to hospital admission. Diabetic patients presented with lower Pfn1_0 concentrations. CONCLUSIONS: This is the first study assessing Pfn1 in type 1 MI patients in relation to the chosen parameters. Pfn1 may be a biochemical tool to objectify information on OPT in MI patients. We found an association between Pfn1 and post-PCI TIMI flow, antiplatelet drug administration and diabetes mellitus.

The role of chemokine CCL5/RANTES and metalloproteinase-9 as inflammatory modulators in symptomatic internal carotid artery stenosis.

Up to 80% of all ischemic strokes (IS) attributed to internal carotid athero-occlusive artery stenosis (ICAS) are related to a thromboembolic mechanism. One athero-occlusive ischemic event increases the risk for ischemia in another vascular territory, resulting from inflammation within the atherosclerotic plaque induced by cytokines. Thus, ultrasonographic characteristics of vulnerable plaques in ICAS, including plaque echolucency and ulceration might correspond to cytokine activity. The present study aimed to investigate the associations between serum cytokines and atherosclerotic plaque characteristics and the 3-year risk of a major adverse coronary and carotid ischemic event (MACCE) in symptomatic patients treated for ICAS. Plaque characteristics on ultrasonography, serum levels of C-C motif chemokine ligand 5 (CCL5)/regulated on activation, normal T-cell expressed and secreted (RANTES), metalloproteinase-9 (MMP-9), interleukin-6 (IL-6), transforming growth factor beta (TGF-ß), C-X-C motif chemokine ligand 16 (CXCL16), FAS ligand (FASL) and high sensivity C-reactive protein (hs-CRP) were analyzed in 103 symptomatic patients with ICAS prior to carotid revascularization. The incidence of MACCE: cardiovascular death (CVD), myocardial infarction (MI) and recurrent ischemic stroke (IS) were recorded prospectively for up to 5 years (median 37; IQR 21 - 40 months). Echolucent plaques, in comparison to echogenic plaques, displayed lower median levels of RANTES (P = 0.042) but higher median levels of IL-6 (P = 0.039). There was no relationship between plaque characteristics and median levels of MMP-9, TGF ß, CXCL16, FASL, or hs-CRP (P = NS). During follow-up, MACCE occurred in 15 (14.6%) patients. Univariate Cox proportional hazard analysis indicated median RANTES levels < 45.5ng/mL (hazard ratio (HR) = 3.95; 95%CI = 1.10 - 14.2; P = 0.035), MMP-9 > 0.6 µg/mL (HR 4.5; 95%CI = 1.4 - 13.9; P = 0.009), renal impairment (HR 3.48; 95%CI = 1.29 - 9.34; P = 0.013) as potential MACCE risk factors. On multivariate Cox proportional hazard analysis, MMP-9 > 0.6 µg/mL and RANTES < 45.5 ng/ml were associated with a 4.72-fold (95%CI = 1.3 - 17.0; P = 0.017) and a 3.8-fold risk increase (95%CI = 1.07 - 13.89; P = 0.038) of MACCE. Kaplan-Meier analysis showed significant differences in MACCE-free survival rates depending on RANTES and MMP-9 median levels. We conclude that serum RANTES, IL-6, and MMP-9 were associated with plaque vulnerability and predicted adverse MACCE in patients treated for ICAS.

Thrombin generation in acute coronary syndrome and stable coronary artery disease: dependence on plasma factor composition.

