The prevalence of erectile dysfunction in men visiting outpatient clinics.

The prevalence of erectile dysfunction (ED) in men visiting outpatient clinics was analyzed using data reported by 1352 randomly chosen physicians who were requested to interview five to 20 consecutive patients aged >or=40 years about the presence of ED. A total of 25.12% of the physicians returned the questionnaires, containing data on 3552 patients, of whom 42.7% had ED, 44.9% had no ED and 12.4% declined to answer the questions. The duration of ED was <1 year in 8.1% of patients, 1-2 years in 32.2% and >2 years in 59.7% of patients. 86.4% of men with ED had >or=1 chronic disease. ED was present in 70.3% of men with coronary heart disease, 67.8% of those with hypertension, 78% of those with diabetes and 70.5% of patients with psychiatric diseases. 93.2% of patients with ED used one or more drugs chronically. In conclusions, 42.7% of men visiting outpatient clinics had ED. Patients with ED often had one or more chronic diseases and used at least one drug chronically. Older patients are less inclined to talk to their physicians about sexual problems.

Inhibition of cell migration by 24-kDa fibroblast growth factor-2 is dependent upon the estrogen receptor.

The single-copy gene for fibroblast growth factor-2 (FGF-2) encodes for multiple forms of the protein with molecular masses of 24, 22.5, 22, and 18 kDa. We reported previously that the 24-22-kDa FGF-2 forms inhibit the migration of endothelial and MCF-7 cells by 50% and 70%, respectively. Here we show that this inhibition of migration is mediated by the estrogen receptor (ER). We have found that depletion of the receptor in either cell line abrogates the inhibitory activity of 24-kDa FGF-2 while re-introduction of the ER into deficient cells once again promotes the inhibitory response. To determine whether exposure to 24-kDa FGF-2 resulted in the activation of the estrogen receptor, 3T3 cells were cotransfected with estrogen receptor cDNA and an estrogen regulatory element-luciferase gene reporter construct and treated with 24- and 18-kDa FGF-2. The high molecular weight form stimulated luciferase activity 5-fold while 18-kDa FGF-2 at the same concentration had no effect. Treatment of ER-positive MCF-7 cells transfected with the reporter construct only showed the same results. Inclusion of the pure estrogen antagonist ICI 182,780 blocked the increase in luciferase activity by 24-kDa FGF-2, further indicating that the response was estrogen receptor dependent. Expression of dominant negative FGF receptor 1 inhibited ER activation, indicating that this was the cell surface receptor mediating the effect. Although growth factor-dependent activation of the ER was reported to require mitogen-activated protein kinase-induced phosphorylation at Ser(118) in COS and HeLa cells, this mechanism is not involved with the activation by 24-kDa FGF-2. These results suggest that the addition of 55 amino acids to the amino-terminal end of 18-kDa FGF-2 by alternative translation alters FGF-2 function and allows for the activation of a second signaling pathway involving the estrogen receptor.

Predictive power of increased QT dispersion in ventricular extrasystoles and in sinus beats for risk stratification after myocardial infarction.

BACKGROUND: QT dispersion, commonly measured in sinus beats (QTd-S), can also be calculated in premature ventricular beats (QTd-V). To date, no studies have addressed the relation between these 2 variables. METHODS AND RESULTS: In 148 patients with remote myocardial infarction and premature ventricular beats on a routine ECG, QT dispersion, defined as the difference between the maximum and the minimum QT interval across the 12-lead ECG, was calculated separately for the ventricular extrasystole and the preceding sinus beat. In the total group of patients, QTd-V was greater than QTd-S (83+/-33 versus 74+/-34 ms, respectively; P=0.001). During a follow-up period of 35+/-17 months, arrhythmic events (sustained ventricular tachycardia, ventricular fibrillation, or sudden death) were noted in 30 patients. A QTd-V of >/=100 ms was a stronger univariate marker of arrhythmic events than was a QTd-S of >/=100 ms, and multivariate analysis selected only prolonged QTd-V (hazard ratio 3.81, 95% CI 2.2 to 11.2) and low ejection fraction (hazard ratio 3.05, 95% CI 1.6 to 7.6) as independent predictors of arrhythmic events. CONCLUSIONS: The magnitude of QTd-V was greater than that of QTd-S in the total group of patients. Prolonged QTd-V is associated with a significantly increased risk for arrhythmic events in postinfarction patients, and the prognostic significance of QTd-V exceeds that of QTd-S.

