PubMed Health⌕ Search

Biomedical subjects

Witold Ruzyłło

Publications and source records attributed to Witold Ruzyłło.

At least 19 recordsLinked to original sources

Serum tissue inhibitor of metalloproteinases-1 and higher risk features of coronary plaque: a volumetric multivessel intravascular ultrasound study.

AIMS: The purpose of this study was to determine the relationship between higher-risk features of coronary plaque and serum levels of matrix metalloproteinase (MMP) family enzymes in the stable angina patients. METHODS AND RESULTS: In 36 patients, 75 coronary lesions were assessed by intravascular ultrasound. For each of the plaques remodelling index, mean calcium arc and plaque burden were measured. Positive remodelling and the values of the calcium arc and plaque burden above the respective medians were regarded as the higher-risk features and summarised for each lesion. Serum levels of MMP-2, -3, -7, -9, and tissue inhibitor of MMP (TIMP)-1 and -2 were measured in all patients. TIMP-1 level was the independent predictor of presence of a lesion with positive remodelling (OR 1.032; 95% CI: 1.004-1.061) and of a lesion with higher plaque burden (OR 1.026; 95% CI: 1.003-1.049) in a given patient. Whereas, MMP-2 level was an independent predictor of presence of a lesion with higher calcium arc (OR 1.035; 95% CI: 1.001-1.071). TIMP-1 level (p=0.003) was also an independent predictor of a number of higher-risk features in the highest-risk plaque in a given patient. CONCLUSIONS: TIMP-1 level correlates with clustering of plaque features associated with higher risk of complications in stable angina patients.

Angina Pectoris↗

White blood cell count adds prognostic information to the thrombolysis in myocardial infarction risk index in patients following primary percutaneous coronary intervention (ANIN Myocardial Infarction Registry).

AIMS: To determine the relationship between baseline white blood cell (WBC) count, Thrombolysis in Myocardial Infarction (TIMI) risk index, and 30-day mortality in unselected patients with ST-elevation myocardial infarction (STEMI) treated with primary mechanical reperfusion (PCI). METHODS AND RESULTS: 903 patients from prospective registry admitted for primary PCI to a tertiary cardiological center. Both baseline WBC count and TIMI risk index data were dichotomized about the respective medians. Overall 30-day mortality was 4.3%. Higher WBC count was associated with adverse clinical outcome (6.3% vs. 2.4%; Kaplan-Meier p=0.004) as were higher TIMI risk index values (7.2% vs. 1.4%; Kaplan-Meier p<0.00001). In addition, median WBC count stratified patients within TIMI risk index strata into very low risk (0%), intermediate risk (3.3%) and high risk (11%) (Kaplan-Meier p=0.023 and p=0.005 for comparison of lower and higher WBC count within TIMI risk index stratas). In multivariate analysis WBC count provided independent and additional to TIMI risk index predictive information (Hosmer-Lemeshow p=0.57 and p=0.88 respectively for predictive value of TIMI risk index alone and combined with WBC count). Other independent predictors of death were current smoking (RR 0.33; 95% CI: 0.13-0.87) and previous MI (RR 3.13; 95% CI: 1.28-7.69). CONCLUSIONS: WBC count may be a simple and useful tool for risk stratification in STEMI patients, providing additional to established risk index prognostic information. Our findings stress the strong correlation of inflammation and poor outcome in STEMI patients, which may indicate directions of development of new therapies.

Aged↗

Coronary artery stent placement as a treatment of acute coronary syndrome in course of variant angina.

High doses of calcium antagonists and nitrates are the treatment of choice in vasospasm angina when no stenosis or mild stenosis is present. In ca. 5-30% patients this kind of treatment is not effective. We present five cases of variant angina with acute coronary syndrome in patients despite standard pharmacological treatment. These patients also did not respond for intracoronary nitroglycerine injection. They were successfully treated with stent implantation in place of vasospasm. Our observations indicate that early enough interventional treatment prevent myocardial infarction. In one case in which stent placement was performed 12 h after clinical manifestation myocardial infarction with Q waves and enzymes release occurred. In others, accurately treated with stent implantation, coronary spasm did not produce myocardial damage. We did not see any clinical and biochemical evidence of myocardial infarction.

Angina Pectoris, Variant↗

Determinants of model of renarrowing after beta radiation for in-stent restenosis.

