Role of serum neopterin level in unstable angina

Coronary artery disease is the most common form of heart disease and the important single cause of death. Unstable angina is a life threatening disorder and a major cause of emergency medical care. Disruption of vulnerable atheromatous plaque is the most common pathogenic mechanism in unstable angina. Macrophage and T cell lymphocytes are critical in the growth and changes of plaques through the secretion of growth factors, cytokines and extracellular matrix digesting enzymes, which weaken fibrous cap. Neopterin, which is a byproduct of guanosine triphosphate degradation in macrophages activated by interferon gamma being a marker of macrophage activation, is a more direct measurement of immune system activation. Immune system activation may play a pathogenic role in acute coronary syndrome. Neopterin can be used as a marker for activity of coronary disease. The purpose of this study to evaluate the neopterin level in patients had unstable angina and complex coronary artery disease lesions vs. patient with chronic stable angina. Prospective study was performed in 50 patients divided in three groups. Group1: [30 patients with unstable angina class IIIb according to Braunwald classification. Group2: 10 patients with chronic stable angina. Group3: 10 patients with normal coronary angiography. The neopterin level was high significantly in group 1 in compare to both other two groups. There was correlation between the neoperin level and the number of angiographically complex lesion. Neopterin level was not correlated vessel score or stenosis score

Intra-uterine fetal echo cardiography in high-risk pregnancies

The purpose of this study was to evaluate the accuracy of prenatal fetal echocardiography in detecting congenital heart defects pregnant women at high and low risk for structural cardiac anomalies. A prospective outcome of two cohorts study was performed, 50 pregnant women with non complicated [low risk] and 100 high risk pregnant patients underwent routine four chamber and left ventricular outflow tract evaluation whereas high risk, patients had detailed fetal echocardiographic examination. Accuracy of the ultrasonographic diagnosis was evaluated from neonatal discharge data. The study detects one fetus, had small sized apical muscular ventricular septal defect [VSD]. Fetuses of high risk group have smaller and diastolic, end systolic left ventricular cavity dimensions, interventricular septal thickness, left ventricular wall thickness, aortic root diameter and left atrial diameter than the matched control. It can be concluded that high risk cause studied showed changes in fetal heart chamber dimensions but not to the extent of known congenital fetal cardiac malformation

Early invasive strategy with facilitated PCI [GPIIBIIIa receptor blocker plus half dose fibrinolytic therapy plus PCI] versus primary PCI in acute ST segment slevation myocardial infarction

This study was done in El-Hussein and Bab Elsharia University Hospitals. From 2002 till 2004. Patients with ST-segment elevation acute myocardial infarction typically require reperfusion therapy either with fibrinolytic therapy or mechincal reperfusion with PTCA and stent implantation. Seventy patients presents within 12 hours of onset of chest pain with St-segment elevation myocardial infarction Half of the patients [group A] undergo aggressive management with facilitated PCI, half dose streptokinase 750000 IU, plus GP IIb/IIIa blocker Tirofiban in weight adjusted dose Coronary angiography done within 90 minutes of presentation with PCI for the infarct related artery [group A].The other half [group B] undergo coronary angiography within 90 minutes to asses TIMI flow with primary PCI to the infarct related artery. Low dose heparin 60 IU bolus then 7 IU/kg infusion for all patients. Aspirin 150 mg at presentation and then once daily. Clopidogrel 300 mg is given to all patients before the procedure and then 75 mg daily for at least one month. Twenty six patients out of thirty five in group A had an anterior wall MI [74.3%] and nine patients had an inferior wall MI [25.7%]. Twenty five patients out of thirty five in group B had an anterior wall MI [71.4%] and ten patients had an inferior wall MI [28.6%]. TIMI flow before PCI, In group A there was fifteen patients out of thirty five had TIMI three flow [42.9%], six patients had TIMI two flow [17.1%], three patients had TIMI one flow [8.6%], and eleven patients had TIMI O flow [3 1.4%]. In group B there was five patients out of thirty five patients had TIMI three flow [14.3%], nine patients had TIMI two flow [25.7%], four patients had TIMI one flow [11.4%], and seventeen patients had TIMI 0 flow [48.6%]. TIMI flow after PCI, in group A there were thirty one patients out of thirty five had TIMI three flow [88.6%], one patient had TIMI two flow [2.9%], and three patients had TIMI 0 flow [8.6%]. In group B there were twenty nine patients out of thirty five patients had TIMI three flow [82.9%], three patients had TIMI two flow [8.6%], one patient had TIMI one flow [2.9%], and two patients had TIMI 0 flow [5.7%]. During the period of follow up nine patients out of thirty five in group A developed chest pain and underwent coronary angiography total occlusion of the stent was present in four patients, significant [more than 50%] lesion was found in three patients, and insignificant [less than 50%] lesion was found in two patients. Nine patients out of thirty five in group B developed chest pain and underwent coronary angiography, total occlusion of the stent was present in one patient, significant [more than 50%] lesion was found in five patients, and insignificant [less than 50%] lesion was found in three patients. There was no statistically significant difference between the incidences of restenosis in both groups. Two patients out of thirty five in group A had a myocardial reinfarction during the period of follow up [5.7%].One patient out of thirty five in group B had a myocardial reinfarction during the period of follow up [2.9%]. In this study we conclude that facilitation of PCI did not affect the use of predilatation or the decrease the incidence of failed PCI. However it increased the incidence of TIMI 2 or 3 flow and decreased the incidence of TIMI 0 or 1 flow before PCI, as expected these incidences became nearly equal in both groups after PCI

