There is substantial evidence indicating that endogenous opioid peptides are involved in the pathophysiology of myocardial ischemia and reperfusion. We measured the myocardial and peripheral concentrations of β-endorphin before and following myocardial ischemia and reperfusion during coronary angioplasty. The results indicate that in patients with coronary artery disease, there was an augmented myocardial concentration of β-endorphin. Moreover, there was an increased peripheral concentration of β-endorphin following myocardial ischemia and reperfusion. The data support the previous notion that endogenous opioid peptides are involved in the pathophysiology of ischemic heart disease.

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Although the damage in myocardial infarction has been demonstrated to be related with the magnitude and number of ST elevation, its relation with terminal distortion of QRS is unclear. The relationship between terminal QRS distortion in ECGs on admission and the results of early low dose dobutamine stress echocardiography (LDSE) performed 6 ± 2 days later was investigated.
Patients admitted to our clinic within the first six hours of their chest pain and without a prior infarction diagnosis were divided into two groups based on the admission electrocardiogram as the absence (QRS-, n = 33) or presence (QRS+, n = 29) of distortion of the terminal portion of the QRS in ≥ 2 leads (QRS+; J point at > 50% of the R wave amplitude in lateral leads or presence of ST elevation without S wave in leads V₁-V₃).
There were no significant differences between the groups with respect to thrombolytic therapy or reperfusion criteria. During LDSE, the infarct zone wall motion score index (WMSI) in the QRS- group was significantly decreased relative to baseline (from 2.93 ± 0.65 to 2.37 ± 0.84, P = 0.02), and it was significantly different compared with WMSI in the QRS+ group (P = 0.005). Improvement of akinetic regions to hypokinetic regions in the infarct zone (IZ) was found to be 33.5% (44/131) in the QRS- group and 17.8% (27/151 P = 0.004) in the QRS+ group. Furthermore, 55.1% (10/29) of the patients in the QRS+ group and only 18.1% (6/33) of those in the QRS- group did not respond to LDSE (P < 0.05). In multiple logistic regression analysis, while there was no relationship between good left ventricular functions (WMSI < 2) and terminal QRS distortion under basal conditions (P = 0.07), an independent relation was observed to exist between them after LDSE (P = 0.03, OR 4.48, 95% CI, 1.13-17.7). Moreover, plasma CK levels were higher in the QRS+ group (P = 0.03), whereas the ejection fraction was worse (P = 0.01). In both groups, there was no correlation between the Selvester score and left ventricle WMSI at baseline, but this correlation was significantly improved with LDSE (QRS-; r = 0.39 P = 0.02 and QRS+; r = 0.44 P = 0.01)
The viability in the IZ is relatively less in those patients with terminal QRS distortion observed in their ECG on admission. This simple classification would be useful in predicting left ventricular function at the time of discharge.

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Existing indices of coronary conductance (hyperemic flow-versus-pressure slope index, FPSI, and zero flow pressure, Pzf) have been developed as measures of microcoronary resistance. These indices, however, refer to cases of normal hearts, and there are no reports studying these indices following acute myocardial infarction. In this study, we investigated whether FPSI and Pzf truly measure the extent of myocardial salvage after successful reperfusion therapy. We also developed a new index of zero pressure flow, Fzp.
Nineteen patients who underwent successful reperfusion therapy to the proximal portion of the left anterior descending artery (LAD) were studied.
After successful reperfusion therapy, a Doppler wire was placed into the LAD. Aortic pressure was recorded in real time. Results from the aortic pressure and flow meter were combined to produce FPSI, Pzf, and Fzp. All cases underwent a resting thallium (Tl) and BMIPP scintigram within five days of successful reperfusion therapy. Infarcted myocardium was estimated using a severity score calculated from the Tl scintigraphy (TlSS), and the BMIPP (BMIPPSS) was estimated using a severity score. Patients with a TlSS/BMIPPSS ratio of less than 0.4 were assigned to the successful salvage group (group S), while the others were assigned to the failed salvage group (group F).
FPSI of group F was 1.91 ± 0.26 m/sec and of group S was 0.92 ± 0.43 m/sec (P < 0.01). Pzf of group F was 51 ± 3 mmHg and of group S was 51 ± 5 mmHg (NS). Fzp of group F was -98 ± 16 cm/sec and of group S was -46 ± 4 cm/sec (P < 0.05).
FPSI and the new index of Fzp were useful in estimating the extent of myocardial salvage. Our results suggest that the Pzf index could not differentiate between the two groups.