UNLABELLED: It is unknown whether model of renarrowing after beta-radiation for in-stent restenosis (ISR) is influenced by the type of geographic miss (GM). METHODS: In 166 ISR treated with Galileo, serial quantitative coronary angiographic analysis was done. Minimal lumen diameters and lengths were measured for (1) stent, (2) peri-stent subsegments subjected to angioplasty with/without irradiation, and (3) irradiation margins. GM was defined as: (Type 1) edge injury within the 32P source dose fall-off: 2.0 mm inside and outside the source end marker or (Type 2) overt, nonirradiated injury: beyond the outer 2.0-mm long dose fall-off zone. RESULTS: Restenosis rate was 28.3% at 8.9+/-4.5 months with 60% located exclusively outside the stent. Type 1 GM was present in 24.7% of proximal edges, whereas Type 2 in 18.1%. Respective percentages for distal edges were 23.5% and 15.7%. Regardless of presence and type of GM, significant late lumen loss occurred only outside the stent. However, the biggest late lumen loss at the proximal edge was induced by the Type 1 GM (0.65+/-0.79, p<0.001), while proximal Type 2 GM was not associated with edge renarrowing (-0.04+/-0.48, p=NS). Both reference lumen diameter and proximal Type 1 GM influenced restenosis independently (OR 0.47; 95%CI 0.24-0.90; p=0.023 and OR 2.46; 95%CI 1.12-5.40; p=0.025). CONCLUSIONS: Regardless of presence and type of geographic miss, late lumen loss after beta-radiation occurs only outside the stent. However, injury within the proximal 32P dose fall-off but not overt edge injury is associated with the biggest late lumen loss at the respective edge, triggering recurrent restenosis.

Aged↗

Assessment of the inflammatory process by endomyocardial biopsy in patients with dilated cardiomyopathy based on pathological and immunohistochemical methods.

INTRODUCTION: Myocarditis may lead to dilated cardiomyopathy (DCM) in immunogenetically predisposed individuals. The diagnosis of myocardial inflammation is currently based on histopathological and immunohistochemical methods. Previous studies indicate that inflammatory cardiomyopathy occurs in approximately 50% of patients with DCM. AIM: The goal of the study was to assess the inflammatory process in patients with DCM by endomyocardial biopsy using histopathological and immunohistochemical methods. METHODS: Endomyocardial biopsy specimens was examined using routine histopathological methods and immunochemical staining for T lymphocytes (CD3(+), n=84), major histocompatibility complex I (HLA ABC, n=48) and II (HLA DPQR, n=84) antigens and the adhesion molecules ICAM-1 (n=51) and VCAM-1 (n=48) in 84 patients (69 male, 15 female; mean age 35.0+/-10.5 years) with angiographically-confirmed DCM. Familial disease occurrence was noted in 14 (16.7%) patients. Cardiac samples obtained from 18 patients who died of non-cardiovascular causes were used as a control group. RESULTS: Myocarditis was diagnosed, according to the Dallas criteria, in 8 (9.5%) patients. The frequency of inflammatory cardiomyopathy, defined as the presence of >2 CD3(+) T lymphocytes per high-power field (hpf) in myocardial biopsy, was 14.3%. When broader criteria were applied (presence of >2.0 CD3(+) lymphocytes/hpf and/or 1.5 CD3(+) lymphocytes/hpf in multiple foci and increased expression of class I/II HLA), inflammatory cardiomyopathy was diagnosed in 32.1% of patients. Inflammatory activation of the endothelium, indicated by increased expression of at least three adhesion molecules (class I and II HLA, ICAM-1, VCAM-1), was present in 22 (45.8%) patients. The expression of HLA DPQR, HLA ABC and ICAM-1 was observed on the endothelium of capillaries and larger vessels, interstitial cells, and the surface of activated lymphocytes; immunohistochemical reactions were diffuse. In patients with markedly elevated expression of the aforementioned adhesion molecules, the expression was also present on cardiomyocyte cell membranes. VCAM-1 was restricted to the endothelium of individual small veins. The control group did not demonstrate any signs of myocarditis, inflammatory cardiomyopathy or inflammatory endothelial activation. CONCLUSIONS: The application of immunohistochemical methods to myocardial biopsy in order to identify the inflammatory cell phenotype and the presence of adhesion molecules permits the diagnosis of inflammatory cardiomyopathy in 14% or 32% of patients, depending on the criteria used, while conventional pathology allows for this diagnosis in 9% of patients. The observed frequency of inflammatory cardiomyopathy, defined as the presence of >2 CD3(+) T lymphocytes/hpf in the myocardium, was lower (14%) than in previous studies, while the frequency of inflammatory endothelial activation was similar (45%).

Adult↗

[Myocardial microabscesses detected by endomyocardial biopsy in a patient with dilated cardiomyopathy and celiac disease: a case report].

A case of an 18-year-old male with a one-month history of progressive heart failure and suspected viral myocarditis is presented. Myocardial biopsy revealed mononuclear infiltration and the presence of granulocytes with micro-abscesses. Small bowel biopsy and autoimmunological examinations documented the presence of celiac disease. The patient's condition gradually improved following antibiotics, standard heart failure treatment, dental caries therapy and introduction of gluten-free diet.

Abscess↗

Dilated cardiomyopathy caused by LMNA mutations. Clinical and morphological studies.

