Diabetes mellitus and female gender are the strongest predictors of poor collateral vessel development in patients with severe coronary artery stenosis.

BACKGROUND: Coronary collateral vessel development (CVD), i.e., arteriogenesis, is regarded as one of the most important mechanisms­along with angiogenesis­to result in protection of the myocardium. Coronary CVD is associated with a reduction in infarct size, future cardiovascular events and improved survival in patients with occlusive coronary artery disease by enhancing regional perfusion in the chronically ischemic myocardium. In the present study, we aimed to investigate the relation of cardiovascular risk factors and hematological parameters with collateral development in patients with severely stenotic (≥95%) and totally occluded coronary artery disease including at least one major coronary artery. MATERIALS AND METHODS: The study population was selected from the patients who underwent coronary angiography between January 2008 and March 2009. Five hundred and two patients who had at least one coronary artery stenosis ≥95% (368 men; mean age 59 ± 10 years) comprised the study population. Of the 502 patients, 228 had total occlusion in at least one major epicardial coronary artery. Collateral artery grading was performed by using Cohen-Rentrop method to the vessel with coronary artery stenosis of ≥95% and patients with chronic total occlusions (CTO). Patients with grade 0-1 collateral development were regarded as the poor collateral group, and patients with grade 2-3 collateral development were regarded as the good collateral group. RESULTS: Two hundred and fifty-eight (51%) of 502 patients had poor collateral development, and 244 (49%) had good collateral development. Logistic regression analysis revealed that DM was independently associated with poor CVD in patients with ≥95% stenosis (p < 0.001). Additionally, female gender and DM were found to be independently associated with poor CVD in patients with CTO (p = 0.005 and p < 0.001, respectively). Monocyte count was found to be independent of CVD neither in patients with ≥95% stenosis nor in patients with CTO. CONCLUSION: Our data show that DM is an independent factor for poor coronary CVD both in patients with severe coronary artery stenosis and in patients with CTO. Female gender or being in post-menopausal period is another negative risk factor for poor CVD in addition to DM in patients with CTO.

Imaging of coronary artery anomalies: the role of multidetector computed tomography.

BACKGROUND: Coronary artery anomalies are evaluated by using catheter-based angiography. Multidetector row-computed tomography (MDCT) is a new noninvasive imaging technique that has excellent spatial resolution for detecting the origin and course of a coronary anomalous vessel. OBJECTIVE: To determine the sensitivity of multidetector computed tomography in patients who had coronary artery anomaly demonstrated by conventional coronary angiography. MATERIAL AND METHODS: A retrospective evaluation to identify 23 patients, who underwent retrospective electrocardiographic (ECG)-gated MDCT, was done and in whom an anomalous coronary vessel was found at a single center. Metoprolol (50-100 mg) was given orally to all patients to reduce heart rate so as to get high-quality MDCT images. After performing MDCT, the CT scans of each patient were analysed and compared with their coronary angiograms by two experienced radiologists and one cardiologist who were unaware about the study, and the sensitivity of MDCT was determined. RESULTS: Twenty-three patients (age range 28-73) with seven different coronary arteries of the anomalous type were evaluated. Nineteen patients had an anomalous left coronary artery; three patients had an anomalous single coronary artery; and one patient had an anomalous right coronary artery. The most common anomaly type was the left circumflex coronary artery (52%). The origin and course of all anomalous vessels were detected by ECG-gated MDCT (Lightspeed 16, GE Medical Systems, Milwaukee, Wisconsin, USA). The sensitivity of 100% of MDCT was detected in patients who had anomalous coronary vessels. CONCLUSION: We suggest that MDCT could be a non-invasive alternative imaging technique to conventional coronary angiography for screening the anomalous vessels of coronary arteries because of its excellent spatial resolution, which is very important for detecting the relationship of anomalous vessels with great arteries and cardiac structures.

Imaging of coronary artery fistulas by multidetector computed tomography: is multidetector computed tomography sensitive?

