Effects on left ventricular function of pindolol added to verapamil in hypertrophic cardiomyopathy.

The aim of the study was to assess the effect of adding pindolol to previously used verapamil monotherapy on left ventricular (LV) systolic and diastolic function in 20 patients with hypertrophic cardiomyopathy. Patients were initially treated with verapamil in maximal well-tolerated doses for 16 +/- 14 months; pindolol, 5 mg twice daily, was added. In a Doppler echocardiographic study all patients had altered LV diastolic filling despite verapamil therapy. The control examination, which consisted of echocardiographic study and New York Heart Association functional status classification, was performed after 20 days and repeated after > or = 6 months of follow-up. Combined pindolol and verapamil therapy caused an increase in LV diastolic filling manifested by beneficial changes of transmitral flow parameters. Also, inhibition of hypercontractile LV function expressed by reduction of LV outflow tract pressure gradient and ejection fraction was observed. New York Heart Association functional class was reduced in 13 patients. The magnitude and distribution of LV myocardial hypertrophy did not change significantly. It is concluded that pindolol and verapamil combined therapy is superior to verapamil monotherapy because of improved LV diastolic function (probably due to partial agonist activity of pindolol) and reduced hypercontractile function in patients with hypertrophic cardiomyopathy.

Effects of acute euglycemic hyperinsulinemia on urinary nitrite/nitrate excretion and plasma endothelin-1 levels in men with essential hypertension and normotensive controls.

Insulin stimulates the production of endothelin-1 (ET-1) and nitric oxide (NO) by isolated endothelial cells. Additionally, insulin-dependent glucose transport and insulin-mediated NO production partially share common elements in signal transduction. There are discordant data on plasma ET-1 levels during acute euglycemic systemic hyperinsulinemia in normotensive men and men with essential hypertension (EH) (known to be insulin-resistant), as well as on the relations between insulin sensitivity and vascular function. Our aim was to assess the response of approximate measures of whole-body generation of NO and ET-1 to acute euglycemic hyperinsulinemia in EH patients and controls. We studied 17 newly diagnosed untreated men with uncomplicated EH and 10 normotensive controls. Plasma ET-1 and urinary excretion of nitrite plus nitrate, stable NO metabolites (Uno(x)), were measured before and during a 3-hour hyperinsulinemic-euglycemic clamp. Both in hypertensives and normotensives, plasma ET-1 levels were reduced after 2 hours of the clamp (EH: baseline, 3.1+/-1.9 pg/mL; 2 hours, 1.9+/-1.2 pg/mL, P = .04 v baseline; controls: baseline, 4.2+/-2.6 pg/mL; 2 hours, 2.8+/-1.4 pg/mL, P = .04 v baseline). No significant changes in Uno(x) during the clamp were observed. Changes in Uno(x) during the clamp (deltaUno(x)) and differences in plasma ET-1 measured before the end and before the beginning of the clamp (deltaET-1) were correlated in the controls (r = .75, P = .01) but not in EH (r = -.01, P = .97). No parameter of glucose metabolism correlated with basal Uno(x), basal plasma ET-1, deltaUno(x), and deltaET-1, whether absolute or percent values, in either group. Thus, acute euglycemic hyperinsulinemia produces a decrease in plasma ET-1 in both EH patients and controls. The lack of correlation between deltaUno(x) and deltaET-1 under these conditions in EH may suggest an impairment of systems governing interactions between the NO-dependent pathway and ET-1. In addition, insulin actions on glucose metabolism and on the endothelial mediators appear dissociated.

Effect of verapamil on systolic and diastolic coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy.