BACKGROUND: Dilated cardiomyopathy (DCM) is familial in about 20-35% of patients. The most frequently encountered mutations associated with DCM are found in LMNA. AIM: To define the frequency of LMNA mutations in a series of consecutive DCM patients and to evaluate the phenotype of mutation carriers. METHODS: We screened the 12 exons of LMNA in a series of 61 Polish patients with DCM diagnosed angiographically, as well as in two DCM families. RESULTS: Two mutations were detected in 5 mutation carriers (D192G in one proband and Y481Stop in one proband and 3 of his offspring), which represents 3.3% (2/61) of the DCM patients. These mutations were absent from 100 controls. The D192G mutation was found in a 26-year-old patient with mild DCM and heart failure leading to death within two years after onset of symptoms. Mild conduction disease was also present. Ultrastructural analysis of the endomyocardial biopsy showed a striking alteration of nuclear morphology. This finding can explain nuclear fragility and is in agreement with the pathophysiological mechanical hypothesis of LMNA mutations. All four Y481Stop mutation-carriers were affected. Three phenotypes were found: in the proband, cardiac dysrhythmia and pacemaker requirement preceded DCM leading to heart transplantation; the proband's 13-year old daughter had conduction disease (2nd degree A-V block) with subtle skeletal muscle involvement documented by immunofluorescence study; ventricular arrhythmia was detected in the proband's son at the age of 11 and in the proband's daughter at the age of 18. Serum creatine kinase was normal in all mutation carriers.

Adolescent↗

[Reversible dilated cardiomyopathy in a patient with acute, advanced heart failure and intense endothelial inflammatory reaction in endomyocardial biopsy--a case report].

Inflammatory response of the endothelium has been increasingly recognized in the aetiopathogenesis of sporadic dilated cardiomyopathy (DCM). It has been shown that up to 2/3 of patients with DCM have immunohistological evidence of enhanced activation of the endothelium. We present a case of a middle-aged patient with a history of hypertension and hyperlipidaemia who developed sudden significant left ventricular dysfunction following flu-like syndrome. Endomyocardial biopsy revealed no myocarditis, but immunohistological features of endothelial activation were present. Additionally, increasing titers of IgG antibodies against PvB19 were observed. During 18 months of standard heart failure treatment along with statin therapy, we observed a significant recovery of left ventricular systolic function, and in this way, reversible dilated cardiomyopathy.

Biopsy↗

Cumulative incidence of coronary lesions with vulnerable characteristics in patients with stable angina pectoris: an intravascular ultrasound and angiographic study.

BACKGROUND: Development of vulnerable lesion may take place simultaneously at many sites of coronary vasculature, therefore causing multisite instability. The prevalence of the phenomenon in stable angina (SA) patients remains unknown. The aim of our study was to assess, in patients with stable angina, the prevalence of coronary plaques with vulnerable characteristics and to ascertain whether the number of such lesions may accumulate. METHODS: Vulnerable plaques are characterised by positive remodelling on intravascular ultrasound (IVUS) and with complex appearance on angiography. We performed preprocedural IVUS in target lesion of 67 patients with SA (46 males, age 55.9). Remodelling index (RI) defined as vessel area at the target lesion divided by that of average reference segments > or = 1.05 was assumed as positive remodelling. Plaques of > or = 30% stenosis on angiography were classified into complex or smooth groups. RESULTS: Positive remodelling was found in 30 (44.8%) and complex plaque in 16 (23.9%) of 67 target lesions. Multiple complex plaques were present in 21 (31.3%) patients. Plaques with positive remodelling more often were complex on angiography (12/30 vs. 4/37, respectively; p=0.005) and were more often associated by complex plaques at other sites (35/30 vs. 23/37; p=0.04) than the remaining lesions. Moreover, the presence of positive remodelling predicted multiple complex lesions at other sites (OR 5.6; 95% CI 1.7-18.3). CONCLUSION: Multiple coronary plaques with vulnerable characteristics are present in nearly one third of patients with stable angina. Incidence of vulnerable lesions may have cumulative character, i.e. the presence of one vulnerable lesion predicts occurrence of further vulnerable plaques.

Angina Pectoris↗

Implantable cardioverter-defibrillators in patients with hypertrophic cardiomyopathy -- dilemmas and difficulties.

