Search

Background: Elevated high-density lipoprotein-cholesterol (HDL-cholesterol) levels have been linked to unfavorable outcomes in various clinical settings, but the association with thyroid nodules remains unclear. We aimed to analyze the correlation between elevated HDL-cholesterol and the presence of thyroid nodules along with certain demographic and clinical findings., Methods: In this retrospective study, the patients were divided into three groups based on their body mass index (BMI): <25, 25-29, and >30 and evaluated. Data of 677 patients aged between 15 and 95 years (52.6 ± 15.6) were evaluated. The entire study population comprised 516 females (76.2%)., Results: Thyroid nodules (67.1%) and left ventricle diastolic dysfunction (LVDD) (58.1%) were the two most frequent findings in the overall cohort. In the multivariate regression model, BMI, heart rate, and HDL-cholesterol values were significant and independent predictors ( p = 0.000 for all) of the presence of thyroid nodules. The presence of thyroid nodules is higher in females, particularly within the higher BMI groups [odds ratio (OR) = 1.048 (CI = 1.02-1.08) for BMI < 25, p = 0.003; OR = 1.094 (CI = 1.05-1.14) for BMI 25-29, p = 0.000; OR = 1.115 (CI = 1.05-1.19) for BMI ≥ 30]. This higher incidence is not observed in males., Conclusion: While the precise mechanisms underlying this association are yet to be fully elucidated, elevated HDL-cholesterol may serve as an indicator of thyroid nodules rather than a marker of cardiovascular protection.

Background: This study aimed to determine whether a high level of high-sensitivity troponin T (hsTnT) predicts a positive treadmill test in patients with suspected stable ischemic heart disease (SIHD)., Methods: In all, 366 patients with suspected SIHD were included in the study. We measured the serum hsTnT levels before the treadmill test. The treadmill test was performed according to the Bruce protocol., Results: Of the 366 patients, 97 had positive treadmill tests. The hsTnT levels were significantly higher in the positive group than in the negative group. In the binary logistic regression analysis, hsTnT, pretest probability, metabolic equivalents (METs), target heart rate (THR) percentage, and Duke treadmill score (DTS) were independent predictors of a positive treadmill test [hsTnT odds ratio (OR): 2.178, P  < 0.001; pretest probability OR: 1.036, P  = 0.007; METs OR: 0.755, P  = 0.008; THR OR: 0.773, P  < 0.001; DTS OR: 2.661, P  = 0.012]. In the receiver operating characteristic (ROC) curve analysis, the area under the curve (AUC) value of the model with the combined parameters of hsTnT, pretest probability, METs, THR, and DTS was statistically significant in predicting a positive treadmill test [combined model AUC: 0.945 (0.922-0.968), P  < 0.001]., Conclusions: In sum, high pretest hsTnT levels predicted a positive treadmill test in patients with suspected SIHD. Analysis of the hsTnT levels before the treadmill test can increase the sensitivity and specificity of the treadmill test. The methods for measuring hsTnT levels are cheap and easily accessible and can be used before the treadmill test in patients with suspected SIHD., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Objective: Recent community-based studies have identified sleep deprivation (SD) as an important modifiable risk factor for hypertension However, the underlying mechanisms linking SD to hypertension remain elusive. Thus, this study investigates blood pressure (BP) responses to cardiac autonomic stress tests in the presence of SD. Furthermore, we analyzed vascular inflammatory biomarkers as a possible underlying factor linking SD to increased BP., Methods: Ten healthy male volunteers (age, 21.6±1.2 years) underwent repeated autonomic stress tests for three consecutive days (baseline, SD, and recovery). The autonomic stress tests included the Valsalva maneuver, mental arithmetic, isometric handgrip, and cold pressor tests. Each day, resting BPs were measured, venous blood samples were collected for intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin measurements, and stress tests were performed between 0900 and 1100. Ambulatory BP was recorded during the entire SD period (24 h)., Results: One-night SD abolished BP reactivity to the Valsalva maneuver, isometric hand grip, and cold pressor tests, which returned after recovery sleep. Ambulatory BP monitoring showed that the mean systolic and diastolic BPs were 121.1±8.5 mm Hg and 72.8±6.3 mm Hg, respectively, between 0700 and 2300 and 120.3±9.6 mm Hg and 74.1±6.1 mm Hg, respectively, between 2300 and 0700 during the SD day (p>0.05 for both). Vascular inflammatory markers seemed unrelated to BP changes., Conclusion: Acute SD altered BP responses to cardiac autonomic stress tests in healthy men without affecting resting BP levels. SD led to a non-dipping pattern in BP oscillation. Collectively, these findings highlight the importance of sleep in regulating BP.