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Lipoprotein (a) (Lp(a)) is an independent risk factor for myocardial infarction (MI). It may also inhibit the fibrinolysis system, and Lp (a) affects the natural course of MI and the results of thrombolytic therapy. The purpose of this study was to investigate the influence of Lp (a) on the residual lesion stenosis of the infarction-related arteries (residual stenosis) in acute MI patients in whom reperfusion therapy was not performed.
We studied 129 MI patients not given reperfusion therapy who underwent coronary angiography in the chronic stage. Morning fasting blood was collected and Lp (a), blood sugar, total cholesterol (TC), triglycerides (TG), and hemoglobin A₁c (HbA₁c) were measured.
Residual stenosis was compared between the low Lp(a) group (< 30 mg/dL) and the high Lp(a) group (≥ 30 mg/dL). It was severe in the high Lp(a) group (85.0 ± 24.9% vs 94.5 ± 15.5%, P = 0.0044). We also compared residual stenosis and TIMI classification between younger and older, non-DM and DM, non-HT and HT, low-TC (< 220 mg/dL) and high-TC (≥ 220 mg/dL), low-TG (< 150 mg/dL) and high-TG (≥ 150 mg/dL), and low-Lp (a) and high-Lp (a) patients. Only the serum Lp (a) level affected the residual stenosis and TIMI classification (P < 0.05). Conclusion: These findings suggest that elevated Lp (a) levels inhibit fibrinolysis.

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Recent studies have shown that percutaneous coronary intervention (PCI) activates systemic hemostatic activity, reflecting platelet activation and thrombin formation in the coronary arteries. The present study compared systemic levels of hemostatic markers induced by plain old balloon angioplasty (POBA), coronary stenting (STENT), and cutting balloon (CB) angioplasty.
Sixty-one patients with stable angina pectoris, who underwent elective PCI or diagnostic coronary angiography (CAG) alone, were investigated. Patients who underwent PCI were divided into the POBA group (n = 11), the STENT group (n = 27), and the CB group (n = 11). Patients who underwent CAG alone were assigned to the CAG group (n = 12). Blood samples were collected before, 24 hours after, and 3 days after PCI or CAG. Plasma concentrations of prothrombin fragment 1+2 (F1+2), fibrinopeptide A (FPA), thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor-1 (PAI-1) were measured.
In the CB group, the F1+2 (1.23 ± 0.4 nmol/L) level 3 days after PCI was significantly smaller than that of the POBA group (2.37 ± 0.5 nmol/L) (P < 0.05). The FPA (1.81 ± 0.9 ng/mL), TAT (3.36 ± 1.2 ng/mL) and PAI-1 (23.0 ± 4.1 ng/mL) levels in the CB group 3 days after PCI were significantly smaller than those of the POBA group (P < 0.05, respectively) and STENT group (P < 0.05, respectively), but similar to the CAG group.
Systemic hemostasis is activated to a greater extent after POBA and stenting than it is after CB angioplasty of the coronary arteries. This may contribute to the favorable long-term outcome of CB angioplasty.