BACKGROUND: Coronary angiography is the gold standard for diagnosing coronary artery fistulas (CAFs). Multidetector computed tomography (MDCT) is a recently developed imaging technique for detecting coronary artery stenosis, coronary artery anomalies, and coronary artery fistulas and their courses. OBJECTIVE: We aimed to determine accuracy or sensitivity of MDCT in patients having CAF. METHOD: We evaluated 13 patients with 15 CAFs detected earlier by coronary angiography. MDCT was carried out on all patients and the results were compared with coronary angiography, following which, sensitivity of MDCT was detected. RESULTS: Eleven of 15 CAFs were shown on MDCT and the overall sensitivity of MDCT was found to be 73%. Seven of 8 CAFs that coursed between two vascular structures were detected and the sensitivity of MDCT in this group was found to be 87%. However, the sensitivity of 58% of MDCT in patients with fistula coursing between coronary arteries and cardiac chambers was found. CONCLUSION: Although coronary angiography is the gold standard diagnostic test for detection of CAF, MDCT may be an alternative test, especially, for CAF coursing between vascular structures, to detect origin, course, and the drainage site of fistula through its excellent spatial resolution and ability to show relationship of anatomic structures.

Increased thrombolysis in myocardial infarction frame count in patients with myocardial infarction and normal coronary arteriogram: a possible link between slow coronary flow and myocardial infarction.

BACKGROUND: Thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. This technique counts the number of cineangiographic frames from initial contrast opacification of the proximal coronary artery to opacification of distal arterial landmarks. We hypothesized that patients with normal coronary artery (NCA) and myocardial infarction (MI) might have impaired coronary flow. Accordingly, we assessed the TIMI frame counts of patients with NCA and MI and compared to patients with NCA and without MI. MATERIALS AND METHOD: This retrospective study included consecutive patients with MI and who were found to have normal coronary angiograms performed between 1999 and 2003. Fifty patients (group I) with NCA and MI were enrolled in the study. Fifty consecutive patients with NCA and without MI were also enrolled in the study as control group (group II). Mean time interval between MI and coronary angiography was 6 +/- 2 days. RESULTS: There were statistically significant differences between groups I and II in respect to gender (11 females (22%) versus 22 females (44%), p = 0.003, respectively) and smoking status (62% (31/50) versus 38% (19/50), p = 0.02). Comparison of TIMI frame counts between two groups revealed that group I patients had significantly higher TIMI frame counts than group two patients for all three coronary arteries (LAD: 40 +/- 12 versus 23 +/- 7, Cx: 47 +/- 14 versus 27 +/- 7, RCA: 36 +/- 10 versus 26 +/- 10, respectively, p < 0.001 for all). Smokers were significantly younger when compared to non-smokers (44 +/- 5 years versus 51 +/- 9 years, p = 0.008, respectively). TIMI frame counts of smokers did not significantly differ from those of non-smokers in group I patients. There were statistically significant differences between smokers and non-smokers in group II patients regarding TIMI frame counts for all three coronary arteries (LAD: 29 +/- 7 versus 18 +/- 3, LCX: 34 +/- 10 versus 22 +/- 4, RCA: 34+ /- 13 versus 20 +/- 4, respectively, p < 0.001 for all). CONCLUSION: We have shown that patients with MI and NCA have higher TIMI frame counts for all coronary arteries when compared to patients without MI and NCA. Absence of difference between smokers and non-smoker in the myocardial infarction group in respect to TIMI frame count, has suggested that smoking does not lead to further increase of TIMI frame counts. On the other hand, in patients without MI and with NCA, smokers have higher TIMI frame counts than non-smokers have.

Elevated level of plasma homocysteine in patients with slow coronary flow.

BACKGROUND: Elevated plasma levels of homocysteine are currently considered a major, independent risk factor for cardiovascular diseases. Recently, several investigators have suggested that even mild elevation in plasma homocysteine level can severely disturb vascular endothelial function and subsequently impair coronary blood flow. Accordingly, we investigated plasma homocysteine level in patients with slow coronary flow. METHOD: Study population included 53 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 21 females, 32 males, mean age=48+/-9 years), and 50 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 22 females, 28 males, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviations above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. The mean TIMI frame count for each patient and control subject was calculated by adding the TIMI frame counts for each major epicardial coronary artery and then dividing the obtained value into 3. Plasma homocysteine level was measured in all patients and control subjects using commercially available homocysteine kits. RESULTS: There was no statistically significant difference between two groups in respect to age, gender, hypertension, diabetes mellitus, hyperlipidemia and cigarette smoking (p>0.05). Plasma homocysteine level of patients with slow coronary flow were found to be significantly higher than those of control subjects (15.5+/-5.7 vs. 8.7+/-4.2 microM/l, respectively, p<0.001). Moreover, we found a significant positive correlation between plasma homocysteine level and mean TIMI frame count (r=0.660, p<0.001). CONCLUSION: We have shown that patients with slow coronary flow have raised level of plasma homocysteine compared to control subjects with normal coronary flow. This data suggests that elevated level of plasma homocysteine may play a role in the pathogenesis of slow coronary flow.

