Complex Ventricular Arrhythmias In Patients Research Articles

Fragmented QRS may be associated with complex ventricular arrhythmias in mitral valve prolapse.

Although mitral valve prolapse (MVP) is a benign disease, several studies have indicated its association with ventricular arrhythmias (VAs). Some histopathological studies have pointed to left ventricular fibrosis as the underlying cause of arrhythmia in MVP patients. Fragmented QRS (fQRS) on electrocardiography (ECG) has been shown to be a marker of myocardial fibrosis. This study aimed to investigate the association between fQRS and complex VAs in patients with MVP. A total of 230 consecutive patients who were diagnosed with MVP were included in the study. The control group consisted of 302 healthy individuals matched according to age and sex. fQRS was defined as additional R' wave or notching/splitting of S wave in two contiguous ECG leads. All patients underwent 24-hour Holter monitoring and VAs were classified using Lown's scoring system. Lown class ≥3 VAs were considered as complex VAs. As compared to the healthy individuals, prevalence of fQRS (40% vs. 9.6%, P<0.001) and complex VAs (18.7% vs. 0%, P<0.001) were significantly higher in patients with MVP. Furthermore, complex VAs (35.9% vs. 7.2%, P=0.001) were significantly higher in MVP patients with fQRS. In multiple logistic regression analysis, the presence of bileaflet prolapse (OR: 2.567, 95%CI: 1.434 to 4.367; P=0.002) and presence of fQRS (OR: 3.021, 95%CI: 1.556 to 6.232; P<0.001) were independent predictors for complex VAs. The presence of fQRS may be associated with complex VAs in patients with MVP. Therefore, fQRS may be used in risk stratification of complex VAs in patients with MVP.

Presence of fragmented QRS may be associated with complex ventricular arrhythmias in patients with type-2 diabetes mellitus

Background Ventricular arrhythmias (VAs) are frequent in diabetes mellitus (DM) patients. Myocardial fibrosis is one of the components of diabetic cardiomyopathy secondary to DM. Fragmented QRS (fQRS) on electrocardiography (ECG) has been shown to be a marker of myocardial fibrosis. In this study, we aimed to investigate the association between fQRS and complex VAs in patients with DM. Methods Three hundred and thirty-six consecutive patients who were diagnosed with DM were included in the study. The control group consisted of 275 age- and sex-matched healthy individuals. ECG and transthoracic echocardiography were performed in all the patients. fQRS was defined as additional R’ wave or notching/splitting of S wave in two contiguous ECG leads. All the patients underwent 24-h Holter monitoring and VAs were classified using Lown’s scoring system. Lown class ≥ 3 VAs were considered as complex VAs. Results As compared to the healthy individuals, prevalence of fQRS (37.5% vs. 6.9%, p < .001) and complex VAs (14% vs. 0%, p < .001) were significantly higher in patients with DM. Furthermore, complex VAs (28.4% vs. 6.4%, p < .001) were significantly higher in DM patients with fQRS. In multiple logistic regression analysis, DM duration (OR: 1.510, 95% CI:1.343 to 1.698; p < .001) and presence of fQRS (OR: 3.262, 95% CI: 1.443 to 7.376; p = .004) were independent predictors for complex VAs. Conclusions The presence of fQRS may be associated with complex VAs in patients with DM. Therefore, fQRS may be used as a predictor of complex VAs and the risk of sudden death in patients with DM.

Presence of fragmented QRS may be associated with complex ventricular arrhythmias in patients with essential hypertension