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Exercise Q, R, and S wave amplitude changes, called the QRS score, have been reported to be a marker of exercise-induced myocardial ischemia. Therefore, in this study, using the exercise QRS score, we sought to determine if slow coronary flow (SCF) phenomenon is associated with the exercise-induced myocardial ischemia.
This retrospective study included 23 patients evaluated for suspected coronary artery disease and found to have SCF (group I) and 19 subjects with angiographically-defined significant coronary artery stenosis (group II). All study subjects underwent treadmill exercise testing using the modified Bruce protocol. For each subject the amplitude of the Q, R, and S waves in leads aVF and V₅ was measured manually using calipers before and immediately after exercise. The QRS score was calculated by subtracting the Q, R, and S wave differences in leads aVF and V₅.
There was no difference between the two groups with respect to demographic properties. The peak heart rate achieved, baseline and peak systolic-diastolic blood pressure, exercise duration, and the metabolic equivalent values were similar in both groups. The maximum ST-segment depression ratio was significantly lower in patients with SCF than those of significant coronary stenosis (0.8 ± 0.4 vs 1.3 ± 0.5 P = 0.001, respectively). However, the exercise QRS score was found to be similar in both groups (3.3 ± 2.3 vs 2.1 ± 3.0 P = 0.2, respectively).
The data suggest that SCF phenomenon may alone lead to myocardial ischemia even in the absence of obstructed major epicardial coronary arteries as detected by similar exercise QRS scores to those of significant coronary artery stenosis.

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Radiofrequency (RF) catheter ablation has become standard therapy for many types of arrhythmias. RF energy may cause deterioration in left ventricular function by damaging the myocardium. The aim of the present study was to assess the changes in left ventricular function after catheter ablation using various echocardiographic parameters.
Forty patients (22 women), aged 37 ± 14 years (range, 15-76 years), underwent catheter ablation for various tachycardias. Routine echocardiogaphic examination was done in all patients. Left ventricular systolic function was evaluated by the modified Simpson method and tissue Doppler. With regard to left ventricular diastolic function parameters, diastolic early (E) and late (A) transmitral filling velocities, deceleration time (DT), isovolumetric relaxation time (IVRT), and tissue Doppler parameters were assessed. All ventricular function parameters were assessed before, and 1 hour, 1 day, and 1 month after the catheter ablation procedure. To avoid any influence of heart rate on diastolic function parameters, the E/A ratio, DT, and IVRT were adjusted to heart rate (cE/A, cDT, cIVRT).
No changes in left ventricular systolic function after the ablation were observed. After the ablation procedure (1 hour, 1 day, and 1 month) the cE/A ratio decreased from 1.42 ± 0.43 to 1.19 ± 0.40, 1.18 ± 0.40, and 1.30 ± 0.33 (P = 0.009), respectively. cDT increased from 210 ± 54 to 272 ± 64, 255 ± 60, 240 ± 64 (P = 0.001), respectively. Likewise cIVRT increased from 113 ± 22 to 133 ± 54, 123 ± 27, 117 ± 19 (P = 0.007), respectively. Significant changes were also observed concerning tissue Doppler parameters in assessing diastolic function.
Although no significant changes were observed in systolic function after RF ablation, this procedure may have some detrimental effects on ventricular diastolic function para-meters.

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To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-α after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.

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The present study was designed to investigate the incidence of benign joint hypermobility syndrome (BJHMS) in mitral valve prolapse (MVP) and the correlation between the echocardiographic features of the mitral valve and elastic properties of the aortic wall and Beighton hypermobility score (BHS) in patients with MVP and BJHMS.
Fourty-six patients with nonrheumatic, uncomplicated, and isolated mitral anterior leaflet prolapse (7 men and 39 women, mean age; 26.1 ± 5.9) and 25 healthy subjects (3 men and 22 women, mean age, 25.4 ± 4.3) were studied. Patients were divided into two groups according to their BHS (group I, MVP+BJHMS; group II, MVP-BJHMS). Individuals with accompanying cardiac or systemic disease were excluded. Echocardiographic examination was performed in all subjects. The presence of BJHMS was evaluated according to Beighton's criteria.
The incidence of BJHMS in patients with MVP was found to be significantly higher than that of controls (45.6%, (21/46) vs 12% (3/25), P < 0.0001). Group I (MVP + BJHMS) had significantly increased anterior mitral leaflet thickness (AMLT, 3.4 ± 0.4 vs 3.1 ± 0.3; P < 0.005), maximal leaflet displacement (MLD, 2.4 ± 0.4 vs 1.7 ± 0.4; P < 0.005), and degree of mitral regurgitation (DMR, 17.1 ± 7.2 vs 11.2 ± 4.4; P < 0.01) compared to group II. However, the index of aortic stiffness (IAOS) was found to be lower (17.6 ± 6.9 vs 23.9 ± 7.6; P < 0.005) and aortic distensibility (AOD) to be higher (0.0035 ± 0.007 vs 0.0024 ± 0.005; P < 0.005) in group I. There was a significant correlation between AMLT, MLD and DMR, and BHS (r = 0.57/P = 0.007, r = 0.55/P < 0.009, r = 0.51/P < 0.01, respectively). In addition, AOD correlated positively with BHS (r = 0.53/P < 0.005), but the index of aortic stiffness correlated inversely with BHS (r = -0.49/P < 0.007).
The incidence of BJHMS in patients with MVP was more frequent than the normal population and there was a significant correlation between the severity of BJHMS (according to BHS) and echocardiographic features of the mitral leaflets and elastic properties of the aortic wall.

