An unusual case of a giant pseudoaneurysm formation after myocardial infarction.

In the era of early and invasive therapeutic approaches, myocardial rupture has become an uncommon complication of myocardial infarction. We report an uncommon complication following inferior myocardial infarction with both left ventricular and right ventricular rupture and subsequent communication via a shared pseudoaneurysm.

Association of plasma osteopontin levels with coronary calcification evaluated by tomographic coronary calcium scoring.

Evidence indicates that proteins controlling bone mineralization are also involved in the regulation of coronary calcification. The aim of the present study is to evaluate the association between plasma osteopontin (OPN) levels and coronary calcification quantified by using tomographic coronary calcium scoring. Plasma OPN levels were measured from samples of 80 intermediate-risk asymptomatic patients (56 +/- 10 years) who underwent tomographic coronary calcium scoring via multislice computed tomography for incremental risk stratification. There was no significant difference regarding OPN levels between patients with and without coronary calcification in the whole study population. Of 49 patients not receiving renin-angiotensin system inhibitors and/or statins, plasma OPN levels of patients with coronary calcification (38.7%) were significantly higher than those without coronary calcification (61.3%) (8.88 +/- 2.85 vs. 6.79 +/- 2.41, P = 0.008, respectively). On a binary logistic regression model, only age and plasma OPN level were found to be significant independent associated variables for the presence of coronary calcification in patients not receiving these medications (odds ratio for age, 1.15, P = 0.017; for plasma OPN levels, 1.63, P = 0.014). Our results indicate that plasma OPN levels may be predictive of coronary calcification, suggesting an important role of OPN in the atherosclerotic calcification pathogenesis.

QT dispersion increases in patients with systemic lupus erythematosus.

Although autopsy studies have documented that heart is affected in most of systemic lupus erythematosus (SLE) patients, clinical manifestations occur in less than 10%. QT dispersion, a new parameter that can be used to assess homogeneity of cardiac repolarization and autonomic function, has not been studied in SLE patients. The aim of our study was to evaluate the QT dispersion (QTd) in SLE patients without overt cardiac involvement. Eighty-three patients with a diagnosis of SLE (mean age 41+/-13) and age- and sex-matched 77 healthy control subjects (mean age 43+/-10) were enrolled in the study. All subjects had their complete history taken, laboratory examination, and transthoracic echocardiography (ECG). Patients with cardiac disease, hypertension, diabetes, or taking medications that may effect QTd or any ECG abnormalities were excluded. Resting 12-lead ECG were recorded for measurement of QTd. None of the patients and control subjects had overt cardiac involvement. The mean SLE duration was 86.5+/-15.4 months. QT dispersion was significantly greater in SLE patients than incontrol subjects (55.2+/-24.7 vs 20.7+/-5.3 ms, respectively; p<0.001). There was no correlation between QTd and duration of SLE, SLEDAI-K score, corticosteroid usage, and presence of anti SS-A antibody. QT dispersion is significantly increased in SLE patients without overt cardiac involvement. Our result suggests that prolonged QT dispersion can be a useful noninvasive and simple method for early detection of cardiac involvement in SLE patients.

B-type natriuretic peptide (BNP) levels in female systemic lupus erythematosus patients: what is the clinical significance?