BackgroundVentricular arrhythmias (VAs) are frequent in hypertensive patients. Myocardial fibrosis is one of the components of left ventricular hypertrophy secondary to hypertension. Fragmented QRS (fQRS) on electrocardiography (ECG) has been shown to be a marker of myocardial fibrosis. In this study, we aimed to investigate the association between fQRS and complex VAs in patients with essential hypertension. MethodsTwo hundreds consecutive patients who were diagnosed with hypertension were included in the study. The control group consisted of 153 age and sex matched healthy individuals. ECG and transthoracic echocardiography were performed to all patients. fQRS was defined as additional R' wave or notching/splitting of S wave in two contiguous ECG leads. All patients underwent 24-hour Holter monitoring and VAs were classified using Lown's scoring system. Lown class ≥3 VAs were considered as complex VAs. ResultsThere was no significant difference with respect to age (52 ± 8 vs 52 ± 6 years, p = 0.836) and gender distribution (female: 64% vs 63%, p = 0.907) between the groups. As compared to the healthy individuals, prevalence of fQRS (67% vs 9.2%, p < 0.001) and complex VAs (19% vs 0%, p < 0.001) were significantly higher in patients with hypertension. Furthermore, complex VAs (25.4% vs 6.1%, p = 0.001) were significantly higher in hypertensive patients with fQRS. In multiple logistic regression analysis, left ventricular ejection fraction (OR: 1.11, 95%CI: 1.025 to 1.183; p = 0.006), left ventricular mass index (OR: 1.04, 95%CI: 1.021 to 1.107; p = 0.001) and presence of fQRS (OR: 5.605, 95%CI: 1.427 to 22.019; p = 0.014) were independent predictors for complex VAs. ConclusionThe presence of fQRS may be associated with complex VAs in patients with essential hypertension. Therefore, fQRS may be used in risk stratification of complex VAs and sudden cardiac death especially in hypertensive patients with left ventricular hypertrophy.

Does the ‘Normal’ QRS (duration

Ventricular arrhythmias (VAs) are frequent in hypertensive patients. Myocardial fibrosis is one of the components of left ventricular hypertrophy secondary to hypertension. Fragmented QRS (fQRS) on electrocardiography (ECG) has been shown to be a marker of myocardial fibrosis. In this study, we aimed to investigate the association between fQRS and complex VAs in patients with essential hypertension.Two hundreds consecutive patients who were diagnosed with hypertension were included in the study. The control group consisted of 153 age and sex matched healthy individuals. ECG and transthoracic echocardiography were performed to all patients. fQRS was defined as additional R' wave or notching/splitting of S wave in two contiguous ECG leads. All patients underwent 24-hour Holter monitoring and VAs were classified using Lown's scoring system. Lown class ≥3 VAs were considered as complex VAs.There was no significant difference with respect to age (52 ± 8 vs 52 ± 6 years, p = 0.836) and gender distribution (female: 64% vs 63%, p = 0.907) between the groups. As compared to the healthy individuals, prevalence of fQRS (67% vs 9.2%, p < 0.001) and complex VAs (19% vs 0%, p < 0.001) were significantly higher in patients with hypertension. Furthermore, complex VAs (25.4% vs 6.1%, p = 0.001) were significantly higher in hypertensive patients with fQRS. In multiple logistic regression analysis, left ventricular ejection fraction (OR: 1.11, 95%CI: 1.025 to 1.183; p = 0.006), left ventricular mass index (OR: 1.04, 95%CI: 1.021 to 1.107; p = 0.001) and presence of fQRS (OR: 5.605, 95%CI: 1.427 to 22.019; p = 0.014) were independent predictors for complex VAs.The presence of fQRS may be associated with complex VAs in patients with essential hypertension. Therefore, fQRS may be used in risk stratification of complex VAs and sudden cardiac death especially in hypertensive patients with left ventricular hypertrophy.

