Cystatin C Is Associated with the Extent and Characteristics of Coronary Atherosclerosis in Patients with Preserved Renal Function.

Cystatin C (CysC), an endogenous inhibitor of cysteine proteases and a sensitive and accurate marker of renal function, is associated with the severity of coronary atherosclerosis assessed by angiography and future cardiovascular events according to previous studies. We aimed to evaluate the association between CysC levels and coronary plaque volume, composition and phenotype assessed by intravascular ultrasound and intravascular ultrasound-derived virtual histology in patients with preserved renal function. Forty-four patients with angiographically documented coronary artery disease and complete intravascular imaging were included in the study. Patients were categorized into tertiles by CysC levels. Subjects in the high CysC tertile had significantly higher mean plaque burden (48.0 % ± 6.9 vs. 42.8 % ± 7.4, P = 0.029), lower mean lumen area (8.1 mm2 ± 1.7 vs. 9.9 mm2 ± 3.1, P = 0.044) and a higher number of 5-mm vessel segments with minimum lumen area < 4 mm2 (17.9 ± 18.9 vs. 6.8 ± 11.7, P = 0.021) compared to patients in the lower tertiles. In addition, CysC levels demonstrated significant positive correlation with the mean plaque burden (r = 0.35, P = 0.021). Neither relative, nor absolute plaque components differed significantly according to CysC tertiles. The Liverpool Active Plaque Score was significantly higher in the high CysC tertile patients (0.91 ± 1.0 vs. 0.18 ± 0.92, P = 0.02). In conclusion, our study demonstrated a significant association of increased CysC levels with more advanced coronary artery disease and higher risk plaque phenotype in patients with preserved renal function.

Feasibility of cerebral blood flow and oxygenation monitoring by continuous transcranial Doppler combined with cerebral oximetry in a patient with refractory cardiac arrest treated by extracorporeal life support.

The adequacy of cerebral blood flow and the level of regional oxygen saturation during CPR and early post-resuscitation phases assuring favorable neurological outcome are not known. We demonstrate the feasibility of cerebral blood flow and oxygenation monitoring by a continuous transcranial Doppler combined with cerebral oximetry in a patient with refractory cardiac arrest treated by extracorporeal life support.

Prediction of coronary vessel involvement on the basis of atherosclerosis risk factor analysis.

The prediction of coronary vessel involvement by means of noninvasive tests is one of the fundamental objectives of preventive cardiology. This review describes the current possibilities of coronary vessel involvement prediction by means of ultrasonographic examination of carotid arteries, analysis of polymorphisms in the genes encoding enzymes responsible for production of nitric oxide and carbon monoxide and assessment of levels of certain proinflammatory cytokines. In the presented work these noninvasive markers are correlated with the extent of coronary vessel involvement as assessed by coronary angiography, intravascular ultrasound and virtual histology (Fig. 5, Ref. 40).

Genetic variants in haem oxygenase-1 and endothelial nitric oxide synthase influence the extent and evolution of coronary artery atherosclerosis.

The genetic basis for atherosclerosis development and progression is poorly characterized. We aimed to assess the relationship between endothelial nitric oxide synthase (ENOS) 894 G/T, haem oxygenase-1 (HO1) dinucleotide-length promoter polymorphisms and coronary artery atherosclerotic invol vement and its changes during statin therapy. Coronary angiography, intravascular ultrasound (IVUS), IVUS-derived virtual histology (VH) and genetic polymorphism analysis were performed at study entry. Patients were randomized 1:1 to standard or aggressive hypolipidaemic treatment, and a follow-up evaluation was performed after twelve months. Plaque magnitude was significantly higher in carriers of HO1 risk variants when compared with carriers of the protective variants (< 25 GT repeats). Similarly, the total coronary atherosclerotic burden was significantly greater in HO1 risk variant carriers than in HO1 protective variant carriers. Both parameters did not differ with respect to the ENOS genotype. A higher prevalence of thin-cap fibroatheroma (TCFA) in HO1 risk variant carriers was observed, compared with the HO1 protective variant carriers. The prevalence of TCFA was not influenced by the ENOS genotype. Baseline plaque composition did not differ significantly with respect to both polymorphisms. Significant interactions between plaque composition changes and ENOS and HO1 genotypes were observed during statin treatment. In conclusion, the protective HO1 promoter polymorphism correlates with a lower coronary artery plaque burden, whereas the protective ENOS 894 G/T polymorphism seems to favourably influence changes of coronary artery plaque composition during statin therapy, but has no significant correlation to the magnitude of coronary atherosclerosis.