Cardiovascular disease is a major cause of death in patients with systemic lupus erythematosus (SLE) especially during the late phase of the disease. This study was conducted to evaluate B-type natriuretic peptide (BNP) levels in female SLE patients without cardiac symptoms and to investigate whether BNP levels correlated with echocardiographic findings. We studied 59 women with SLE and 33 healthy women. SLE patients with history of cardiac disease, diabetes mellitus, hypertension, and other inflammatory diseases were excluded from the study. All subjects had a complete history and physical examination. Overall disease activity assessment in SLE patients at the time of the study were derived by calculation of SLE disease activity index (SLEDAI). BNP levels were determined, and transthoracic echocardiography were performed in all subjects. There was no difference between SLE patients and controls in terms of age, blood pressure, smoking status, plasma glucose, creatinine levels, and lipid profiles. Nine patients had SLEDAI score greater than 5. All subjects had an EF greater than 55%. Diastolic dysfunction was more frequent in lupus patients than in controls (15 [25.4%] vs. 2 [6%]; p = 0.022). BNP levels of SLE patients were significantly higher than controls (median 17.9 range [5-211] pg/ml vs. median 14.7 range [5-39.7] pg/ml; p = 0.033). Twenty-seven of the SLE patients (46%) and seven of the controls (21%) had BNP levels greater than or equal to 20 pg/ml (p = 0.019). There were no differences in BNP levels of SLE patients with and without diastolic dysfunction (median 17.8 range [5-117] pg/ml vs. median 18.5 range [5-211] pg/mL; p = NS). BNP levels were positively correlated with left atrium diameter (r (2) = 0.39, p = 0.001). BNP levels did not correlate with erythrocyte sedimentation rate/C-reactive protein levels, SLEDAI scores, total steroid dosage used, or other echocardigraphic parameters. BNP levels were increased in female SLE patients without cardiac symptoms as compared to healthy controls. Although none of the SLE patients in our study had clinical signs of ischemic heart disease, increased levels of BNP in SLE patients might be a reflection of a ischemic myocardial tissue.

QT interval dispersion changes according to the vessel involved during percutaneous coronary angioplasty.

Increased QT dispersion (QTd) is a noninvasive marker of an electrophysiologic abnormality associated with high mortality in coronary artery disease. The purposes of this study were to measure changes in QTd and ST-segment changes immediately before, during and after intracoronary balloon inflation and to determine whether the coronary artery vessel involved and/or the duration of inflation affect(s) QTd. A total of 45 patients (32 men, 13 women, mean age 58 +/- 11 years) who were referred for elective percutaneous transluminal coronary angioplasty were included. The mean QT interval dispersions for all patients before the inflation, during the balloon inflation at 60 sec and after the balloon deflation at 5 min were 68 +/- 13 ms, 82 +/- 16 ms and 71 +/- 13 ms, respectively. There was no significant difference between baseline and 5 min after deflation. The increase in QTd during the balloon inflation was significant (p<0.01). There was no significant QTd change in patients with left circumflex artery (Cx) lesions during inflation and after deflation compared with baseline. The differences were statistically significant only in patients with left anterior descending (LAD) lesions and right coronary artery (RCA) lesions at 60 sec during balloon inflation (p=0.001 vs. p=0.04). Acute reversible myocardial ischemia induced by balloon inflation causes an increase in QTd limited to the LAD and RCA vessels. Therefore, when using QTd as a marker of myocardial repolarization abnormality due to acute reversible ischemia, the involved coronary artery vessel must be taken into account.

Plasma soluble osteopontin concentrations are increased in patients with rheumatic mitral stenosis and associated with the severity of mitral valve calcium.

Although the severity of valvular calcification is an important prognostic indicator, the cellular mechanisms of the calcification process are unknown. Osteopontin modulates inflammation and biomineralization, and increased osteopontin expression has been demonstrated in calcified degenerative or rheumatic cardiac valves. The present study evaluated soluble plasma osteopontin in 32 patients with echocardiographically determined rheumatic mitral stenosis and compared the results to those of a control group of 22 healthy patients. Patients were evaluated with routine echocardiographic techniques, Wilkins scoring, and 2-dimensional echocardiographic calcium scoring. Patients with rheumatic involvement other than in the mitral valve were excluded. Plasma osteopontin and high-sensitivity C-reactive protein levels in patients with mitral stenosis were significantly higher those of the control group (p = 0.006 and p = 0.0001, respectively). A significant correlation was found between plasma osteopontin levels and the severity of mitral valve calcification (p = 0.003) and also between high-sensitivity C-reactive protein levels and Wilkins score (p = 0.009). There was a stepwise and statistically significant increase in soluble plasma osteopontin levels in association with the severity of mitral valve calcification. In conclusion, increased osteopontin levels were correlated with the severity of mitral valve calcification in patients with rheumatic mitral stenosis, suggesting an important role of osteopontin in the modulation of valvular calcification. Elevated levels of high-sensitivity C-reactive protein concentrations suggest the presence of ongoing inflammation in those patients.

