Ahmet Camsari

Slow coronary flow may be a sign of diffuse atherosclerosis. Contribution of FFR and IVUS.

Objective. — Slow coronary flow (SCF) is a phenomenon characterized by delayed opacification of coronary arteries in the absence of epicardial occlusive disease, in which many aetiological factors such as microvascular and endothelial dysfunction, and small vessel disease have been implicated. We aimed to investigate the epicardial resistance in relation with SCF by using fractional flow reserve (FFR) and intravascular ultrasound (IVUS). Both have been combined to disclose the related epicardial flow resistance and the arterial anatomy. Methods and results. — Coronary pressure and FFR measurement were performed in 19 (8 (42.1%) men, 11 (57.9%) women; age = 55.9 ± 9.4 years) patients with SCF. All patients underwent subsequent IVUS investigation at the same setting. As compared with expected normal values, FFR values were significantly lower (1.0 vs. 0.83 ± 0.13, p < 0.0001). In patients with SCF, a strong negative correlation was seen between TIMI frame count and FFR (r = –0.551, p < 0.05). Upon IVUS investigation, the common finding was longitudinally extended massive calcification throughout the epicardial arteries and increased intimal thickness (0.59 ± 0.18mm). A negative correlation between intimal thickness and FFR was determined (r = –467, p < 0.05). Conclusion. — We have demonstrated the decreased FFR in the patients with SCF. Decreased FFR levels have been attributed to increased resistance in the epicardial coronary arteries due to diffuse atherosclerotic disease which has been demonstrated by IVUS.

Increased levels of high sensitive C‐reactive protein in patients with chronic rheumatic valve disease: evidence of ongoing inflammation

The precise pathogenetic mechanism(s) of rheumatic fever and rheumatic heart disease have never been defined. C‐reactive protein (CRP) is increased in patients with acute rheumatic fever, but it is not known whether plasma levels increase in patients with chronic rheumatic valve disease. The aim of this study was to determine the role of inflammation detected by high sensitivity CRP (hs‐CRP) levels in the progression of chronic rheumatic valve disease. A total of 113 patients with chronic rheumatic valve disease (81 women, 32 men; mean age 40±14 years, range 13–70), 51 patients with prosthetic valve(s) (31 women, 20 men; mean age 48±13 years, range 21–71) and 102 healthy subjects (68 women, 34 men, mean age 41±12 years, range 25–73), as a control group, were assessed. Patients with acute rheumatic fever, acute infection, inflammatory disease, malignancy, acute myocardial infarction and trauma were excluded. hs‐CRP was determined using latex‐enhanced immunonephelometric assays on a BN II analyzer (Behring). Transthoracic echocardiography was performed in all patients in order to evaluate valvular disease. Levels of hs‐CRP were significantly higher in patients with chronic rheumatic heart disease than in patients with prosthetic valve(s) and healthy subjects (0.62±0.64 vs. 0.35±0.41 vs. 0.24±0.18 mg/l, P<0.01 and P<0.001 respectively). No correlation was observed between CRP and age, sex or functional capacity. We found that hs‐CRP is increased in chronic rheumatic heart disease; this may indicate that inflammatory response still persists in the chronic phase.

Glutathione S-transferase gene polymorphism as a susceptibility factor in smoking-related coronary artery disease

Abstract.Coronary artery disease (CAD) is the leading cause of morbidity and mortality in the world, and cigarette smoking is a major contributing factor to the disease. Glutathione S-transferase (GST) enzyme is implicated in the detoxification of carcinogens present in tobacco smoke and consequent polymorphisms in this gene may confer susceptibility to cardiovascular disease if DNA damage is important in CAD. Therefore, we examined this question in a case-control study of subjects having coronary atheroma by angiography and with a past history of myocardial infarction (MI). The study population consists of 247 healthy controls and 148 consecutive patients who had undergone coronary angiography for suspicion of coronary artery disease. DNA was extracted from whole blood, and the GSTM1 and GSTT1 polymorphisms were determined using a real-time polymerase chain reaction (PCR). We found that the null GSTM1 and GSTT1 genotypes were associated with an increase in the risk of developing coronary heart disease (OR = 1.14; 95% CI: 0.71 – 1.82; OR = 1.38; 95% CI: 0.82 – 2.32), respectively, but this increase was not significant. Patients who smoke having the null genotypes of GSTM1 (OR: 1.63 (1.10 – 2.63)) and GSTT1 (2.66 (1.50 – 4.72)) and both (3.20 (1.37 – 7.45)) were at a higher risk for developing coronary heart disease. In conclusion, the finding of a significant association between GSTM1 and T1 with smoking status may influence cardiovascular disease via DNA damage.