Objective: This study was an investigation of the role of left ventricular (LV) apical rotation seen in the early period after myocardial infarction (MI) in predicting infarct localization., Methods: A total of 124 patients with a ST-Segment elevation myocardial infarction (STEMI) diagnosis who underwent primary percutaneous coronary intervention (PCI) and 50 healthy volunteers with similar demographic characteristics were included in the study. The relationship between 2-dimenstional speckle tracking echocardiography (STE)-guided LV apical rotation angle measurements and technetium-99m sestamibi-single-photon emission computed tomography (SPECT)-guided infarct localization was evaluated. Conventional echocardiography and STE were performed on average 2 days after PCI, and gated SPECT myocardial perfusion imaging (MPI) was performed within an average of 60 days., Results: The apical rotation angle was lower in patients with an anterior MI compared with those who had an inferior MI and the control group (AntMI-InfMI: 6.51±2.4°, AntMI-Control: 13.20±2.5°, InfMI-Control: 14.3±2.1°; p value: 0.00, 0.00, 0.15, respectively). SPECT MPI analysis revealed the presence of an LV apical scar in all patients with acute anterior MI, but only 14 of those with inferior MI group (usually the inferoapical wall). The apical rotation angle recorded in patients with apical scar was lower than that of the patients without apical scar (7.6±2.8° and 14.5±2°, respectively; p=0.00). Receiver operating characteristic curve analysis yielded an area under the curve for apical rotation of 0.799 (p<0.01). The optimal cutoff value of 12.1° had a sensitivity of 78.3% and a specificity of 68.2% for predicting LV apical scar following STEMI., Conclusion: Detection of apical rotation angle decrease in the early period after STEMI may be useful in predicting extension of infarct scarring to the LV apex.

In the setting of acute myocardial infarction (AMI), adverse myocardial remodeling (AMR) has been universally regarded as an early-onset phenomenon generally arising within the first few weeks (usually within days in the infarct zone) following myocardial injury. On the other hand, onset of cardiac morphological changes in this setting may potentially extend far beyond this time frame (usually beyond several months after the index AMI), suggesting a prolonged latent period in certain cases. In clinical practice, this delayed form of post-AMI remodeling, namely late AMR, has emerged as an interesting and underrecognized phenomenon with poorly understood mechanisms. Notably, systemic inflammation and associated growth factors seem to play a pivotal role in this setting. Accordingly, the present article primarily aims to discuss potential mechanisms and clinical implications of late AMR (in a comparative manner with its classical early counterpart) among AMI survivors along with a particular emphasis on potential benefits of certain anti-inflammatory strategies in this setting.

Natriuretic peptides have long been introduced into clinical practice. These biomarkers have certainly been shown to provide useful information in the diagnosis, prognosis and risk stratification in heart failure and also may have a role in the guidance of heart failure therapy. Although, there are some limitations in using of these markers such as lack of specificity, aging, renal dysfunction or obesity, among the huge number of candidates for heart failure biomarkers, only natriuretic peptides are currently widely used in daily clinical practice in heart failure. Recent heart failure guidelines recognize natriuretic peptides as an essential tool in the new diagnostic and therapeutic algorithms. Furthermore, natriuretic peptides are not only used in the diagnosis or prognosis of heart failure, but also these biomarkers are referred to have some potential role in primary prevention, cardio-oncology, advanced heart failure, assessment of response to cardiac resynchronization therapy, pulmonary arterial hypertension, acute coronary syndromes, atrial fibrillation and valvular heart disease. In this article, natriuretic peptides have been reviewed for their updated information and new recommendations in heart failure and also potential role of these biomarkers in the management of various clinical conditions have been addressed in the form of expert opinion based on the available data in the literature.

In the past years, transcatheter aortic valve implantation (TAVI) has emerged as a promising option for the treatment of aortic valve pathologies particularly in the the presence of surgically high-risk situations. Importantly, a variety of specific procedural complications including acute coronary osteal occlusion, though very rare, has been reported in major clinical studies. However, little is known about the late impact of TAVI on coronary system at the macro and microvascular levels. On the other hand, clinical studies as well as real life experiences have shown variable rates of acute coronary syndrome (ACS) readmissions among TAVI recipients in the short and long terms. Within this context, it may be suggested that even though late coronary ischemic events arising after TAVI, to some extent, appears to be spontaneous or attributable to certain stressors, TAVI may also have the potential to directly account for, accelerate or contribute to the evolution of these ischemic events on follow-up. Accordingly, the present review primarily focuses on potential association of TAVI with late coronary ischemic syndromes along with a particular emphasis on its mechanistic basis and clinical implications among TAVI recipients., (Copyright © 2018. Published by Elsevier B.V.)

