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Prof.Dr.Bengi Başer

The aim of this study was to assess the effect of paraprosthetic regurgitation of mitral mechanical valves to myocardial tissue and lactate dehydrogenase (LDH) level. We compared 19 patients (study group) who had mitral mechanical valve with severe mitral paravalvular regurgitation with 20 patients (control group) who had native valve with severe rheumatic mitral regurgitation. None of the patients had clinical hemolytic anemia. On transesophageal echocardiographic examination, semiquantative evaluation and spatial distribution of regurgitant jets were noted in both of the groups. Five LDH isoenzymes were studied in two groups. Myocardial tissue specimens were taken from the left atrial wall during reoperation. Grids randomly taken were studied under the transmission electron microscope. Total serum LDH levels of the study group (578 +/- 12 IU/L) were higher than the control group (495 +/- 6.2 IU/L) (p < 0.001). We found LDH1/LDH2 more than 1 in all patients; the ratio was not statistically different in the control group. Electron microscopy revealed the same degree of injury in both groups. Haptoglobin levels were decreased and reticulocyte counts were increased in patients with paraprosthetic valve regurgitation. Electron microscopic findings support that myocardial injury contributes to increase of total LDH level and high LDH1/LDH2 ratio. But statistically significant elevation in total LDH level in study group and the stable state of LDH1/LDH2 ratio between two groups showed that hemolysis caused by paraprosthetic regurgitation is the most important factor for the increase of total LDH level, so that high LDH level can be used as a reliable parameter for the diagnosis of intravascular hemolysis in paraprosthetic regurgitation.

A reduction in velocity in coronary artery contrast filling during coronary arteriography that is called slow coronary flow is one of the reasons of myocardial ischemia. Ischemia mechanism hasn’t been understood. We evaluated coronary arteriographic and scintigraphic properties in patients with a slow flow pattern (SFP). The study included 60 patients who revealed SFP in their coronary arteriograms. The control group consisted of 50 patients with normal myocardial perfusion and normal coronary arteries in their coronary arteriograms. The Thrombolysis in Myocardial Infarction (TIMI) flow count method was used for the assessment of slow coronary flow. Single day rest-stress Technetium-99m hexakis-2-methoxy-isobutyl isonitrile (Tc-99m MIBI) myocardial perfusion tomography was performed to all study patients. Patients with SFP revealed both higher frame counts in native coronary arteries and higher average frame counts. In control patients, the average frame count was 26.4 3.5 (LAD: 35.4 3.3, LCx: 22.5 4.5, RCA: 21.5 2.8). In patients with SFP the average frame count was 64.40 16.64 (LAD: 85.75 24.39, LCx: 57.21 15.25, RCA: 53 75 17.81) (p < 0.001). Myocardial perfusion tomography showed ischemia in 17 patients (Group 1), while 43 patients in Group 2 revealed no perfusion defect. There were no statistically significant differences between Groups 1 and 2 in frame counts. In conclusion, no correlation was observed between the time needed to fill a native coronary artery and ischemia even if there is SFP.

Patients with aortic stenosis (AS) may have classic angina pectoris. The safety of exercise testing in adults with AS is controversial and, in fact, exercise testing in such patients is considered to be contraindicated especially in severe aortic stenosis (SAS). Furthermore, exercise testing has low specificity in uncovering coronary artery disease (CAD) in patients with AS, because the baseline ECG is frequently abnormal. We wished to assess the safety and diagnostic accuracy of dipyridamole stress myocardial perfusion tomography (DMPT) in the detection of CAD in patients with SAS. The study included 30 patients with SAS (mean aortic valve area 0.57 +/- 0.09 cm(2)). All patients underwent dipyridamole myocardial perfusion scintigraphy (SPECT), coronary arteriography and catheterization, as well as Doppler echocardiography. Myocardial perfusion tomography was applied with (99m)Tc hexakis-2-methoxyisobutyl isonitrile (MIBI) by a single day rest-dipyridamole infusion protocol. Hemodynamic, electrocardiographic and clinical responses were compared with those of 50 control patients without AS. Hemodynamic responses during dipyridamole stress tests demonstrated no significant differences between the controls and the AS patients in the following parameters: systolic blood pressure, heart rate, rate-pressure product or incidence of headache, chest pain, dyspnea, flushing and dizziness. A reversible perfusion defect was observed in 10 patients with DMPT. The existence of coronary lesions was determined by coronary arteriography in 8 of 10 patients (sensitivity 100%, specificity 91%). The results showed that DMPT is well tolerated, even by patients with SAS and is of high diagnostic value in assessing CAD.

