Aortic arch calcification predicts the extent of coronary atherosclerosis in patients with or without type 2 diabetes: short communication.

AIM OF THE STUDY: The aim of this study was to evaluate the sensitivity and specificity of aortic arch calcification for detection of severe coronary atherosclerosis in patients suffering from coronary artery disease (CAD), with or without type 2 diabetes. PATIENTS AND METHODS: This study included 107 type 2 diabetic patients (68 men) with a mean age of 62.4 +/- 10.7 years and a mean diabetes duration of 14.2 +/- 5.9 years and 104 patients (63 men) with a mean age of 64.5 +/- 9.3 years who did not have diabetes. All patients had CAD, documented by coronary arteriography. Severe CAD was defined as atherosclerosis of the left main branch or atherosclerosis of three coronary arteries or atherosclerosis of the proximal part of the left anterior descending artery. Aortic arch calcification was assessed by means of posteroanterior chest X-rays, studied by a radiologist kept blind to the result of coronary arteriography. RESULTS: In type 2 diabetic patients, diagnosis of aortic arch calcification had 65.6% sensitivity and 86.9% specificity for detection of severe CAD. In patients without diabetes, diagnosis of aortic arch calcification had 47.7% sensitivity and 96.7% specificity for detection of severe CAD. CONCLUSIONS: Aortic arch calcification has a high specificity for detection of severe coronary atherosclerosis in patients with CAD. Sensitivity is higher in patients with type 2 diabetes, while specificity is slightly higher in non-diabetic patients.

Could sustained monomorphic ventricular tachycardia in the early phase of a prime acute myocardial infarction affect patient outcome?

OBJECTIVES: Sustained monomorphic ventricular tachycardia (SMVT) in the course of a prime acute myocardial infarction is not a common arrhythmia and its prognostic significance has not been specifically elucidated. The aim of the study was to estimate the prognostic implications of the occurrence of sustained monomorphic ventricular tachycardia in the early phase (<72 h) of a prime acute myocardial infarction. METHODS: We studied 690 consecutive patients admitted to the coronary care unit with a diagnosis of a prime myocardial infarction. SMVT was observed in 18 (2.6%) patients and we followed these patients for establishing the prognostic value of the arrhythmia according to the clinical characteristics. RESULTS: Patients with SMVT had a more extensive myocardial infarction based on the peak of the CK-MB isoenzyme activity (480+/-290 IU/L, vs 270+/-190 IU/L, P < .01), and higher mortality rate (40% vs 9%, P < .001). The independent predictors of SMVT were CK-MB (odds ratio [OR] 12.4), presence of complex ventricular arrhythmias (OR = 5.7), a wide QRS complex > or =130 milliseconds (OR = 4.8) and Killip class (OR = 4.8). The SMVT was itself an independent predictor of mortality (OR = 5.0). Compared with patients with ventricular fibrillation or polymorphic ventricular tachycardia, those with SMVT had a higher CK-MB activity, higher rate of wide QRS > or =130 milliseconds (33% vs 8%, P < .002), had a worse hemodynamic condition (Killip class >I:58% vs 23%, P < .04) and higher recurrence rate of ischemic events (68% vs 16%, P < .05). During the one year follow-up period, 4 patients (36.3%) of the 11 survivors from those with SMVT died of cardiac related causes. CONCLUSIONS: SMVT during the first 72 h of a prime myocardial infarction is an index of a larger healing myocardium with acute very complexed electrophysiological changes and it is an independent predictor of in-hospital mortality and a prognostic factor of a poor one year outcome.

Revisiting the frequency of peripheral arterial disease in patients with coronary artery disease: is there a difference between diabetic and non-diabetic patients?