Takotsubo cardiomyopathy (TTC) is primarily regarded as a form of acute and transient myocardial disease with a variety of characteristic wall-motion abnormalities. Importantly, a significant portion of TTC cases generally present with variable degrees of acute left ventricular (LV) dysfunction with or without clinical HF. On the other hand, LV dysfunction in the setting of TTC has been universally and exclusively considered as a synonym for systolic dysfunction, potentially overlooking other forms of myocardial pathologies, including transient diastolic dysfunction, in this setting. More interestingly, recent observations suggest that TTC, despite its macroscopic recovery, may not always manifest as a fully reversible phenomenon, suggesting persistence of microscopic changes at the cellular level to some degree. In clinical practice, these residual changes might largely account for the evolution of certain pathologies, including persistent diastolic dysfunction and subclinical LV dysfunction with variable symptomatology (particularly those arising during high levels of myocardial workload, including exercise, etc.) among TTC survivors. Within this context, the present review aims to highlight various clinical patterns and implications of LV dysfunction in the setting of TTC, and to provide basic information regarding morphological and mechanistic characteristics of wall-motion abnormalities in this setting., Competing Interests: Disclosure: The authors have no conflicts of interest to declare.

Objective: The purpose of this study was to identify patient characteristics and statin discontinuation-related factors in patients with hypercholesterolemia., Methods: A total of 532 patients (age mean±SD: 57.4±11.5 years; 52.4% women, 47.6% men) with hypercholesterolemia and statin discontinuation were included in this national cross-sectional non-interventional observational study. Data on socio-demographic characteristics of patients, cardiovascular risk factors, past treatment with and discontinuation of statin treatment were collected in one visit., Results: Mean±SD duration of hypercholesterolemia was 4.9±4.2 years at time of discontinuation of statin treatment. Statin treatment was initiated by cardiologists in the majority of cases (55.8%), whereas discontinuation of statin treatment was decided by patients in the majority of cases (73.7%), with patients with higher (at least secondary education, 80.4%) more likely than those with lower (only primary education, 69.7%) to decide to discontinue treatment (p=0.022). Negative information about statin treatment disseminated by TV programs-mostly regarding coverage of hepatic (38.0%), renal (33.8%), and muscular (32.9%) side effects (32.9%)-was the most common reason for treatment discontinuation., Conclusion: The decision to discontinue statin treatment was made at the patient's discretion in 74% of cases, with higher likelihood of patients with higher educational status deciding to discontinue treatment and switch to non-drug lipid-lowering alternatives. Cardiologists were the physicians most frequently responsible for the initiation of the statin treatment; coverage of several non-life-threatening statin side effects by TV programs and patients' lack of information regarding high cholesterol and related risks were the leading factors predisposing to treatment discontinuation.

Early administration of glycoprotein IIbIIIa inhibitors results in improved angiographic parameters, including thrombolysis in myocardial infarction (TIMI) flow grade, corrected TIMI frame count, and TIMI myocardial perfusion grade (TMPG) among patients with ST-segment elevation myocardial infarction. Whether the same is true in the setting of non-ST-segment elevation acute coronary syndrome is unknown. The goal of the early glycoprotein IIbIIIa inhibition in non-ST-segment elevation acute coronary syndrome (EARLY ACS) angiographic substudy was to compare angiographic outcomes among patients with non-ST-segment elevation acute coronary syndrome who were administered early routine versus delayed provisional eptifibatide. Of 9,406 patients in the EARLY ACS trial, 2,066 patients were included in the angiographic substudy (early routine eptifibatide [n=1,042] or early placebo [n=1,024] with delayed provisional eptifibatide after angiography and before percutaneous coronary intervention [PCI]). The angiographic substudy primary end point was the incidence of TMPG 3 before and after PCI. TMPG 3 before (43.7% vs 44.9%, p=0.58) and after PCI (52.4% vs 50.1%, p=0.73) was similar for early routine versus delayed provisional eptifibatide, respectively. Angiographic procedural complications consisting of a composite of loss of side branch, abrupt vessel closure, distal embolization, and no reflow occurred less frequently in early routine group versus delayed provisional group (9.3% vs 13.6%, respectively, p=0.01). In the EARLY ACS angiographic substudy, the use of early routine eptifibatide resulted in fewer angiographic procedural complications. These data provide support for the use of eptifibatide in the catheterization laboratory during high-risk cases merely to prevent angiographic procedural complications., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: The aim of this study was to evaluate the serum soluble CD40 ligand (sCD40L) levels, serum uroten- sin II levels, and serum leptin levels as an indirect indicator of endothelial dysfunction, inflammation, and atherosclerosis at the microvascular level, and the comparison of those values with those of the control group with a nor- mal coronary flow pattern., Methods: The study included 35 consecutive patients (17 women, 18 men; average age: 51.20 ± 10.93 years) in our hospital who underwent coronary angiography due to objective myocardial ischemia and in whom slow coronary flow was detected. The control group included 34 consecutive patients with normal coronary flow pattern (18 women, 16 men; average age: 54.59 ± 12.40 years). The coronary flow rates of all patients and control subjects were documented by the thrombolysis in myocardial infarction (TIMI) frame count. Serum sCD40L concentrations, serum urotensin II concentrations and serum leptin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available kits., Results: The corrected TIMI frame count for LAD, Cx, RCA, and mean TIMI frame count were significantly higher in patients with slow coronary flow (SCF), compared to subjects with normal coronary flow (43.8 ± 1.7 vs. 17.7 ± 4.7, p < 0.001; 27.9 ± 6.9 vs. 11.9 ± 4.8, p < 0.001; 25.4 ± 8.4 vs. 11.1 ± 3.1, p < 0.001; and 32.3 ± 6.4 vs. 13.7 ± 5, p < 0.001, respectively). The serum soluble CD40 ligand and serum urotensin II levels were significantly higher in the slow coronary flow group compared to the control group (12.00 ± 5.43 ng/mL--6.49 ± 5.03 ng/mL, p < 0.001; and 50.94 ± 34.28 pg/mL--26.91 ± 11.52 pg/mL, p < 0.001, respectively). In addition, there was no statistically significant difference between the slow coronary flow group and the control group with regard to serum leptin levels and hs-CRP levels (both p > 0.05)., Conclusions: This study suggests that soluble CD40 ligand and urotensin II likely play a role in the pathogenesis of slow coronary flow.