Patients with aortic stenosis (AS) may have classic angina pectoris. The safety of exercise testing in adults with AS is controversial and, in fact, exercise testing in such patients is considered to be contraindicated especially in severe aortic stenosis (SAS). Furthermore, exercise testing has low specificity in uncovering coronary artery disease (CAD) in patients with AS, because the baseline ECG is frequently abnormal. We wished to assess the safety and diagnostic accuracy of dipyridamole stress myocardial perfusion tomography (DMPT) in the detection of CAD in patients with SAS. The study included 30 patients with SAS (mean aortic valve area 0.57 +/- 0.09 cm(2)). All patients underwent dipyridamole myocardial perfusion scintigraphy (SPECT), coronary arteriography and catheterization, as well as Doppler echocardiography. Myocardial perfusion tomography was applied with (99m)Tc hexakis-2-methoxyisobutyl isonitrile (MIBI) by a single day rest-dipyridamole infusion protocol. Hemodynamic, electrocardiographic and clinical responses were compared with those of 50 control patients without AS. Hemodynamic responses during dipyridamole stress tests demonstrated no significant differences between the controls and the AS patients in the following parameters: systolic blood pressure, heart rate, rate-pressure product or incidence of headache, chest pain, dyspnea, flushing and dizziness. A reversible perfusion defect was observed in 10 patients with DMPT. The existence of coronary lesions was determined by coronary arteriography in 8 of 10 patients (sensitivity 100%, specificity 91%). The results showed that DMPT is well tolerated, even by patients with SAS and is of high diagnostic value in assessing CAD.

Several studies have indicated that the velocity of contrast dye increases after intravenous dipyridamole infusion in patients with a slow-flow pattern (SFP). In this study we compared the results of coronary arteriography and exercise myocardial perfusion single photon emission computed tomography (SPECT) in patients with SFP. We also investigated the changes in myocardial perfusion in patients with abnormal exercise myocardial perfusion SPECT by using a pharmacological stress test with dipyridamole. This study included 60 patients who revealed SFP in their coronary arteriograms. Slow coronary flow diagnoses were made using the frame count method. A single day rest-exercise technetium-99m hexakis-2-methoxy-isobutyl isonitrile (Tc-99m MIBI; Du Pont Pharma SA, Belgium) SPECT was performed in all patients. Patients who had reversible perfusion defect (RPD) on the exercise SPECT were evaluated with dipyridamole myocardial perfusion scintigraphy. RESULTS Patients with SFP revealed both higher frame counts in native coronary arteries and higher mean frame counts. The coronary frame count was 26.4 +/- 3.5 in control patients and 64.40 +/- 16.64 in patients with SFP, respectively (P < 0.001). Exercise perfusion SPECT showed RPD in 17 patients (group 1), but was normal in 43 others (group 2). There were no statistically significant differences between groups 1 and 2 in frame counts. Myocardial perfusion was normalized in all 17 patients of group 1 after dipyridamole infusion. In patients with SFP perfusion, changes may improve with dipyridamole infusion. This study indicates that this improvement can be shown by dipyridamole SPECT. Furthermore, no correlation was observed between the time needed to fill a native coronary artery and RPD of the myocardium.