BACKGROUND: Acute coronary syndrome (ACS) is associated with thrombin formation, triggered by ruptured or eroded coronary atheroma. We investigated whether thrombin generation based on circulating coagulation protein levels, could distinguish between acute and stable coronary artery disease (CAD). METHODS AND RESULTS: Plasma coagulation factor (F) compositions from 28 patients with ACS were obtained after onset of chest pain. Similar data were obtained from 25 age- and sex-matched patients with stable CAD. All individuals took aspirin. Patients on anticoagulant therapy were excluded. The groups were similar in demographic characteristics, comorbidities and concomitant treatment. Using each individual's coagulation protein composition, tissue factor (TF) initiated thrombin generation was assessed both computationally and empirically. TF pathway inhibitor (TFPI), antithrombin (AT), factor II (FII) and FVIII differed significantly (P < 0.01) between the groups, with levels of FII, FVIII and TFPI higher and AT lower in ACS patients. When thrombin generation profiles from individuals in each group were compared, simulated maximum thrombin levels (P < 0.01) and rates (P < 0.01) were 50% higher with ACS while the initiation phases of thrombin generation were shorter. Empirical reconstructions of the populations reproduced the thrombin generation profiles generated by the computational model. The differences between the thrombin generation profiles for each population were primarily dependent upon the collective contribution of AT, FII and FVIII. CONCLUSION: Simulations of thrombin formation based on plasma composition can discriminate between acute and stable CAD.

Chemokine RANTES is increased at early stages of coronary artery disease.

Cardiovascular diseases, and in particular coronary artery disease (CAD), are the leading causes of death in Europe and represent around 50% of overall mortality. Numerous cardiovascular markers have been proposed in relation to cardiovascular risk prediction, in relation to cardiac and vascular and cerebral events. Chemokines which regulate immune cell vascular chemotaxis, including CCL5/RANTES are points of great interest. We hypothesized that chemokine RANTES level measured in peripheral blood may be associated with severity of atherosclerosis in patients with stable angina undergoing coronary angiography. RANTES and interleukin 18 (IL-18) levels were measured by ELISA. Classical and novel cardiovascular risk factors like brachial flow mediated dilation and intima-media thickness were analyzed in the context of chemokine levels and severity of atherosclerosis. Study included 62 consecutive patients with coronary atherosclerosis demonstrated by coronary angiography, (mean age 59.3 years (S.D. = 7.4)), divided into two groups: group I with lower severity of atherosclerosis, (n = 45) and group 2 with severe CAD (n = 17) based on coronary angiography. Groups were well balanced for classic risk factors for atherosclerosis. Mean RANTES level were significantly higher in patients in group I (67.9 ng/ml, S.E.M. = 3.97) than in group II (50.5 ng/ml, S.E.M. = 7.49; P = 0.03). In contrast, IL-18 levels were similar in both groups (255 pg/ml in group I and 315 pg/ml, S.E.M. = 40.91 in group I, P = 0.12), as well as hsCRP concentration (3.45 S.E.M. = 2.66 ng/ml and 4.69 ng/ml S.E.M.= 1.64 ng/ml respectively; P = 0.47). Flow-mediated dilatation (FMD) values have been significantly lower in group II than in group I (6.31; S.E.M. = 0.61; vs 4.41; S.E.M. = 0,56, respectively, P = 0.026), while nitroglycerine-mediated dilatation (NMD) did not differ, indicating more pronounced endothelial dysfunction. No significant correlations between chemokine RANTES levels and intima-media thickness (IMT), FMD measurements have been found in the total population studied. Chemokine RANTES level could become a useful marker of severity of coronary artery disease. Its lower levels were observed in patients with more diffuse disease. Elevated level of chemokine RANTES in patients with stable angina pectoris may evaluate patients to high risk group in plaque formation at early stages of atherosclerosis.

Early intravenous administration of metoprolol enhances myocardial salvage by thrombolysis with recombinant tissue-type plasminogen activator after thrombotic coronary artery occlusion in the dog by improvement of the collateral blood flow to the area at risk.