BACKGROUND: The aim of this study was to investigate whether frequency of concomitant peripheral arterial disease (PAD) is associated with angiographic severity of coronary artery disease (CAD), as well as to ascertain if diabetic patients differ from those without diabetes in the association between these two manifestations of atherosclerosis. PATIENTS AND METHODS: This study included 302 patients (229 men, mean age 62.2 +/- 11.5 years) with documented CAD, divided into groups I-III, according to the angiographic severity of coronary atherosclerosis. Group I comprised 140 patients (104 men) with severe CAD, group II comprised 63 patients (48 men) with moderate CAD and group III comprised 99 patients (77 men) with mild CAD. Each of the groups I-III was further divided into the subgroups of diabetic and non-diabetic patients. Included were also 88 patients (42 men, mean age 61.7 +/- 9.5 years) without CAD and a control group of 60 healthy volunteers (30 men), aged 18-40 years. PAD was diagnosed by means of a Doppler apparatus. RESULTS: Frequency of PAD was associated with angiographic severity of CAD (p = 0.0001). This association was shown both in diabetic (p = 0.012) and in non-diabetic patients (p = 0.0041). Significantly (p < or = 0.01) higher frequency of PAD among diabetic patients was found in each of the groups I-III. CONCLUSIONS: Among patients with CAD, frequency of concomitant PAD is associated with angiographic severity of coronary atherosclerosis. This association is demonstrated both in diabetic and in non-diabetic patients. Finally, PAD is significantly more frequent in diabetic patients, irrespective of the angiographic severity of CAD.

Gliclazide treatment lowers serum ICAM-1 levels in poorly controlled type 2 diabetic patients.

OBJECTIVE: To investigate the potential effect of gliclazide on serum ICAM-1 (intercellular adhesion molecule-1) and VCAM-1 (vascular cell adhesion molecule-1) levels in poorly controlled type 2 diabetic patients. PATIENTS AND METHODS: The study included 104 patients, randomly divided into two groups. Group A comprised 53 patients (26 men) treated with gliclazide with a mean age of 67.5+/-9.9 years, a mean diabetes duration of 13.4+/-5.4 years and a mean HbA1c of 8.6+/-1.1%. Group B comprised 51 patients (25 men) treated with glibenclamide with a mean age of 66.4+/-10.9 years, a mean diabetes duration of 13.2+/-6.1 years and a mean HbA1c of 8.4+/-1.3%. A third group of 30 healthy controls (15 men) with a mean age of 63.3+/-10.4 years was also included. Serum levels of ICAM-1 and VCAM-1 were measured at the beginning of the study and after six months of treatment. RESULTS: Pretreatment serum ICAM-1 and VCAM-1 levels did not differ between groups A and B, while they were significantly higher (P=0.0001) than in healthy controls. No significant difference in HbA1c, body mass index, blood pressure control and lipid profile between the two groups was observed after the sixth month of treatment. In group A, serum ICAM-1 levels after six months of treatment were significantly reduced from 623.12+/-61.17 ng/ml to 370.14+/-49.92 ng/ml (P=0,01), while no reduction was found in VCAM-1 levels. In group B, no reduction was found in serum ICAM-1 and VCAM-1 levels after the end of the study. CONCLUSIONS: Our results suggest that gliclazide treatment reduces serum ICAM-1 levels in poorly controlled type 2 diabetic patients. This reduction is independent of the hypoglycaemic action of gliclazide.

The control of dyslipidemia in outpatient clinics in Greece (OLYMPIC) Study.

The objective of this study was to determine the proportion of Greek patients referred to outpatient clinics for dyslipidemia who achieved the low-density lipoprotein cholesterol (LDL-C) goal defined by the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guidelines, using lifestyle changes, lipid-lowering drug treatment (LLDT), or both. Adult patients with dyslipidemia, who had been receiving a hypolipidemic diet and/or LLDT for at least 3 months were assessed in a multicenter study performed at 66 sites across Greece. Patients were followed up for an additional 3-month treatment period. Lipid levels were recorded at baseline and at the end of the study. The primary endpoint was the proportion of patients achieving their individual LDL-C target at the end of the study, according to their coronary heart disease (CHD) risk status or its equivalents, as defined by the NCEP-ATP III guidelines. Multivariate logistic models were used to identify determinants of undertreatment. The study included 2,660 adults (20-75 years) from 7 regions of Greece. Of the evaluable sample (n = 2,211; men 51%; mean age 62 +/-9 years) 81% were receiving LLDT (96% with statins and 3% with fibrates), 44% had a history of CHD, 61% arterial hypertension, 36% diabetes, and 26% a family history of premature CHD. Overall, 6% were at low CHD risk, 30% at medium CHD risk, and 63% at high CHD risk. At the end of the study, 26% of all patients and 30% of those receiving LLDT achieved the NCEP-specified LDL-C target levels. The percentage of patients at LDL-C goal according to CHD risk status was: low risk 67% (95% CI = 59-75), medium risk 29% (95% CI = 26-33), and high risk 20% (95% CI = 18-22). Statins proved to be more effective than fibrates (p <0.0001). Atorvastatin-treated subjects (n = 1,222, mean dose 19 mg/day) attained the LDL-C target (31% of the cases) at a higher rate than those receiving other LLDT (n = 574, 26% at target, p <0.01) or not receiving drug treatment (n = 415, 8%, p <0.001). This outcome was more evident in the high-CHD risk group (n = 1,402, 26% with atorvastatin vs 16% with other LLDT and 3% not receiving LLDT attained the LDL-C goal, ANOVA, p <0.001). The majority of dyslipidemic patients receiving LLDT, mainly those with high-CHD risk, are not achieving the NCEP LDL-C target. This is mainly explained by inadequate dose titration to ensure target goals are met. Promoting healthy lifestyle and appropriate LLDT (potent statins with sufficient dose titration) must be implemented to ensure that patients attain LDL-C treatment goals and thus benefit from the reduction in individual CHD risk.