Dispersion of QT interval following ventricular premature beats and mortality after myocardial infarction.

In a group of 193 postinfarction patients with ventricular premature beats on a resting 12-lead ECG, the dispersion of QT and JT intervals was calculated as a difference between maximum and minimum QT and JT intervals in ventricular premature beats. During a follow-up of 38 +/- 17 months, death from all causes was noted in 56 patients. Univariate predictors of mortality included QT dispersion >/=100 ms, JT dispersion >/=100 ms, left ventricular ejection fraction <40%, complete bundle branch block, 'R-on-T' index of ventricular premature beats <1 and age of patients >60 years. At multivariate Cox proportional hazards survival analysis, only QT dispersion >/=100 ms, left ventricular ejection fraction <40% and complete bundle branch block had an independent relation to postinfarction mortality. The final model selected increased QT dispersion as the prognostic factor which was the most strongly related to mortality (chi(2) = 23.60, p = 0.0000).

Dual activities of 22-24 kDA basic fibroblast growth factor: inhibition of migration and stimulation of proliferation.

Basic fibroblast growth factor (FGF2) is synthesized as four isoforms with molecular weights of 24, 22.5, 22, and 18 kDa, with each of the three higher molecular weight forms (hmwFGF2) produced by the initiation of translation at one of three upstream CUG codons. We have shown that bovine arterial endothelial cells export the high molecular weight forms of FGF2 (hmwFGF2) in a 17beta-estradiol-dependent manner (Piotrowicz et al., 1997, J Biol Chem 272:7042-7047). To determine whether the hmwFGF2 forms affected cell behavior after release, we evaluated the effect of recombinant hmwFGF2 on the growth and migration of endothelial cells and mammary carcinoma cells (MCF-7). Treatment with the recombinant protein resulted in the inhibition of endothelial cell migration by 45% and MCF-7 cell migration by 70%. HmwFGF2-dependent inhibition was observed when endothelial cell migration was stimulated by 18 kDa FGF2 or vascular endothelial growth, and MCF cell migration was stimulated with insulin-like growth factor. In each case, inclusion of an antibody against the 55 amino acid amino terminal end of 24 kDa FGF2 abrogated the inhibition of migration, while antibodies to the 18 kDa FGF2 domain had no effect. When endothelial cells were cultured under conditions which promoted export of hmwFGF2, a 40% decrease in motility was observed which was reversed by the antibodies to the 24 kDa FGF2. Thus, both recombinant and endogenously produced hmw-FGF2 are capable of inhibiting migration. In contrast to the ubiquitous effect on migration, hmwFGF2 had no effect on endothelial cell growth but stimulated MCF-7 growth equally as well as the 18 kDa FGF2 (threefold). Antibodies to the 18 kDa domain of 24 kDa FGF2 blocked the growth-promoting activity of hmwFGF2, but those to the amino terminal end were ineffective. These data suggest that hmwFGF2 has dual activities, an inhibitory effect on cell migration and a growth-stimulating effect. The two activities can be localized to different parts of hmwFGF2: inhibitory activity to the amino terminal 55 amino acids (which are absent from the 18 kDa FGF2) and growth-promoting activity to the 18 kDa domain. Therefore, the ratio of hmwFGF2 and 18 kDa FGF2 in the extracellular space may provide a mechanism of control for angiogenesis and mammary tumor development.

Dispersion of QT interval in premature ventricular beats as a marker of susceptibility to arrhythmic events.