Objective: Renal dysfunction commonly accompanies the course of cardiac disorders and strongly associates with increased morbidity and mortality. Elevated central venous pressure is related to worsening renal function in patients with heart failure. However, predictors of worsening renal function in mitral stenosis-whose pathophysiologic process is similar to heart failure with regard to right heart dysfunction-are unknown. This study aimed to evaluate whether clinical and echocardiographic parameters might predict worsening renal function in patients with mild-to-moderate mitral stenosis., Methods: The current study has a prospective cohort design. Sixty consecutive patients (9 male, 51 female, mean age 50±13 years) with mild-to-moderate mitral stenosis were followed up for 34±13 months (range 1-60) and their renal functions were monitored. Worsening renal function was defined as a decline in glomerular filtration rate of ≥ 20% on follow-up. In order to presence or absence of worsening renal functions, study patients divided into two groups. Statistical analysis was performed using the Chi-square, Independent samples t / Mann-Whitney U tests, univariate and multivariate Cox proportional hazards analyses, receiver operating characteristic (ROC) and Kaplan-Meier curve analyses., Results: Worsening renal function was observed in 14 patients (23%). In univariate analysis, male gender, mean pulmonary artery pressure (mPAP), peak tricuspid regurgitation velocity, systolic pulmonary artery pressure, digitalis and antiplatelet usage, right atrial size, and TEI index were determined to be predictors of worsening renal function. In a multivariate Cox proportional hazards model, mPAP (HR=1.136, 95% CI: 1.058-1.220, p<0.001) and male gender (HR=4.110, 95% CI: 1.812-9.322, p=0.001) were associated with increased risk of worsening renal function during the follow-up period. In ROC curve analysis, the optimal cut-off value of mPAP to predict worsening renal function was measured as more than 21 mmHg, with 78.6% sensitivity and 58.7% specificity (AUC 0.725, 95% CI 0.595-0.838). According to the Kaplan-Meier curve, a significant difference was found between those who had mPAP of >21 mmHg, and those who did not have, in terms of worsening renal function (p=0.006), and the difference between the groups increased after 30 months of follow-up., Conclusion: Elevated mean pulmonary artery pressure at the time of initial evaluation, in patients with mild-to-moderate mitral stenosis, might help to predict worsening renal function.