OBJECTIVE: To assess non-invasively the effect of verapamil treatment on coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy. DESIGN: High frequency transthoracic Doppler echocardiography was used to compare resting phasic coronary blood flow velocity before and after a one month period of verapamil treatment in 17 patients (14 men and three women) with non-obstructive hypertrophic cardiomyopathy. Eighteen healthy subjects formed an age and sex matched control group. Systolic and diastolic coronary blood flow velocity was measured in the distal portion of left anterior descending coronary artery using high frequency transthoracic Doppler echocardiography. Blood flow velocity before and after verapamil was compared in the patients with cardiomyopathy and with the results in the control group. RESULTS: Compared with the controls, patients with hypertrophic cardiomyopathy had increased diastolic coronary blood flow velocity (41.8 (8.1) v 59.9 (21.9) cm/s, p < 0.01) and a lower mean systolic coronary blood flow velocity (18.7 (10.8) v -11.2 (27.5) cm/s, p < 0. 01) before verapamil treatment. A backward pattern of systolic flow, manifested by negative values of coronary blood flow velocity, was recorded in eight of the patients, while no negative values were found in the controls. After verapamil treatment the retrograde systolic blood flow was restored to an anterograde pattern in only one patient. The mean value of systolic coronary blood flow velocity did not change significantly and remained lower than the systolic forward flow velocity in the controls (-3.6 (31.8) v 18.7 (10.8) cm/s, p < 0.05). However, diastolic coronary blood flow velocity decreased significantly after verapamil (59.9 (21.9) v 50.7 (19.5) cm/s p < 0.05), reaching a level comparable with that in the controls (50.7 (19.5) v 41.8 (8.1) cm/s, p > 0.05). CONCLUSIONS: In contrast to healthy subjects, in non-obstructive hypertrophic cardiomyopathy the systolic pattern of coronary blood flow was heterogeneous (both retrograde and anterograde), and diastolic coronary blood flow velocity was abnormally increased, despite a lack of significant symptoms. Verapamil treatment did not restore the forward pattern of systolic blood flow but decreased diastolic blood flow velocity to a level comparable with that in healthy subjects.

The frequency and functional impact of hypertension overlapping on hypertrophic cardiomyopathy: comparison between older and younger patients.

BACKGROUND AND AIM: In a previous report, when hypertension (HT) overlapped on hypertrophic cardiomyopathy (HTHCM), the decreased survival rate was associated with higher NYHA classes. The study concerned only elderly patients and therefore we decided to extend it by: (1) assessment of the frequency and age-distribution of HTHCM in HCM population; and (2) the comparison of NYHA class between HTHCM and HCM both in younger and older patients. PATIENTS AND METHODS: We retrospectively viewed 123 HCM patients with regard to the presence of hypertension as a concomitant disease. The HTHCM and HCM patients were compared with regard to NYHA functional classes within younger (<50 years of age) and older (>50 years of age) subgroups. RESULTS: Of the 123 HCM patients, 24 (19.5%) had associated hypertension. Among younger patients, 15.7% had concomitant hypertension, while in older patients the percentage of HTHCM significantly increased to 38%. In younger patients, the mean values of the NYHA class were significantly higher in HTHCM in comparison to HCM patients (2.19 +/- 0.37 vs 1.94 +/- 0.56, P < 0.05), whereas in the older patients, the mean values of NYHA class were comparable between HTHCM and HCM patients (2.13 +/- 0.33 vs 2.23 +/- 0.42, P > 0.05). CONCLUSION: Hypertension associated with HCM is not rare in young patients, and this coincidence significantly increases in older patients. Hypertension overlapping on HCM additionally deteriorates functional status in younger patients whereas in the older patients NYHA class the difference between HTHCM and HCM narrows and becomes insignificant.

Progression of asymmetric pattern of left ventricular hypertrophy in patients with hypertrophic cardiomyopathy accompanied by hypertension in the elderly.

OBJECTIVE: The aim of the study was to determine the potential influence of hypertension overlapping hypertrophic cardiomyopathy (HCM) on left ventricular hypertrophy (LVH) pattern. We compared the magnitude of LVH asymmetry between younger and older patients with HCM and concomitant hypertension. MATERIAL AND METHODS: We studied 18 patients (age range from 18 to 77 years) in whom HCM was accompanied by mild-to-moderate hypertension. Patients were subdivided into two groups: (I) <50 years of age (11 patients); and (II) >50 years of age (seven patients). The thickness of ventricular septum and posterior wall was assessed by M-mode echocardiography. The pattern of LVH was determined based on the value of ventricular septum/posterior wall thickness (VS/PW) ratio and LVMI was calculated according to Devereux formula. RESULTS: The more asymmetric LVH pattern was revealed in older HCM with hypertension patients than in younger patients (VS/PW thickness ratio 2.62 +/- 0.81 vs 1.58 +/- 0.56, P < 0.05). The LVMI was similar in both groups (210 + 87 vs 191 + 30 g/m2, P > 0.5). CONCLUSION: Asymmetric pattern of LVH aggravated with increasing age in HCM with hypertension patients while LVMI was comparable between younger and older patients. Thus, the primary myocardial disease, ie, HCM, so significantly determined the asymmetric LVH pattern with aging that coexistent hypertension was not a sufficiently strong stimulus to alter LVH pattern into a more concentric one in the elderly.

