Aytac Oncul

The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events.

AbstractBackground: Aspirin resistance may increase up to more then threefold the risk of major cardiovascular events (MACE) in patients with stable coronary artery disease. Aim:The aim of our study was to determine; the prevalence of aspirin resistance in patients with acute coronary syndromes, the role of aspirin resistance on outcome in the follow-up and the effect of clopidogrel therapy in the prevention of MACE in aspirin resistant subjects. Material and methods: We detected the prevelance of aspirin resistance in 105 patients with acute coronary syndrome. Platelet functions were analyzed in Platelet Function Analyzer (PFA)-100 (Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP (Col/ADP) cartridges. Primary end points of the study were myocardial infarction, unstable angina, cardiac death. Results: 19% (n = 20) of patients were aspirin resistant by PFA-100. In the follow-up, MACE occured in 9 patients (45%) with aspirin resistance and in 10 patients (11.7%) with aspirin sensitive platelet aggregation (p = 0.001). Multivariate analysis showed that aspirin resistance was an independant predictor of MACE. The prevalence of MACE in patients who were on clopidogrel treatment for 12 months were lower compared to those who were on a clopidogrel treatment for the first six months (p = 0.040). Conclusions: We determined that the MACE risk in patients with acute coronary syndromes having detected aspirin resistance, was higher at statistically significant levels compared to patients having aspirin sensitive platelet aggregation. Our results showed that aspirin resistance, was an independant predictor of MACE in patients with acute coronary syndrome.

Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR).

Aspirin resistance may increase the risk of major adverse cardiac events (MACE) more than threefold in patients with stable coronary artery disease (CAD). This study aimed to determine the prevalence of aspirin resistance in patients with stable CAD, the role of aspirin resistance on outcome in the follow-up, and the effect of clopidogrel therapy in MACE prevention in aspirin-resistant individuals. We detected the prevalence of aspirin resistance in 234 patients with stable CAD. Platelet function was determined by PFA-100 with collagen and/or epinephrine and collagen and/or ADP cartridges. The mean follow-up time was 20.6 ± 6.9 months. The primary endpoints of the study were occurrence of myocardial infarction, unstable angina, stroke and cardiac death. Of patients, 22.2% (n = 52) were aspirin resistant by PFA-100. During follow-up, MACE occurred in eight patients (15.4%) with aspirin resistance and in 20 patients (11.0%) with aspirin-sensitive platelet aggregation (P = 0.269). MACE increased in aspirin-resistant patients after termination of clopidogrel therapy. Eleven patients experienced MACE after cessation of clopidogrel therapy (P < 0.001). The MACE risk in patients with stable CAD having detected aspirin resistance was similar compared with patients having aspirin-sensitive platelet aggregation by PFA-100. The MACE prevalence increased during follow-up, however, just after cessation of clopidogrel therapy.

Effect of carvedilol on silent anthracycline-induced cardiotoxicity assessed by strain imaging: A prospective randomized controlled study with six-month follow-up.

BACKGROUND The use of antracycline (ANT) in breast cancer has been associated with adverse cardiac events. Two-dimensional (2D) strain imaging (SI) can provide a more sensitive measure of altered left ventricular (LV) systolic function. We aimed to evaluate the preventive effect of carvedilol administration assessed by SI in a patient with breast cancer treated with ANT. METHODS Patients receiving ANT were randomly assigned to the carvedilol- or placebo-receiving group. Each received an echocardiographic examination with conventional 2D echocardiography, pulsed tissue Doppler, and 2D SI prior to and 6 months post ANT treatment. RESULTS During the 6-month follow-up period there were no patient deaths or interrupted chemotherapy treatments due to doxorubicin-induced cardiotoxicity. Both left ventricular ejection fraction (LVEF) and fractional shortening (FS) were within normal limits for all patients before and after ANT therapy. EF, FS and LV dimensions were measured using M-mode echocardiography and found to be similar in both groups before and after ANT therapy. The mean EF, FS, and LV echocardiograph baseline and control dimensions were similar in both groups after 6 months. Though baseline SI parameters were similar between the groups, there was a significant decrease in LV basal septal and basal lateral peak systolic strain in the control group compared to the carvedilol group. CONCLUSIONS These results indicate that carvedilol has a protective effect against the cardiotoxicity induced by ANT.