BACKGROUND: Clinical observations indicate that increased QT interval dispersion in sinus beats may portend malignant ventricular arrhythmias and sudden cardiac death. The purpose of this study was to test the hypothesis that measures of QT dispersion in ventricular premature beats (QTd-V) may be also useful in identifying patients at high risk of arrhythmic events. METHODS: In the group of 303 patients with ventricular premature beats on standard 12-lead ECG, the QTd-V was calculated as a difference between maximum and minimum QT interval in premature ventricular beats. During follow-up for 26 +/- 19 months the arrhythmic events (sustained ventricular tachycardia, ventricular fibrillation or sudden cardiac death) were noted in 42 patients. RESULTS: Patients with arrhythmic events had significantly (P < 0.005) greater values of QTd-V than those without arrhythmic events. Univariate predictors of arrhythmic events included QTd-V > or = 100 ms, left ventricular ejection fraction < 40%, QRS complex duration of ventricular premature beats > 150 ms, underlying heart disease and complete bundle branch block. Multivariate analysis using the Cox proportional hazard model showed that only QTd-V > or = 100 ms and ejection fraction < 40% were independent predictors of arrhythmic events. CONCLUSIONS: The results of this study indicate a significant relationship between QTd-V and the risk of arrhythmic events. The assessment of QTd-V may be useful for identifying patients with ventricular premature beats at high and low risk of subsequent arrhythmic events.

Heat shock protein 27 kDa expression and phosphorylation regulates endothelial cell migration.

The effects of enhanced HSP27 expression or expression of a nonphosphorylatable form of HSP27 on the migration of bovine arterial endothelial cells was assessed. Expression of the wild-type protein enhanced migration by twofold compared to control transfectants, whereas expression of the mutant protein retarded migration by 40%. Since homologs of the small heat shock protein inhibit F-actin polymerization in vitro and may alter basolateral F-actin content in vivo, it was postulated that the 27 kDa heat shock protein affects microfilament extension essential for cell motility. Expression of the wild-type protein promoted the generation of long cellular extensions, whereas expression of the dominant negative mutant protein resulted in a marked reduction of lamellipodia and generated aberrant microfilament morphology at the wound edge. Immunofluorescence combined with phalloidin staining demonstrated the colocalization of the HSP27 gene products with lamellipodial microfilament structures. These data suggest that the 27 kDa heat shock protein regulates migration by affecting the generation lamellipodia microfilaments.

Low variability of cycle lengths in nonsustained ventricular tachycardia as an independent predictor of mortality after myocardial infarction.

In a group of 191 postinfarction patients, the low variability of cycle lengths in nonsustained ventricular tachycardia was associated with poor prognosis during follow-up. By use of Cox model analysis it was found that reduced ventricular rate variability was a powerful independent predictor of sudden death and all-cause mortality in this group of patients.

Basolateral membrane-associated 27-kDa heat shock protein and microfilament polymerization.

The in vivo activity of the 27-kDa heat shock protein, a barbed-end microfilament capping protein, may be localized to the plasma membrane. To investigate this putative association, bovine endothelial cells expressing the human wild type or a mutant nonphosphorylatable 27-kDa heat shock protein were subjected to subcellular fractionation and immunoblot analysis. The 25-kDa endogenous bovine homolog and both exogenous gene products partitioned with cytosolic or plasma membrane components, indicating that phosphorylation is not required for membrane association. Phorbol ester treatment resulted in phosphorylation of only membrane-associated 25-kDa and wild type 27-kDa heat shock protein and did not induce redistribution. In a second fractionation protocol, streptavidin-agarose precipitation of extracts prepared from cells biotinylated at either the apical or basal surface localized membrane 25- and 27-kDa heat shock protein exclusively to the basolateral surface. Stimulation of transfectants expressing the wild type 27-kDa heat shock protein resulted in its phosphorylation and a doubling in the amount of membrane-associated F-actin precipitated, whereas the mutant protein decreased the amount of F-actin precipitated. These data suggest that membrane-associated 25- and 27-kDa heat shock proteins inhibit the generation of basolateral microfilaments and that phosphorylation releases this inhibition.

The 27-kDa heat shock protein facilitates basic fibroblast growth factor release from endothelial cells.