A Low-cost Version of the Fridericia´s Formula for QT Correction

Ventricular arrhythmias (VAs) are frequent in hypertensive patients. Myocardial fibrosis is one of the components of left ventricular hypertrophy secondary to hypertension. Fragmented QRS (fQRS) on electrocardiography (ECG) has been shown to be a marker of myocardial fibrosis. In this study, we aimed to investigate the association between fQRS and complex VAs in patients with essential hypertension.Two hundreds consecutive patients who were diagnosed with hypertension were included in the study. The control group consisted of 153 age and sex matched healthy individuals. ECG and transthoracic echocardiography were performed to all patients. fQRS was defined as additional R' wave or notching/splitting of S wave in two contiguous ECG leads. All patients underwent 24-hour Holter monitoring and VAs were classified using Lown's scoring system. Lown class ≥3 VAs were considered as complex VAs.There was no significant difference with respect to age (52 ± 8 vs 52 ± 6 years, p = 0.836) and gender distribution (female: 64% vs 63%, p = 0.907) between the groups. As compared to the healthy individuals, prevalence of fQRS (67% vs 9.2%, p < 0.001) and complex VAs (19% vs 0%, p < 0.001) were significantly higher in patients with hypertension. Furthermore, complex VAs (25.4% vs 6.1%, p = 0.001) were significantly higher in hypertensive patients with fQRS. In multiple logistic regression analysis, left ventricular ejection fraction (OR: 1.11, 95%CI: 1.025 to 1.183; p = 0.006), left ventricular mass index (OR: 1.04, 95%CI: 1.021 to 1.107; p = 0.001) and presence of fQRS (OR: 5.605, 95%CI: 1.427 to 22.019; p = 0.014) were independent predictors for complex VAs.The presence of fQRS may be associated with complex VAs in patients with essential hypertension. Therefore, fQRS may be used in risk stratification of complex VAs and sudden cardiac death especially in hypertensive patients with left ventricular hypertrophy.

Local Activation Delay Exacerbates Local J-ST Elevation in the Epicardium: Electrophysiological Substrate in Brugada Syndrome

Ventricular arrhythmias (VAs) are frequent in hypertensive patients. Myocardial fibrosis is one of the components of left ventricular hypertrophy secondary to hypertension. Fragmented QRS (fQRS) on electrocardiography (ECG) has been shown to be a marker of myocardial fibrosis. In this study, we aimed to investigate the association between fQRS and complex VAs in patients with essential hypertension.Two hundreds consecutive patients who were diagnosed with hypertension were included in the study. The control group consisted of 153 age and sex matched healthy individuals. ECG and transthoracic echocardiography were performed to all patients. fQRS was defined as additional R' wave or notching/splitting of S wave in two contiguous ECG leads. All patients underwent 24-hour Holter monitoring and VAs were classified using Lown's scoring system. Lown class ≥3 VAs were considered as complex VAs.There was no significant difference with respect to age (52 ± 8 vs 52 ± 6 years, p = 0.836) and gender distribution (female: 64% vs 63%, p = 0.907) between the groups. As compared to the healthy individuals, prevalence of fQRS (67% vs 9.2%, p < 0.001) and complex VAs (19% vs 0%, p < 0.001) were significantly higher in patients with hypertension. Furthermore, complex VAs (25.4% vs 6.1%, p = 0.001) were significantly higher in hypertensive patients with fQRS. In multiple logistic regression analysis, left ventricular ejection fraction (OR: 1.11, 95%CI: 1.025 to 1.183; p = 0.006), left ventricular mass index (OR: 1.04, 95%CI: 1.021 to 1.107; p = 0.001) and presence of fQRS (OR: 5.605, 95%CI: 1.427 to 22.019; p = 0.014) were independent predictors for complex VAs.The presence of fQRS may be associated with complex VAs in patients with essential hypertension. Therefore, fQRS may be used in risk stratification of complex VAs and sudden cardiac death especially in hypertensive patients with left ventricular hypertrophy.

Pathogenesis of the Novel Autoimmune-Associated Long-QT Syndrome.

Emerging clinical evidence demonstrates high prevalence of QTc prolongation and complex ventricular arrhythmias in patients with anti-Ro antibody (anti-Ro Ab)-positive autoimmune diseases. We tested the hypothesis that anti-Ro Abs target the HERG (human ether-a-go-go-related gene) K(+) channel, which conducts the rapidly activating delayed K(+) current, IKr, thereby causing delayed repolarization seen as QT interval prolongation on the ECG. Anti-Ro Ab-positive sera, purified IgG, and affinity-purified anti-52kDa Ro Abs from patients with autoimmune diseases and QTc prolongation were tested on IKr using HEK293 cells expressing HERG channel and native cardiac myocytes. Electrophysiological and biochemical data demonstrate that anti-Ro Abs inhibit IKr to prolong action potential duration by directly binding to the HERG channel protein. The 52-kDa Ro antigen-immunized guinea pigs showed QTc prolongation on ECG after developing high titers of anti-Ro Abs, which inhibited native IKr and cross-reacted with guinea pig ERG channel. The data establish that anti-Ro Abs from patients with autoimmune diseases inhibit IKr by cross-reacting with the HERG channel likely at the pore region where homology between anti-52-kDa Ro antigen and HERG channel is present. The animal model of autoimmune-associated QTc prolongation is the first to provide strong evidence for a pathogenic role of anti-Ro Abs in the development of QTc prolongation. It is proposed that adult patients with anti-Ro Abs may benefit from routine ECG screening and that those with QTc prolongation should receive counseling about drugs that may increase the risk for life-threatening arrhythmias.