Impact of gender on the left ventricular cavity size and contractility in patients with hypertrophic cardiomyopathy.

BACKGROUND: The aim of the study was to assess gender-specific differences in left ventricular cavity size, contractility and left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. METHODS: We studied retrospectively 129 referred patients with hypertrophic cardiomyopathy (77 males and 52 females). The echocardiographically measured left ventricular end-systolic, end-diastolic dimensions, fractional shortening and occurrence of left ventricular outflow tract gradient > or =30 mmHg were compared between sexes. Logistic regression analysis was used to calculate the predictive values of left ventricular dimensions and contractility for left ventricular outflow tract obstruction for each gender separately. RESULTS: Left ventricular end-diastolic and end-systolic dimensions were significantly smaller in females than males (41.7+/-5.3 vs. 45.1+/-4.9 mm, P=0.0003; 23.1+/-44 vs. 25.6+/-5.3 mm, P=0.007 respectively). On the contrary, the value of fractional shortening was comparable in both sexes (44.7+/-7.3 vs. 43.6+/-7.9%, P>0.05). The left ventricular outflow tract gradient occurred in females as frequently as in males (28.8 vs. 33.8%, P>0.05). By logistic regression analysis the predictors of left ventricular outflow tract gradient in females were left ventricular end-systolic diameter (relative risk=0.74; confidence interval (CI) 0.61 to 0.91; P=0.0038), left ventricular end-diastolic diameter (relative risk=0.82; CI 0.72 to 0.96; P=0.0061) and fractional shortening (relative risk=1.11; CI 1.01 to 1.22; P=0.036). The most potent predictor appeared to be left ventricular end-systolic dimension. In males none of these parameters identified patients with left ventricular outflow tract obstruction. CONCLUSIONS: Females with hypertrophic cardiomyopathy featured smaller left ventricular cavity size, which predisposed to left ventricular outflow tract obstruction (the most potent predictor of left ventricular outflow tract obstruction was left ventricular end-systolic dimension). Higher left ventricular contractility also determined left ventricular outflow tract gradient occurrence in females with hypertrophic cardiomyopathy. In males despite a larger left ventricular cavity size the left ventricular outflow tract obstruction occurred with a similar frequency as in females. Left ventricular outflow tract obstruction was not predicted by left ventricular cavity size or contractility in males.

Plasma ANP and cyclic GMP after physical exercise in patients with mitral valve disease and in healthy subjects.

Plasma levels of both atrial natriuretic peptide (ANP) and cyclic GMP are elevated in patients with various heart diseases as compared to healthy subjects. In this study patients with advanced mitral valve disease (Group A) and healthy subjects (Group B) were exposed to symptom-limited upright stepwise physical exercise on a cycle ergometer. Concentrations of ANP and cyclic GMP were measured in plasma at rest (20 min in supine position) or 5 min after physical exercise by specific radioimmunoassays. Here we show that short dynamic exercise caused a significant increase in plasma levels of ANP and cyclic GMP, in both groups. In Group A strong correlation between plasma ANP and cyclic GMP was found at rest (r = 0.91, P < 0.001, n = 11) and after physical exercise (r = 0.85, P < 0.001, n = 11). In contrast, there was no correlation between plasma concentrations of ANP and cyclic GMP in Group B at rest (r = -0.16, P > 0.05, n = 10) or after exercise loading (r = 0.14, P > 0.05, n = 10). Absolute increases in circulating levels of both substances were not found to correlate in either group. These data suggest that exercise-induced elevations in plasma cyclic GMP may be due not only to ANP release but also to an as yet undetermined factor, possibly EDRF/NO.

Circulating N-terminal brain natriuretic peptide precursor and endothelin levels in patients with syndrome X and left bundle branch block with preserved systolic function.