Reduced thrombin generation and soluble P-selectin after intravenous enoxaparin during PCI.

PURPOSE: The objective of our study was to identify changes in the coagulation and serum concentration of soluble P-selectin (sP-sel) after i.v. bolus of 0.75 mg/kg enoxaparin in a group of 33 patients during PCI. METHODS AND RESULTS: As compared to baseline, i.v. enoxaparin increased anti -Xa activity and FIIa inhibition together with APTT and thrombin time tests within 20 min, that persisted for 60 min. At 6 h, the results of all tests had returned to baseline. In contrast, the level of prothrombin fragments (F1 + 2) decreased persistingly for a period of 6 h (baseline 1.19 ± 0.42 nmol/l, after 20 min 1.03 ± 0.46 nmol/l, after 60 min 1.06 ± 0.43 nmol/l, after 6 h 0.95 ± 0.40 nmol/l, p < 0.001 vs. baseline for all values). In addition, i.v. enoxaparin decreased serum sP-sel level (baseline 111.80 ± 37.05 ng/ml, after 20 min 87.80 ± 33.17 ng/ml, after 60 min 86.45 ± 29.15 ng/ml, after 6 h 92.24 ± 31.34 ng/ml, p < 0.001 vs. baseline value for all). sP-sel level mildly correlated with both F Xa inhibition (r = -0.275, p < 0.05) and F1 + 2 level (r = 0.274, p < 0.05). CONCLUSION: Intravenous enoxaparin induced target F Xa inhibition (>0.6 IU/ml) for 60 min in 82% of study patients. During the 6 h of monitoring, a decrease of thrombin generation (F1 + 2) and sP-selectin levels were observed.

Fabry disease - Vascular manifestations.

Fabry disease (FD) is an X-linked disorder of glycosphingolipid metabolism caused by the deficient activity of alpha-galactosidase A which results in the accumulation of neutral glycosphingolipids in various tissues leading particularly to vasculopathy, cardiomyopathy, neuropathy, and chronic kidney disease. It results in substantial morbidity and premature death in affected patients. Although there are some signs and symptoms suggestive of FD including painful crisis, angiokeratomas, and corneal changes, the majority of FD complications are non-specific (left ventricular hypertrophy, conduction abnormalities, vascular spasms, proteinuria, renal insufficiency), which is why FD still remains largely underdiagnosed. The mechanism by which accumulating glycosphingolipids cause multiorgan disorder is not yet completely understood as it cannot be explained by pure substrate storage. Besides standard therapy of different medical problems in FD patients, specific enzyme replacement therapy has been introduced in the last few years.

Intravascular ultrasound assessment of coronary artery involvement in Fabry disease.