OBJECTIVES: We studied the effects of beta 1-adrenergic blockade preceding thrombolysis on hemodynamic variables, myocardial blood flow and infarct size in a canine model of thrombotic occlusion of the left anterior descending coronary artery. BACKGROUND: Previous work suggested a reduction in infarct size and improvement in left ventricular function by intravenous beta-blockade preceding thrombolysis. METHODS: Experiments were conducted in 34 anesthetized dogs; 17 received 0.975 mg/kg body weight of metoprolol intravenously starting 15 min after occlusion, and thrombolysis was initiated 60 min after occlusion. Seventeen dogs received saline solution followed by thrombolysis. Coronary blood flow was measured by radioactive microspheres, infarct size by a dye method, hemodynamic variables by catheter-tipped pressure transducers and cardiac output by the thermodilution method. RESULTS: Infarct size in metoprolol- and placebo-treated dogs was 23.62 +/- 18.04% and 41.50 +/- 16.03% of area at risk, respectively (p < 0.01). Before occlusion, myocardial blood flow and hemodynamic variables were similar. Sixty minutes after occlusion, cardiac output (1.94 +/- 0.41 vs. 2.32 +/- 0.68 liters/min, p < 0.01) was lower in the metoprolol-treated dogs. Collateral flow to the area at risk (17.27 +/- 7.44 vs. 10.25 +/- 5.33) and to its epicardial (21.68 +/- 8.04 vs. 11.5 +/- 6.10), midmyocardial (14.30 +/- 8.63 vs. 7.35 +/- 4.94) and endocardial (13.18 +/- 8.21 vs. 6.26 +/- 5.34 cm3/min per 100 g) layers was higher (p < or = 0.05) in the metoprolol-treated dogs. The ratio of epicardial flow area at risk/circumflex territory was inversely correlated to infarct size (r = -0.69, p < 0.01). After 5 min of occlusion, collateral flow was comparable in the five dogs of each group; over the next 55 min it remained constant in the metoprolol group but decreased in the placebo dogs. CONCLUSIONS: Intravenous metoprolol, administered before thrombolysis, enhances infarct size limitation, partly by improvement of collateral flow to area at risk.

Determinants of depressed left ventricular ejection fraction in pure mitral stenosis with preserved sinus rhythm.

BACKGROUND AND AIM OF THE STUDY: Although depressed left ventricular ejection fraction is present in a considerable proportion of subjects with pure mitral stenosis (MS), its mechanisms are not clearly identified. The purpose of this study was to identify determinants of depressed ejection fraction in young patients with isolated mitral stenosis in sinus rhythm. METHODS: We retrospectively analyzed 320 records of patients with MS (mitral valve area < or = 2.0 cm2) who underwent invasive diagnostic procedure in our center. Of these 39 subjects aged 20-40 years with isolated MS in sinus rhythm were selected for the final analysis. RESULTS: An ejection fraction not exceeding 50% was found in 12 patients (group A). When comparing group A to the remainder (group B), group A patients had lower left ventricular end-diastolic volume indices (60.5 +/- 21.6 ml/m2 vs. 76.1 +/- 16.1 ml/m2, p = 0.02) and stroke volume indices (28.0 +/- 10.4 vs. 47.9 +/- 12.0, p < 0.001). No significant differences between the groups in patients' age, end-systolic volume index, mitral valve area, mean transmitral gradient, left-sided cardiac pressures, pulmonary wedge pressure, systemic vascular resistance, and cardiac output were found. Indices of left ventricular isovolumic contraction and relaxation as well as end-systolic indices of left ventricular function were also comparable. Group A had significantly higher pulmonary vascular resistance, pulmonary artery pressures, and higher heart rate. An approximate index of left ventricular compliance was significantly lower in group A with similar left ventricular minimal and end-diastolic pressures. CONCLUSIONS: Depressed ejection fraction in pure mitral stenosis with preserved sinus rhythm seems attributable to left ventricular underfilling that appears to be precipitated by other factors in addition to a narrowed mitral orifice, e.g. decreased passive left ventricular compliance and/or altered interventricular interactions.

Influence of an early adrenergic blockade on thrombotic infarct size and myocardial metabolism.