Plasma osteopontin levels are elevated in non-ST-segment elevation acute coronary syndromes.

BACKGROUND: The regions of ruptured atherosclerotic plaques have numerous macrophages. Osteopontin that modulates macrophage function has been shown in atherosclerotic plaques. We aimed to study the plasma levels of osteopontin in patients with unstable angina or non-ST-seg ment elevation myocardial infarction (NSTEMI) and the rela tionship between osteopontin and the extent of the coronary artery disease (CAD). METHODS: We studied 65 patients with unstable angina or NSTEMI, 25 patients with stable angina and 18 patients as the control group. The extent of coronary artery stenosis was determined by the number of vessels with >50% stenosis. Plasma osteopontin concentrations were measured from the blood samples that were drawn immediately after admission to the emergency department in unstable angina/NSTEMI patients and before the coronary angiograph in the stable angina and control groups. RESULTS: The plasma osteopontin concentration was (495 118 ng/ml) significantly higher in the patients with unstable angina/NSTEMI compared to the stable angina group (319 106 ng/ml) and control group (125+/-54 ng/ml) (p=0.0001 The plasma osteopontin levels were lower in the patients with stable angina pectoris who had one-vessel disease compared to those with two-vessel disease (p=0.01). How ever, in the unstable angina/NSTEMI group, the plasma osteopontin levels were statistically not different among the patients with one-vessel, and two-vessel and three-vessel disease (p=NS). There was no correlation between the plasma osteopontin levels and the extent of coronary stenosis. CONCLUSIONS: The plasma osteopontin levels are elevatedin patients with unstable angina/NSTEMI, but there appears to be no correlation with the extent of CAD. These results ma suggest that osteopontin may have a role in the pathobiology of ACS.

Right ventricular outflow tract thrombus in a case of Behcet's disease.

Behcet's disease is known as a chronic systemic vasculitic syndrome, the hallmark of which is recurrent oral aphthous and genital ulcerations and uveitis. Vascular involvement, mainly thrombosis, reportedly affects as many as one-third of patients. Cardiac involvement, however, is very rare. We present in this report a young female patient developing right ventricular thrombus while being treated medically.

Impaired fibrinolytic capacity in rheumatic mitral stenosis with or without atrial fibrillation and nonrheumatic atrial fibrillation.

Chronic atrial fibrillation (AF) has often been associated with systemic embolization, and patients with mitral stenosis (MS) have the highest thromboembolic risk. Increased risk of thromboembolism could be in part due to impaired fibrinolytic function. Global fibrinolytic capacity (GFC) is an innovative technique for evaluating the entire fibrinolytic system. The aim of our study was to evaluate fibrinolytic activity in patients with rheumatic and nonrheumatic chronic AE To investigate fibrinolytic activity, we assessed GFC in peripheral blood samples of 32 patients with nonrheumatic AF (14 women; mean age, 56 +/- 1 years), 30 patients with rheumatic MS and AF (23 women; mean age, 35 +/- 9 years), and 32 patients with rheumatic MS and sinus rhythm (24 women; mean age, 36 +/- 8 years). The control group comprised 30 healthy adult subjects in normal sinus rhythm. Patients with chronic AF (rheumatic and nonrheumatic) had lower GFC than did the controls (P = .0001). The rheumatic AF group also showed decreased levels of GFC compared with the nonrheumatic AF group, with the rheumatic MS and sinus rhythm group, and with controls (P = .03, P = .02, P = .0001, respectively). GFC was lower in patients with rheumatic MS and sinus rhythm than in controls (P = .003). Although there were correlations between GFC and mitral valve area, transmitral mean gradient, left atrial diameter, and mitral calcification in patients with rheumatic MS, multivariate analysis showed only transmitral gradient as an independent factor affecting GFC. Patients with AF have decreased GFC, a finding that suggests the presence of a hypofibrinolytic state. Fibrinolytic dysfunction was more pronounced in rheumatic MS patients with AF than in those with nonrheumatic AF. Moreover, patients with rheumatic MS and sinus rhythm had decreased global fibrinolytic activity. Hypofibrinolysis documented by decreased GFC can be one of the important causes of increased risk of embolism in patients with AF and rheumatic MS.