AIM: We used intravascular ultrasound (IVUS) to characterize coronary artery involvement in patients with Fabry disease (FD). METHODS: Nine FD patients (5 women) were matched to 10 control patients (5 women) chosen from our IVUS database. Standard volumetric IVUS analyses were performed along with assessment of plaque echodensity. RESULTS: Plaques in FD patients were diffuse and hypoechogenic compared with more focal and more echogenic lesions in control patients. Echogenicity of plaques was significantly lower in FD patients (median 30.7 +/- 12.9 vs 55.9 +/- 15.7, p = 0.0052, mean 37.2 +/- 15.6 vs 66.2 +/- 13.3, p = 0.0014). Diffusiveness was assessed as differences between mean and median plaque burden versus the plaque burden in each of the analysed cross-sections. These differences were lower in FD vs controls (5.8 +/- 4.8 vs 8.7 +/- 6.6, p < 0.001 for mean, and 5.8 +/- 4.9 vs 8.8 +/- 7.3, p < 0.001 for median) indicating a more diffuse involvement. The occurrence of lipid cores was significantly higher in FD patients than in controls (2.4 +/- 1.5 vs 1.0 +/- 0.94, p = 0.02). CONCLUSION: IVUS showed diffuse hypoechogenic plaques in patients with FD. The explanation may be higher lipid content in plaques and accumulation of glycosphingolipid in smooth-muscle and endothelial cells.

[Overcooling during mild hypothermia in cardiac arrest survivors--phenomenon we should keep in mind]. / Nadmerné othlazení behem mírné hypotermie po srdecní zástave--fenomén zasluhující pozornost.

BACKGROUND: Mild hypothermia (MH) in cardiac arrest survivors has became a routine part of early postresuscitative support. Overcooling is a frequent phenomenon with the unknown outcome. AIM OF THE STUDY: To analyze the incidence and outcome ofovercooling below body core temperature (BT) of 32 degrees C. MATERIAL AND METHODS: We performed retrospective analysis of all 56 consecutive cardiac arrest survivors treated by MH who reached therapeutic BT in the 2nd Department of Internal Medicine, General Teaching Hospital, Prague. MH was initiated as soon as possible after the return of spontaneous circulation to reach BT of 33 degrees C followed by maintainance of BT 32-34 degrees C for 12 hours. Patients were cooled by surface cooling via ice-packs and by interavenous infusion of cold crystaloids. RESULTS: Overcooling below BT of 32 degrees C was observed in 23 patients (41%). This group of patients had more frequently asystole as the initial rhythm (34.8 vs 9.1%), more frequently were cooled by combinatory cooling approach (56.5 vs 27.3%), more frequently had lower baseline BT (35.3 +/- 1.3 vs 36.2 +/- 1.2 degrees C), higher cooling rate (the interval required for a decrease of BT by 1 degrees C 61.5 +/- 53.1 vs 90.1 +/- 50.0 min) (all p < 0.05) than patients with proper profile of BT during MH. Overcooling was independent negative predictor of discharge favourable neurological outcome (OR 0.16, 0.022-0.77, p = 0.037). CONCLUSION: Induction of MH by conventional cooling approach is burdened by high risk of overcooling. This phenomenon is probably associated with worse outcome.

Induction of mild hypothermia in cardiac arrest survivors presenting with cardiogenic shock syndrome.

BACKGROUND: Induction of mild hypothermia (MH) in patients resuscitated from cardiac arrest improves their outcome. However, benefits and risks of MH in patients who remain in cardiogenic shock after the return of spontaneous circulation (ROSC) are unclear. We analysed all cardiac arrest survivors who were treated with MH in our intensive coronary care unit (CCU) and compared the outcome of patients with cardiogenic shock syndrome (CSS) with those who were circulatory stable. METHODS: We performed retrospective analysis of all consecutive cardiac arrest survivors treated by MH in our CCU from November 2002 to August 2006. They were classified into two groups, according to whether they met the criteria for cardiogenic shock or not before MH initiation. RESULTS: Out of 56 consecutive patients, 28 fulfilled criteria of cardiogenic shock before MH initiation (group A) and 28 were relatively stable (group B). In-hospital mortality was 57.1% in group A and 21.4% in group B patients (P=0.013). Favourable neurological outcome anytime during hospitalization was found in 67.9% of group A patients and in 82.1% of group B subjects (P=0.355). Favourable discharge neurological outcome was reached in 39.3% in group A and in 71.4% in group B (P=0.031). The complication rate in both groups did not differ. CONCLUSION: While in-hospital mortality in cardiac arrest survivors treated by MH was expectably higher in those with cardiogenic shock than in stable patients, the favourable neurological outcome during hospitalization was comparable in both groups. Therefore, induction of MH should be considered in cardiac arrest survivors with CSS after ROSC.