BACKGROUND: Deterioration of left ventricular function during follow-up was reported in some patients with syndrome X and concomitant left bundle branch block. The patients with syndrome X and left bundle branch block has been frequently presented with elevated Endothelin-1 (ET-1) level while brain natriuretic peptide (BNP) (a sensitive marker of left ventricular dysfunction) has not been measured in patients with syndrome X. METHODS: The purpose of the present study was to assess left ventricular diastolic function, levels of N-terminal Brain Natriuretic Peptide (NT-proBNP) precursor and biochemical parameters of endothelial function in patients with syndrome X complicated by left bundle branch block but preserved left ventricular systolic function (group A, n=8). The echocardiographic and neurohormonal measures in these patients were compared to those in patients with syndrome X without left bundle branch block (group B, n=13), and controls (group C, n=15). RESULTS: At rest and after exercise the serum concentration of NT-proBNP was significantly higher in group A than in the controls (at rest: 232+/-96 vs. 133+/-23 fmol/ml, P=0.03; after exercise: 313+/-96 vs. 180+/-33 fmol/ml, P=0.02). The highest concentration of endothelin-1 was also found in group A, being significantly higher than in the controls (6.81 vs. 4.52 pg/ml, P<0.05). Mitral flow abnormalities were detected in left bundle branch block patients. Accordingly, the lowest E/A ratio was in group A and it differed significantly from that in group C (0.85 vs. 1.1, P<0.05). E/A ratio inversely correlated with plasma NT-proBNP concentration in patients with left bundle branch block (r=-0.48, P=0.02). CONCLUSIONS: Elevated NT-proBNP and endothelin-1 plasma concentrations were demonstrated in patients with syndrome X complicated by left bundle branch block even when left ventricular systolic function was still preserved. In this subgroup the magnitude of left ventricular diastolic dysfunction correlated with the increase of BNP level which reflects neurohormonal activation.

Comparison of dual-chamber pacing with nonsurgical septal reduction effect in patients with hypertrophic obstructive cardiomyopathy.

OBJECTIVES: The aim of the study was to compare the influence of dual-chamber pacing vs. nonsurgical septal reduction on hemodynamic and morphological parameters in patients with obstructive form of hypertrophic cardiomyopathy. METHODS: Nineteen patients with dual-chamber pacing (group I) and 9 patients who underwent nonsurgical septal reduction (group II) were studied at baseline and after a 6-month follow-up. The changes of left ventricular outflow tract gradient and posterior wall thickness (as an index of left ventricular hypertrophy regression) were compared. RESULTS: The baseline left ventricular outflow tract gradient was comparable between group I and group II (77+/-25 vs. 82+/-25 mm Hg, p>0.05). At 6-month follow-up, the left ventricular outflow tract gradient was reduced to a similar level in both groups (28+/-19 vs. 25+/-12 mm Hg, p>0.05). At baseline, posterior wall hypertrophy was comparable between groups (12.9+/-1.7 vs. 13.6+/-2.2 mm, p>0.05). During follow-up, the posterior wall thickness was unchanged in the pacing group (12.9+/-1.7 vs. 12.6+/-1.6 mm, p>0.05), whereas nonsurgical septal reduction induced regression of left ventricular hypertrophy in myocardial region remote from the infarcted septal segment (13.6+/-2.2 vs. 10.5+/-2.3 mm, p<0.003). CONCLUSION: Despite comparable reduction of instantaneous left ventricular outflow tract gradient, the nonsurgical septal reduction decreased posterior wall thickness, whereas pacing did not reduce left ventricular hypertrophy. Thus, regression of left ventricular hypertrophy that appeared solely after nonsurgical septal reduction may reflect the more permanent reduction of left ventricular pressure overload. Thus, not only hemodynamic but also morphological benefit from nonsurgical septal reduction seems to indicate the superiority of this method over dual-chamber pacing.

Successful coronary stent implantation in a patient with primary antiphospholipid syndrome.

We report a 22-year-old man who successfully underwent coronary stent implantation after an acute myocardial infarction. Lupus anticoagulant and antibodies against cardiolipin and prothrombin were detected despite the absence of any underlying disease. Therefore, long-term oral anticoagulation was instituted and appeared to be effective. To our knowledge this is the first report on coronary stenting in primary antiphospholipid syndrome.

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.

Impaired response of the forearm resistance but not conductance vessels to reactive hyperemia in hypertrophic cardiomyopathy.