Effects of long-term beta-blocker therapy on P-wave duration and dispersion in patients with rheumatic mitral stenosis.

BACKGROUND: P-wave dispersion (PWD), has been defined as the difference between maximum and minimum P-wave duration. Prolonged P-wave duration and increased PWD have been reported to be related with increased risk for atrial fibrillation (AF). AF is the most common sustained arrhythmia encountered in patients with rheumatic mitral stenosis (MS). Beta-blockers are the mainstay of therapy in patients with rheumatic MS to control ventricular rate both during sinus rhythm and AF. In the present study, we aimed to evaluate the effect of long-term beta-blocker therapy on P-wave duration and PWD in patients with rheumatic MS. METHOD: Study population includes 46 patients (group I, 8 men, 38 women, mean age = 34+/-8 years) with newly diagnosed moderate-to-severe rheumatic MS who have not taken any medication before and prescribed oral beta-blocker therapy and 46 healthy control subjects without any cardiovascular disease (group II, 8 men, 38 women, mean age = 35+/-7 years). Mitral valve area, maximum and mean diastolic mitral gradients, left atrial diameter, and systolic pulmonary artery pressure were evaluated by transthoracic echocardiography before initiation of beta blocker therapy and repeated at the end of the first month. Baseline maximum and minimum P-wave duration and PWD were determined on 12-lead electrocardiogram recorded for each patient and control subject and repeated at the end of the first month after initiation of beta-blocker therapy in patient group. RESULTS: Maximum P-wave duration and PWD were found to be significantly higher in patients with MS than those in control subjects (Maximum P-wave duration: 128+/-7 ms vs. 104+/-4 ms and PWD: 52+/-6 ms vs. 27+/-3 ms, p < 0.001 for both). Both groups had comparable minimum P-wave duration (75+/-4 ms vs. 76+/-4 ms, p = 0.093). Maximum P-wave duration and PWD were found to be significantly decreased by long-term beta blocker therapy (Maximum P-wave duration; 128+/-7 ms vs. 122+/-6 ms, p < 0.001, PWD; 52+/-6 ms vs. 47+/-5 ms, p < 0.001). However, there was no significant difference between the values of minimum P wave duration measured before and at the end of the first month of beta-blocker therapy (75+/-4 ms vs. 75+/-3 ms, p = 0.678). Statistically significant decrease were detected on maximum and mean mitral gradient and systolic pulmonary artery pressure and resting heart rate at the end of the first month of beta-blocker therapy. However, only the change in resting heart rate was found to be significantly correlated with the decrease in maximum P-wave duration and PWD (Maximum P-wave duration: r = 0.327, p = 0.026, PWD: r = 0.378, p = 0.01). CONCLUSION: We have shown for the first time that long-term beta-blocker therapy causes a significant decrease in maximum P-wave duration and PWD in patients with rheumatic MS.

A pericardial hydatid cyst masquerading as acute inferolateral myocardial infarction--a case report.

A case of pericardial hydatid cyst adjacent to the inferoposterial wall of the left ventricle is reported. Significant ST segment elevations in leads D2, D3, aVF, V5, and V6 on surface electrocardiography and sudden onset of severe chest pain mimicked acute inferolateral myocardial infarction. However, cardiac catheterization and coronary angiography showed normal coronary arteries and normal left ventricular cavity. The ST segment elevation in the inferolateral leads disappeared a few days after surgical resection of the cyst. Cardiac hydatid cyst should be considered in the differential diagnosis of patients with angina-like chest pain in endemic areas.