[Regression of atherosclerotic plaques during treatment with statins]. / Regrese aterosklerotických plátu pri lécbe statiny.

Atherosclerosis and its complications represent the most frequent cause of death in the developed countries. Pathophysiology of the atherosclerosis development has been described in details. Much less is known what is the extent of reversibility of pathophysiological changes. Several angiographic studies have proved that statin administration can slow down the progression of the coronary arteries atherosclerosis. However, only intravascular ultrasound analysis is able to give a detailed description of atherosclerotic plaque development during the treatment with statins. Studies have shown apparent stagnation of atherosclerosis progression and in voluminous plaques also signs of regression. Beside changes in the size of atherosclerotic plaques, alteration in their chemical composition was described. During the treatment with statins, amount of lipids in plaque decreases, which indicates the stabilisation of plaques. Plaques are less prone to a rupture and to the subsequent development of an acute coronary syndrome. Beside statins, which influence namely LDL cholesterol, attention is given to drugs enabling to elevate HDL cholesterol level, because it is the way in which cholesterol is transported from tissues back to the liver. It appears that elevation of HDL cholesterol level could bring about more effective regression of atherosclerotic plaques and together with stagnation of the plaque progression it can significantly improve the conservative methods in the treatment of atherosclerotic disease of the coronary and peripheral arterial system.

How does delaying treatment affect the long-term prognosis for patients with acute myocardial infarction treated with primary coronary angioplasty?

BACKGROUND: The benefit of thrombolysis in patients with acute myocardial infarction (AMI) strongly depends on the time from the onset of symptoms to the initiation of treatment. For AMI patients treated with percutaneous coronary interventions (PCI) this delay of treatment seems to be important only up to a certain time level. AIM: To assess the effects of time to treatment of AMI with PCI on the short- and long-term prognosis. METHODS: We followed 339 consecutive AMI patients treated with PCI from 1995 to 1999 in our centre. Patients were divided into five groups according to the time to treatment and ischaemic time (time from symptom onset to reperfusion). RESULTS: Time to treatment <90 min was achieved in 35 (10.5%) patients; 91-210 min in 105 (31%); 211-330 min in 72 (21%); 331-690 min in 74 (22%); and >691 min in 53 (15.5%) patients. According to ischaemic time, the patients were divided into groups: <2 h, 2-4 h, 4-6 h, 6-12 h, and >12 h. The ejection fraction of the left ventricle 3-5 days after AMI was 50%, 51%, 45%, 40%, and 46%, and the 30 day mortality - 5.7%, 2.9%, 11.1%, 10.8%, and 11.3%, respectively. Compared with patients treated later, patients with time to treatment <3.5 h had a significantly higher rate of TIMI 3 flow (93.6% vs 83.9%, p=0.007), lower 30-day mortality (3.6% vs 11.1%, p=0.012), lower 3-year mortality (8.6% vs 19.1%, p=0.003), lower frequency of heart failure during hospitalisation (11.4% vs 28.1%, p<0.001) as well as lower maximal level of creatine kinase (32+/-29 vs 44+/-39 micro kat/l, p=0.005). CONCLUSIONS: The success rate of primary PCI to achieve normal flow in an infarct-related artery is high, but it decreases when treatment is started later than 3,5 h from AMI onset. The short-term and long-term mortality as well as the incidence of heart failure during the acute phase of MI are the lowest when PCI is started within 3,5 h from the onset of symptoms.

[Effect of primary coronary angioplasty on long-term prognosis in patients with diabetes mellitus]. / Vliv prímé koronární angioplastiky na dlouhodobou prognózu nemocných s diabetes mellitus.