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Few data have been published on the reproducibility of baseline subtracted peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography. We investigated the reproducibility of the peak intensity measured from intravenous intermittent triggered myocardial contrast echocardiography in 10 young healthy males. The contrast echocardiography was obtained using the second harmonic mode with an intravenous bolus injection of Levovist (first study). The same myocardial contrast echocardiography was repeated after the first study (second study). The myocardial opacification and peak intensity in the 12 segments of the apical 4 and 2 chamber views were assessed visually and quantitatively. The differences in the peak intensity between the initial and repeated measurements in the first study (intraobserver reproducibility) and between the initial measurements in the first and second studies (interinjection reproducibility) were assessed using the Bland and Altman method. The degree of opacification was good or intermediate in 207/228 (91%) of the segments. The agreement of myocardial opacification between the first and second studies was 87/114 (76%). However, significantly higher peak intensity was obtained in apical septal (8200 ± 6300 au²) and mid septal (8500 ± 6000 au²) segments in the 4 chamber view and in the mid inferior (12400 ± 9300 au²) and apical inferior (10700 ± 6300 au²) segments in the 2 chamber view compared with other segments. The mean differences of the peak intensities according to the Bland and Altman analysis was -1600 ± 5000 au² in the intraobserver reproducibility study, and -1100 ± 5300 au² in the interinjection reproducibility study. Thus, the measurement error was determined to range from 8400 au² to 9500 au² in both studies. We conclude that the peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography using Levovist varies significantly among segments in the left ventricular myocardium. Large intraobserver and interinjection variability exists in the measurement of peak intensity, suggesting that the reproducibility of this technique is limited for quantitative assessment of myocardial perfusion.

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A whole-heart coverage MRI sequence, which employes a hybrid of fast gradient echo and echo planar acquisition imaging (FastCard EchoTrain), has recently been developed. Using this sequence, a first-pass myocardial perfusion MRI was shown to be a good noninvasive modality for detecting coronary artery disease (CAD) in a clinical setting. In addition, the clinical usefulness of delayed enhanced MRI has recently been reported. The objectives of this study were (1) to investigate the accuracy of dipyridamole stress first-pass myocardial perfusion MRI for diagnosing CAD (> 50% stenosis) and (2) to clarify whether additional delayed enhancement MRI has any clinical significance. We performed first-pass myocardial perfusion MRI in 102 consecutive patients (66 ± 9 years old) suspected to have CAD or new lesions in patients with well-documented prior myocardial infarction (MI). Using a 1.5 T cardiac MR imager (GE CV/i), eight short axis MR images of the left ventricle were acquired by injecting gadolinium (0.1 mmol/kg) under dipyridamole infusion stress (0.56 mg/kg). Fifteen minutes later, aminophylline (250 mg) was injected and first-pass perfusion MRI was repeated in the resting state in order to evaluate both the presence of perfusion defect and delayed enhancement. The presence of perfusion defect and delayed enhancement was determined based on a visual qualitative analysis by the agreement of two separate readers who were blinded to any clinical information. Based on the stress and rest findings, no defect, reversible defect, or fixed defect with or without delayed enhancement was recorded in any patient. The MR findings revealed 76 CAD patients, including 24 MI patients with new lesions and 26 patients without CAD on coronary angiography. The presence of stress perfusion defect had a 93% sensitivity and an 85% specificity for diagnosing CAD. A fixed defect showed an 86% sensitivity and a 66% specificity for diagnosing a prior MI. Patients with a fixed defect with delayed enhancement had more significant stenosis in the infarct related artery than in those without any enhancement (11/26 vs 15/20, P < 0.05).
Dipyridamole stress first-pass myocardial perfusion MRI using the FastCard EchoTrain was found to be a clinically useful and accurate modality for diagnosing CAD.