Effects of short-term atorvastatin treatment on global fibrinolytic capacity, and sL-selectin and sFas levels in hyperlipidemic patients with coronary artery disease.

BACKGROUND: The beneficial effects of HMG-CoA reductase inhibitors (statins) in patients with coronary artery disease (CAD) appear to be attributable not only to their lipid-lowering properties, but also to their therapeutic effects on the coagulation system, and anti-inflammatory effect. Furthermore, statins mitigate the apoptosis of vascular smooth muscle cells (VSMC) and macrophages in atherosclerotic plaques. HYPOTHESIS: The purpose of this study was to evaluate the effects of short-term atorvastatin treatment on the fibrinolytic system and systemic inflammatory status, and on apoptosis in hyperlipidemic patients with CAD. METHODS: The study population consisted of 36 hyperlipidemic patients (14 women and 22 men, mean age 53+/-9 years) with stable CAD, untreated with lipid-lowering medications. Serum lipoproteins, fibrinogen levels, sFas and sL-selectin, and global fibrinolytic capacity (GFC) were measured at baseline and after 12 weeks of treatment with atorvastatin, 10 mg/day. RESULTS: Atorvastatin treatment decreased serum low-density lipoprotein (-39%, P=0.0001), total cholesterol (-32%, P=0.0001), and triglycerides (-22%, P=0.0001), and increased high-density lipoprotein (+13%, P=0.0001) at 12 weeks compared to baseline. These effects were associated with a decrease in plasma fibrinogen from 331+/-73 to 298+/-58 mg/dl (P=0.0001), and sL-selectin levels from 666+/-201 to 584+/-162 ng/ml (P=0.0001). sFas levels and GFC increased from 3754+/-1264 to 4873+/-1835 pg/ml and from 3.5+/-2.4 to 5.6+/-2.9 microg/ml, respectively (both P=0.0001). CONCLUSIONS: These results suggest that lipid lowering with atorvastatin therapy significantly increases GFC, decreases fibrinogen levels, and causes leukocyte deactivation. Our findings also suggest that atorvastatin treatment mitigates apoptosis of VSMC in the atherosclerotic plaque. These effects of atorvastatin may, in part, explain the early decrease in cardiovascular events observed in clinical trials of statins.

Detection of patients with hypertrophic cardiomyopathy at risk for paroxysmal atrial fibrillation during sinus rhythm by P-wave dispersion.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) in hypertrophic cardiomyopathy (HCM) is associated with poor prognosis. Previous studies have shown good correlation between P-wave dispersion (Pd) and occurrence of PAF. However, Pd in patients with HCM for predicting PAF has not been studied. HYPOTHESIS: The aim of the study was to determine whether Pd could identify patients with HCM who are likely to suffer from PAF. METHODS: Twenty-two patients with HCM with a history of PAF (Group 1) and 26 patients with HCM without a history of PAF (Group 2) were studied. Maximum (Pmax) and minimum (Pmin) P-wave durations, as well as P-wave dispersion (Pd = Pmax - Pmin) were calculated from 12-lead surface electrocardiograms (ECG). RESULTS: P-wave dispersion was significantly different between the groups (Group 1: 55 +/- 6 ms vs. Group 2: 37 +/- 8 ms; p<0.001), while Pmax (Group 1: 134 +/- 11 ms vs. Group 2: 128 +/- 13 ms; p = 0.06) and Pmin (Group 1: 78 +/- 9 ms vs. Group 2: 81 +/- 7 ms; p = 0.07) was not significantly different. Patients with a history of PAF had higher left atrial diameter than the patients without PAF (Group 1: 52 +/- 8 mm vs. Group 2: 48 +/- 10 mm; p = 0.02). A cut-off value of 46 ms for Pd had a sensitivity of 76% and a specificity of 82% in discriminating between patients with and without PAF. CONCLUSION: This study suggests that P-wave dispersion could identify patients with HCM who are likely to develop PAF.