To evaluate the extent to which the protective effect of metoprolol was accompanied by changes in myocardial oxygen consumption and metabolism, thrombotic occlusion of coronary artery followed by infusion of metoprolol or placebo was performed in twenty four German Shepherds. To restore a coronary blood flow rt-PA was administered. Plasma levels of oxygen, glucose, lactic acid, non esterified fatty acids, triacylglyceride and adenosine breakdown products were measured before and at the end of the occlusion and in the early and late reperfusion periods. Regional myocardial blood flow was measured by means of radioactive tracer microspheres. Infarct size was estimated after perfusion and staining of excised hearts with Evans blue. Plasma levels of metoprolol were determinated before the end of occlusion and during reperfusion and therapeutic concentrations were confirmed. The infarct size was smaller in dogs receiving metoprolol (21.6 +/- 20.7 vs 43.0 +/- 17.3% p. < 0.02). Coronary collateral blood flow was greater in metoprolol than in placebo dogs (18.68 +/- 7.58 vs 11.05 +/- 6.10 ml/min/100g, p. < 0.01). As a consequence of myocardial ischemia a shift toward carbohydrate utilization, the myocardial lactate release and the accompanying symptoms of diminished myocardial lipid uptake were observed. A washout of adenosine degradation products during early reperfusion was also noticed. In beta 1 blocked animals the reduction of myocardial oxygen consumption and preserved myocardial uptake of lactate and non esterified fatty acids were documented.

Lack of beneficial effects of L-arginine infusion in primary pulmonary hypertension.

The aim of this study was to assess the effects of L-arginine in primary pulmonary hypertension (PPH). Diagnostic cardiac catheterization was performed in 4 patients (pts) (1 man and 3 women, aged 18-47 years) with suspected PPH. In all of them diagnosis of PPH was confirmed; mean pulmonary artery pressure (PAP) ranged from 46 to 83 mmHg. Then 61/min oxygen was administered for 10 min through the oxygen mask (first oxygen test). After another 15 min, L-arginine was infused into an antecubital vein at a dose of 12.63g of L-arginine hydrochloride in 300 ml of 0.9% NaCl over 90 min. 15 min before the planned termination of the infusion the second oxygen test was performed in the same way as the first one. Hemodynamic data were collected by means of two catheters placed in the main pulmonary artery and in the aortic root. Cardiac output (CO) was estimated by the thermodilution technique. Blood samples were drawn from both catheters to estimate oxygen tension and cyclic GMP (cGMP) levels. In pts 1 and 2 differences between baseline values and following L-arginine did not exceed 9% for mean PAP (mPAP), total pulmonary resistance (TPR), mean aortic pressure (mAP), systemic resistance (SR), CO and HR. In patient 3 mAP and SR dropped by about 30%. In patient 4 after 15 min of the infusion mAP and SR fell by about 50%, whereupon we stopped L-arginine administration. Thus, for ethical reasons, we decided not to recruit new subjects for the study. In pts 1-3 aortic oxygen tension diminished by 10-15% on L-arginine.(ABSTRACT TRUNCATED AT 250 WORDS)

Simvastatin-induced myopathy in a patient treated for hypercholesterolemia. Morphological aspects.

Functional and histological changes in skeletal muscle developing during hypolipemic therapy, especially with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are rare. This paper reports a case of simvastatin-induced myopathy confirmed histopathologically and ultrastructurally.

[Comparative study of acute and chronic effects of nifedipine in patients with secondary pulmonary hypertension]. / Porównanie ostrego i przewleklego dzialania nifedipiny u chorych z wtórnym nadcisnieniem plucnym.

The effects of nifedipine in a single dose of 10 mg on the pulmonary circulation and the selected right and left ventricular function indices were studied in a group of 10 patients with secondary pulmonary hypertension (mean systolic pressure 55.2 mm Hg). In 8 patients hemodynamic studies were repeated after seven days treatment (3 x 10 mg). Acute treatment with nifedipine resulted in a reduction in mean systolic arterial pressure by 21.8%, diastolic by 12.2% and systemic resistance by 25.5%, and in an increase in cardiac index by 14.3%. After 7 days a similar pattern of changes was observed, however with less intensity: systolic pressure was reduced by 10.3% diastolic by 5.5%, and systemic resistance by 17.1%. Pulmonary artery wedge pressure did not change after a single dose, and mean pulmonary artery pressures showed a tendency toward lower levels: systolic by 8.9% and diastolic by 8.6%, whereas total pulmonary resistance decreased markedly (by 22.7%), as well as pulmonary vascular resistance. Right ventricular filling pressure was reduced. After chronic treatment we found a further slight fall in the pulmonary arterial pressure. Although per cent changes were similar to those in the arterial pressure, alterations in the mean values were not statistically significant. The total pulmonary resistance remained reduced. While analysing the changes in the pulmonary circulation and right ventricular indices it should be noted that they were less intense and less homogeneous than the left ventricular function parameters. Some of the patients showed certain similarities in the direction and intensity of changes in the hemodynamic indices of the pulmonary circulation in the acute and chronic experiment.