Increased levels of soluble adhesion molecules E-selectin and P-selectin in patients with cardiac syndrome X.

The role of endothelial dysfunction and platelet activation in patients with cardiac syndrome X is controversial. The aim of this study was to investigate the plasma levels of circulating E- and P-selectin molecules in patients with syndrome X. The study included 21 patients with cardiac syndrome X (11 men and 10 women, mean age = 56 +/- 5 years) and 20 patients with significant coronary artery disease who had stable angina pectoris (11 men and 9 women, mean age = 60 +/- 8 years). Twenty-two age- and sex-matched subjects (12 men and 10 women, mean age = 58 +/- 8 years) undergoing diagnosis of atypical chest pain in whom coronary arteries were found normal and exercise test had no signs of ischemia served as the control group. Syndrome X was defined as presence of typical chest pain on exertion or at rest with positive exercise test and angiographically normal epicardial coronary arteries with no evidence of coronary spasm after intracoronary infusion of ergonovine maleate. The mean plasma concentrations of P-selectin were significantly elevated both in patients with coronary artery disease and syndrome X as compared with control subjects (49.15 +/-7.47 and 42.80 +/- 8.93 vs 22.63 +/-6.47 ng/mL, p < 0.001). Similarly, both patients with coronary artery disease and syndrome X had higher plasma concentrations of E-selectin than the control group (78.85 +/- 16.69 and 68.38 +/- 15.30 vs 36.43 +/- 4.72 ng/mL, p < 0.001). In conclusion, patients with syndrome X had increased plasma concentrations of soluble adhesion molecules, E-selectin and P-selectin, reflecting an ongoing chronic inflammation involved with endothelial dysfunction and enhanced platelet activation/damage in this setting.

Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events.

Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in IE patients with and without embolic events by measuring the plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasminogen activator inhibitor-1, beta-thromboglobulin, and platelet factor 4. The study included 76 consecutive patients with definite IE according to the Duke criteria. Among them, 13 (17.1%) had major embolic events. Plasma concentrations of prothrombin fragment 1 + 2 (3.2 +/- 1.3 vs 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/L, p <0.001, respectively) and thrombin-antithrombin (7.3 +/- 1.5 vs 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p <0.001, respectively) were elevated in patients with embolic events compared with both patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-thromboglobulin (63.3 +/- 10.9 vs 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p <0.001, respectively) and platelet factor 4 (106.0 +/- 28.7 vs 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p <0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher plasminogen activator inhibitor-1 levels than both nonembolic patients and healthy subjects (14.4 +/- 6.4 vs 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). In conclusion, IE patients with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state that may contribute to the increased risk of thromboembolic events in this particular group.

P-wave duration and P-wave dispersion in patients with dilated cardiomyopathy.

BACKGROUND: P-wave dispersion (PWD) has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses. In the present study, we aimed to investigate PWD in patients with dilated cardiomyopathy. METHOD: The study population consisted of 72 patients with dilated cardiomyopathy and 72 healthy control subjects. Left atrial diameter, left ventricular end-diastolic and end-systolic diameters and left ventricular ejection fraction of all patients and control subjects were measured by means of transthoracic echocardiography. Maximum P-wave duration (Pmaximum) and minimum P-wave duration (Pminimum) were measured from the 12-lead surface electrocardiogram. PWD was calculated as the difference between Pmaximum and Pminimum. RESULTS: Pmaximum and PWD of patients with dilated cardiomyopathy were significantly higher than those of control subjects (Pmaximum: 126+/-12 ms vs. 116+/-10 ms, PWD: 47+/-6 ms vs. 38+/-7 ms, respectively, P<0.001 for all). However, there was no statistically significant difference between patient group and control group regarding Pminimum (79+/-7 ms vs. 78+/-6 ms, respectively, P=0.27). Left atrial diameter was significantly higher in patients with dilated cardiomyopathy compared to control subjects (4.51+/-0.62 cm vs. 3.60+/-0.43 cm, respectively, P<0.001). Left ventricular ejection fraction was found to be significantly lower in patients with dilated cardiomyopathy compared to control subjects (33+/-5% vs. 63+/-7%, respectively, P<0.001). CONCLUSION: PWD was found to be significantly higher in patients with dilated cardiomyopathy than in healthy control subjects.

