Cuneyt Turkoglu

Early use of pravastatin in patients with acute myocardial infarction undergoing coronary angioplasty.

AIM To determine whether statin therapy initiated early in acute myocardial infarction together with thrombolytic therapy in patients with acute myocardial infarction results in clinical benefit through early plaque stabilization. METHODS AND RESULTS The study population consisted of 77 patients who underwent coronary balloon angioplasty of the infarct-related artery during the first month of acute myocardial infarction. These patients belonged to the cohort of the Pravastatin Turkish Trial (PTT). Forty of them were assigned randomly to have immediate pravastatin (40 mg/day) therapy adjunctive to thrombolytic therapy regardless of serum lipid levels and received statin treatment throughout the study. Lipid levels were determined immediately after admission and before angioplasty and at the end of 6 months. Patients were re-evaluated clinically and angiographically for cardiovascular adverse events and restenosis after a 6-month follow-up period. The baseline angiographic and clinical characteristics of the two groups were similar. The incidence of angina was significantly lower in the pravastatin group (30.0%, 12 patients) compared to the control group (59.5%, 22 patients) (p = 0.018). The cumulative major adverse cardiac events in the pravastatin group were significantly lower when compared to the control group (32.5% vs. 75.6%, p = 0.0001). CONCLUSIONS Early initiation of pravastatin therapy immediately after an acute myocardial infarction significantly decreased the frequency of major cardiac adverse events. Such early potential clinical benefits further strengthen the rationale for starting statin treatment as soon as possible after acute coronary events particularly in patients in whom invasive intervention is planned.Aim — To determine whether statin therapy initiated early in acute myocardial infarction together with thrombolytic therapy in patients with acute myocardial infarction results in clinical benefit through early plaque stabilization. Methods and results — The study population consisted of 77 patients who underwent coronary balloon angioplasty of the infarct-related artery during the first month of acute myocardial infarction. These patients belonged to the cohort of the Pravastatin Turkish Trial (PTT). Forty of them were assigned randomly to have immediate pravastatin (40 mg/day) therapy adjunctive to thrombolytic therapy regardless of serum lipid levels and received statin treatment throughout the study. Lipid levels were determined immediately after admission and before angioplasty and at the end of 6 months. Patients were re-evaluated clinically and angiographically for cardiovascular adverse events and restenosis after a 6-month follow-up period.The baseline angiographic and clinical characteristics of the two groups were similar.The incidence of angina was significantly lower in the pravastatin group (30.0%, 12 patients) compared to the control group (59.5%, 22 patients) (p = 0.018).The cumulative major adverse cardiac events in the pravastatin group were significantly lower when compared to the control group (32.5% vs. 75.6%, p = 0.0001). Conclusions — Early initiation of pravastatin therapy immediately after an acute myocardial infarction significantly decreased the frequency of major cardiac adverse events. Such early potential clinical benefits further strengthen the rationale for starting statin treatment as soon as possible after acute coronary events particularly in patients in whom invasive intervention is planned.

Impaired Endothelial Function in Patients with Myocardial Bridge

Objective: The relationship between myocardial bridging (MB) and ischemic heart disease is still controversial. In this study, we aimed to evaluate the existing atherosclerosis and noninvasive endothelial function of brachial artery in patients with MB. Methods: The present study included 50 patients (group I) who had MB in left anterior descending (LAD) on coronary angiography. All of the coronary artery segments were evaluated by intravascular ultrasound (IVUS). Endothelial function was assessed with measurement of flow‐mediated dilatation (FMD) and nitrate‐dependent dilatation in the brachial artery. The study also included 30 healthy control subjects (group II). Patients in the group I were further subdivided into two subgroups based on the findings on IVUS: group IA included 20 patients without atherosclerotic lesions and group IB included 30 patients with atherosclerotic coronary artery disease in addition to MB. Results: FMD values were found to be significantly lower in the patients with MB (group I) than in the control (6.4 ± 3% vs 11 ± 4%, P <0.001). In regard to FMD values in subgroups, FMD was 7 ± 2% in the group IA and 5.8 ± 1% in the group IB (P = 0.023). On IVUS, atherosclerotic plaque was found proximal to the bridge in the same coronary artery segment in addition to MB in 75% of the patients in group I (group IB). No atherosclerotic plaque was found in within or distal segments of MB. Conclusion: Endothelial function is impaired in patients with MB and there is an increased tendency for atherosclerosis proximal to the bridge in the patients with MB. Endothelial dysfunction is more severe in the patients with atherosclerosis proximal to the bridge.