Diminished global fibrinolytic capacity in patients with mitral valve prolapse is associated with transient ischemic attacks.

Although mitral valve prolapse (MVP) has shown to be associated with thromboembolic complications, the cause of thromboembolic events in those patients is still unknown. The purpose of this study was to evaluate the fibrinolytic activity in MVP patients. The study included 35 consecutive patients (25 women, mean age 25+/-11 years) with echocardiographically documented MVP and 25 age- and sex-matched subjects as a control group. Four of MVP patients have a history of transient ischemic attack (TIA). Global fibrinolytic capacity (GFC), a new technique that examines the effectiveness of the entire fibrinolytic system, was measured. Global fibrinolytic capacity was found to be nonsignificantly increased in MVP patients (3.14+/-1.42 microg/mL) compared to those in control subjects (2.36+/-1.33 microg/mL) (p>0.05). However, in four of these MVP patients who had a history of transient ischemic attack, the GFC level was significantly lower than in patients who have no history of transient ischemic attack (1.67+/-0.6 microg/mL vs 3.27+/-1.46 (microg/mL, p=0.003). Furthermore, the GFC levels of these four patients were less than those of controls (p=0.04). These results showed that global fibrinolytic activity was similar in MVP patients without a history of TIA and control subjects. However, MVP patients with a history of TIA had significantly decreased global fibrinolytic activity compared to controls and as well as MVP patients without a history of TIA.

Prevalence of coronary artery disease before valvular surgery in patients with rheumatic valvular disease.

BACKGROUND: Although many patients with valvular heart disease have concomitant coronary artery disease (CAD), there are limited data on the association between rheumatic valvular disease (RVD) and CAD. In this study, we aimed to investigate the prevalence of CAD in a group of patients with RVD and undergoing coronary angiography before valvular surgery. METHODS: In this retrospective analysis, we enrolled a total of 1075 patients (658 women, 61.2%; mean age: 53.2 ± 9.9 years) who underwent coronary angiography for the evaluation of CAD before valvular surgery between January 2003 and May 2010. RESULTS: The overall prevalence of significant CAD was 11.1%. Patients with significant CAD were older than patients without significant CAD (55.16 ± 10.4 vs. 51.45 ± 9.1; P<0.001). In addition, hypertension, smoking, diabetes mellitus, and dyslipidemia were more prevalent among patients with significant CAD (P<0.05). After adjustment for several risk factors, only aortic stenosis remained the predictor of significant CAD (odds ratio: 1.66; 95% confidence interval: 1.26-2.19; P<0.001). However, aortic regurgitation was inversely associated with the presence of CAD (odds ratio: 0.56; 95% confidence interval: 0.21-1.01; P<0.001). CONCLUSION: The overall prevalence of CAD in our population with RVD was low. Rheumatic aortic stenosis is associated with an increased prevalence of CAD, whereas the prevalence of CAD is lower in those patients with aortic regurgitation.

Intron 4 VNTR polymorphism of eNOS gene is protective for cardiac syndrome X.