Changes in plasma levels of adhesion molecules after percutaneous mitral balloon valvuloplasty.

BACKGROUND: Adhesion molecules are expressed on vascular endothelium and on immune and inflammatory cells. Recently increased levels of adhesion molecules have been shown in patients with rheumatic mitral stenosis. This study examined the serum levels of the adhesion molecules intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in patients with rheumatic mitral stenosis and the effects of percutaneous mitral balloon valvuloplasty (PMBV) on these adhesion molecules. MATERIALS AND METHODS: Thirty five patients (3 men, 32 women, mean age 39+/-5 years) with severe rheumatic mitral stenosis who underwent percutaneous balloon mitral valvuloplasty, and 35 age and sex matched healthy control subjects were included in the study. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients who underwent PMBV and in all control subjects. Blood samples were taken for measurement of adhesion molecules immediately before and 24 h after the mitral balloon valvuloplasty. RESULTS: The plasma levels of soluble adhesion molecules E-selectin, ICAM-1 and VCAM-1 were significantly elevated in patients with mitral stenosis compared to control subjects: E-selectin, 97+/-59 vs. 45+/-24 ng/ml (P=.001), sICAM-1, 874+/-301 ng/ml vs. 238+/-82 ng/ml (P<.0001); sVCAM-1, 3056+/-763 ng/ml vs. 985+/-298 ng/ml (P<.0001). Plasma levels of VCAM-1 significantly increased 24 h after the valvuloplasty procedure (3056+/-763 ng/ml vs. 3570+/-1225 ng/ml P=.013). Plasma levels of E-selectin showed a significant decrease after PMBV (97+/-59 vs. 70+/-58 ng/ml, P=.043) and plasma levels of ICAM-1 did not show any change after PMBV (874+/-301 vs. 944+/-377 ng/ml, P=.356). CONCLUSION: Cellular adhesion molecules, sICAM-1, E-selectin, sVCAM-1 have shown changes in different directions in response to PMBV. These results necessitate further studies to clarify the mechanism underlying the association between adhesion molecules and PMBV as well as rheumatic mitral stenosis.

Activation of coagulation system in dilated cardiomyopathy: comparison of patients with and without left ventricular thrombus.

OBJECTIVES: We aimed to investigate plasma levels of molecular markers for platelet activity, thrombin activation and fibrinolytic status in patients with dilated cardiomyopathy (DCM) with and without left ventricular (LV) thrombus and to compare these markers between patients with DCM and control participants. MATERIALS AND METHODS: The study population comprised 60 patients with DCM who met the inclusion criteria. Patients were divided into two groups: 22 patients with LV thrombus and 38 patients without LV thrombus. The age-matched control group consisted of 23 healthy participants (18 men and five women with a mean age of 49). Patients with DCM and healthy participants were compared with respect to platelet activity, thrombin activation and fibrinolytic status. These comparisons were also performed in patients with DCM with and without LV thrombus. RESULTS: Platelet factor 4 (28.2+/-4.4 ng/ml compared with 20+/-3.1 ng/ml, P<0.01) and beta-thromboglobulin (40+/-2 ng/ml compared with 17+/-3 ng/ml) levels, reflecting platelet activity, were significantly higher in patients with DCM than in control participants. Fibrinopeptide A (6.94+/-0.69 ng/ml compared with 1.96+/-0.1 ng/ml, P<0.001) and thrombin-antithrombin III complex (5.26+/-2.60 ng/ml compared with 3.17+/-1.23 ng/ml, P<0.001) levels, as markers of fibrin generation, were also higher in patients with DCM than in normal participants. Plasma levels of D-dimer (118+/-16 ng/ml compared with 85+/-3 ng/ml, P<0.001) and plasmin-alpha2-plasmin inhibitor complex (0.8+/-1.1 microg/ml compared with 0.6+/-1.7 microg/ml, P<0.001) in patients with DCM significantly exceeded those in the normal participants. There were no statistically significant differences between patients with and without LV thrombus in DCM with respect to platelet activity, thrombin activation and fibrinolytic status. CONCLUSION: We have shown that platelet activation, thrombin activation and fibrinolytic activity are increased in patients with DCM compared to control participants. However, these markers reflecting coagulation activation in patients with LV thrombus are comparable to those in patients without LV thrombus.