Is there any influence of elevated diastolic blood pressure on ventricular arrhythmias in hypertensive patients with left ventricular hypertrophy?

Cardiologia CROATICA Objective: To investigate the prevalence of ventricular arrhythmias in a patient with isolated systolic hypertension (ISHT) and left ventricular hypertrophy (LVH) in comparison to patients with systolic and diastolic hypertension and LVH. Patients and Methods: 192 (87 men) patients with essential hypertension and LVH were divided into two groups: 98 patients with ISHT and 94 patients with systolic and diastolic hypertension. After discontinuing all medications for a period of 48 hours, the blood pressure was measured, electrocardiography, echocardiography, Holter monitoring and bicycle ergometry were performed. The number of ventricular arrhythmias was recorded. Antihypertensive drugs and the duration of previous treatment were taken into consideration. Results: Isolated systolic hypertension (systolic blood pressure >140 mmHg and diastolic blood pressure <90 mmHg) was recorded in 98 patients (51%), 47 men and 51 women (Table 1). The frequency of ventricular arrhythmias did not differ according to Lowns classification categories I-II and IIIIV in patients with and without isolated systolic hypertension (Table 2). There was no difference in the treatment duration between the groups (p=0.858), or in the type of the applied medication. We found 44% complex ventricular arrhythmias in patients with ISHT. No significant difference was found in the frequency of ventricular arrhythmias between the groups that were observed. Conclusions: No significant difference was found in the frequency of ventricular arrhythmias in patients with isolated systolic hypertension and LVH in comparison to patients with systolic and diastolic hypertension and LVH. Diastolic blood pressure does not seem to have any influence on the frequency of ventricular arrhythmias in such patients.

Comparison of Frequency of Complex Ventricular Arrhythmias in Patients With Positive Versus Negative Anti-Ro/SSA and Connective Tissue Disease

A previous study of electrocardiography at rest showed that anti-Ro/SSA-positive patients with connective tissue disease (CTD) frequently had corrected QT (QTc) interval prolongation. Because QTc interval prolongation is a definite risk factor for arrhythmic sudden death in the general population, a 24-hour electrocardiographic monitoring study was performed to investigate the possible relation between QTc interval prolongation and incidence of ventricular arrhythmias as a possible expression of immunomediated electric instability of the myocardium in anti-Ro/SSA-positive patients with CTD. The study population consisted of 46 patients with CTD; 26 anti-Ro/SSA-positive and 20 anti-Ro/SSA-negative (control group) patients (Sjögren's syndrome, 9 and 3 patients; systemic lupus erythematosus, 4 and 9 patients; systemic sclerosis, 2 and 4 patients; undifferentiated CTD, 8 and 1 patients; mixed CTD, 2 and 2 patients, and polymyositis/dermatomyositis, 1 and 1 patient, respectively). All patients underwent ambulatory Holter electrocardiography to obtain 24-hour monitoring of the QTc interval and ventricular arrhythmias. With respect to the control group, anti-Ro/SSA-positive patients with CTD (1) commonly showed QTc interval prolongation (46% vs 5%), and this abnormality, when present, persisted for the 24 hours (global mean 24-hour QTc interval 440.5+/-23.4 vs 418.2+/-13.2 ms); (2) had a higher incidence of complex ventricular arrhythmias (i.e., Lown classes 2 to 5, 50% vs 10%) also in the absence of detectable cardiac abnormalities; and (3) in patients with CTD, there is a direct relation between global mean 24-hour QTc interval and ventricular arrhythmic load independently of age and disease duration. In conclusion, anti-Ro/SSA-positive patients with CTD seemed to have a particularly high risk of developing ventricular arrhythmias. The risk appeared related mainly to abnormalities in ventricular electrophysiologic characteristics emerging in the clinical setting as QTc interval prolongation.