Several studies have indicated that the velocity of contrast dye increases after intravenous dipyridamole infusion in patients with a slow-flow pattern (SFP). In this study we compared the results of coronary arteriography and exercise myocardial perfusion single photon emission computed tomography (SPECT) in patients with SFP. We also investigated the changes in myocardial perfusion in patients with abnormal exercise myocardial perfusion SPECT by using a pharmacological stress test with dipyridamole. This study included 60 patients who revealed SFP in their coronary arteriograms. Slow coronary flow diagnoses were made using the frame count method. A single day rest-exercise technetium-99m hexakis-2-methoxy-isobutyl isonitrile (Tc-99m MIBI; Du Pont Pharma SA, Belgium) SPECT was performed in all patients. Patients who had reversible perfusion defect (RPD) on the exercise SPECT were evaluated with dipyridamole myocardial perfusion scintigraphy. RESULTS Patients with SFP revealed both higher frame counts in native coronary arteries and higher mean frame counts. The coronary frame count was 26.4 +/- 3.5 in control patients and 64.40 +/- 16.64 in patients with SFP, respectively (P < 0.001). Exercise perfusion SPECT showed RPD in 17 patients (group 1), but was normal in 43 others (group 2). There were no statistically significant differences between groups 1 and 2 in frame counts. Myocardial perfusion was normalized in all 17 patients of group 1 after dipyridamole infusion. In patients with SFP perfusion, changes may improve with dipyridamole infusion. This study indicates that this improvement can be shown by dipyridamole SPECT. Furthermore, no correlation was observed between the time needed to fill a native coronary artery and RPD of the myocardium.

Primary malignant cardiac tumors are extremely rare neoplasms. About three-quarters of all cardiac tumors are histologically benign. A 24-year-old man presented to the hospital with dyspnea and chest pain. A solid, dense, nonhomogeneous and rough-surfaced mass (89 x 90 x 36 mm) with protrusion into the right heart cavities was observed on transthoracic echocardiography. The findings were confirmed by transesophageal echocardiography and magnetic resonance imaging. The histopathology of the mass confirmed a diagnosis of angiosarcoma. No evidence of an extracardiac origin of the tumor was found by radiological body imaging. The patient died 2 months after presentation to the hospital.

Prostheses used to treat heart valve disease improve patient survival, but have certain disadvantages. Paravalvular leakage (PVL) is a rare complication after mitral valve replacement (MVR), and can impair cardiac function and reduce the patient’s functional capacity, depending on the degree of periprosthetic regurgitation. Between 1985 and July 1999, 2,502 patients underwent MVR with or without concomitant cardiac procedures. Of these patients, 33 (18 males, 15 females; mean age 39.8+/-15.3 years; range: 12-62 years) had PVL of differing degree. The interval between MVR and observation of PVL was 30.5+/-31.5 months (range: 1-126 months), and the period after diagnosis was 22.6+/-31.5 months (range: 2-114 months). Fourteen patients (42.4%) underwent reoperation (RO group), and 19 (57.6%) were followed medically (ME group). Indications for reoperation were reduction of functional capacity, echocardiographically proven serious mitral regurgitation, and hemolysis. Reoperative mortality was 3.0% (1/33), and late mortality 3.1% (1/32) for all patients. Cumulative survival after PVL was 90.2+/-6.7% at both five and ten years. Annular calcification (33.0%) and infective endocarditis (18.2%) were important predictive factors for development of PVL. Only one patient required second re-do surgery. Univariate and forward stepwise logistic regression analyses showed that there was no predictor for the development of severe PVL requiring a second reoperation. No difference was observed between left ventricular dimensions before and after periprosthetic regurgitation. The only significant finding between groups was an increase in left atrial diameter in RO patients after the development of PVL (p <0.05). Among patients undergoing MVR there are no clinical features to distinguish who will develop severe PVL during follow up. If PVL reduces the patient’s functional capacity or causes serious hemolysis, or if severe PVL is evaluated echocardiographically, then reoperation must be performed. Mild or moderate mitral regurgitation without impairment of functional capacity may be followed medically. In asymptomatic patients, enlargement (>5%) of the left atrial diameter following development of moderate PVL may be a valuable criterion for deciding when to reoperate.