Metoprolol, a Β-1 selective blocker, can be used safely in coronary artery disease patients with chronic obstructive pulmonary disease

The coexistence of coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD) is frequent because of common etiological factors. Β-Blockers remain underutilized in patients with CAD who also have COPD. This study was performed to evaluate the safety of Β-1 selective blocker agents in CAD patients with COPD. Fifty patients (aged 57.3 ± 10.1 years) were enrolled in this study; 27 patients received metoprolol CR (controlled release), and 23 received metoprolol (conventional). The patients were stratified according to the severity of COPD (21 severe, 21 moderate, and 8 mild), started on metoprolol CR or conventional metoprolol, and titrated up to the maximum tolerated dose. The clinical controls were done during the first week and then at the first and third month. Patients received a mean total daily dose of 92.5 ± 18 mg of metoprolol CR or 189 ± 36.7 mg of metoprolol. Seven patients could not receive the maximum dose. There was no significant decrease in forced expiratory volume in 1 s (FEV1) in either group (basal vs last FEV1: 54.5% ± 13.4% vs 54.3% ± 13% in the metoprolol CR group and 49.6% ± 14.5% vs 53.2% ± 12.8% in the metoprolol group). No adverse event was experienced. Metoprolol, a Β-1 selective blocker, can be used safely at the maximum dose in CAD patients with COPD.

The Relationship between Plasma Endothelin-1, Nitric Oxide Levels, and Heart Rate Variability in Patients with Coronary Slow Flow

Background: Coronary slow flow (CSF) is characterized by delayed opacification of coronary arteries in the absence of epicardial occlusive disease. In this study, we aimed to determine endothelin‐1 (ET‐1), nitric oxide (NOx) levels and time domain heart rate variability (HRV) parameters in patients with CSF and relationship among these parameters.

Two episodes of anuria and acute pulmonary edema in a losartan-treated patient with solitary kidney.

Atherosclerotic renal artery stenosis (RAS) is an increasingly important cause of end-stage kidney disease, and may cause hypertension, progressive renal failure, and recurrent pulmonary edema. Herein, we report two episodes of anuria and acute pulmonary edema associated with losartan treatment in a hypertensive patient with preexisting severe renal artery stenosis in a solitary kidney. After successful percutaneous renal balloon angioplasty procedure, urine flow was started immediately, despite 10 days of anuria. Blood pressure measurements were still at acceptable levels with a low dose Β blocker, and serum creatinine levels were normal even after eight months. PTRA should be done in such patients, even with prolonged anuria. Physicians who recommend angiotensin receptor blockers in patients with RAS, especially in patients wih hypovolemia or a solitary kidney, should be careful about this complication.

The correlation of thrombolysis in myocardial infarction frame count with insulin resistance in patients with slow coronary flow

BackgroundIt has been reported that coronary endothelial dysfunction plays an important pathogenetic role in patients with slow coronary flow (SCF). Insulin resistance is defined as impairment of insulin-stimulated glucose and/or lipid metabolism, while endothelial dysfunction is defined as paradoxical or inadequate endothelial-mediated vasodilation. In this study, we aimed to evaluate insulin resistance in patients with SCF. MethodsThe study population included 25 patients with SCF and 28 healthy controls. Insulin resistance was estimated via homeostasis model assessment insulin resistance index (HOMA-IR). ResultsPatients with SCF had higher high-sensitive C-reactive protein (hs-CRP) and HOMA-IR scores (P<0.05) than controls. Mean thrombolysis in myocardial infarction frame count had significant correlation with hs-CRP, fasting plasma insulin levels and HOMA-IR score (r=0.566, P<0.05; r=0.883, P<0.05; r=0.884, P<0.05, respectively). ConclusionIn patients with SCF, thrombolysis in myocardial infarction frame counts and hs-CRP are correlated with increased insulin resistance and thus, it can be suggested that insulin resistance and inflammation may, in part, have a role in the pathogenesis of SCF.