Basic fibroblast growth factor is an important mitogenic and angiogenic factor that stimulates endothelial cell growth and migration. This hormone is not secreted via the classical vesicular pathway, and the identification of intracellular proteins that facilitate its release remains lacking. Transfection and expression of the 27-kDa human heat shock protein in bovine arterial endothelial cells doubles the rate of estrogen-induced basic fibroblast growth factor secretion, preferentially inducing the release of high molecular weight forms of the hormone. The secreted basic fibroblast growth factor is mitogenic to breast adenocarcinoma cells cultured in the conditioned medium obtained from the transfected endothelial cells. In contrast, decreasing the level of the endogenous heat shock protein homolog with an antisense vector markedly decreases basic fibroblast growth factor release. Anti-heat shock protein or anti-basic fibroblast growth factor antibodies co-precipitate both proteins from endothelial cell extracts, demonstrating a direct association between the two proteins. This interaction is likely to be an important step in the mechanism of basic fibroblast growth factor secretion.

Ventricular tachycardia rate variability as a new predictor of sudden death in patients with remote myocardial infarction.

BACKGROUND: Clinical data have shown that evaluation of sinus rhythm variability is a useful test for selection of high-risk patients after myocardial infarction. The purpose of this study was to test the hypothesis that measures of ventricular rate variability (VRV) during non-sustained ventricular tachycardia (NSVT) may be helpful in predicting sudden death in patients with a remote myocardial infarction. METHODS: The study group comprised 162 patients with remote myocardial infarction who showed NSVT on 24 h ECG recording. Temporal changes in up to 10 beat-to-beat V-V intervals of NSVT episodes were assessed. The following parameters of VRV-NSVT were calculated: average value of successive differences in V-V intervals (ADVV); normalized average value of successive differences in V-V intervals (nADVV). RESULTS: During a mean follow-up of 4 years, 57 patients (35%) had died; sudden death was identified in 34 (21%). Patients who died suddenly had significantly (P < 0.001) lower values of ADVV and nADVV variables compared with survivors or those whose death was not sudden. The incidence of sudden death was assessed in the group of patients with more stable cycle durations in the episodes of NSVT (expected to be at high risk) and in the group with more variable cycle durations (expected to be at low risk). The relative risk of sudden death for patients with ADVV values less than 30 ms was 3.2 compared with those with ADVV values of at least 30 ms (P < 0.001), and that for patients with nADVV values less than 6% was 3.0 compared with those with nADVV values of at least 6% (P < 0.001). CONCLUSIONS: These results indicate a relationship between regularity of NSVT rhythm and risk of sudden death. The assessment of VRV-NSVT can be used to identify patients with NSVT who remain at high risk after myocardial infarction.

Fluid shear stress induces the phosphorylation of small heat shock proteins in vascular endothelial cells.

The small molecular mass heat shock protein of 27 kDa (HSP27) has been shown to influence actin filament dynamics and endothelial cell behavior in ways similar to those observed during laminar flow. We have employed human umbilical vein endothelial cells to determine whether fluid shear stress affects HSP27 expression or phosphorylation. After a shear stress of 16 dyn/cm2, HSP27 became more highly phosphorylated, with maximum increase in phosphorylation levels (3-fold) attained by 30 min and sustained for at least 20 h. HSP27 antigen levels did not change; however, HSP27 mRNA levels decreased by 20% after 16 h. In bovine aortic endothelial cells stably transfected with the wild-type human HSP27 gene, shear stress induced the phosphorylation of both the exogenous human HSP27 and the endogenous bovine HSP25. The product of a transfected mutant HSP27 gene in which the putative phosphorylation sites Ser-15, Ser-78, and Ser-82 had been replaced with Gly was not phosphorylated. Thus the modulation of HSP27 and its activity by shear stress is mediated through a posttranslational mechanism and differs from the shear stress induction of immediate early genes at the level of transcription.

Distribution of ligand-occupied alpha IIb beta 3 in resting and activated human platelets determined by expression of a novel class of ligand-induced binding site recognized by monoclonal antibody AP6.