Objectives: The PLATO (Platelet Inhibition and Patient Outcomes) angiographic substudy sought to compare the efficacy of ticagrelor versus clopidogrel with respect to angiographic outcomes before and after PCI in the setting of acute coronary syndrome., Background: Greater platelet inhibition has been associated with improved angiographic outcomes before and after percutaneous coronary intervention (PCI). Therefore, it was hypothesized that treatment with ticagrelor, which achieves more rapid, higher, and more consistent platelet inhibition, would be associated with improved angiographic outcomes when compared with those of clopidogrel treatment., Methods: The angiographic cohort consists of 2,616 patients drawn from the 18,624-patient PLATO trial. Clopidogrel naïve or pre-treated patients were randomized to 180 mg of ticagrelor or 300 mg of clopidogrel (75 mg for clopidogrel pre-treated patients). PCI patients were administered, as per treatment group: 1) an additional 90 mg of ticagrelor if >24 h following the initial loading dose; or 2) an optional further 300 mg of clopidogrel or placebo (total 600 mg) prior to PCI. The substudy primary endpoint was the incidence of post-PCI TIMI (Thrombolysis In Myocardial Infarction) myocardial perfusion grade 3 (TMPG 3) among patients who received a study drug prior to PCI., Results: In total, 21.3% of patients were pretreated with clopidogrel prior to randomization. There was a short time interval between randomization and PCI (median: 0.68 [interquartile range (IQR): 0.30 to 2.21] h) among all patients. Post-PCI TMPG 3 was similar between the ticagrelor and clopidogrel groups (47.1% vs. 46.9%; p = 0.96). Likewise, the following pre-PCI outcomes were similar in the ticagrelor and clopidogrel groups, respectively: TMPG 3 (30.5% vs. 31.2%), TIMI flow grade 3 (37.1% vs. 39.3%), corrected TIMI frame count (median: 100 vs. 71 frames), TIMI thrombus grade 0 (24.1% vs. 27.6%), minimum lumen diameter (median: 0.3 [IQR: 0.0 to 0.6] vs. 0.3 [IQR: 0.0 to 0.6] mm) and percentage of diameter stenosis (median: 89 [IQR: 78 to 100] vs. 89 [IQR: 77 to 100])., Conclusions: Neither coronary flow nor myocardial perfusion, evaluated on coronary angiograms performed before or following PCI procedures within a few hours after the start of oral antiplatelet treatment in the setting of acute coronary syndromes, demonstrated a difference with ticagrelor versus clopidogrel. (A Comparison of Ticagrelor [AZD6140] and Clopidogrel in Patients With Acute Coronary Syndrome [PLATO]; NCT00391872)., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objective: This study aims to identify possible determinants of coronary collaterals in patients with severe coronary artery disease., Methods: The current study has a retrospective cohort design. Seventy four patients with ≥90% stenosis or total occlusion of the left anterior descending artery (LAD) were enrolled; coronary collateral grades, high-sensitive C-reactive protein (hs-CRP), fibrinogen, protein C and S, lipids, uric acid levels and medications applied before coronary angiography were noted and compared. Multiple logistic regression analysis was used for the multivariate analyses of independent variables associated with the development of adequate coronary collateral vessels., Results: The presence of coronary collaterals was significantly higher in males (p=0.018), with higher hs-CRP (p=0.023), prior statin use (p=0.022), and higher Gensini scores (p<0.001). In multiple logistic regression analysis, hs-CRP levels (OR=0.94, 95.0% CI=0.883-1.000, p=0.048), male gender (OR=4.73, 95.0% CI=1.441-15.539, p=0.010) and prior statin usage (OR=4.70, 95.0% CI=1.264-17.452, p=0.021) were identified as independent predictors of coronary collateral development., Conclusion: Male gender, prior statin usage, and higher hs-CRP levels are determinants of coronary collaterals in patients with coronary artery disease.

ST-elevation myocardial infarction (STEMI) causes 12.6% of deaths worldwide. Treatment strategies involve early revascularization by percutaneous coronary intervention and/or fibrinolytics, with adjunctive pharmacologic therapy. While antiplatelet therapy remains the cornerstone of pharmacologic management, newer antithrombotic therapies are showing benefit in the reduction of long-term thrombotic events following acute vessel occlusion. Future directions in adjunctive STEMI management include the use of hematopoietic stem cell therapy or growth factors to induce proliferation and differentiation of cardiac myocytes., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Objectives: The goal of this analysis was to determine the association between intraprocedural complications and clinical outcomes among patients with high-risk non-ST-segment elevation acute coronary syndrome (NSTEACS) undergoing percutaneous coronary intervention (PCI)., Background: Among patients undergoing PCI for NSTEACS, the relationship between intraprocedural complications and clinical outcomes, independent of epicardial and myocardial perfusion, has not been well characterized., Methods: The EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Non-ST-Segment Elevation Acute Coronary Syndrome) trial enrolled 9,406 patients with high-risk NSTEACS undergoing an early invasive strategy. Of these, 1,452 underwent angiographic assessment in an independent core laboratory and did not have a myocardial infarction (MI) between enrollment and angiography. We assessed the relationship between abrupt closure, loss of side branch(es), distal embolization, and no-reflow phenomenon and 30-day clinical outcomes in these patients., Results: Of the patients, 166 (11.4%) experienced an intraprocedural complication. Baseline clinical characteristics were similar between patients who did and did not have complications. The 30-day composite of death or MI was significantly higher among patients with an intraprocedural complication (28.3% vs. 7.8%, odds ratio [OR]: 4.68, 95% confidence interval [CI]: 3.2 to 7.0, p < 0.001). Individually, both mortality (3.0% vs. 0.9%, OR: 3.60, 95% CI: 1.2 to 10.5, p = 0.019) and MI (27.1% vs. 7.4%, OR: 4.66, 95% CI: 3.1 to 7.0, p < 0.001) were significantly increased. After adjusting for differences in post-PCI epicardial and myocardial perfusion, the association with 30-day death or MI remained significant., Conclusions: Among high-risk NSTEACS patients undergoing an invasive strategy, the incidence of intraprocedural complications is high, and the occurrence of these complications is associated with worse clinical outcomes independent of epicardial and myocardial perfusion. (Early Glycoprotein IIb/IIIa Inhibition in Patients With Non-ST-segment Elevation Acute Coronary Syndrome [EARLY ACS]; NCT00089895)., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: This study sought to determine angiographic and clinical outcomes among patients with acute coronary syndrome (ACS) presenting with isolated anterior ST-segment depression on 12-lead electrocardiogram (ECG)., Background: In patients with ACS, anterior ST-segment depression on 12-lead ECG may represent plaque rupture with: 1) acute thrombotic occlusion with elevation of cardiac biomarkers (+Tn); 2) a patent artery with +Tn; or 3) a patent artery with -Tn., Methods: The TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis In Myocardial Infarction 38) enrolled 13,608 ACS patients. Those with isolated anterior (leads V(1) to V(4)) ST-segment depression were analyzed. Angiograms and ECGs were interpreted by local investigators., Results: There were 1,198 (8.8%) patients with isolated anterior ST-segment depression. Of those, 314 (26.2%) had an occluded culprit artery (TIMI flow grade 0/1) and +Tn, 641 (53.5%) had a patent culprit artery (TIMI flow grade 2/3) and +Tn, and 243 (20.3%) had TIMI flow grade 2/3 and -Tn. Among patients with an occluded artery, the culprit artery was most often the left circumflex artery (48.4%). The 30-day incidence of the composite of death and MI was significantly higher among patients with an occluded artery (8.6%) than among those with a patent culprit artery and either +Tn (6.3%) or -Tn (2.9%) (3-way p = 0.006). Among patients with an occluded artery, the median time from ECG to percutaneous coronary intervention was 29.4 h (interquartile range 26.1 to 44.1 h)., Conclusions: Among ACS patients presenting with isolated anterior ST-segment depression, over one-quarter had an occluded culprit artery and elevated cardiac biomarkers. These patients had significantly worse clinical outcomes, and few underwent urgent angiography., (Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Since its introduction, the TIMI frame count method has contributed to the understanding of the pathophysiology of coronary artery disease. In this article, the evolution of the TFC method and its applicability in the assessment of various therapeutic modalities are described.