[Percutaneous renal artery angioplasty--review of current indicators]. / Angioplastyka tetnic nerkowych--aktualne wskazania.

The most frequent cause of secondary arterial hypertension is renal artery stenosis. The aetiology of renal artery stenosis is mainly atherosclerotic (75-80%), in the remaining cases fibromuscular dysplasia is the causative factor. Renovascular hypertension has a poorer prognosis than spontaneous because it is more resistant to antihypertensive treatment, signifies an increased risk for the development and progression of malignant hypertension and may lead to irreversible renal dysfunction due to ischaemia. Renal revascularisation has been proved an effective treatment modality in patients with arterial hypertension or renal failure due to renal artery stenosis. However, surgical treatment is associated with the mortality rate of 6-9% due to the concomitant presence of ischaemic heart disease, cerebral and peripheral arteriosclerosis. Percutaneous transluminal renal angioplasty is equally effective in the treatment of arterial hypertension as surgical operation, leading to the improvement or stabilisation of renal function. The advent of renal stenting has markedly changed the efficacy and safety of procedures with PTRA becoming an alternative to surgery. The high efficacy of PTRA is associated with low mortality and relatively few complications as compared with surgical treatment. However, there is continuous discussion concerning the efficacy of percutaneous and surgical renal revascularisation in arterial hypertension. PTRA is currently increasingly frequently recommended in patients with renovascular hypertension not only to control blood pressure but also to protect renal function.

[Subendocardial blood flow index in relation to selected parameters of left-ventricular function in patients with aortic valve stenosis]. / Wskaznik przeplywu podwsierdziowego w odniesieniu do wybranych parametrów czynnosci lewej komory u chorych ze zwezeniem lewego ujscia tetniczego.

The aim of our studies was to estimate the relation between the reduction of the subendocardial blood flow, expressed by DPTI/TTI ratio and the grade of aortic stenosis determined by the maximal systolic aortic gradient. Additionally the influence of subendocardial blood flow reduction of left ventricular function and ECG alterations was assessed. The analyzed data were obtained during the cardiac catheterizations in a group of 30 patients (average age 32 years). The mean value of DPTI/TTI ratio was decreased (0.49 +/- 0.2) and associated with the elevated mean value of AGmax (72.2 +/- 38.1 mmHg). Negative correlation between DPTI/TTI and AGmax (r = -0.73; p less than 0.003), DPTI/TTI and LVEDP (r = -0.53; p less than 0.005) occurred. Depression of ST-T segment in EEG and episodes of anginal pain accompanied the reduction of subendocardial blood flow. We concluded that reduction in subendocardial blood flow in patients with SA-may lead subendocardial ischaemia of the left ventricular wall with subsequent of its function.

[Personality and restenosis after percutaneous transluminal coronary angioplasty]. / Osobowosc a restenoza po zabiegu przezskórnej angioplastyki wiencowej.

The paper is an attempt to find out which personality traits predispose to increased risk of restenosis in patients after first percutaneous transluminal coronary angioplasty (PTCA). The Eysenck Personality Questionnaire-Revised (EPQ-R) was used in 87 consecutive men (31 persons with university education, 26 secondary, and 20 occupational education; mean age 50 years, range from 32 to 72) on the second day after PTCA. Raw data were used in statistical analysis of EPQ-R. Restenosis was identified in coronary angiography within several weeks to 6 months after PTCA. Restenosis was detected in 25 patients. Groups with and without restenosis were compared with respect to EPQ-R parameters referring to neurotism (14.8 +/- 3.26 vs. 12.4 +/- 5.63; p < 0.01), extroversion (13.7 +/- 3.82 vs. 13.7 +/- 3.95; NS) and psychotism (5.7 +/- 3.20 vs. 7.2 +/- 4.8; p = 0.08). There was positive correlation between the level of neurotism and the frequency of restenosis (logistic regression coefficient = 0.225; OR = 1.252; p = 0.03), but not with age and the level of education. In contrast, psychotism did not correlate significantly with frequency of restenosis. In conclusion, neurotism appears to affect the frequency of restenosis, which means that emotional imbalance through reducing immunity to stress and skills of effective coping with it increases the risk of restenosis. Psychological intervention directed at developing the skills of coping with stress should be a part of the therapy in patients after PTCA.