Ventricular arrhythmias in Takayasu arteritis

We studied the prevalence, severity and clinical significance of ventricular arrhythmias in 78 female patients with Takayasu arteritis by 24-h ambulatory electrocardiography monitoring. Fifty (64%) of 78 patients had no or less than 30 beats/h premature ventricular contractions (Group A). The remaining 28 (36%) patients exhibited frequent or complex premature ventricular contractions (Group B). The frequency of HLA Bw 52 which is closely associated with this morbid condition, echocardiographic and thallium-201 stress myocardial scintigraphic findings were then compared between these two groups. The frequency of positive HLA Bw52 was not significantly different between these two groups. Echocardiographically determined left ventricular mass (309 ± 94 vs. 166 ± 64 g; P < 0.01), frequency of complicated aortic regurgitation (77% vs. 24%; P < 0.01) and abnormal thallium-201 scintigraphic findings (76% vs. 38%; P < 0.05) were found higher in Group B as compared with those in Group A. These data indicate that frequent or complex ventricular arrhythmias in patients with Takayasu arteritis were associated with the presence of left ventricular hypertrophy, aortic regurgitation and decreased coronary reserve.

Should complex ventricular arrhythmias in patients with congestive heart failure be treated? A protagonist's viewpoint

Should complex ventricular arrhythmias in patients with congestive heart failure be treated? A protagonist's viewpoint

Effects of milrinone on complex ventricular arrhythmias in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

To determine whether oral milrinone therapy has an effect on complex ventricular arrhythmias in patients with severe congestive heart failure and, if so, whether a change in the severity of complex ventricular arrhythmias after 1 week of milrinone therapy is associated with a change in the mode or frequency of cardiac mortality, a retrospective analysis was performed to determine the frequency of ventricular tachycardia and the density of ventricular couplets on 24-hour ambulatory electrocardiographic recordings performed before and 1 week after initiation of oral milrinone therapy in 74 consecutive patients with New York Heart Association functional class III or IV congestive heart failure. The endpoints of mortality and mode of death were assessed during a mean follow-up of 6 months. In 91% of the patients, 1 week of oral milrinone therapy was associated with no significant change (85%) or a significant decrease (6%) in the density of ventricular couplets and frequency of ventricular tachycardia. However, in 9% of patients the frequency of complex ventricular arrhythmias increased significantly at the end of 1 week of oral milrinone therapy. In this subgroup, neither total cardiac mortality nor the incidence of sudden cardiac death was significantly higher than that in patients with no change or a decrease in complex ventricular ectopic activity.

Complex ventricular arrhythmias in patients with Q wave versus non-Q wave myocardial infarction.

We examined whether or not subsets of patients with complex ventricular arrhythmias after myocardial infarction are at high risk with respect to 1 year mortality after hospital discharge. Based on previous studies showing increased risk for those with non-Q wave infarcts, we hypothesized that complex PVCs (premature ventricular complexes) in this group might be associated with a poorer prognosis than complex PVCs in patients with Q wave infarcts. Seven hundred seventy-seven patients entering our study with acute infarction were followed prospectively for 1 year after undergoing a predischarge 24 hr ambulatory electrocardiographic examination. Patients were classified by electrocardiographic criteria into the following groups: Non-Q wave (n = 191), Q wave anterior (n = 261), and Q wave inferior infarction (n = 325). The following arrhythmias were classified as complex: multiform PVCs, couplets, and ventricular tachycardia. Sixty-two percent of patients with non-Q wave infarcts who did not survive 1 year had complex PVCs, compared with 32% of survivors (p less than .01). No differences were seen in the Q wave subgroup. The survival for patients with Q wave and non-Q wave infarction without complex PVCs were nearly identical at 1 year (93% and 90%), whereas in patients with complex PVCs survival for those with Q wave and non-Q wave infarction was 92% and 76%, respectively (p less than .001). Of those with non-Q wave infarction, only 4% of nonsurvivors were free of any PVCs, as compared with 28% of nonsurvivors in the Q wave group (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)