INTRODUCTION: The implantation of a cardioverter-defibrillator (ICD) is an established method of sudden cardiac death (SCD) prevention. The value of ICD therapy in secondary prevention of SCD is unquestionable. Precise identification of high-risk patients and ICD use for primary prevention of SCD, especially in patients with hypertrophic cardiomyopathy (HCM), remain controversial. Problems include the high prevalence of complications associated with ICD implantation and optimal selection of ICDs. AIM: To estimate the frequency and type of complications after ICD implantations in HCM patients in a long-term follow-up. METHOD: The efficacy and safety of ICD therapy were estimated in 46 HCM patients with devices implanted for a secondary (n-18) or primary prevention (n-28) of SCD. RESULTS: During the mean follow-up period of 28.2+/-26.1 months (from 2 to 68) appropriate ICD interventions occurred in 10 (55%) patients of the secondary prevention group and in 3 (10%) patients of the primary prevention group. Complications were documented in 15 (33%) patients. The most frequent were inappropriate ICD interventions recorded in 14 (30%) patients. The causes of these inappropriate ICD shocks were: T-wave oversensing (7 patients), atrial fibrillation with rapid ventricular rhythm (3 patients), lead failure (2 patients), and sinus tachycardia (2 patients). In two patients infections of the ICD pocket requiring removal of the system occurred. Displacement of the lead occurred in one patient. There were no significant differences in the prevalence of complications between the primary and secondary prevention groups or in the number of inappropriate interventions with respect to ICD type. CONCLUSIONS: The high rate of appropriate ICD shocks provides proof of high ICD-based SCD prevention efficacy. There is a high rate of complications observed after ICD implantation with inappropriate interventions being the most frequent among them. This indicates that careful programming of the device as well as the use of a programme with T-wave oversensing prevention should be ensured.

Adult↗

Familial form of arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is characterised by fatty and fibrous infiltration of myocardial muscle. Clinical symptoms include dangerous cardiac arrhythmias and heart failure in the advanced form of the disease. ARVD is genetically determined in at least 50% of cases and is characterised by a marked variability of clinical presentation within one family. AIM: To assess the prevalence of the familial form of ARVD in Poland, the mode of inheritance and the risk of sudden cardiac death as well as heart failure development in asymptomatic patients, in whom ARVD was detected during family screening. METHODS: 211 relatives of 40 patients with ARVD were examined. Thirty two families were identified in which at least two members had the disease. The analysed parameters included family history, physical examination, ECG, echocardiography and magnetic resonance. RESULTS: Abnormalities of the right ventricle and/or cardiac arrhythmias suggesting ARVD were found in 71 subjects (mean age 32.4 years). In 28 cases ARVD was diagnosed. From this group, one patient had aborted sudden death. In the remaining 43 subjects a borderline form of the disease was detected. Of this group, one patient died suddenly. The degree of morphological changes in cardiac muscle correlated with patients' age. CONCLUSIONS: 1. The familial form of ARVD is frequent in Poland. 2. ARVD is inherited in an autosomal dominant mode. 3. Sudden cardiac death may be the first symptom of the disease, even in subjects with borderline ARVD. 4. ARVD is a progressive disease. Concomitant left ventricular involvement is not rare and probably represents a late stage of the disease.

Adolescent↗

Transcatheter closure of patent foramen ovale in patients with cryptogenic stroke.

BACKGROUND: Paradoxical embolism due to the presence of patent foramen ovale (PFO) is a well-established possible mechanism of ischaemic stroke of unknown origin. Mechanical sealing of the interatrial septum seems to be the most effective method for the prevention of stroke recurrences. AIM: To assess prospectively the short- and mid-term results of transcatheter closure of PFO in consecutive patients with a history of cryptogenic ischaemic stroke. METHODS: Between March 1999 and December 2002, thirty two patients with PFO (15 males, age from 19 to 55 years, mean 41 years) with a history of documented ischaemic stroke of unknown origin underwent transcatheter closure of PFO using an Amplatzer occluder. All procedures were performed under general anaesthesia and with transesophageal echocardiographic guidance. RESULTS: In all patients the procedure was effective and no complications were observed. During the follow-up period of a mean of 25.9 months (>12 months in 22 patients), no new neurological events were recorded. Control transesophageal echocardiography was performed in 28 patients mean 22.3 months after the procedure and confirmed the correct positioning of the occluder. A significant (>30 bubbles of contrast) residual shunt was detected in two patients. One patient developed episodes of paroxysmal supraventricular tachycardia which were effectively cured by radiofrequency ablation. CONCLUSIONS: Transcatheter closure of PFO is safe, effective and devoid of side effects connected with extracorporeal circulation. This procedure may become the treatment of choice in patients with the highest risk of recurrent ischaemic stroke.

Adult↗

[Recurrent ventricular fibrillation during a febrile illness as the first manifestation of Brugada syndrome--a case report].

A case of a 33-year-old male who was admitted to the hospital due to recurrent ventricular fibrillation during a febrile illness is presented. Initially, the patient was diagnosed with acute myocardial infarction and received thrombolytic treatment. Echocardiography and coronary angiography were normal. Right precordial ECG leads recorded one and two intercostal spaces higher than normal as well as ECG obtained following ajmaline administration revealed a typical Brugada pattern.

Adult↗