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Mitral annulus calcification (MAC) is a chronic degenerative noninflammatory process. The goal of this study was to determine endothelin-1 (ET-1) and nitric oxide (NOx) levels in patients with MAC and compare them with those in normal subjects. The study group included 39 patients [26 females (66%), age, 63 ± 8 years] with MAC and 20 [11 females (55%), age, 61 ± 7 years] healthy subjects. The patients were divided into two subgroups, group A with severe MAC and group B with mild MAC, according to the severity of the MAC. Plasma ET-1 levels were higher and NOx levels were lower in patients than controls [(6.5 ± 5.6 pg/mL vs 3.7 ± 2.9 pg/mL for ET-1 and 35.0 ± 10.6 μmol/L vs 42.3 ± 9.9 μmol/L for NOx; P < 0.05 for both)]. In the subgroups, ET-1 levels were higher in group A than group B (8.65 ± 6.84 pg/mL vs 4.74 ± 3.45 pg/mL, P < 0.05) and the control group (8.65 ± 6.84 pg/mL vs 3.70 ± 2.88 pg/mL, P < 0.05). There was no difference between group B and the control group. Plasma NOx levels were significantly decreased in group A compared to controls (32.22 ± 11.88 μmol/L vs 42.25 ± 9.99 μmol/L, P < 0.05). However, no significant difference was observed between group B (37.38 ± 9.06 μmol/L) and the other groups. Diabetes mellitus, coronary artery disease, and dyslipidemia were significantly associated with ET-1 levels. However, this association was not observed for NOx. In conclusion, patients with MAC have increased ET-1 and decreased NOx levels. This seems to be more prominent in patients with severe MAC.

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In patients with end stage renal disease on hemodialysis (HD), left ventricular (LV) function is frequently impaired. However, the mechanism of the LV dysfunction is totally unknown. It has been suggested that overproduction of nitric oxide induced by inflammatory cytokines may contribute to the LV dysfunction in some diseased states. In this study, we examined whether inflammatory cytokines play a role in the altered LV function in HD patients.
The plasma concentrations of 5 major inflammatory cytokines, including interleukin (IL)-1α, IL-1β, IL-6, tumor necrosis factor-α, and macrophage-colony stimulating factor (M-CSF) were measured by enzyme immunoassay with horseradish peroxidase in 18 consecutive patients on HD and in 16 control subjects. Then, we examined the relationship between plasma concentrations of M-CSF and LV ejection fraction (EF) on echocardiography.
Among the inflammatory cytokines examined, only the plasma concentrations of M-CSF were significantly elevated in patients on HD as compared to the control subjects. There was no significant change in the M-CSF concentrations before and after HD. Furthermore, there was a significant negative correlation between the plasma concentrations of M-CSF and LVEF.
These results suggest that elevated levels of plasma M-CSF may exist prior to the development of LV dysfunction observed in HD patients.