Potent antiplatelet and antithrombotic agents have significantly reduced mortality in the setting of acute coronary syndromes and percutaneous coronary intervention. However these agents are associated with increased bleeding which is in turn associated with adverse clinical outcomes. In many centers, transfusion is often used to correct for blood loss. Blood transfusion in the setting of acute coronary syndrome has been associated with adverse clinical outcomes including increased mortality. Transfusion associated microchimerism (TA-MC) is a newly recognized complication of blood transfusion. There is engraftment of the donor's hematopoietic stem cells in patients who then develop microchimerism. This article discusses the association of bleeding/blood transfusion with adverse outcomes and the potential role of TA-MC in clinical outcomes.

Although percutaneous coronary intervention restores optimal epicardial blood flow in most cases, abnormal myocardial perfusion may still persist. This might be as a result of macro and microembolization, neutrophil plugging, vasoconstriction, myocyte contracture, local intracellular and interstitial edema, intramural haemorrhage, and endothelial blistering. Local delivery of intracoronary pharmacotherapy via the coronary arteries may increase local drug concentration several fold, and may improve drug efficacy. Several pharmacological agents such as adenosine, calcium channel blockers, alpha blockers, beta2 receptor activators, vasodilators, antithrombotics, and antiplatelet agents have been used to treat coronary microvascular dysfunction. This article reviews the results of trials of intracoronary pharmacotherapy to date.

Background: Currently available fibrinolytic agents are limited by their ability to restore normal blood flow in only half of patients, the risk of reocclusion, and the risk of intracranial hemorrhage. The genetically engineered agent BB-10153 is activated by thrombin, not plasminogen activator enzymes, which limits its activity to the site of thrombus which may in turn reduce the risk of systemic bleeding. BB-10153 also has a relatively long half-life of 3-4 hours, which may also limit the potential for early reocclusion [1, 2]., Methods: The study was a phase II, open-label, multi-center, dose escalation, single-dose administration study to determine the efficacy, safety, tolerability, pharmacokinetics and pharmacodynamics of BB-10153 in ST segment elevation MI (STEMI). STEMI patients (n = 50) received a single dose of BB-10153 at one of six dose levels (1.0, 2.0, 3.0, 5.0, 7.5 and 10 mg/kg). The primary endpoint was TIMI flow grade (TFG) 3 at 60 minutes following the intravenous bolus of BB-10153., Results: Mean area under the curve for drug concentration ranged from 48.0 microg.h/mL in the 1 mg/kg dose group to 788.6 microg.h/mL in the 10 mg/kg dose group. Likewise, mean Cmax generally increased with dose over the entire dose range, from 4.9 microg/mL in the 1 mg/kg dose group to 139.6 microg/mL in the 10 mg/kg dose group. The mean apparent terminal half-life (t1/2) was 4.4 hours (range 2.2 to 7.6 hours). Few patients in the 1-3 mg/kg dosage groups achieved TFG 3 on the one-hour post-dose angiogram (4/20, 20%), and no patients achieved complete ST segment resolution. The 5, 7.5 and 10 mg/kg doses were associated with similar rates of TIMI grade 3 flow of approximately three per seven patients. Pooling TFG 3 data from the 5, 7.5 and 10 mg/kg groups yielded a TIMI grade 3 flow rate of 34% (n = 10/29; range 29-43%). No patients experienced 30-day death, recurrent acute MI, cardiogenic shock, stroke or anaphylaxis during the study. One patient experienced recurrent angina and developed recurrent myocardial ischemia requiring urgent revascularization. Three patients sustained TIMI major bleeding events (one in 1 mg/kg group, two in 7.5 mg/kg group), six patients sustained TIMI minor bleeds (one in the 2, 3, 7.5 and 10 mg/kg groups, two in the 5 mg/kg group), twp patients sustained TIMI minimal bleeds (one in each of the 2 and 10 mg/kg groups) and no patients sustained intracranial hemorrhage (ICH)., Conclusion: In a dose escalation study of a single intravenous bolus, the novel fibrinolytic agent, BB-10153 was associated with a rise in the mean area under the curve and Cmax for drug concentration over the dose range 1 to 10 mg/kg. Higher doses were associated with a range of TIMI grade 3 flow of 29-43%, and no patients experienced 30-day death, recurrent acute MI, cardiogenic shock, stroke or anaphylaxis during the study. In a dose escalation study of a single intravenous bolus, the novel fibrinolytic agent, BB-10153 was associated with a rise in the mean area under the curve and Cmax for drug concentration over the dose range 1 to 10 mg/kg. Higher doses were associated with a range of TIMI grade 3 flow of 29-43%, and no patients experienced 30-day death, recurrent acute MI, cardiogenic shock, stroke or anaphylaxis during the study.