Risk factors for concomitant peripheral arterial occlusive disease in patients with coronary artery disease: is there a difference between diabetic and non-diabetic patients?

AIM OF THE STUDY: The aim of the present study was investigation of cardiovascular risk factors for concomitant Peripheral Arterial Occlusive Disease (PAOD) in diabetic vs. non-diabetic patients with coronary artery disease (CAD). PATIENTS AND METHODS: This study included 302 patients (229 men) with a mean age of 62.2 +/- 11.5 years and angiographically documented CAD. These were divided into Group A comprising 116 diabetic patients (79 men) and Group B comprising 186 non-diabetic patients (150 men). Peripheral Arterial Occlusive Disease (PAOD) was diagnosed using a Doppler apparatus. Cardiovascular risk factors that were investigated included age, history of myocardial infarction, smoking, Body-Mass Index, Waist-Hip-Ratio, hypertension and serum lipids. RESULTS: PAOD was diagnosed in 49 patients of Group A (42.4%) and 20 patients of Group B (10.8%). In Group A concomitant PAOD was associated with significantly (p = 0.0001) longer diabetes duration and significantly (p = 0.0001) higher frequency of insulin treatment, as well as significantly (p = 0.02) higher triglycerides and significantly (p = 0.039) lower HDL-Cholesterol. In Group B patients with PAOD had significantly (p = 0.0001) higher age and significantly higher (p = 0.041) LDL-Cholesterol levels than those without PAOD. No association was found between PAOD and presence of remaining risk factors in either group. In multiple regression analysis, concomitant PAOD was associated with diabetes duration (p = 0.0026) and insulin treatment (p = 0.0004) in Group A, while it was associated with age (p = 0.01) in Group B. The associations with serum lipids were no longer significant. CONCLUSIONS: Among non-diabetic patients with CAD, those who have concomitant PAOD are significantly older. Among diabetic patients with CAD, those who have concomitant PAOD show significantly longer diabetes duration and significantly higher frequency of insulin treatment.

Impact of diabetes mellitus on severity of concomitant peripheral arterial occlusive disease in patients with coronary artery disease.

AIM OF THE STUDY: The aim of the study was to evaluate the impact of Diabetes Mellitus (DM) on severity of concomitant Peripheral Arterial Occlusive Disease (PAOD) in patients with Coronary Artery Disease (CAD). PATIENTS AND METHODS: This study included 302 patients (229 men) with a mean age of 62.2 +/- 11.5 years who had angiographically documented CAD. Patients were divided into Group I (severe CAD), Group II (moderate CAD) and Group III (mild CAD). Each of the groups I-III was divided into subgroups comprising diabetic patients (subgroups Ia, IIa, IIIa) and non-diabetic patients (subgroups Ib, IIb, IIIb). PAOD was evaluated by measurement of Toe-Brachial Index (TBI). RESULTS: PAOD was diagnosed in 69 patients (22.8%). Symptoms of PAOD (intermittent claudication or rest pain) were present in 38 patients (55%), while 31 patients (45%) were asymptomatic. Frequency of symptoms attributable to PAOD did not differ (p = 0.43) between diabetic patients (25 out of 49 patients, 51%) and non-diabetic patients (13 out of 20 patients, 65%). TBI was significantly (p = 0.04) lower in diabetic (0.41 +/- 0.03) than in non-diabetic patients with PAOD (0.51 +/- 0.03). This significant difference was found in each of the Groups I-III. Severity of PAOD was significantly associated with angiographic gravity of CAD, both in diabetic (p = 0.046) and in non-diabetic patients (p = 0.047). CONCLUSIONS: DM has an adverse impact on severity of concomitant PAOD in patients with CAD. This impact does not depend on angiographic gravity of CAD. However, the association between severity of PAOD and angiographic gravity of CAD is demonstrated both in diabetic and in non-diabetic patients.