Predictors of left ventricular thrombus formation in patients with dilated cardiomyopathy: role of activated protein C resistance.

OBJECTIVES: The aim of this study was to investigate the association between left ventricular thrombus formation and natural anticoagulant systems including the protein C, protein S and antithrombin in patients with dilated cardiomyopathy. MATERIALS AND METHODS: Sixty patients with dilated cardiomyopathy who met the inclusion criteria were included in the study. Patients were divided into two groups: group I consisted of 22 patients with left ventricular thrombus and group II consisted of 38 patients without left ventricular thrombus. Our main inclusion criteria were ejection fraction /= 6.0 cm. These two groups were compared for clinical and hematologic parameters (activated protein C resistance, protein S and antithrombin). RESULTS: There were no statistically significant differences between patients with or without left ventricular thrombi with respect to left ventricular end-diastolic and end-systolic dimensions, ejection fraction, fractional shortening and left atrial diameter. There were no statistically significant differences between patients with and without left ventricular thrombus with respect to platelet count (252 +/- 64/mm3 x 10(3) compared with 260 +/- 74/mm3 x 10(3) respectively, P=0.68), prothrombin time (12.94 +/- 1.9 s compared with 12.86 +/- 1.3 s respectively, P=0.82), activated partial thromboplastin time (32 +/- 5 compared with 30 +/- 4 s respectively, P=0.32) and fibrinogen levels (36 +/- 9 mg/dl compared with 34 +/- 8 mg/dl respectively, P=0.41). None of the patients had protein S and antithrombin deficiency. Activated protein C resistance was found in 12 patients (12 out of 22, 54%) in group I and four patients (four out of 38, 9.5%) in group II (P < 0.01). It was also shown to be an independent predictor of left ventricular thrombus (P < 0.05). CONCLUSION: Activated protein C resistance is found to be an independent predictor of left ventricular thrombus in patients with dilated cardiomyopathy who have ejection fractions less then 35% and left ventricular end-diastolic dimensions > 6.0 cm.

Comparison of low-dose dobutamine stress echocardiography and echocardiography during glucose-insulin-potassium infusion for detection of myocardial viability after anterior myocardial infarction.

BACKGROUND: Low-dose dobutamine stress echocardiography (LDDSE) is one of the methods most used to assess myocardial viability. Glucose-insulin-potassium (GIK) infusion has been shown to increase contraction of the ischemic zone. The aim of this study was to compare LDDSE and echocardiography during GIK infusion for detection of myocardial viability. METHODS: Thirty-two patients who had first anterior myocardial infarction (MI) without previous MI were included in the study. Echocardiographic evaluation was carried out on the 7th +/- 2 days after MI. During continuous electrocardiographic, blood pressure and echocardiographic monitoring, an intravenous infusion of dobutamine (3 microg/kg body weight/min) was started with an infusion pump, continued for 5 min and then increased to 5 microg/kg/min and 10 microg/kg/min for another 5 min. The GIK protocol consisted of a fixed dose of insulin (100 microU/kg/h intravenously) and a variable glucose/potassium infusion rate. GIK echocardiography was done at baseline and after 60 min of GIK. The detected viable myocardium was defined as one or two scores decreasing in at least two adjacent abnormal segments during LDDSE and GIK echocardiography. RESULTS: Under resting conditions 225 segments (44%) were normokinetic, 21 segments (4%) dyskinetic, 117 segments (23%) akinetic and 149 segments (29%) hypokinetic. Viability was detected in 20% (57 segments) of the asynergic segments at baseline with GIK echocardiography and in 22% (62 segments) of those segments with LDDSE (P < 0.05). Left ventricular wall motion score index at baseline was 1.87 and it decreased significantly indicating improvement in left ventricular systolic function during both LDDSE and GIK echocardiography (P < 0.001, versus 1.75 and 1.76 respectively). The agreement between LDDSE and GIK echocardiography for detection of myocardial viability was 96%. CONCLUSION: We have shown that GIK echocardiography is similar to LDDSE for detection of myocardial viability. With the support of further clinical studies GIK echocardiography could be used to detect myocardial viability after acute MI.