[Risk of hypertension after heart transplantation in the follow-up period]. / Ryzyko nadcisnienia tetniczego po przeszczepieniu serca w obserwacji odleglej.

From October 1988 to March 2000, 58 patients underwent orthotopic heart transplantation (HTX). Data of 220 heart recipients with the follow up > or = 3 months after HTX were analyzed using the average values of blood pressure measured with the sphigmo-manometer. 65% of patients were diagnosed with the hypertension (HA). 39.9% of those patients (NTA group) had the systolic blood pressure < or = 140 mmHg and diastolic blood pressure < or = 90 mmHg during pharmacotherapy. 60.1% of hypertensive patients (NTB group) had the systolic pressure > 140 mmHg and/or diastolic pressure > 90 mmHg despite pharmacotherapy. 35% of all patients had normal blood pressure after HTX (HNA group). Patients with hypertension were older and the end stage ischemic cardiomyopathy was more frequently indication for HTX. Significantly more females were in NTA group. We observed no influence of the daily dose of cyclosporine or other immunosuppressive drugs on HA. The average blood concentration of cyclosporine A and mycophenolate mofetil was similar in all groups. The calcium channel blockers and inhibitors of angiotensin converting enzyme were main tool of pharmacotherapy used. In NTA group calcium channels blockers were used more frequently. In NTB group there was a statistically significant higher blood level of creatinine. After HTX there is a high risk of HA, which: increases with age, with the ischemic cardiomyopathy as indication to HTX, is significantly higher in males, there is no correlation between HA and the dosage and blood level of cyclosporine, increases with kidney insufficiency. In monotherapy calcium channel blockers seem to be especially effective.

[Clinical outcome in patients after single vessel PTCA with multiple stent implantation]. / Ocena chorych leczonych angioplastyka wiencowa i implantacja dwóch i wiecej stentów do jednej tetnicy.

Multiple stenting in a coronary artery may improve the angiographic result of unsatisfactory percutaneous coronary angioplasty (PTCA) but little is known about its clinical outcome. We evaluated 42 patients who underwent multiple contiguous stent implantation (2-4 stents) within a single coronary artery in order to achieve optimal vessel reconstruction. Procedural success rate was 95%. In-hospital events included myocardial infarction in 2 patients (5%) and acute stent thrombosis in 2 patients (5%). Acute stent thrombosis was successfully treated with repeated PTCA and abciximab infusion. The mean stented segment length was 33.5 +/- 9.9 mm. In 23 patients (54.8%) stents were implanted due to abrupt or threatened artery closure (bailout), in 9 (21.4%) following total chronic artery occlusion and in 10 (23.8%) due to a suboptimal result of angioplasty (i.e. provisional stenting). The bailout stent implantation was most frequent in the left anterior descending artery (15 out of 23 patients, i.e. 65.2%). Long-segment multiple stenting was performed mainly in the right coronary artery to maintain recanalization after the chronic artery occlusion (6 out of 9 patients, i.e. 66.7%). Mean data for all studied patients revealed a significant improvement in the exercise stress test parameters after the procedure (exercise time: 8.5 +/- 3.9 vs. 11.4 +/- 3.5 min, maximal load: 5.4 + 3.0 vs. 7.6 +/- 2.9 METS, percent of the maximal predicted effort 75.5 +/- 10.3 vs. 83.2 +/- 9.2%, p < 0.01 for all). Although the sub-group analysis showed a significant increase in exercise test parameters in patients treated with stent implantation due to the bailout (p < 0.05), the increase did not reach statistical significance in the group of patients who underwent multiple stent implantation to maintain recanalization after chronic artery occlusion or to improve the result of angioplasty. At 14.9 +/- 8.3 months follow-up restenosis was found in 14 (33%) patients. It was successfully treated either with re-PTCA (10 patients, i.e. 23%) or with bypass surgery (4 patients, i.e. 10%). Interestingly, the length of the stented segment was not significantly higher in those patients who developed restenosis. No patient died sustained myocardial infarction or subacute stent thrombosis. We conclude that multiple stent implantation is a safe procedure, with an insignificant complication rate. Best outcome is seen when multiple stent implantation is performed for the left anterior descending artery bailout. Reconstruction of the right coronary artery due to chronic total occlusion usually requires multiple stent implantation. When multiple contiguous stent implantation is performed due to the suboptimal PTCA result, it does not seem to improve the clinical outcome as evaluated by exercise stress test. Although the risk of restenosis is increased, subacute stent thrombosis seems rare with multiple one-vessel stenting.