A rare indication for stenting: Persistent coronary artery spasm

SummaryA 34-year-old man presenting with angina both at rest and on exertion was investigated. He developed severe ST segment elevation and a brief period of ventricular tachycardia during an exercise tolerance test. On coronary angiography, 60% fixed luminal narrowing was observed in the proximal left anterior descending coronary artery and a severe spasm developed at this site, leading to temporary total occlusion of the vessel. Successful coronary angioplasty (PTCA) was performed on this lesion, with a residual 15% narrowing. However, the patient had a recurrence of angina 3 weeks later, despite being administered high doses of nitrate and calcium antagonist. During control angiography, the lesion severity was unchanged, but spasm developed again following contrast injection. At this time, a Palmaz-Schatz stent was implanted. Calcium antagonist, nitrate, Ticlopidine and low molecular weight heparin therapy was started. There was no recurrence of symptoms during a 3-month follow-up. The exercise tolerance test, and myocardial perfusion scintigraphy findings were normal and the stent was patent without restenosis at the end of the 3-month follow-up. Intracoronary stent implantation for persistent coronary spasm refractory to conventional medical therapy can be considered a feasible and attractive treatment modality for the control of symptoms.

Levosimendan versus Dobutamine in Heart Failure Patients Treated Chronically with Carvedilol

INTRODUCTION Although beta-blockers are highly effective in the treatment of heart failure (HF), many patients with HF receiving a beta-blocker continue to become decompensated and require hospitalization for worsening HF. Levosimendan and dobutamine are used to manage decompensated HF, but their comparative effects on left ventricular (LV) function in patients prescribed beta-blockers are unknown. AIMS The aim of this study was to compare the effects of dobutamine and levosimendan on LV systolic and diastolic functions in chronic HF patients treated chronically with carvedilol. Forty patients with chronic HF who had NYHA class III to IV symptoms, a LV ejection fraction (LVEF) <40%, and ongoing treatment with carvedilol were enrolled in this randomized (1:1), dobutamine controlled, open-label study. Before and 24 h after treatment, LVEF, mitral inflow peak E and A wave velocity, E/A ratio, the deceleration time of the E wave (DT), isovolumic relaxation time (IVRT), peak systolic (Sm) and early diastolic (Em) mitral annular velocity, and systolic pulmonary artery pressure (SPAP) were measured by echocardiography. RESULTS Levosimendan produced a statistically significant increase in LVEF (28+/-5% vs. 33+/-3%), Sm (6.5+/-1.2 cm/s vs. 7.4+/-0.9 cm/s), DT (120+/-10 ms vs. 140+/-15 ms), and Em (7.5+/-0.4 cm/s vs. 8.1+/-0.5 cm/s) and significant decrease in E/A ratio (2.1+/-0.3 vs. 1.7+/-0.4) and SPAP (55+/-5 mmHg vs. 40+/-7 mmHg). No significant change occurred in LV systolic and diastolic function parameters, or SPAP with dobutamine treatment. Levosimendan did not significantly alter the heart rate (72+/-4 bpm vs. 70+/-3 bpm), systolic (105+/-5 mmHg vs. 102+/-4 mmHg), or diastolic blood pressure (85+/-5 mmHg vs. 83+/-5 mmHg) whereas with dobutamine treatment, all these parameters significantly increased. CONCLUSIONS Dobutamine and levosimendan have different effects on LV functions in patients treated chronically with carvedilol. These differences should be considered when selecting inotropic therapy for decompensated HF receiving long-term carvedilol.