The sequence beta (3)203-228 is involved, in a yet undetermined manner, in alpha IIb beta 3 function. We now show that murine monoclonal antibody (MoAb) AP6, specific for beta (3)211-221, binds to alpha IIb beta 3 on adenosine diphosphate (ADP)-activated platelets only when the receptor is occupied by intact fibrinogen. The ligand-induced binding-site reported by AP6 is unique in that it is not expressed following occupancy by either RGD peptides or the gamma-chain carboxy-terminal dodecapeptide. Binding of AP6 to platelets coincides temporally with the binding of the MoAb 9F9, specific for a receptor-induced binding site on fibrinogen. Thus, AP6 reports the binding of fibrinogen to the recognition pocket of alpha IIb beta 3. Its binding to thrombin-stimulated washed platelets correlates with secretion as determined using an MoAb to P-selectin. When ultrathin sections of nonactivated platelets were examined by immunogold staining and electron microscopy, AP6 identified a pool of alpha IIb beta 3 colocalizing with P-selectin and suggesting the presence of alpha IIb beta 3-ligand complexes in the alpha-granule membrane. There was little binding of AP6 to surface alpha IIb beta 3 of unstimulated platelets. After ADP-induced activation, AP6 was abundantly distributed over the entire platelet surface, including pseudopods, but only when fibrinogen was present in the medium. ADP had little effect on AP6 reactivity within platelets. This contrasted with washed platelets and thrombin, where extensive AP6 binding was observed within internal membrane pools as early as 10 to 15 seconds after stimulation. Surface labeling with AP6 followed slower kinetics. Flow cytometry on Triton X-100 permeabilized fixed platelets confirmed AP6 binding to alpha IIb beta 3 within the platelet. Thus, our results provide evidence of (1) a pool of alpha-granule alpha IIb beta 3 occupied by ligand in nonactivated platelets; (2) thrombin-induced activation of alpha IIb beta 3 within the platelet, and (3) thrombin-induced mobilization of ligand-bound alpha IIb beta 3 to the surface.

Accelerated growth and senescence of arterial endothelial cells expressing the small molecular weight heat-shock protein HSP27.

Bovine arterial endothelial cells were stably transfected with the human wild-type (wt) HSP27 or a mutant gene (mu) encoding a nonphosphorylatable form of the protein. At early passage both cultural and cellular morphology were similar, although the vacuole content in wtHSP27 was much higher than muHSP27 cells. As the cultures aged, wtHSP27 cells became large, polymorphic, highly vacuolated, and reached senescence before muHSP27 transfected cultures, which remained small and polygonal with few detectable vacuoles. Vector control cells showed an intermediate phenotype. Tritiated thymidine incorporation studies were performed with multiple wtHSP27 and muHSP27 clones and the results compared with 11 vector control clones. The results showed an average increase in growth rate for the wtHSP27 cells of 3.0 +/- 0.6 times. The growth rate of eight muHSP27 clones showed a slight decrease. Estradiol treatment of endothelial cells resulted in an increase in both bovine and human HSP27, with peak expression at 100 nM. Treatment of the vector-transfected cells with 100 nM estradiol resulted in a 1.44 +/- 0.18 fold increase in growth rate, which was blocked by expression of muHSP27. These data demonstrate a role for HSP27 in controlling the growth rate of endothelial cells in an estrogen-responsive manner.

24-h ECG monitoring in patients with rheumatoid arthritis.

Although the main cardiac complication in patients with rheumatoid arthritis is subclinical pericarditis, mononuclear cell infiltrations into myocardium may cause cardiac arrhythmias and conduction defects. In order to examine these problems we evaluated 70 patients (53 women and 17 men) aged 18-83 years (average 56.7 +/- 11.2) with classic or definite rheumatoid arthritis, according to diagnostic criteria. Duration of the disease was 1-35 years (average 8.7 +/- 8.4). The control group comprised 70 patients admitted to hospital with degenerative joint disease, a duodenal ulcer, or who required treatment for ophthalmological or laryngeal reasons; these patients were matched for sex and age. In all patients standard 12-lead ECG investigations were performed, as well as 24-h ECG monitoring, using an Oxford Medical System device with two precordial leads CM5 and CS2, according to the Holter method. We analysed heart rate, conduction disturbances, and occurrence of arrhythmias, on the basis of generally assumed ECG criteria. Cardiac arrhythmias were found in 50% of patients with rheumatoid arthritis, and their occurrence was similar to that in the control group. Observed arrhythmias were independent of the progression of arthritis, the type of treatment administered, the familial occurrence of arthritis, the presence of manifestations pertaining to organs, the presence of rheumatoid factor, the stage of the disease according to Steinbrocker, or the presence of immune complexes in serum and HLA Dr antigens, which are regarded as fundamental in the pathogenesis of rheumatoid arthritis.