Microvascular abnormalities caused by endothelial dysfunction seem to be responsible for the myocardial ischemia in patients with cardiac syndrome X (CSX). Nitric oxide is a key mediator of endothelial function and is synthesized by endothelial nitric oxide synthase (eNOS). We investigated if the 3 potential polymorphisms of the eNOS gene (VNTR in intron 4, T786C polymorphism in the promoter region, and G894T polymorphism in exon 7) are independent risk factors for CSX. Sixty-nine patients with CSX and 73 healthy controls were studied. Genotypes were determined through polymerase chain reaction with or without restriction endonuclease digestions. Genotype distribution was significantly different between patients with CSX and controls for intron 4aa (allele for 4 repeats of 27 bp), intron 4aa genotype frequency being 3.2% and 6.8%, respectively. The presence of intron 4a is 3.2 (odds ratio) times protective (95% confidence interval, 1.5-6.8) for the risk of CSX disease. The protective effect of intron 4a polymorphism also holds after adjustment for age and sex and when the study group is limited to those without hypertension and hyperlipidemia. No significant difference was observed in genotype distribution of G894T and T786C polymorphism between patients with CSX and controls. In conclusion, intron 4aa genotype of eNOS gene is protective for CSX. No association was found between promoter and exon 7 polymorphisms of eNOS gene and CSX.

[Mean systolic annular velocity and strain score index: new and non-invasive parameters for the evaluation of acute myocardial infarction patients]. / Ortalama sistolik anüler velosite ve strain skor indeksi: akut miyokart enfarktüsü hastalarinin degerlendirilmesinde yeni ve invazif olmayan parametreler.

OBJECTIVE: To evaluate the diagnostic value of mean annular velocity (MAV) and strain score index (SSI) for determination of the left ventricular systolic dysfunction in patients with first acute myocardial infarction (AMI). METHODS: Seventy-one patients (55 male, mean age: 59+/-12 years) with first acute ST-elevation myocardial infarction and 30 healthy subjects were included in this cross-sectional and observational study. Echocardiography with tissue Doppler and strain analysis was performed during initial hospital admission. Peak systolic myocardial velocities were recorded from 4 different sites on the mitral annulus. A MAV value was calculated and the peak systolic strain values of 12 segments were measured and a mean SSI was calculated. ROC curve analysis was used in order to determine cut-off values for MAV and SSI. RESULTS: The patients with AMI had a significantly reduced MAV compared with healthy subjects (5.52+/-1.78 cm/s vs 9.80+/-1.13 cm/s, p<0.001). In ROC analysis, a cut-off value of 8.41 cm/s (AUC 0.915, 95%CI 0.887-0.952, p<0.001) for MAV differentiated AMI patients from controls with 97.2% sensitivity and 93.3% specificity. The patients with AMI have also decreased SSI (11.23+/-2.83 vs 19.11+/-2.05, p<0.001). A cut-off value of 15.35% differentiated AMI patients from controls with 94.4% sensitivity and 100% specificity (ROC AUC 0.945, 95%CI 0.901-0.972, p<0.001). There was a good correlation between left ventricular EF and MAV (r=0.73, p<0.001) and SSI (r=0.66, p<0.001). CONCLUSION: The patients with first myocardial infarction have decreased mean systolic annular velocity and mean systolic strain score index.

[The early predictors of ventricular remodeling after myocardial infarction: the role of tumor necrosis factor-alpha]. / Akut miyokard infarktüsü sonrasi ventriküler yeniden biçimlenme erken belirleyicileri: Tümör nekrozis faktör-alfa'nin rolü.