Background: Tissue perfusion during acute myocardial infarction (AMI) may be assessed by means of the angiographic method -- TIMI myocardial perfusion (TMP). We hypothesised that TMP grade (TMPG) after primary coronary angioplasty (PCI) implicates immediate and long-term clinical outcomes., Methods: We studied 588 consecutive patients (mean age 58.7+/-10.8 years) with ST-segment elevation AMI treated with PCI. Infarct-related TMPG was evaluated before and after PCI. Myocardial injury was expressed as an area under the curve (AUC) of CK-MB release in the first 48 hours of reperfusion. Left ventricular ejection fraction (LVEF) was assessed by 2-dimensional echocardiography one day after PCI. Clinical end-points during a 12-month follow-up included death, recurrent MI and repeated revascularisation or hospitalisation. At the end of the follow-up, NYHA functional class was evaluated in all patients., Results: Before PCI, TMPG -3, -2 and -0/1 values were observed in 52 (8.8%), 77 (13.1%) and 459 (78.1%) patients, respectively. After PCI, TMPG-3, -2 and -0/1 were achieved in 196 (33.3%), 174 (29.6%) and 218 (37.1%) patients, respectively. Patients with TMPG-3, -2, and -0/1 had AUC of 10341+/-1194, 12330+/-1272 and 16718+/-1860 (U/l x h) (p<0.01) and LVEF of 53.6+/-8.6%, 45.5+/-9.5% and 41.7+/-10.4% (p<0.001), respectively. In-hospital mortality rate in patients with TMPG-3, -2 and -0/1 was 0%, 4% and 11.9%, respectively (p<0.001), and after 12-months - 2%, 6.3% and 16.5%, respectively (p<0.001). The event-free survival rate after 1-year was 83.2%, 74.1% and 65.1% respectively (p<0.001). The percentage of patients in NYHA class > or =2 was 10.2%, 16.1% and 20.6% (p=0.003), respectively., Conclusions: The TIMI myocardial perfusion grade after primary coronary angioplasty in acute myocardial infarction effects left ventricular injury and function as well as early and long-term clinical outcome.

Background: Subjects with diabetes constitute 13-25% of patients with ST segment elevation acute myocardial infarction (STEMI). In spite of the introduction of thrombolytic therapy, patients with STEMI and diabetes continue to have worse prognosis than those without diabetes. Primary percutaneous coronary intervention (PCI) has been shown in recent years to be the most effective therapy in patients with STEMI., Aim: To compare the outcome of STEMI patients with or without diabetes who underwent primary PCI., Methods: The study group consisted of 500 consecutive patients with STEMI. The occurrence of major adverse cardiac events (MACE) which included death, reinfarction or repeated PCI of the target vessel, was analysed peri-operatively and during a six-month follow-up period.Results. Diabetes was diagnosed in 68 (13.6%) patients. The mean time duration from the onset of STEMI symptoms to treatment was similar in patients with or without diabetes (230+/-97 min vs 231+/-139 min, NS). Patients with diabetes were older (61.9+/-8.9 vs 57.9+/-10.8 years, p=0.004), had higher body mass index (29+/-4 vs 27+/-5, p=0.002), more frequent history of coronary artery disease (57.4% vs 37.9%, p=0.002), higher prevalence of arterial hypertension (71.6% vs 56.8%, p=0.02) and more frequently the left anterior descending artery as the infarct-related artery (58.8% vs 42.1%, p=0.01). Immediately after PCI, epicardial and myocardial reperfusion rates were lower in patients with rather than without diabetes (TIMI 3: 84.9% vs 91.3%, p=NS, cTFC: 32+/-26 vs 22+/-16, p<0.0001, and MPG3: 25% vs 41.9% p=0.008). Diabetes increased the risk of MACE during in-hospital period by 2.7 times. The rate of MACE during a six-month follow-up period was almost two times higher in patients with rather than without diabetes (death: 8.8% vs 5.1%, reinfarction: 1.5% vs 1.2%, repeated PCI: 11.8% vs 6.9%)., Conclusions: Primary PCI-achieved epicardial and myocardial reperfusion rate is lower in STEMI patients with rather than without diabetes. The presence of diabetes almost doubles the risk of MACE during a six-month follow-up.