Recent stents in patients of acute myocardial infarction clinically and angiographic results

Conronary thrombosis plays a major role in the pathogenesis of acute myocardial infarction. Between December 1998 to November 2000. 57 patients with acute myocardial infarction who were admitted at coronary care unit [CCU] of Sayed Galal and Al Housein University Hospital were included in this study. The patients were divided into two groups: G1: they had primary PCI. G2: [25 patients] they had received streptokinase followed by percutaneaus coronary intervention [PCI] within 24hs after failed thrombolysis [Persistent chest pain and/or extension of ST segment elevation]. The primary goal of therapy for acute myocardial infarction is rapid, complete and sustained restoration of infarct related artery [IRA] blood flow. Both fibrinolytic and mechanical restoration of antegrade coronary blood flow in patients have been shown to improve left ventricular function, reduce infarct size and reduce mortality. Although intravenous fibrinolytic therapy is effective in improving outcome after myocardial infarction and can be administered early to a great proportion of patients than is possible with percutaneaus coronary intervention, its effectiveness profile is disappointing to most cardiologists. The advantages of PCI include immediate visual assessment of reperfusion success and identification of the entire coronary and ventricular anatomy. This assessment often obviate the need for noninvasive testing befor hospital discharge and can lead to an accelerated discharge and recovery of low risk patients. The benefit of primary angioplasty seems greatest in elderly and those with high risk characteristics. The presence of the platelet rich thrombus in acute myocardial infarction and the central role of platelet activation in stent thrombosis suggest a potentially, advantagious role for the new class glycoprotein Ilb; llla receptor antagonists during PCI. Stenting in acute MI and in thrombus containing lesion has become a feasible and safer procedure in an expert hands, with new devices, high pressure deployment and with the use of [GPIIbIIIa blockers

Qualitative and quantitative coronary angiography in patients with Q-wave myocardial infarction versus patients with non-Q wave myocardial infarction

The classification of myocardial infarction into transmural and subendocardial types has been based on the presence or absence of abnormal Q-waves in the ECG; it is more appropriate to describe myocardial infarction as Q-wave and non-Q wave infarction. Visual evaluation of CA lesions was associated with inter observer and intraobserver variability of about 30%. In the present study 40 patients [20 patients with Q-wave and 20 patients with non Q-wave myocardial infarction] have been assessed for the presence or absence of significant difference regarding all risk factors for CAD, echocardiographic findings, cardiac enzymes and various QCA [Quantitative Coronary Angiography] variables [percentage of stenosis, plaque area, length of lesion, type of lesion, number of vessels affected and site of lesion]. The distribution of risk factors [age. sex, smoking, hypertension, diabetes, hyperlipmdemia] between both groups revealed no statistically significant difference. The history of previous ischemic insult was significantly higher in group II [40% in group II and 5% in group I]. Echocardiographic findings: Regional wall motions abnormalities [RWMA]: in group 1, 95% of patients have hypokinesia and 5% have akinesia in one or more left ventricular wall segments. In goup 2, 20% of patients have normal wall motions, 65% have hypokinesia and 15% have akinesia in one or more of left ventricular wall segments [P<0.05]. However the ejection fraction, fractional shortening, end-systolic and end-diastolic volumes were not statistically different between the two groups. In evaluation of cardiac enzymes, CPK; ranged from 550 to 2001 IU, in group I. with a mean value of 997 +/- 425 IU, in group 2, it ranges from 220 to 900 IU with a mean value of 451 +/- 149 IU [P<0.001]- LDH; it ranges from 550 IU tol900 IU with a mean value of 1657 +/- 198 IU while in group 2 it ranges from 301 IU to 860 IU with a mean value of 618 +/- 168 IU [P<0.05]. CPK MB fraction; values were ranging from 28 IU to 60 IU with a mean value of 53 +/- 21.7 IU for group I. In group 2 it ranges from 22 to 30 IU with a mean value of 32.9 +/- 9.1 IU [P<0.001]. As regard the parameters of QCA, Percentage stenosis; in group I, it ranges from 61% to 99.6% with a mean value of 87.66 +/- 12.4. In group 2, it ranges from 59% to 99.9% with a mean value of 90 +/- 14.1%, [P>0.05]. Plaque area; in group 1, it range from 1.09 to 16.8 mm2 with a mean value of 5.15 +/- 2.4 mm2. In group 2 it ranges from 0.33 to 21.66 mm2 with a mean value of 7.12 +/- 6.6 mm2 [P>0.05]. Length of lesion; in group 1, it range from 4.42 to 25.75 mm with a mean value of 16.68 +/- 3.7 mm. In group 2. it ranges from 4.72 to 29.3 mm with a mean value of 17.65 +/- 4.6 mm [P>0.05]. Number of vessels affected; in group 1, 60% of patients have single vessel disease, 20% two-vessel disease and 20% multi-vessel disease. In group 2, 50% of patients have single vessel disease, 25% two-vessel disease and 25% multi-vessel disease [P>0.05]. So we concluded that there is no significant difference between Q-wave and non Q-wave myocardial infarction except in the following points: the history of previous myocardiat infarction and ischemia is commoner in non Q-wave myocardial infarction. Regional wall motions abnormalities occur more frequently in patients with Q-wave myocardial infarction. Cardiac enzymes are more elevated in Q-wave myocardial infarction than non Q-wave myocardial infarction. It is clear from the study that the magnitude of myocardial infarction should be judged on the anatomical and functional basis rather than the designation of Q-wave or non Q-wave type of myocardial infarction. It is also apparent that quantitative coronary angiography is an accurate and reproducible method for assessing the coronary artery lesion