Prostheses used to treat heart valve disease improve patient survival, but have certain disadvantages. Paravalvular leakage (PVL) is a rare complication after mitral valve replacement (MVR), and can impair cardiac function and reduce the patient’s functional capacity, depending on the degree of periprosthetic regurgitation. Between 1985 and July 1999, 2,502 patients underwent MVR with or without concomitant cardiac procedures. Of these patients, 33 (18 males, 15 females; mean age 39.8+/-15.3 years; range: 12-62 years) had PVL of differing degree. The interval between MVR and observation of PVL was 30.5+/-31.5 months (range: 1-126 months), and the period after diagnosis was 22.6+/-31.5 months (range: 2-114 months). Fourteen patients (42.4%) underwent reoperation (RO group), and 19 (57.6%) were followed medically (ME group). Indications for reoperation were reduction of functional capacity, echocardiographically proven serious mitral regurgitation, and hemolysis. Reoperative mortality was 3.0% (1/33), and late mortality 3.1% (1/32) for all patients. Cumulative survival after PVL was 90.2+/-6.7% at both five and ten years. Annular calcification (33.0%) and infective endocarditis (18.2%) were important predictive factors for development of PVL. Only one patient required second re-do surgery. Univariate and forward stepwise logistic regression analyses showed that there was no predictor for the development of severe PVL requiring a second reoperation. No difference was observed between left ventricular dimensions before and after periprosthetic regurgitation. The only significant finding between groups was an increase in left atrial diameter in RO patients after the development of PVL (p <0.05). Among patients undergoing MVR there are no clinical features to distinguish who will develop severe PVL during follow up. If PVL reduces the patient’s functional capacity or causes serious hemolysis, or if severe PVL is evaluated echocardiographically, then reoperation must be performed. Mild or moderate mitral regurgitation without impairment of functional capacity may be followed medically. In asymptomatic patients, enlargement (>5%) of the left atrial diameter following development of moderate PVL may be a valuable criterion for deciding when to reoperate.

The pathophysiology of angina pectoris is not precisely known yet in patients who have no coronary lesion but slow coronary flow by angiography. In this study we aim to display metabolic ischemia via atrial pacing to determine the difference of lactate production and arterio-venous O2 content difference (AVO2). Thirty-four patients with slow coronary flow detected by coronary angiography via the TIMI ‘frame count’ method were included in this study. The resting and stress images from the patients undergoing myocardial perfusion tomography were recorded, pre and postpacing lactate extraction and AVO2 content difference values were calculated. Patients were classified according to their metabolic responses to atrial pacing stress. Group I consisted of 28 patients (18 male, 10 female, mean age 54.42 +/- 9.61) who did not demonstrate metabolic ischemia and group II consisted of six patients (four male, two female, mean age 60 +/- 5.76) who had metabolic ischemia after the procedure. There was no statistically significant difference between prepacing AVO2 content difference in group I (57.38+/-2.05%) and group II (58.23 +/- 2.11%) (P = NS). However postpacing AVO2 content difference of group I and group II was statistically significant (respectively, 57.96+/-2.65 vs. 68.35 +/- 2.15%, P < 0.001). In other words, postpacing AVO2 content difference was unchanged from the basal AVO2 content difference level in group I (respectively, 57.38 +/- 2.05 vs. 57.96 +/- 2.65%; P = NS) in contrast to the postpacing AVO2 content difference which increased significantly in group II (58.23 +/- 2.11 vs. 68.35 +/- 2.15%; P < 0.028). Although basal lactate extraction rates were similar in groups I and II (respectively, 0.24 +/- 0.1 vs. 0.23 +/- 0.18; P = NS), postpacing lactate extraction rates were decreased significantly in the two groups, prominently in group II (0.154 +/- 0.15 vs. -0.471 +/- 0.27; P < 0.0001) which indicated that lactate extraction converted to lactate production. Metabolic ischemia was detected in only 17.6% of patients included in this study and 83.4% of these six patients with proven metabolic ischemia had perfusion defects in scintigraphy. Our data confirmed that angina pectoris was not originated from myocardial ischemia in most of the patients with slow coronary flow. We conclude that perfusion scintigraphy is a reliable and accurate method for detection of true ischemia in this group of patients.

