Many contradictory reports have been published investigating the relationship between coronary artery disease (CAD) and the increased intima-media thickness (IMT) in the common carotid artery (CCA). However, only a limited number of studies evaluate the relationship between CAD and CCA disease as reflected by both the plaque morphology (fibrous and calcific plaques) and IMT. We have studied the associations between CAD and the wall morphology of CCA by B-mode ultrasound (US). One hundred and forty-four subjects, whose angiography was planned on the basis of suspected CAD, were included into the study. The patients were divided into 4 groups on the basis of B-mode US findings; Group I: normal, Group II: increased IMT (IMT >/= 0.8 mm and plaque absent), Group III: fibrous plaque, Group IV: calcific plaque. Coronary artery disease was diagnosed in 63 patients. A statistically significant correlation was found between CAD and CCA wall morphology (r =0.42, CI (95%) = 0.30-0.51, p<0.001). Positive predictive values were 45.0%, 48.4%, and 75.0% in patients with increased IMT, fibrous plaque, and calcific plaque, respectively. None of the women with normal CCA wall morphology had significant coronary artery lesion. With respect to the normal group, the risk for CAD increased by 4.3 fold with the existence of fibrous plaque (p=0.02) and by 9.9 fold with the existence of calcific plaque (p<0.001). It has been shown that the CCA wall morphology determined by B-mode US is correlated with CAD in patients with chest pain, and the presence of calcific plaque is a better predictor for CAD than that of fibrous plaque and increased IMT. Women with chest pain and normal CCA wall morphology may not need coronary angiography.
As a result, the dependence of cardiac autonomic neuropathy on the disease duration and degree of left ventricular function impairment was shown in the patients undergoing chronic hemodialysis.
We investigated the effects of atorvastatin on inflammation and cardiac events during the inpatient period and initial 6-month follow-up in acute coronary syndrome (ACS) patients with low low-density lipoprotein (LDL) cholesterol level. One hundred and twelve consecutive ACS patients with LDL cholesterol less than 100 mg/dl were included in the study (mean 78.2+/-12.3 mg/dl). While 70 randomly selected patients received a dose of 40 mg atorvastatin within the first 24 h on top of their standard treatment as the atorvastatin group, the remaining 42 patients considered as the control group were given the standard treatment only, i.e., without any lipid-lowering drug therapy. Lipid profile, high-sensitivity C-reactive protein (hsCRP), and plasma amyloid A (SAA) levels were measured in all patients within the first 24 h of chest pain, on the 5th day, and in the 6th month. During the inpatient period and subsequent 6-month follow-up, all episodes of angina, reinfarction, revascularization, heart failure, rehospitalization, cardiac mortality, and total number of cardiac events were recorded. In the atorvastatin group, hsCRP and SAA values on the 5th day and in the 6th month compared to the first 24 h were significantly lower than those of the control group (P<0.0001). Mean LDL cholesterol level was significantly decreased in the atorvastatin group (55.7+/-17.7 mg/dl), but there was no significant change in the control group at the 6th month. The frequency of heart failure during the inpatient period and angina, unstable angina pectoris, heart failure, and revascularization in the first 6 months were also significantly reduced in the atorvastatin group. Atorvastatin started in the first 24 h reduces inflammation and improves the prognosis during both the inpatient period and the first 6 months of clinical follow-up in ACS patients with low LDL cholesterol levels.
The aim of this study was to evaluate the left ventricular systolic and diastolic functions in patients with sickle cell anemia. Fifty-four patients (34 male, 20 female, mean age 22.6 +/- 7.3 years) and 23 healthy persons (12 male, 11 female, mean age 26.7 +/- 6.8 years) were studied. After clinical examination and routine biochemical evaluation by a hematologist, patients with sickle cell anemia were admitted to the study. M-mode and 2-dimensional and Doppler echocardiographic measurements of patients and controls were performed according to criteria of the American Echocardiography Society. The values of the patient groups were compared with the values of normal healthy subjects (controls). Left ventricular systolic and diastolic diameters of sickle cell patients were greater than those of controls (p < 0.001). All of the sickle cell anemia patients had reduced systolic cardiac function (EF: 0.57 +/- 0.1 vs 0.63 +/- 0.06 and FS: 0.30 +/- 0.06 vs 0.34 +/- 0.04, p < 0.02) and abnormal diastolic left ventricular function parameters compared with the control group (IRT: 114 +/- 20 msec vs 65 +/- 7 msec, p < 0.0001; E/A ratio: 1.2 +/- 0.5 vs 1.6 +/- 0.04, p < 0.01). Left ventricular mass (LVM) was greater in patients than in controls (222 +/- 78 g vs 177 +/- 46 g, p < 0.01). Left ventricular systolic and diastolic functions were abnormal in patients with sickle cell anemia, and the left ventricular mass was greater in the patients compared with controls.
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