Accessory mitral valve tissue manifesting cerebrovascular thromboembolic event in a 34-year-old woman.

Accessory mitral valve tissue is an extremely rare congenital cardiac anomaly. Most of the cases reported in the medical literature were associated with left ventricular outflow tract obstruction. The majority of cases of accessory mitral valve tissue, causing left ventricular outflow tract obstruction, occur in association with other congenital cardiac anomalies. In this reported case, a patient with accessory mitral valve tissue complicated with thromboembolic cerebrovascular event is presented. The patient also had an associated idiopathic hypertrophic subaortic stenosis.

Right coronary artery originating from distal left circumflex: an extremely rare variety of single coronary artery.

Single coronary artery is a rare congenital anomaly of the coronary circulation which is often associated with other congenital cardiac malformations. Right coronary artery arising from the distal left circumflex artery is an extremely rare variety of single coronary artery. We report a patient with a single coronary artery system, in whom the right coronary artery originated from the distal left circumflex. No other associated cardiac anomaly was detected.

Relationship between myocardial viability and the predischarge electrocardiographic pattern in patients with first anterior wall acute myocardial infarction.

BACKGROUND: The assessment of residual viability in the infarcted area after an acute myocardial infarction is relevant to subsequent management and prognosis. OBJECTIVE: The aim of this study was to investigate the correlation between myocardial viability after an acute anterior myocardial infarction (AMI) as assessed by low dose dobutamine stress echocardiography (LDDSE) and the electrocardiographic patterns of ST segment and T wave abnormalities at the end of the first week of the acute event. METHODS: Sixty-nine consecutive patients (51 men, 18 women, mean age+/-standard deviation=57+/-11 years) who admitted to our clinic due to a first episode of transmural AMI were included in this study. Two-dimensional echocardiography was performed to all patients during rest and low dose dobutamine administration at the end of the first week of admission (7+/-2 days). Patients were classified into four groups according to ST segment and T wave morphology: group A, ST elevation < or =0.1 mV and negative T waves; group B, ST elevation < or =0.1 mV and positive T waves; group C, ST elevation > or =0.1 mV and negative T waves and group D, ST elevation > or =0.1 mV and positive T waves. RESULTS: Myocardial viability was detected more often in patients with isoelectric ST segments (22/24, 92%) than those with elevated ST segments (21/45, 47%) (P<0.001). Similarly patients with negative T waves had myocardial viability more frequently compared to those with positive T waves (32/45, 71% vs. 11/24, 46%, P<0.01). Seventeen (94%) of 18 patients in group A and 5 (83%) of six patients in group B had viable myocardium (P>0.05). Myocardial viability was found in 15 (56%) of 27 patients in group C and six (33%) of 18 patients in group D (P<0.01). As a marker of viable myocardium, isoelectricity of ST segment was specific (92%) but only moderately sensitive (51%), with a 92% positive predictive accuracy and a poor (53%) negative predictive value. T wave negativity was less specific but more sensitive than isoelectricity of ST segment for myocardial viability. CONCLUSION: The presence of isoelectric ST segment and negative T wave indicates a high probability of myocardial viability. However, absence of these electrocardiographic patterns does not exclude the presence of viable myocardium.

Decreased platelet activation and endothelial dysfunction after percutaneous mitral balloon valvuloplasty.