The effect of atorvastatin on platelet function in patients with coronary artery disease

Background — Lipid-lowering therapy was shown to have several beneficial effects in patients with coronary artery disease (CAD). Aim — The objective of this study was to investigate the effect of atorvastatin on platelet aggregation in patients with CAD. Methods — Twenty-five hypercholesterolaemic patients who had angiographically proven CAD and 16 normal subjects were enrolled. All patients received 10 mg/day atorvastatin for two months. Anti-platelet agents were discontinued 15 days prior to blood sampling at the beginning and at the end of the atorvastatin therapy. Aggregometric curves of the platelets in response to ADP, collagen and epinephrine were obtained using the aggregometry (turbidimetric) technique. Results — In patients with CAD, total cholesterol (TC) and LDL cholesterol (LDL-C) basal levels were measured (230 ± 49 mg/dl, 140 ± 41 mg/dl, respectively). Following lipid-lowering therapy, TC and LDL-C decreased significantly (p < 0.05). The activation measurements of aggregometric curves decreased significantly compared with basal parameters in response to ADP but not in response to collagen and epinephrine. Conclusion — Lipid-lowering therapy with the HMG-CoA reductase inhibitor, atorvastatin, had a marked reduction effect on platelet aggregation.

Takayasu arteritis in Turkey

Takayasu arteritis is a non-specific inflammatory process of unknown etiology affecting the aorta and its branches. A retrospective study was done in 14 patients diagnosed as Takayasu arteritis. Eleven patients were female and three were male. Ages ranged from 12 to 30 years. Seven patients had type I arteritis, three patients type II arteritis, and four patients type III Takayasu arteritis. Successful angioplasty was performed in five cases.

Soluble P-selectin and the success of thrombolysis in acute myocardial infarction

BACKGROUND P-Selectin mediates adhesive interactions between platelets, leukocytes and endothelium to form thrombi. Our purpose was to investigate plasma soluble(s) P-selectin levels in patients with acute myocardial infarction (aMI) and the effect of thrombolysis on P-selectin levels. METHODS Patients with aMI within the first 6 h of chest pain were enrolled prospectively. sP-selectin levels were determined by ELISA in the plasma of patients with aMI (n=32), stable angina (n=18), and healthy controls (n=15). Samples were obtained before, 3 and 24 h after reperfusion therapy with tissue plasminogen activator. Seven patients showed recurrent angina or failure to reperfuse. RESULTS sP-selectin levels were significantly higher in aMI group than other groups (86.7+/-8.7 ng/ml, P<0.05). sP-selectin levels were similar in stable angina and control groups (28.8+/-4.4 vs. 25.4+/-7.3 ng/ml, P=NS). A significant increase in sP-selectin levels was observed 3 h after successful thrombolysis and this was followed by a decrease to near the baseline level late after reperfusion. But patients with failed reperfusion showed sustained high sP-selectin levels after 24 h of thrombolysis (P<0.05). CONCLUSION The plasma sP-selectin level is elevated in aMI and it increases further following thrombolytic therapy. This increase is probably induced by activation of endothelial cells or platelets after myocardial ischemia and reperfusion during aMI. As the elevated levels are sustained in patients with failed reperfusion, serial P-selectin levels may be used as a non-invasive indicator of successful thrombolysis in aMI.

The Effect of Myocardial Surgical Revascularization on Left Ventricular Late Potentials

Background: The presence of ventricular late potentials (LP) is an important indicator for the development of ventricular tachyarrhythmias due to ischemic heart disease. The effect of myocardial revascularization on LP has remained controversial. The purpose of this study was to determine whether complete myocardial surgical revascularization (CABG) documented by myocardial perfusion scintigraphy might alter the substrate responsible for LP.

Relationship Between Echocardiographic Determinants of Left Atrial Spontaneous Echo Contrast and Thrombus Formation in Patients with Rheumatic Mitral Valve Disease.

Spontaneous echo contrast (SEC) may be detected by ultrasonography in environments favoring blood stasis. It is most commonly seen through the use of transesophageal echocardiography in the left atrium of patients with rheumatic mitral valve disease especially in the presence of atrial fibrillation. We studied the predictors of SEC, such as cardiac rhythm, left atrium and left atrial appendage functions, and mitral and pulmonary vein flow parameters, in patients with rheumatic mitral valve disease. The relationship between these parameters and the severity of SEC and appearance of thrombus was evaluated.

Brugada syndrome, Brugada phenocopy or none?

Brugada syndrome is a form of inherited arrhythmia syndrome characterized by a distinct ST‐segment elevation in the right precordial leads. Brugada phenocopies are clinical entities that present with an electrocardiographic pattern identical to Brugada syndrome and may obey to various clinical conditions. We present a case of a suicidal attempt using a high dose of propafenone causing a Brugada‐type electrocardiographic pattern. Is this a Brugada syndrome case, a Brugada phenocopy or something else?