Ligand and cation binding are dual functions of a discrete segment of the integrin beta 3 subunit: cation displacement is involved in ligand binding.

The alpha IIb beta 3 integrin binds Arg-Gly-Asp-containing (RGD-containing) ligands in a cation-dependent interaction. A fourteen amino acid sequence, beta 3 (118-131), and an antibody to it, inhibited ligand binding functions of alpha IIb beta 3, and a 1:1 stoichiometric beta 3 (118-131)-RGD complex was detected by mass spectroscopy. Cation binding to beta 3 (118-131) was demonstrated by terbium luminescence and mass spectroscopy. Notably, ligand displaced cation from the beta 3(118-131) peptide and also from purified alpha IIb beta 3. Thus, beta 3 (118-131), a highly conserved region in integrin beta subunits, binds both ligand and cation. Formation of a ternary complex between cation, ligand, and receptor, with subsequent displacement of cation from beta 3 (118-131) and a second site within the receptor, may be central to the mechanism of ligand recognition by integrins.

A mechanism for divalent cation regulation of beta 3-integrins.

Integrins alpha IIb beta 3 and alpha V beta 3 mediate numerous cell-matrix and cell-cell contacts. Both integrins contain multiple divalent cation-binding motifs that regulate ligand binding. Here, we elucidate a major difference in the regulation of alpha IIb beta 3 and alpha V beta 3 by divalent ions. Fibrinogen binding to alpha IIb beta 3 in Ca(2+)-containing buffer is rapid, with an apparent association rate constant (k1app) of 8.2 x 10(5) M-1 s-1, but Ca2+ does not support association between fibrinogen and alpha V beta 3. Interestingly, Mn2+ supports fibrinogen binding to both integrins, albeit with a relatively slow association rate (k1app = 10(4) M-1 s-1). This influence of divalent ions on ligand association rates accounts for the opposite divalent ion requirements for platelet aggregation and tumor cell adhesion to fibrinogen. Furthermore, the regulation of fibrinogen binding to alpha V beta 3 is complex when both Ca2+ and Mn2+ are present. Physiological concentrations of Ca2+ completely ablated adhesion. Kinetic analysis demonstrated that Ca2+ is a mixed-type inhibitor of Mn(2+)-supported fibrinogen binding to alpha V beta 3. Consequently, the data presented here suggest a mechanism in which two separate cation-binding sites regulate ligand binding to beta 3-integrins.

[Unexplained syncope. Likelihood of inducing sustained ventricular tachycardia with electrophysiologic examination]. / Napadowa utrata przytomnosci niewyjasnionego pochodzenia. Prawdopodobienstwo wywolania trwalego czestoskurczu komorowego w badaniu elektrofizjologicznym.

In patients with unexplained syncope and documented nonsustained VT or complex premature ventricular beats indication for programmed ventricular stimulation (PVS) should be considered. However, the variables derived from noninvasive methods that predict diagnostic yield of PVS are incompletely defined. The purpose of this study was to elucidate the role of noninvasive testing variables in predicting inducible monomorphic sustained ventricular tachycardia (SVT) in 116 patients (pts) presenting with syncope. The study group consisted of 45 pts with remote Q wave myocardial infarction. 5 pts with non-Q wave myocardial infarction, 21 pts with another heart disease and 45 pts without organic heart disease. All pts underwent standard ECG, Holter monitoring, echocardiography, signal-averaged ECG and PVS with 1, 2 and 3 extrastimuli at three basic cycle lengths. Nonsustained VT, low ejection fraction, prolongation of QTc interval, abnormal Q waves in postinfarction pts (Q-MI) and late potentials (LP) indicate a greatly increased probability of inducible SVT. Inducible SVT was present in 15 of 45 (33%) pts with Q-MI. Although in the group of 71 pts without Q-MI, nonsustained VT on Holter monitoring was detected in 20 pts, LP in 16 pts, prolongation of QTc interval in 3 pts and low ejection fraction in 2 pts, the positive yield of PVS was documented in only one case (1%). The combination of Q-MI and LP best predicted inducible SVT showing a sensitivity of 75%, specificity of 93%, overall predictive accuracy of 91%, predictive value of positive response of 63% and negative response of 69% to identify pts who would have inducible SVT. Thus, the combination of Q-MI and LP variables was shown as the best predictor of inducible SVT in pts with unexplained syncope. In pts without Q-MI the noninvasive testing variables have considerably less value in selection of pts to PVS, because inducible SVT is very rare in this population.