Diabetes mellitus is a major risk factor for coronary artery disease and aortic dysfunction. The aim of this study was to determine the changes in the aortic elastic properties in patients (pts) with diabetic coronary artery disease and to search the effect glycerol trinitrate (GT). Method: Patients with coronary artery disease were allocated into two groups. Study group (SG) consisted of 17 pts (13 women 4 men; mean age 58.4±9.4 years) with diabetes mellitus, and the control group (CG) 20 pts (14 women, mean age 56.0±10.7 years) without diabetes mellitus. Aortic systolic and diastolic dameter indexes and aortic distensibility and stiffness index were measured before and after 200 μg GT (intravenously) by transthorasic echocardiography. Results: There were no statistically significant differences between the two groups before GT with regard to age, sex, smoking, systolic and diastolic blood pressures, aortic systolic and diastolic diameter indexes. Aortic distensibility was found to be lower and stiffness index was found to be higher in SG (for the distensibility 0.0015± 0.0005 vs 0.0026±0.0007 mmHg-1, p<0.001 and for the stiffness index 43.74 ± 13.76 vs 24.62 ± 6.33, p<0.001). After GT aortic distensibility increased and stiffness index decreased significantly in both groups. However, the differences between SG and CG for aortic distensibility and stiffness index disappeared after GT. High-degree negative correlation was found between aortic distensibility and stiffness index in both groups before and after GT. Conclusion: Aortic distensibility is lower and stiffness index is higher in coronary artery pts with diabetes mellitus than without diabetes mellitus. Glycerol trinitrate induced significant increase in aortic distensibility and decrease in aortic stiffness index in both groups. Improvement in aortic functions after GT was higher nominally in the diabetic group.

Valva semilunaris sinistra and the aortic root complete to left ventricle morphologically and form to left ventricular outflow tract physiologically. This study was designed to investigate the relationship of diameters and geometric features of human aortic valve and root in static state. The morphological effects of geometry and dimensions of the aortic valve and root were examined using of 18 adult hearts from fixed male cadavers who had expired due to noncardiac causes. The aortic valve measurements were performed on the free edge of the leaflets and the annullar edge from tomographic cross-sectional views obtained from magnetic resonance imaging (MRI). Morphological assessement of the aortic root was done with cross-sectioned sequentially for measurements at four levels: at the ventriculoarterial junction (annulus), at the sinuses of Valsalva (sinus), at the sinotubular junction, and at 1 cm above the sinotubular junction. Mathematical relationship and comparisons were made by level setting using Euclidean radiation and a computerized morphometric analysis programming among the values from four different aortic root levels. The diameters of the annulus and the sinus level were represented by a value of one, and all other values were represented by a fraction (percentage) of these values. Statistical analysis among the variation of the diameters at the four levels of aortic root was achieved using ANOVA test (one-way analysis of variance). The free edge of left coronary cusp was the shortest among three leaflets (p < 0.05). Our data obtained from mathematical modelling showed that the aortic root was the narrowest at the sinotubular junctional level, and the widest at the sinus level (p < 0.05). The mean thickness of the aortic root wall was variable within each MRI cross-section. The aortic wall was thicker at the commissural level than at the sinus level. The analysis of our mathematical data implied that the production of the design to aortic root anatomy and geometry by 3-dimentional geometrical solution could resemble the surgical anatomy and could be adapted to the aortic root replacement and the procedures of the aortic valve preservation.

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