Impact of vitamin D insufficiency on the epicardial coronary flow velocity and endothelial function.

ObjectiveIncreasing evidence suggests a relationship between vitamin D (VD) insufficiency and cardiovascular disease. The present study evaluated the effect of VD insufficiency on epicardial coronary flow rate, subclinical atherosclerosis, and endothelial function. MethodsThe present study was cross-sectional and observational. We enrolled 222 consecutive patients who had undergone coronary angiography for suspected ischemic heart disease and were found to have normal or near-normal coronary arteries. Thereafter, 25(OH)D3 levels were measured and the coronary flow rate was assessed using the thrombolysis in myocardial infarction frame count. Slow coronary flow (SCF) was defined as a thrombolysis in myocardial infarction frame count greater than 27/frame. Endothelial function was assessed by brachial artery flow-mediated dilatation. Carotid intima-media thickness, an indicator of subclinical atherosclerosis, was measured using B-mode ultrasonography. ResultsThe mean level of 25(OH)D3 was 31.8 ng/ml, and 47% (n=106) of the patients had insufficient 25(OH)D levels (<30 ng/ml). Baseline characteristics were similar between VD-insufficient and VD-sufficient groups. The incidence of SCF was significantly higher in the VD-insufficient group than in patients with sufficient VD (relative risk=3.5, 95% confidence interval=1.1–10.5, P=0.01). After adjusting for cardiovascular disease risk factors, VD insufficiency was independently associated with SCF. The linear regression analysis showed that VD insufficiency was correlated independently with % flow-mediated dilatation (&bgr;=0.424, P<0.001) and carotid intima-media thickness (&bgr;=0.43, P<0.001). ConclusionA strong association was found between VD insufficiency and the SCF phenomenon. In addition, VD insufficiency was associated with endothelial dysfunction and subclinical atherosclerosis. We believe that further studies are required to clarify the role of VD in patients with SCF.

Aspirin-resistant platelet aggregation in a cohort of patients with coronary heart disease.

Aspirin resistance could be defined as thrombotic and embolic cardiovascular events despite regular aspirin therapy. The study aimed to determine the profile and prevalence of aspirin resistance in coronary artery disease patients. We evaluated the prevalence of aspirin resistance in a cohort of 505 patients with the diagnosis of coronary artery disease taking 80–300 mg regular aspirin daily. Platelet functions were analyzed by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine cartridges and collagen and ADP cartridges. A closure time of 186 s or less with the collagen and epinephrine cartridge was defined as aspirin resistance. Of the patients, 118 (23.4%) were aspirin resistant by the PFA-100. Aspirin-resistant patients were more likely to be older than aspirin-sensitive patients (P = 0.024). No statistically significant differences between the aspirin-resistant and aspirin-sensitive individuals were present in gender, major risk factors of coronary artery disease, number and localization of involved coronary vessels, serum lipid levels, and blood counts. According to the high prevalence of coronary heart disease, many people are affected by aspirin resistance, which may play a role in adverse cardiovascular events. Monitoring of platelet function in patients with coronary heart disease may support the optimization of antiplatelet therapy with additional and/or alternative agents.

Does aspirin use prevent acute coronary syndrome in patients with pneumonia: multicenter prospective randomized trial.