OBJECTIVE: Ventricular remodeling (VR) is a pathologic process characterized by progressive ventricular dilatation occurring after acute myocardial infarction (MI) leading to left ventricular systolic dysfunction. The purpose of the study was to evaluate the efficacy of plasma tumor necrosis factor alpha (TNF-alpha) levels to predict the left VR. METHODS: This prospective observational cohort study included 72 consecutive patients with newly diagnosed MI with age ranging between 38-87 years (mean 59 +/- 12 years). Control group was consisted of 30 patients with no additional systemic disease and normal coronary arteriograms. Transthoracic echocardiography was performed to all patients and controls both in the beginning of the study and in the 6th follow-up. A coronary arteriography was also performed to all patients. Patients with an increment in the diastolic volume index more than 20% in the follow-up compared with basal values included in the VR subgroup. The patient subgroup with VR consisted of 19 patients. Statistical analyses were performed using ANOVA and Kruskal Wallis tests for comparison of variables between groups. Logistic regression and ROC analyses were used for evaluation of accuracy of TNF-alpha in prediction of VR. RESULTS: There were no significant differences between groups according to demographic characters. The basal plasma levels of TNF-alpha were higher in the patient subgroup with VR as compared with patients without VR and controls (14.59 +/- 4.28 pg/ml vs 7.30 +/- 4.48 pg/ml, and 1.64 +/- 1.49 pg/ml, p< 0.001). In logistic regression analysis only TNF-alpha predicted the VR (OR-1.356, 95% CI 1.117-1.647). Plasma TNF-alpha levels with a cut-off > or = 10.33 pg/ml were found to have 89.5% sensitivity and 79.3% specificity to predict the development of VR. CONCLUSION: These results demonstrate the increment of plasma TNF-alpha levels in the acute phase of MI and the close relationship between the TNF-alpha levels and VR in the patients with first MI.

Early electrocardiographic diagnosis of acute coronary ischemia on the paced electrocardiogram.

BACKGROUND: Twelve-lead electrocardiography (ECG) is the most important source for the early diagnosis of an acute myocardial ischemia. However, its diagnostic value when the sequence of ventricular activation is altered by ventricular pacing is unknown. The aim of the study was to evaluate the ECG changes on the paced ECG during percutaneous coronary intervention (PCI) by doing temporary pacing. METHODS AND RESULTS: Standard 12 lead baseline and temporary pacing ECG records were taken before the intervention in elective PCI patients. Standard 12 lead and temporary pacing ECG records were repeated during the balloon inflation. Fifteen (12 men and 3 women; age 57.2+/-9.7 years) subjects who were undergoing routine PCI were studied. Mean Delta ST deviation on the normal conduction ECG during inflation was 1.03+/-1.02 mV and mean Delta ST deviation on the paced ECG during inflation was 1.7+/-1.6 mV. The pre-inflation mean QRS duration on the paced ECG was 143.2+/-2.8 ms and during inflation mean QRS duration was 157.8+/-12.5 ms. The mean QRS prolongation was 14.6+/-13.6 ms on the paced ECG. Despite the presence of paced ECG abnormalities, significant ischemic ST segment deviations were seen after referencing the ST segment deviations to the pre-PCI. Also, there is significant QRS prolongation on the paced ECG during ischemia. CONCLUSIONS: The present study extends the correlation between normal and paced ECG during ischemia and the QRS prolongation could be a marker of myocardial ischemia on the paced electrocardiogram.

Comparison of strain doppler echocardiography and radiologic left ventriculography for quantitative assessment of regional myocardial function.

OBJECTIVE: We aimed to study the comparison of strain and strain rate parameters with conventional left ventriculography derived regional function. METHOD: Forty patients were included in the study. The study group was selected from patients who had undergone left ventriculography and coronary angiography for clinical indications. Regional myocardial function was assessed using the centerline method via ACOM PC Quantcor LVA measurement system. Patients were also evaluated with echocardiography. Strain and strain rate Doppler echocardiographic measurements were compared with conventional left ventriculography at anterobasal, anterolateral, inferior and posterobasal segments. RESULTS: Radiological left ventricular radial shortening was found to correlate with longitudinal strain shortening in all ventriculographic segments examined (anterobasal, r = 0.771, P < 0.0001; anterolateral, r = 0.790, P < 0.0001; posterobasal, r = 0.861, P < 0.0001; inferior, r = 0.815, P < 0.0001). Correlation was persistent both in patients with or without coronary artery disease. The sensitivity of a peak systolic longitudinal strain >12.5% for prediction of patients with radial shortening >or=20% was 75%, with a specificity of 100%. However, no relationship could be demonstrated between radiological left ventricular radial shortening and strain rate measurements. CONCLUSIONS: In our study it was shown that regional wall motion can be measured quantitatively via strain Doppler echocardiography with the left ventriculography as reference.