[Paroxysmal loss of consciousness. Comparison of electrophysiologic and holter monitoring results]. / Napadowa utrata przytomnosci. Porównanie wyników badania elektrofizjologicznego i monitorowania holterowskiego.

Holter monitoring is one of the most commonly done test in the evaluation of patients with syncope. As Holter monitoring may miss an arrhythmia or document an asymptomatic arrhythmia invasive electrophysiologic testing has been applied in patients with syncope. The purpose of this study was to compare Holter monitoring and electrophysiologic tests in patients with syncope of unexplained origin. The group consisted of 100 patients with syncope of unknown origin. Coronary artery disease was present in 43 patients, other heart disease in 19 patients and no structural heart disease was found in 38 patients. Electrophysiological testing consisted of (1) recording of His bundle electrogram, (2) atrial stimulation, (3) ventricular stimulation with 1.2 and 3 extrastimuli at three basic cycle lengths. The results of Holter monitoring were classified by severity of abnormalities into three classes: I--normal study; II--moderate abnormalities; III--severe abnormalities: sinus rhythm with pauses longer than 3 s, Mobitz II or complete atrio-ventricular block, supraventricular arrhythmia faster than 180 bpm, sustained ventricular tachycardia. Abnormalities of electrophysiologic testing were grouped as: I normal study; II--moderate abnormalities; III--severe abnormalities: sinus nodal recovery time more than 3 s, HV interval longer than 100 ms, supraventricular arrhythmia faster than 200 bpm, sustained ventricular tachycardia. Class III abnormalities were documented in 17 patients on Holter monitoring and in 20 patients by electrophysiologic testing. Compatibility between class III abnormalities in Holter monitoring and electrophysiological testing was noted in 4 patients, discordance of class III results in 33 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

[Diurnal variability of heart rate during paroxysmal ventricular tachycardia]. / Zmiennosc dobowa czestotliwosci rytmu serca podczas napadowego czestoskurczu komorowego.

The aim of this study was to assess the diurnal variability of heart rate during VT. For the purpose of this investigation VT was considered to be a minimum of 3 consecutive ventricular beats in duration at a rate more than 100 bpm. From the group of 287 patients with VT during 24-hour ECG monitoring, a selection was made of 52 patients in whom episodes of monomorphic VT occurred in the day-time and night-time without any changes of the QRS morphology. Thirty one patients had ischemic heart disease, 10--dilated cardiomyopathy, 2--mitral valve prolapse and 10 patients had no evidence of heart disease. In these patients the rate of VT (HR-V), basic heart rate (HR-S) before VT, and coupling interval (CI) of VT initiating beat were measured during day-time and night-time. The mean VT rate was 170 +/- 34 bpm during day-time and 149 +/- 36 bpm during night-time (p < 0.001). The mean sinus rhythm rate was significantly (p < 0.001) greater during day-time (88 +/- 16 bpm) than at night (78 +/- 19 bpm). There was significant difference in the mean values of the CI between day-time and night-time (504 +/- 122 vs 589 +/- 181 ms). A significant correlation was noted between HR-V and HR-S at night (r = 0.73; p < 0.001) but not during day-time (r = 0.38). Thus, HR-V similarly as HR-S is greater during day-time than during night-time. Diurnal variability of HR-V may be related to changes in autonomic nervous system tone.