Gelatinases [matrix metalloproteinase-2 (MMP-2) and MMP-9] induce carotid plaque instability but their systemic levels are not predictive of local events.

Matrix metalloproteinases (MMPs) appear to play a central role in atherosclerotic plaque remodeling; however, the relationship of increased MMP levels in inducing carotid plaque instability remains controversial. We investigated whether gelatinases (MMP-2 and MMP-9) are implicated in carotid intraplaque hemorrhage and whether their serum levels may predict local carotid events. Nineteen carotid specimens obtained by endarterectomy of 18 patients were studied. The presence of gross intraplaque hemorrhage was recorded before plaque removal and quantification of MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1 (TIMP-1) in extracts from (1) the more stenotic area of the plaque, (2) the periphery of the plaque, and (3) serum was performed by enzyme-linked immunosorbent assay. MMP-9 levels measured in extracts from the most stenotic area were significantly higher in patients with intraplaque hemorrhage (p = 0.007); however, serum levels showed no difference, while those taken from the periphery of the lesion were also increased but did not reach a statistically significant level (p = 0.06). An increase in MMP-2 values was observed in the periphery of the lesion (p = 0.04) in patients with intraplaque hemorrhage. TIMP-1 levels showed no difference between the two groups regardless of the presence or absence of intraplaque hemorrhage. No significant differences in MMP levels were observed between symptomatic and asymptomatic patients. Increased levels of MMPs, particularly MMP-9, have been implicated in carotid intraplaque hemorrhage without their serum levels being predictive of local events.

Peripheral arterial occlusive disease as a predictor of the extent of coronary atherosclerosis in patients with coronary artery disease with and without diabetes mellitus.

We evaluated the sensitivity and specificity of a diagnosis of peripheral arterial occlusive disease (PAOD) as a predictor of the severity of coronary artery disease (CAD) in patients with and without diabetes. A total of 302 patients were assigned to groups according to the angiographic severity of their CAD and their diabetes status. Both PAOD and severe PAOD were diagnosed by measuring the ankle-brachial index (ABI) and toe-brachial index (TBI). A diagnosis of PAOD had a low sensitivity (34.3%) but a high specificity (87.0%) for detecting patients with severe CAD. Sensitivity was higher in patients with diabetes (52.4%) than without (19.5%), whereas specificity was higher in patients without diabetes (95.4%) than those with diabetes (69.8%). A diagnosis of severe PAOD had a higher specificity (96.0%), but a very low sensitivity (16.4%). We conclude that a diagnosis of PAOD among patients with CAD had a low sensitivity but a high specificity for detecting those with severe CAD, particularly in patients without diabetes.

Detection of Mycobacterium tuberculosis complex DNA in pericardial fluid, bone marrow and peripheral blood in a patient with pericardial tuberculosis. A case report.

Definitive diagnosis of tuberculous pericarditis requires identification of bacilli in pericardial fluid or tissue. Conventional diagnostic methods are time-consuming and have a low sensitivity making bacteriological confirmation of the disease very difficult. Hereby, we report the case of molecular detection of Mycobacterium tuberculosis in pericardial fluid, bone marrow and peripheral blood from a 63-year-old woman with pericardial tuberculosis, using a nested PCR assay specific for IS6110 insertion element of M. tuberculosis complex. The patient had an excellent response to a three-drug combination anti-tuberculous regimen and 1 year later was asymptomatic, without evidence of constrictive pericarditis.