Acute right ventricular infarction (RVI) is usually caused by proximal occlusion of the right coronary artery. RVI is frequent, as it occurs in as many as one out of every two left ventricular interior and/or posterior wall infarctions. The involvement of the right ventricle in acute myocardial infarction has been shown to be associated with an increased risk of life-threatening arrhythmias and sudden cardiac death. Clinical course of RVI can vary from being completely silent to cardiogenic shock (seen in 10-15% patients with inferior wall infarction). RVI diagnosis is based on clinical signs (hypotension and increased jugular venous pressure while pulmonary fields are clear), ECG (ST elevation by > or = 1 mm in V4R), echocardiography (right ventricular wall regional motion abnormalities and/or right ventricle distension, paradoxical motion of the interventricular septum, tissue Doppler), technetium pyrophosphate scanning with ventriculography, and invasive patient monitoring. In addition to its important diagnostic part, the invasive patient monitoring plays a key role in risk stratification and can dynamically guide the treatment (such as fluid loading). In most cases, successful reperfusion in the infarct-related artery territory can be achieved by interventional management (i.e. angioplasty) or--if the latter is not available--by thrombolytic therapy. Patients with arterial hypotension require volume expansion which is best guided by the central venous pressure (CVP; a measure of the right atrial pressure, RAP) and the pulmonary capillary wedge pressure (PCWP). If the hemodynamics does not improve despite optimal fluid loading, pharmacological (catecholamine infusion) or mechanical (intra-aortic balloon pump) circulatory assistance needs to be implemented. Patients with significant sinus bradycardia or 3rd degree AV block may require temporary cardiac pacing. In addition, inhalatory nitric oxide (iNO) has been shown to reduce right ventricular afterload in a selective manner and its potential clinical role is currently being evaluated. Within several months after RVI, the right ventricular performance improves in most patients, including those without successful reperfusion of IRA. Such patients, however, have an increased risk of complications (including sudden death) while the recovery of right ventricular function is slow.

Unlabelled: Facilitated percutaneous coronary intervention (facilitated PCI) in acute myocardial infarction--the use of planned PCI after pharmacological reperfusion therapy, can fuse the best aspects of thrombolysis and primary angioplasty. The aim of the study was to assess microvacular reperfusion in patients with acute myocardial infarction treated with half dose of alteplase and full dose of abciximab followed by primary PCI., Methods: The study enrolled 100 patients with myocardial infarction within 12 hrs of chest pain onset in hospitals with at least 90 minutes of transportation time to interventional center. All patients received intravenous boluses of 60 U/kg heparin, 15 mg alteplase (r-tPA) and 0.25 mg/kg abciximab, and then infusions of: alteplase (35 mg/60 min) and abciximab (0.125 micrograms/kg/min for 12 hours) before transportation to interventional facility, Results: Coronary angiography was performed at a mean 123 +/- 38 minutes after lytic therapy administration. In baseline angiography 73% of patients had TIMI 3 flow in infarct related artery. In 88 patients (90%) there was TIMI 2 + 3 flow. In 82 patients PCI was performed immediately after diagnostic catheterization, with angiographic procedural success rate of 92% (TIMI 3). Corrected TIMI frame count was 29.8 +/- 25.9 before and 17.2 +/- 9.5 after PCI. TIMI Myocardial Perfusion Grade 3 and 2 (MPG 3 + 2) was present in 77% of patients before and in 72% after PCI., Conclusions: Combination of abciximab and half dose of alteplase was a very effective strategy in restoring flow in infarct related artery and achieving microvascular reperfusion. This model of pharmacological treatment could be utilized as pre-treatment for patients referred for primary PCI from remote hospitals.

Almost one in five patient has reperfusion abnormalities despite the type of percutaneous interventional procedure after acute myocardial infarction. It has been shown with myocardial contrast echocardiographic and coronary angiographic studies that infarct related artery patency does not always correlate with the presence of adequate myocardial perfusion in the infarct related artery territory. Therefore, it is necessary to obtain further diagnostic and evaluation tools to assess coronary microcirculation and reperfusion failure. ST segment resolution time, TIMI flow grade, TIMI Frame Count and TIMI Myocardial Perfusion Grade (blush score) are helpful tools to assess myocardial perfusion and diagnosis of reperfusion abnormalities.