OBJECTIVES: To investigate feasibility and safety of primary PCI in diabetic patients. BACKGROUND: Diabetic patients with acute myocardial infarction (AMI) have been shown to be at high risk for adverse clinical outcomes. Limited data is available on long term prognosis of diabetics treated with primary PCI. METHODS: Retrospective analysis of consecutive 67 diabetic patients and 211 non diabetic patients treated with primary PCI from 1/1995 to 12/1999, follow up for 38 +/- 12 months. RESULTS: The baseline characteristics were comparable in both groups. The mean age was 62 years in diabetic patients and 59 years in non diabetic patients. Hypertension (50% vs. 36%, p = 0.05), contraindications to thrombolytic treatment (13.4% vs. 5.7%, p = 0.037), cardiogenic shock (16.4% vs. 7.1%, p = 0.023), multivessel disease (34% vs. 23%, p = 0.07) and longer time delay to treatment (240 vs. 180 min., p = 0.05) were more often present in diabetic group. 47% of diabetic and 42% of nondiabetic patients received stents. The TIMI 2 or 3 flow rates were reached in 91% of diabetic patients and in 90% of nondiabetic patients, but TIMI 2 flow was found more often in diabetics (9% vs. 2.4%, p = 0.016). Higher rate of bleeding complications leading to significant change in the blood count (7.5% vs. 1.4%, p = 0.01) and higher 30 day mortality (11.9% vs. 5.2%, p = 0.05) was observed in diabetic group. However when the shock patients were excluded from the analysis, the 30 day mortality was different insignificantly in both groups (4.5% vs. 2.4%, p = 0.36). During follow up of 259 acute phase survivors 24 patients died. There was a trend to higher total long term mortality (22.3% vs. 13.2%, p = 0.07) and higher rate of nonfatal reinfarction (13.4% vs. 6.2%, p = 0.05) in diabetic group. CONCLUSIONS: Primary PCI is safe and effective treatment of diabetic patients presenting with AMI. The higher rate of slow flow in infarct related artery after PCI observed in diabetics can be one of reasons for higher 30 day mortality in this group. Mean ischemic time in diabetics is behind the 4 hour border, where the possible benefit from reperfusion decreases. The main reason for higher mortality in our diabetic group was the higher rate of cardiogenic shock. Higher risk of bleeding complications at puncture site in diabetic patients can be explained by the lower quality of vessel wall.

[Comparison of the morphology of atherosclerotic plaques in patients with stable angina pectoris and acute coronary syndrome using intravascular ultrasonography]. / Srovnání morfologie aterosklerotických plátu u nemocných se stabilní anginou pectoris a akutním koronárním syndromem pri vysetrení intravaskulárním ultrazvukem.

The article summarises present knowledge on the differences in the structure of atherosclerotic plaques in patients with stable angina pectoris and in those with acute coronary syndrome during intravascular ultrasound examination. Authors describe differences in the pathologic anatomy and also in the clinics. The review includes pictures of the typical structural features and references of papers with similar topics.

[Cardiogenic shock--a complex therapeutic approach]. / Kardiogenní sok--komplexní terapeutický prístup.

Cardiogenic shock belongs to the most severe and immediately life-threatening complications of the acute myocardial infarction. Despite development of modern diagnostic and therapeutic methods the incidence and mortality of cardiogenic shock has not significantly declined in the past decades. Early reperfusion strategy with percutaneous revascularization has become a cornerstone of therapy. The complex approach to cardiogenic shock comprises pharmacological and mechanical hemodynamic support, ventilatory support utilizing new ventilator regimens, metabolic and renal support/replacement with continuous renal replacement therapies and psychological, eventually psychopharmacological support. All these measures enable prevention of the multiple organ failure syndrome development and positively influence high mortality of patients suffering from cardiogenic shock.

[Comparison of the occurrence of positive and negative vascular remodeling in patients with stable vs unstable angina pectoris]. / Srovnání výskytu pozitivní a negativní cévní remodelace u nemocných se stabilní vs. nestabilní anginou pectoris.