ObjectivesThe aim of this study was to test the hypothesis that aspirin would reduce the risk for acute coronary syndromes (ACSs) in patients with pneumonia. BackgroundsPooled data suggest that pneumonia may trigger an ACS as a result of inflammatory reactions and the prothrombotic changes in patients with pneumonia. Hypothetically considering its antiaggregating and anti-inflammatory effects, aspirin might also be beneficial for the primary prevention of ACS in patients with pneumonia. MethodsOne hundred and eighty-five patients with pneumonia who had more than one risk factor for cardiovascular disease were randomized to an aspirin group (n=91) or a control group (n=94). The patients in the aspirin group received 300 mg of aspirin daily for 1 month. ECGs were recorded on admission and 48 h and 30 days after admission to assess silent ischemia. The level of high-sensitivity cardiac troponin T was measured on admission and 48 h after admission. The primary endpoint was the development of ACS within 1 month. The secondary endpoints included cardiovascular death and death from any cause within 1 month. ResultsThe &khgr;2-test showed that the rates of ACS at 1 month were 1.1% (n=1) in the aspirin group and 10.6% (n=10) in the control group (relative risk, 0.103; 95% confidence interval 0.005–0.746; P=0.015). Aspirin therapy was associated with a 9% absolute reduction in the risk for ACS. There was no significant decrease in the risk of death from any cause (P=0.151), but the aspirin group had a decreased risk of cardiovascular death (risk reduction: 0.04, P=0.044). ConclusionThis randomized open-label study shows that acetyl salicylic acid is beneficial in the reduction of ACS and cardiovascular mortality among patients with pneumonia.

Predominant Tricuspid Stenosis Secondary to Bacterial Endocarditis in a Patient With Permanent Pacemaker and Balloon Dilatation of the Stenosis

In a 49‐year‐old woman with sick sinus syndrome and a pemanent VVI pacemaker, severe tricuspid stenosis and its clinical consequences developed 4 years after the attack of endocarditis. Besides the quite unusual occurrence of lead related tricuspid stenosis, successful treatment with balloon dilatation is the unique feature of this case.

Coronary artery aneurysm development after successful primary stent implantation

This case report describes a patient who developed an aneurysmatic dilation of a coronary artery 6 months after successful primary stent implantatIon. The dilation occurred within the stented segment of the artery. To our knowledge, this is the first report of the development of an aneurysm, in the absence of angiographically visible dissection or other possible causative factors.

Intracoronary autologous bone marrow-derived mononuclear cell transplantation improves coronary collateral vessel formation and recruitment capacity in patients with ischemic cardiomyopathy: a combined hemodynamic and scintigraphic approach.

This study investigated the effects of intracoronary autologous bone marrow−derived mononuclear cell (BMC) transplantation on coronary microcirculation. Fifteen patients with ischemic cardiomyopathy were treated by intracoronary infusion of BMCs via the patent infarct-related artery. The thermodilution-derived coronary flow reserve, index of microvascular resistance, pressure-derived collateral flow index, and coronary wedge pressure were measured at baseline and at 6 months. Successive balloon inflations during BMC transplantation were performed to observe the recruitment in pressure-derived collateral flow index and coronary wedge pressure, and the percentage changes between baseline and 6 months were calculated. The mean (SD) coronary flow reserve increased from 1.3 (0.4) to 2.1 (0.5), and the mean (SD) index of microvascular resistance decreased from 44.9 (24.4) to 21.2 (14.1) (P = .001 for both). The mean (SD) improvement in pressure-derived collateral flow index (from 0.14 [0.05] to 0.22 [0.08]) was also statistically significant (P = .001). Similarly, the percentage improvements in pressure-derived collateral flow index and coronary wedge pressure were statistically significant (P = .01 for both). The percentage improvement in perfusion assessed by single-photon emission computed tomography strongly correlated with the percentage changes in pressure-derived collateral flow index (r = 0.88, P = .001) and coronary wedge pressure (r = 0.69, P = .01). These results demonstrate for the first time (to our knowledge) that intracoronary autologous BMC transplantation improves coronary collateral vessel formation and recruitment capacity in human subjects.

An example of apparently normal electrocardiogram originating from incorrect electrocardiographic acquisition in a patient with ST-segment elevation myocardial infarction

Electrocardiography (ECG) is proved to be an invaluable tool for diagnosis of ischemic heart disease for a long while. Importance of ECG in acute management decision makes it a crucial method that must be known in depth by every physician, and the clinicians should also be aware of the dangerous pitfalls of ECG. We present a patient with ST-segment elevation myocardial infarction in whom incorrect interpretation of an inaccurately taken ECG might have led to disastrous consequences.