It has been suggested that in hypertrophic cardiomyopathy (HC), vascular abnormalities are not restricted to the heart. Flow-mediated dilation of peripheral conductance arteries (reflecting their endothelial function) has not yet been studied in HC. Our aim was to assess both flow-dependent dilation of the brachial artery and flow responses (dependent on resistance vessels) during forearm reactive hyperemia (RH) in nontreated HC patients. The authors studied 13 HC patients and 14 age- and sex-matched healthy controls. None of them exhibited any factors known to be associated with endothelial dysfunction. Using 7 MHz ultrasound, brachial artery diameter and Doppler flow velocity were measured continuously at baseline and throughout 1 min of RH following 5 min of forearm ischemia induced by inflation of a blood pressure cuff. Arterial diameter and RH flow are expressed as percent changes with respect to the baseline. Flow-dependent dilation was similar in the HC patients and control subjects (7.2 +/- 9.5% vs 9.9 +/- 10.4%, p>0.05). Compared to the control group, RH flow in HC was decreased; however, differences did not reach statistical significance until 60 sec of RH (112 +/- 102% vs 261 +/- 217%, p<0.05; HC vs controls). In HC patients, endothelial function of peripheral conductance arteries is preserved. Hence, a defect in the forearm arterial bed in HC seems to be limited to mechanisms maintaining the dilation of resistance vessels during decreasing RH flow.

Determinants of left ventricular function two weeks and one year after an acute myocardial infarction.

This study examines possible covariates of left ventricular function two weeks and sixteen months after an acute infarction. It was performed in a group of 312 patients randomized double blindly to recombinant tissue plasminogen activator (rt-PA) (n = 156) or placebo treatment and followed thereafter for at least one year. Two weeks after the infarction, enzymatic infarct size, infarct-related vessel, and number of diseased coronary arteries were significant determinants of the infarct-related regional wall motion (centerline method) (R2 = 0.25 to 0.60, P = 0.0001). Enzymatic infarct size, regional wall motion of both infarct-related and remote areas, reinfarction, and treatment allocation were significant independent correlates of ejection fraction (R2 = 0.76), end-diastolic volume (R2 = 0.20), and end-systolic volume (R2 = 0.69, P < 0.0001). Infarct-related coronary artery and predischarge end-systolic volume were significant independent covariates of ejection fraction at rest (R2 = 0.47) after sixteen months. Age, enzymatic infarct size, and predischarge end-diastolic volume were independent determinants of the maximal (R2 = 0.49, P < 0.0001) and peak exercise ejection fraction (R2 = 0.49, P < 0.0001).

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)

[Depressive disturbance and quality of life in patients with coronary artery disease]. / Zaburzenia depresyjne a jakosc zycia u pacjentów z choroba niedokrwienna serca.

The aim the study was to evaluate the impact of mood disturbances on the subjective quality of life in patients with coronary artery disease after an effective angioplasty. The study covered 100 patients with the optimum result of PTCA. Their condition was evaluated one day before and four weeks after angioplasty. Significant differences in the subjective quality of life assessment were detected depending on the occurrence and dynamics of depressive symptoms. The authors postulate evaluation of psychological state and introduction of anti-depressive therapy in patients with coronary artery disease subjected to revascularisation.

[Intracoronary ultrasound assessment of balloon angioplasty with "stent-like' angiographic result]. / Ultrasonograficzna ocena skutecznosci balonowej angioplastyki wiencowej z wynikiem angiograficznym "porównywalnym do stentowania".

The aim of the study was to evaluate by intracoronary ultrasound (ICUS) the efficacy of optimal coronary balloon angioplasty (POBA) guided by quantitative coronary angiography (QCA). The study population included 40 patients who underwent conventional coronary balloon angioplasty, in whom a stent-like result was achieved (percent diameter stenosis (%DS) < 35% in QCA). In all patients diagnostic ICUS assessment was performed after the procedure. The site of stenosis and the proximal and distal reference segments were analysed with respect to residual plaque burden (RPB), true vessel dimension (the media-to-media diameter) and type of vascular remodelling. Despite an optimal angiographic result residual plaque burden was 70 +/- 6% at the site of stenosis, whereas in the reference segments it was around 45% indicating the severity of atherosclerosis in angiographically normal vascular segments. No significant differences were seen between averaged reference vessel diameter in QCA (Ref.D) and averaged luminal reference diameter in ICUS. In contrast, true vessel diameter in ICUS was significantly larger than Ref.D in QCA (p < 0.001). Positive vascular remodelling at the site of stenosis was observed in most patients. Optimal angiographic result of QCA-guided POBA does not indicate optimal dilatation of the lesion. In most patients ICUS reveals marked residual plaque burden, which is an independent predictor of restenosis after percutaneous coronary interventions.

[Restenosis after coronary balloon angioplasty. Prevention and treatment]. / Restenoza po balonowej angioplastyce. Zapobieganie i leczenie.