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Several studies claim that prothrombin 20210GA and factor V Leiden mutations are related to arterial thrombosis. We investigated the frequencies of these mutations and their significance in the development of early atherosclerosis in acute myocardial infarction (AMI) patients younger than 55 years of age. We investigated 96 patients with AMI and 77 control subjects. The diagnosis of AMI was established by typical chest pain and ST elevations on the presentation electrocardiogram and characteristic cardiac enzyme elevations. None of the control subjects had evidence of cardiovascular disease. DNA samples were isolated from all subjects and prothrombin 20210GA and factor V Leiden mutations were determined by the RealTime PCR technique with the aid of a Light Cycler device. The prevalence of factor V Leiden mutation was 6.3% and 5.2% in the patient and control groups, respectively (OR 0.6 [95% CI 0.1- 3.9], P = 0.6), whereas the prevalence of prothrombin G20210A mutation was 4.2% and 2.6% in the patient and control groups, respectively (OR 2.8 [95% CI 0.2 - 32.2], P = 0.4). None of the patients had both mutations. Prothrombin 20210GA and factor V Leiden mutations are not significant risk factors for the development of myocardial infarction in patients less than 55 years old in Southern Turkey.

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We investigated the use of a catheter-based cryoablation system on atrioventricular (AV) junction ablation in dogs. In five dogs, the cryoablation catheter was introduced to the AV junction area in order to create transient high degree or complete AV block. Cryo-freezing energy was applied by lowering the temperature to -75°C for five minutes as a single cycle. This cycle was repeated until significant impairment of the AV conduction appeared. Transient high degree and complete AV block was obtained in all five dogs without any adverse effects. The iceball formation was identified by intracardiac echocardiography. Ablation of the AV junction is effective with several freeze-thaw cycles using a transvenous catheter cryoablation system.

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A 62-year-old man with hypertension and hypercholesterolemia was referred to our unit for evaluation of chest pain. A very rare variant of single coronary artery, in which the anomalous right coronary artery originated as a separate branch from the left anterior descending artery, was incidentally found on his coronary angiography. The anomalous right coronary artery in our case appears to be unique in that it courses intraseptally rather than rightwards proximally and has obstructive atherosclerotic lesions resulting in inferior ischemia. Moreover, the acute angle made by the anomalous right coronary artery to turn toward the atrioventricular groove may have reduced the flow velocity and contributed to the development of inferior ischemia.

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A 60-year-old male with exertional dyspnea was referred to our hospital. Right pulmonary artery stenosis due to external compression by a calcified band was diagnosed by echocardiography, computed tomography, and magnetic resonance imaging. Percutaneous transluminal angioplasty was conducted in vain due to vascular recoil and failure of stent delivery. Pulmonary bypass grafting was performed successfully. The surgery indicated a probable etiology of chronic pericarditis. This is an extremely rare case of adult pulmonary artery stenosis without a known history of congenital disease, constrictive pericarditis, tuberculosis, or surgery.

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Chylous ascites is a clinical entity characterized by accumulation of milky fluid containing high amounts of triglycerides in the peritoneal cavity. The cause is usually lymphatic obstruction secondary to neoplastic processes. Constrictive pericarditis rarely causes cylous ascites through elevated venous pressure and lymphatic stasis. To the best of our knowledge, there is no report of constrictive pericarditis leading to chylous ascites in a patient presenting with objective lymphangiographic findings of lymphatic obstruction rather than stasis. We present a case of chylous ascites and pleural effusion secondary to constrictive pericarditis presenting with signs of lymphatic obstruction in lymphangio-graphy, in whom complete clinical and laboratory improvement was achieved after pericardiectomy.

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Cases with cardiac hydatid cyst disease are uncommon, being approximately 0.2-2% of all cases. Most cardiac hydatid cysts are located in the interventricular septum or left ventricular wall. Pericardial location is very rare. We report a 42-year old Turkish man with pericardial hydatid cyst disease who was otherwise asymptomatic, having no cardiac symptomatology. The most appropriate therapeutical option for a hydatid cyst is surgical removal of the cyst mass. However, our patient refused surgical treatment and thus medical treatment with albendazole was initiated. Following the first month of the drug therapy, pericardial effusion disappeared. The cystic nature of the mass disappeared and was solidified at the 6^th month of treatment. The patient has been followed-up by us asymptomatically.

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