BACKGROUND: The vascular remodelling refers to the increase or decrease in EEM (external elastica membrane) area that occurs during development of atherosclerosis. The positive remodeling, which was thought only as a compensatory factor during atheroma development, was also found as a one of the main features of unstable plaque. The intravascular ultrasound is very good tool to measure different type of arterial remodelling. These findings correlate with histologic post-mortem specimen with excellent results. AIM OF THE STUDY: To correlate the remodelling index from patients suffered from stable angina pectoris (SAP) and from patients suffered from unstable angina (UA). METHOD: We performed IVUS in 51 patients. In the group of patients with unstable angina were included patients with worsening angina symptoms in last six weeks or with angina in rest. We used IVUS--endosonics In-Vision with 30 MHz probe Awanar with mechanical pull-back. We studied the occurrence of positive remodelling, negative remodeling (an index that describes remodeling is expressed as: lesion EEM CSA/reference EEM CSA. If the lesion EEM area is greater than the reference EEM area, positive remodelling has occurred, and the index will be > 1.0. If the lesion EEM area is smaller than the reference EEM area, negative remodelling has occurred, and the index will be < 1.0). RESULTS: We performed the intravascular ultrasound in 51 patients, 22 patients (43.1%) with unstable angina (UA) and in 29 patients (56.9%) stable angina (SAP). The positive remodelling was found in 14 patients (63.6%) in UA group vs. 5 patients (17.2%) in group with SAP, p < 0.05. The negative remodelling was found in 6 patients (27.3%) in UA group vs. 23 patients (79.3%) in SAP group, p < 0.05. CONCLUSION: Positive remodelling is more often found in patients with UA vs. in patients with SAP. Positive arterial remodelling is therefore one of the features of unstable atherosclerotic plaque.

[Contrast nephropathy and its prevention]. / Kontrastová nefropatie a moznosti její prevence.

Contrast-induced nephropathy is one of the adverse events of diagnostic and therapeutic intravascular application of contrast agent. In general, the condition was defined as an increase in the serum creatinine concentration of more than 44 mmol/l or of more than 25% within 48 hours after the contrast agent administration. Other cause of creatinine increase should be excluded. Contrast-induced nephropathy has been reported to be the third leading cause of acute nephropathy in hospitalized patients, occurring at a rate of 1-6% in unselected population and of 30-50% in high-risk patients. One year mortality can be as high as 45% in high-risk patient population. The most important risk factors are chronic renal insufficiency, diabetes mellitus and high volume of contrast agent. Clinical presentation is mostly asymptomatic, but in some patients acute renal failure with necessity of hemodialysis can occur. Prevention is underlying tool in reducing of contrast-induced nephropathy incidence. It is based on the identification of risk patients, stop of medication which can increase risk of contrast-induced nephropathy and proper hydratation of patients before, during and after the contrast agent administration. In high-risk patients, non-ionic and low-osmolarity contrast agent should be used. Several clinical studies testing different drugs to prevent contrast-induced nephropathy were performed, but no convincing result has been found. Promising substancies are N-acetylcysteine and fenoldopam.

[Direct percutaneous transluminal coronary angioplasty in patients with acute myocardial infarct treated at the Cardiac Center of the General Medical School Hospital in Prague: a 1-year retrospective study]. / Prímá perkutánní transluminální koronární angioplastika u pacientu s akutním infarktem myokardu v Kardiocentru Vseobecné fakultní nemocnice Praha: jednorocní retrospektivní studie.