The paper describes the mechanisms as well as clinical and angiographic risk factors for the development of restenosis after balloon coronary angioplasty. Based on literature findings and personal experience the ways of preventing restenosis were reviewed taking into account the optimisation of immediate angioplasty results based upon intracoronary ultrasound and physiological measurements of the coronary flow reserve. The paper also reviews the available techniques in the management of restenosis after balloon coronary angioplasty.

[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.

[The assessment of safety of enoxaparin administration during percutaneous transluminal coronary angioplasty after ticlopidine pretreatment. Application of low molecular weigh heparins in prevention of coronary micro-embolization]. / Ocena bezpieczenstwa stosowania enoxaparyny podczas zabiegów przezskórnej rewaskularyzacji serca u pacjentów uprzednio otrzymujacych tiklopidyne Zastosowanie heparyn drobnoczasteczkowych w zapobieganiu zatorowosci mikrokrazenia wiencowego.

BACKGROUND: Administration of enoxaparin to patients with acute coronary syndromes can result in better outcomes in comparison to patients treated with unfractionated heparin. Use of enoxaparin during percutaneous coronary interventions (PCI) can also improve the outcome. Administration of ticlopidine and aspirin for a few days before PCI decreases frequency of ischaemic complications. There is lack of data about safety and efficacy of combined administration of enoxaparin, ticlo-pidine and aspirin during PCI. METHODS: 61 patients with coronary artery disease were involved in the study. All patients were pretreated with aspirin (75-325 mg/d) and ticlopidine (2 x 250 mg) for at least 3 days before PCI. PCI procedures were conducted after i.v. administration of 1 mg/kg of enoxaparin. After PCI bleeding and ischaemic complications were monitored. RESULTS: In the treated group, no major bleeding occurred, while minor bleeding was noted in 6.5% of patients. No periprocedural major adverse cardiac events (death, Q wave infarction, urgent revascularisation) were observed. Microembolisation was present in 4.9% patients (expressed as CK-MB > 3 times the reference level). CONCLUSIONS: Intravenous administration of enoxaparin 1 mg/kg during PCI in patients pretreated with aspirin and ticlopidine for at least 3 days before intervention appears to be safe. Safety and high efficacy of enoxapirine in this pilot trial justify initiating the randomized, multicenter trial comparing use of low molecular weight heparin to unfractionated heparin during PCI.

[Clinical predictors of left ventricular function improvement after percutaneous coronary interventions in patients with ejection fraction below 45%]. / Kliniczne wskazniki poprawy funckji lewej komory u pacjentów z frackja wyrzutowa ponizej 45% poddanych zabiegom przezskórnej rewaskularyzacji wiencowej.

BACKGROUND: The value of clinical predictors of left ventricle function recovery after surgical revascularization in patients with decreased ejection fraction is well documented. However, there are no clinical studies assessing factors which can influence left ventricle function in patients with coronary disease and low ejection fraction (LVEF) undergoing percutaneous coronary interventions (PCI). OBJECTIVE: We tried to assess clinical prognostic factors of left ventricle function improvement after PCI in patients with coronary artery disease and impaired LVEF. PATIENTS AND METHODS: We studied patients with LVEF < 45% undergoing PCI. We assessed duration and grade of symptoms of heart failure, angina class and echocardiographic parameters of LV systolic function. After 6 months follow-up LVEF was obtained again. We analyzed influence of baseline clinical factors on LVEF recovery after PCI. RESULTS: We studied 29 patients (mean age 54.4 +/- 11 years) before and after PCI. In the whole group of patients we found significant increase in EF (38.4 +/- 6% vs 50.4 +/- 15%, p = 0.005) at follow up examination. There was significant improvement of EF in patients with NYHA class I or II (from 40.4 +/- 5% to 58.1 +/- 9%, p < 0.0001) as compared to NYHA class III or IV (from 31.4% +/- 9% to 31.8 +/- 11, p = NS). In multivariate regression analysis correlation between NYHA class and LVEF at control examination (beta = -0.54, p = 0.03) was independent from epidemiological variables and baseline LVEF. There was significant increase in LVEF in patients with severe angina (CCS III or IV) as compared to patients without angina (DEF 21.3 +/- 5% vs 7.9 +/- 10%, p = 0.009). There was also higher increase in LVEF in patients with chest pain during balloon inflation (delta EF 17.4 +/- 9% vs 5.7 +/- 9%, p = 0.01). CONCLUSIONS: Mild symptoms of heart failure and independent predictors of left ventricle function recovery after PCI in patients with impaired LVEF. The lack of angina symptoms negatively influence LVEF recovery after PCI.