OBJECTIVE: This study was conducted to assess the changes in platelet activation and endothelial dysfunction in patients with mitral stenosis (MS) and sinus rhythm (SR) following percutaneous mitral balloon valvuloplasty (PMBV). BACKGROUND: Systemic thromboembolism is a serious complication in patients with valvular heart disease, and its incidence is highest in those with mitral stenosis. A hypercoagulable state has also been reported in patients with mitral stenosis and sinus rhythm. A recent study has shown that patients with previous PMBV had a lower incidence of thromboembolism. METHODS AND RESULTS: The study was conducted in 21 patients (two men, 19 women, mean age=34+/-6 years) with mitral stenosis and sinus rhythm (SR) who underwent percutaneous mitral balloon valvuloplasty and 17 healthy control subjects (two men, 15 women, mean age=33+/-6 years). Biochemical markers of platelet activity (beta thromboglobulin, BTG, and soluble P-selectin, sPsel) and endothelial dysfunction (von Willebrand Factor, vWF) were measured in both control subjects' and patients' serum samples taken immediately before PMBV and 24 h after PMBV procedure. All patients underwent successful PMBV. Significant improvement of mitral valve area, pulmonary artery pressure, mean mitral gradients, and left atrial diameter were achieved in all patients after PMBV. Compared with control subjects, patients with MS had higher plasma levels of BTG (66+/-26 ng/ml vs. 14+/-6 ng/ml, P<0.001), vWF (177+/-67 units/dl vs. 99+/-37 units/dl, P<0.0001), sPsel (226+/-74 ng/ml vs. 155+/-66 ng/ml, P<0.001). There was a significant reduction of plasma levels of BTG (66+/-26 ng/ml vs. 48+/-20 ng/ml, P=0.002), vWF (177+/-67 units/dl vs. 134+/-60 units/dl, P=0.001) and P-selectin (226+/-74 ng/ml vs. 173+/-71 ng/ml, P=0.008,) 24 h after PMBV. CONCLUSION: We have shown that patients with severe MS and SR have increased platelet activation and endothelial dysfunction compared with control subjects and PMBV results in decreased platelet activity and improvement of endothelial injury.

Relationship between control of ventricular rate in atrial fibrillation and systemic coagulation activation in patients with mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Systemic thromboembolism is a major complication in patients with mitral stenosis (MS), especially in those who have atrial fibrillation (AF). It has been suggested that systemic coagulation activity may be increased in these patients. The study aim was to investigate the relationship between control of ventricular rate and systemic coagulation factors in patients with MS and AF by measuring plasma levels of prothrombin fragment (PF) 1+2, thrombin-antithrombin III complex (TAT) and plasminogen activator inhibitor-1. METHODS: Fifty-four consecutive patients with moderate to severe MS and AF were included in the study. Patients with resting heart rates < 100 beats per min were considered as having a controlled ventricular response rate (group A; n = 28) and those with > 100 beats per min as an uncontrolled ventricular response rate (group B; n = 26). RESULTS: Group A patients had a lower mean mitral gradient and pulmonary artery pressure than group B patients (11 +/- 6 versus 15 +/- 5 and 35 +/- 7 versus 39 +/- 8; p < 0.05, respectively). Plasma concentrations of PF 1+2 (4.17 +/- 2.1 versus 2.95 +/- 1.21; p < 0.01) and TAT III (4.61 +/- 1.75 versus 3.12 +/- 1.01; p < 0.01) were elevated in group B compared with group A. Similarly, group B patients had higher plasminogen activator inhibitor-1 levels than group A patients (7.87 +/- 3.8 versus 5.8 +/- 2.9; p < 0.05). A significant correlation was found between heart rate and plasma PF 1+2 and TAT levels. Multiple logistic regression analysis revealed that heart rate and mean mitral gradient were independent predictors of systemic coagulation activation. CONCLUSION: Besides contributing towards hemodynamic and symptomatic relief, the control of AF rate in MS patients induces a drastic decline in coagulation activation, and may also reduce the incidence of thromboembolism.

Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events.

BACKGROUND: Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). HYPOTHESIS: The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in patients with IE with and without embolic events by measuring the plasma levels of prothrombin fragment 1+2 (PF1+2), thrombin-antithrombin III complex (TAT), plasminogen activator inhibitor-1 (PAI-1), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF4), respectively. METHODS: The study included 76 consecutive patients (female = 55, male = 21, mean age 26 years, range 8-64 years) with definite IE according to the Duke criteria; of these, 13 (17.1%) had embolic events. RESULTS: Plasma concentrations of PF1+2 (3.2 +/- 1.3 vs. 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/l, p < 0.001, respectively) and TAT (7.3 +/- 1.5 vs. 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p < 0.001, respectively) were elevated in patients with embolic events compared with patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-TG (63.3 +/- 10.9 vs. 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p < 0.001, respectively) and PF4 (106.0 +/- 28.7 vs. 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p < 0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher PAI-1 levels than nonembolic patients and healthy subjects (14.4 +/- 6.4 vs. 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). CONCLUSION: Patients with IE and with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state, which contributes to the increased risk of thromboembolic events in this particular group.