UNLABELLED: Direct percutaneous transluminal coronary angioplasty (d-PTCA) in patients with acute myocardial infarctions (AIM) has become an alternative of thrombolytic treatment. If the involved department has adequate experience the success rate of the procedure is high and the immediate and long-term results are better than those of thrombolysis. Moreover contrary to thrombolytic treatment successful percutaneous coronary intervention in AIM is more beneficial for patients also later than 6 hours after the development of infarction pain. In the Cardiocentre of the General Faculty Hospital (GFH) patients with AIM are constantly attended, i.e. those indicated for reperfusion therapy are treated solely by the d-PTCA method. OBJECTIVE AND METHOD: Retrospective analysis of d-PTCA in AIM made during the annual period from Jan. 1 2000 to Dec. 31 2000. Into the observation study patients were included with clinical and/or ECG signs of AIM when the period from the onset of pain to the beginning of intervention did not exceed 12 hours. All patients were given before the procedures 500 mg of acetylsalicylic acid and 10,000 u. heparin. Cardiac catheterization was implemented by the percutaneous Seldinger technique via the a. femoralis l.dx., in exceptional cases from the left femoral artery. An approach via the a. radialis and/or a. brachialis was not used in any of the patients. From the investigation patients were excluded who had before the percutaneous coronary intervention (PCI) a thrombolytic preparation (so-called rescue-PTCA). RESULTS: During the mentioned period in the Cardiocentre of the GFH a total of 673 PTCA were performed, incl. 127 (18.9%) d-PTCA in patients with AIM. In the mentioned group of 127 patients subjected to intervention were 87 (68.5%) men and 40 (31.5%) women. The mean age of the men was 59.1 +/- 12 years and the mean age of the women 68.2 +/- 12 years. As to the main risk factors of coronary atherosclerosis arterial hypertension was present in 48%, smoking in 42%, diabetes in 23% and hyperlipoproteinaemia in 31% of the treated patients. More than one third of the patients had a history of myocardial infarction (38%). The infarcted artery was the r. interventricularis anterior (LAD) in 51 (40.2%), the right coronary artery (RCA) in 54 (42.5%), the r. circumflex (LCX) in 16 (12.6%), the left main coronary artery in 2 (1.6%) and the bypass in 4 (3.1%). Multiple coronary affections were recorded in 80 (63%) patients, affections of one artery in 47 (37%). Primary procedural success (flow TIMI 3/2) was achieved in 121 patients (95.3%). Normal flow through the infarcted artery TIMI 3 was achieved in 118/127 (85.8%) patients. In 91 (71.7%) into the infarcted artery a coronary stent was implanted, during hospitalization no subacute stenosis of the stent developed. The mean period between the onset of infarction pain--injection was 4.4 +/- 2.3 hours. The mean period of the entire procedures was 48 +/- 14.5 minutes. As contrast material only non-ionic contrast substances were used (Iomeron 350) with a mean consumption of 150 ml per patient. The mean skiascopic time was 13.6 +/- 1.8 min. A total of 9 (7.1%) patients were treated with GP IIb/IIIa receptor blockers (abciximab). The total hospitalization mortality of the intervened group was 7.1% (9 patients). In a sub-group of 9 patients who at the onset of the procedure were in cardiogenic shock 3 (33%) died. The hospitalization mortality of the sub-group of patients with AIM without cardiogenic shock, treated with d-PTCA was 5.1% (6/118). During hospitalization the authors did not observe any intracranial haemorrhage. DISCUSSION: The group of subjects with AIM subjected to catheterization who are treated by d-PTCA is relatively numerous in our department. According to a number of clinical studies successful d-PTCA in AIM gives better short-term and long-term results as compared with thrombolytic therapy. The primary success rate of d-PTCA was high and the hospital mortality was low and comparable with contemporary data in the literature. CONCLUSION: Direct PTCA is effective treatment in patients with acute myocardial infarction. The authors results confirm the high procedural success rate and acceptable hospital mortality. These favourable results of an invasive approach to treatment of AIM must be compared in future with bolus thrombolytic treatment by new types of thrombolytic preparations in combination with anti-platelet treatment with blockers of platelet glycoprotein receptors IIb/IIIa with/or without subsequent percutaneous coronary intervention.