Left Ventricular Function in Patients with Ventricular Arrhythmias and Aortic Valve Disease

Forty patients having aortic valve replacement were evaluated preoperatively for ventricular arrhythmia and left ventricular ejection fraction. Arrhythmias were classified as complex or simple using the Lown criteria on the 24-hour ambulatory electrocardiogram; ejection fractions were determined by radionuclide gated blood pool analysis and contrast angiography. The ejection fractions determined by radionuclide angiography were 59.1 ± 13.1% for 26 patients with simple or no ventricular arrhythmias, and 43.9 ± 20.3% for 14 patients with complex ventricular arrhythmias ( p < 0.01). Ejection fractions determined by angiography, available for 31 patients, were also lower in patients with complex ventricular arrhythmias (61.1 ± 16.3% versus 51.4 ± 13.4%; p < 0.05). Seven of 9 patients showing conduction abnormalities on the electrocardiogram had complex ventricular arrhythmias. Eight of 20 patients with aortic stenosis had complex ventricular arrhythmias, while 2 of 13 patients with aortic insufficiency had such arrhythmias. It is concluded that decreased left ventricular ejection fraction, intraventricular conduction abnormalities, and aortic stenosis are associated with an increased frequency of complex ventricular arrhythmias in patients with aortic valve disease.

Complex ventricular arrhythmias in patients with valvular regurgitation: A potentially important, clinically overlooked phenomenon?

Complex ventricular arrhythmias in patients with valvular regurgitation: A potentially important, clinically overlooked phenomenon?

Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction.

HomeCirculationVol. 57, No. 5Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBClinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction. K P Anderson, J DeCamilla and A J Moss K P AndersonK P Anderson Search for more papers by this author , J DeCamillaJ DeCamilla Search for more papers by this author and A J MossA J Moss Search for more papers by this author Originally published1 May 1978https://doi.org/10.1161/01.CIR.57.5.890Circulation. 1978;57:890–897 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByZaman S and Kovoor P (2014) Sudden Cardiac Death Early After Myocardial Infarction, Circulation, 129:23, (2426-2435), Online publication date: 10-Jun-2014.Josephson M (1986) Treatment of ventricular arrhythmias after myocardial infarction., Circulation, 74:4, (653-658), Online publication date: 1-Oct-1986.Kuo C, Atarashi H, Reddy C and Surawicz B (1985) Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes., Circulation, 72:2, (370-376), Online publication date: 1-Aug-1985.Maisel A, Scott N, Gilpin E, Ahnve S, Le Winter M, Henning H, Collins D and Ross J (1985) Complex ventricular arrhythmias in patients with Q wave versus non-Q wave myocardial infarction., Circulation, 72:5, (963-970), Online publication date: 1-Nov-1985.Roy D, Marchand E, Théroux P, Waters D, Pelletier G and Bourassa M (1985) Programmed ventricular stimulation in survivors of an acute myocardial infarction., Circulation, 72:3, (487-494), Online publication date: 1-Sep-1985.Bigger J, Fleiss J, Kleiger R, Miller J and Rolnitzky L (1984) The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction., Circulation, 69:2, (250-258), Online publication date: 1-Feb-1984.Gomes J, Hariman R, Kang P, El-Sherif N, Chowdhry I and Lyons J (1984) Programmed electrical stimulation in patients with high-grade ventricular ectopy: electrophysiologic findings and prognosis for survival., Circulation, 70:1, (43-51), Online publication date: 1-Jul-1984.Kleiger R, Miller J, Thanavaro S, Province M, Martin T and Oliver G (1981) Relationship between clinical features of acute myocardial infarction and ventricular runs 2 weeks to 1 year after infarction., Circulation, 63:1, (64-70), Online publication date: 1-Jan-1981. May 1, 1978Vol 57, Issue 5Article InformationMetrics Copyright © 1978 by American Heart Associationhttps://doi.org/10.1161/01.CIR.57.5.890 Originally publishedMay 1, 1978 PDF download Advertisement