[Stents for treatment of transluminal percutaneous coronary angioplasty (PTCA) complications]. / Stenty w leczeniu powiklanej angioplastyki wiencowej (PTCA).

UNLABELLED: This study describes initial results of stent implantation in bailout situations in 38 patients with obstructive dissection after percutaneous transluminal coronary angioplasty (PTCA). Before stent introduction 1.8% of all patients after PTCA required emergency bypass grafting (CABG) because of postprocedural complications. In 1997 the rate of such emergency operations decreased to only 0.5% (p < 0.05). The success rate of stent deployment in patients included in the study was 95%. Mean final inflation pressure used for stent deployment was 12.0 +/- 2.3 atm. After stent implantation average residual stenosis was -0.81 +/- 5.75%. Of the 38 patients, 15 (40%) were treated before stent implantation with prolonged inflations with perfusion catheter. Bailout stenting was performed in 10 (25%) patients undergoing PTCA for restenotic lesions. The stents were placed in the left anterior descending coronary artery in 26 patients (69%), left circumflex coronary artery in 3 patients (8%), and in the right coronary artery in 9 patients (23%). Before bailout stenting 28 patients (75%) presented with type C and D dissection. One patient (2.5%) developed acute stent thrombosis. No episodes of subacute stent thrombosis were noted. During six-months clinical follow up no death and no Q-MI were observed. Angiographic follow up restenosis rate was 13/30 (43%), predominantly in patients treated with prolonged perfusion balloon inflations before stent implantation. The incidence of repeated PTCA and elective CABG due to restenosis was 12/30 (40%) and 1/30 (3%), respectively. There were no vascular complication at the puncture site. IN CONCLUSION: the introduction of coronary stenting has provided an excellent non-surgical modality for treatment of imminent or acute vascular closure complicating coronary angioplasty.

[Coronary bypass grafting after failed percutaneous angioplasty (PTCA)]. / Pilne pomostowanie tetnic wiencowych po powiklanych angioplastykach wiencowych (PTCA).

Between January 1991 and September 1997, in the Cardiovascular Surgery Department of the Institute of Cardiology of Jagiellonian University Medical School, 23 patients underwent emergency CABG due to acute myocardial ischaemia in result of failed PTCA. Over the same period of time invasive cardiologists performed 1883 PTCAs out of which 23 (1.2%) were emergency cardiosurgical procedures, and in 38 patients, stents were implanted in the damaged coronary arteries. The patients' age ranged from 37 to 67 years (median 52.2). In all patients good left ventricular function was preserved, median ejection fraction being 64%. Two patients required IABP to support left ventricular function. 1-4 bypass grafts were implanted (median 1.9 per patient). In one patient, internal mammary artery was collected and then implanted into anterior interventricular branch. The most common complication was myocardial infarction which occurred in 12 patients (52%). In ten patients low output was observed postoperatively. One operated patient (a female died (4.3%). The mean time of hospitalization was 11 days. Emergency myocardial revascularisation procedures performed after failed PTCA, bring higher risk of mortality and dangerous postoperative complications.