Effects of acute exercise on fibrinolysis and coagulation in patients with coronary artery disease.

Acute physical exertion may trigger an acute coronary syndrome. Furthermore, acute physical exercise may influence hemostatic markers in healthy individuals. However, the effect of acute exercise on blood fibrinolysis and coagulation in patients with coronary artery disease (CAD) is still not well understood. Nineteen untrained patients with angiographically proven CAD (age, 58 +/- 9 years, 12 males), and 25 age- and sex-matched controls without CAD (age, 56 +/- 6 years, 16 males) underwent a treadmill exercise test. Global fibrinolytic capacity (GFC) and prothrombin fragment 1 + 2 (F 1 + 2) levels were measured before exercise, at peak exercise, and 2 hours after recovery. There were no differences between the groups with respect to left ventricular ejection fraction, history of hypertension, body mass index, and serum lipids. Before exercise, GFC was significantly lower in patients with CAD when compared with controls (1.40 +/- 0.43 versus 3.28 +/- 1.19 microg/mL, respectively; P < 0.001). In patients with CAD, F 1 + 2 levels were significantly higher than those of controls (1.15 +/- 0.43 versus 0.79 +/- 0.10 nmol/L, respectively; P = 0.002). In both study groups, GFC levels increased significantly at peak exercise and decreased to baseline values 2 hours after recovery. At peak exercise, F 1 + 2 levels significantly increased in both study groups. However, while F 1 + 2 levels of controls decreased to baseline values 2 hours after recovery (0.79 +/- 0.10 versus 0.80 +/- 0.10 nmol/L; P > 0.05), F 1 + 2 levels of patients with CAD were still significantly elevated (1.15 +/- 0.43 versus 1.84 +/- 0.06 nmol/L; P = 0.002). Acute exercise increases coagulation and fibrinolysis both in untrained subjects with and without CAD. However, in patients with CAD, the equilibrium between fibrinolysis and coagulation during peak exercise is disturbed in favor of coagulation after recovery.

Impaired systemic endothelial function in patients with pseudoexfoliation syndrome.

Pseudoexfoliation syndrome (PEX) is the most common clinical precursor of open-angle glaucoma. Recent studies have shown that pseudoexfoliative material is widely distributed throughout the body, including blood vessels. The aim of our study was to evaluate endothelial function in the brachial artery of patients with pseudoexfoliation syndrome. We prospectively examined 23 patients with PEX (mean age, 70 +/- 8 years) and 20 healthy age- and sex-matched individuals (mean age, 68 +/- 9 years) as a control group. Brachial artery endothelial function was assessed by vascular response to reactive hyperemia (flow-mediated dilation (FMD) and sublingual nitroglycerin (NTG-mediated dilation) using high-resolution ultrasound. Flow-mediated and NTG-induced dilation were expressed as the percent change in diameter after reactive hyperemia and after NTG administration relative to the baseline value, respectively. Patients with cardiovascular disease and other conditions associated with endothelial dysfunction were excluded. When compared with controls, patients with PEX had significantly lower flow-mediated dilation (4.5 +/- 2.8 versus 8.2 +/- 3.7, P = 0.01) and NTG-mediated dilation (10.9 +/- 3.1 versus 15.8 +/- 3.8, P = 0.0001). Flow-mediated dilation and NTG-mediated dilation were similar in PEX patients with glaucoma (n = 11) and without glaucoma (n = 12). Flow-mediated and NTG-mediated dilation did not correlate with any measured parameter in any patient or control subject. The findings indicate that systemic endothelial function is impaired in PEX syndrome patients.