A comparison of 1-month and 6-month clopidogrel therapy on clinical and angiographic outcome after stent implantation

In this study, we aimed to disclose the net effect of long-term (6-month) clopidogrel treatment as compared to that of short-term (1-month) treatment in the poststenting period. A total of 278 patients with successful stent implantation were involved in the study. After preloading with 300 mg of clopidogrel orally (p.o.) 24 h prior to the procedure, randomly selected patients were given either 75 mg p.o. for 1 month (group A) or 75 mg p.o. for 6 months (group B). The patients were followed up clinically and underwent control angiography at 6 months regardless of their clinical status to delineate the coronary anatomy and assess quantitative computer-assisted (QCA) analysis. In 140 (50.4%) patients (group A), 244 (50.6%) stents were used to treat 237 coronary lesions, and in 138 patients (group B), 238 (49.4%) stents were used to treat 238 coronary lesions. There was no difference between the groups with respect to any of the clinical characteristics, intracoronary thrombus, antiaggregant therapy, the type of lesion, vessel score index, and baseline QCA parameters. In 62 patients binary in-stent restenosis (ISR) was determined with no statistical difference between the groups (group A: 20.7% vs group B: 23.9%, P = not significance). There was also no difference between the two groups at 6 months regarding QCA parameters. Thirty-seven of the 62 patients with restenosis have developed major adverse coronary events such as death, myocardial infarction, and target vessel revascularization (group A: 12.9% vs group B: 13.8%, P = not significant). In patients with chronic coronary syndrome, in the poststenting period, 6-month clopidogrel use as an adjunct to aspirin has shown no benefit over 1 month use with respect to clinical outcome and angiographic outcome, such as restenosis rate, follow-up, minimal luminal diameter, late loss, lost index, and net gain.

Predictive Value of P‐Wave Signal‐Averaged Electrocardiogram for Atrial Fibrillation in Acute Myocardial Infarction

Background: Atrial fibrillation (AF) is a common complication of acute myocardial infarction (AMI) with a reported incidence of 7–18%. Recently, P‐wave signal‐averaged electrocardiogram (P‐SAECG) has been used to assess the risk of paroxysmal AF attacks in some diseases. The aim of this study was to determine prospectively whether patients with AMI at risk for paroxysmal AF would be identified by P‐SAECG and other clinical variables.

The relationship between paraoxonase-1 activity and coronary artery disease in patients with metabolic syndrome.

OBJECTIVES We investigated the correlation of serum paraoxonase-1 (PON-1) activity with coronary artery disease (CAD) in patients with metabolic syndrome (MetS). STUDY DESIGN The study included 21 patients (mean age 55 ± 9 years) with MetS, stable angina pectoris, and angiographically shown CAD, 24 patients (mean age 51 ± 10 years) with MetS and angiographically normal coroner arteries, and 28 healthy controls (mean age 49 ± 12 years). Demographic and clinical characteristics, insulin levels, homeostasis model assessment of insulin resistance index, and PON-1 activity were assessed in all the groups. Severity of CAD was assessed using the Gensini score. RESULTS Paraoxonase-1 activity was significantly lower in patients with MetS compared to the control group (p=0.02). The two MetS groups with and without CAD exhibited similar characteristics in all the parameters including PON-1 activity (p>0.05). Univariate correlation analysis performed in MetS-CAD patients showed a significant negative correlation between the Gensini score and PON-1 activity (r=-0.48, p=0.02). The overall PON-1 activity of all the subjects showed no correlation with the parameters examined. CONCLUSION Decreased PON-1 activity in patients with MetS compared to the control group suggests increased oxidative stress in MetS. Detection of similar PON-1 activity levels in MetS groups with and without CAD suggests that disturbance of oxidative-antioxidative balance occurs before the development of CAD. The negative correlation between the Gensini score and PON-1 activity implies that decreased PON-1 activity may be one of the etiologic causes of atherosclerotic progress in MetS.