Antiplatelet agents play an essential role in the treatment of acute coronary syndrome (ACS). Aspirin and thienopyridines comprise the major classes of antiplatelet therapies demonstrated to be of benefit in the treatment of ACS. Thienopyridines are a class of drugs that function via inhibition of the adenosine diphosphate (ADP) P2Y12 platelet receptors. While clopidogrel remains in extensive use in clinical practice, it cannot meet the needs in many clinical conditions because of its pharmacological limitations. In recent years, newly developed P2Y12 antagonists, such as prasugrel and ticagrelor, have proven to be of higher efficacy and less resistance. As a third generation thienopyridine, prasugrel exerts a much more rapid and consistent inhibitory effect on platelet aggregation than clopidogrel. Treatment with ticagrelor, nonthienopyridine oral antiplatelet drug, significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in the rate of overall major bleeding as compared with clopidogrel. The present review aims to discuss the current knowledge on the safety and efficacy of new oral antiplatelet agents including prasugrel and ticagrelor.
Acute Coronary Syndrome ; Adenosine ; Adenosine Diphosphate ; Aspirin ; Blood Platelets ; Hemorrhage ; Myocardial Infarction ; Piperazines ; Platelet Aggregation ; Platelet Aggregation Inhibitors ; Pyridines ; Stroke ; Thienopyridines ; Thiophenes ; Ticlopidine ; Prasugrel Hydrochloride

The explosive epidemics of diabetes and obesity as well as an aging population have led to cardiovascular diseases as the leading cause of world-wide morbidity and mortality beyond cancer. The recent introduction of drug-eluting stents and medications such as statins, dual anti-platelet therapy, and angiotensin converting enzyme inhibitors has dramatically improved clinical outcomes in patients with cardiovascular diseases. However, mortality is still increasing despite state-of-the-art therapeutics, as current diagnostic and therapeutic strategies against cardiovascular disease center on "locking the barn door after the horse has been stolen". Novel diagnostic solutions that identify individuals at risk before the disease is overt are needs. Imaging approaches that visualize molecular targets rather than anatomical structures aim to illuminate vital molecular and cellular aspects of atherosclerosis biology in vivo. Recent technological advances in small animal imaging systems and dedicated targeted/activatable molecular imaging probes have positioned molecular imaging to greatly impact atherosclerosis imaging in the next decade. However, several issues must be addressed before its clinical translation.
Aging ; Angiotensin-Converting Enzyme Inhibitors ; Animals ; Atherosclerosis ; Biology ; Cardiovascular Diseases ; Drug-Eluting Stents ; Horses ; Humans ; Molecular Imaging ; Obesity ; Primary Prevention

The main cause of acute myocardial infarction is plaque rupture accompanied by superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested as a type of lesion with a vulnerability that can cause plaque rupture. However, not only the existence of a TCFA but also the fine and complex interactions of other anatomical and hemodynamic factors, such as microcalcification in the fibrous cap, cholesterol crystal-induced inflammasome activation, the apoptosis of intraplaque macrophages, and endothelial shear stress distribution should precede a clinical event caused by plaque rupture. Recent studies are being conducted to identify these mechanisms through molecular imaging and hemodynamic assessment using computational fluid dynamics, which will result in better clinical results through selective coronary interventions.
Apoptosis ; Cholesterol ; Coronary Artery Disease ; Coronary Thrombosis ; Hemodynamics ; Hydrodynamics ; Inflammasomes ; Macrophages ; Molecular Imaging ; Myocardial Infarction ; Plaque, Atherosclerotic ; Rupture

The main cause of acute myocardial infarction is plaque rupture accompanied by superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested as a type of lesion with a vulnerability that can cause plaque rupture. However, not only the existence of a TCFA but also the fine and complex interactions of other anatomical and hemodynamic factors, such as microcalcification in the fibrous cap, cholesterol crystal-induced inflammasome activation, the apoptosis of intraplaque macrophages, and endothelial shear stress distribution should precede a clinical event caused by plaque rupture. Recent studies are being conducted to identify these mechanisms through molecular imaging and hemodynamic assessment using computational fluid dynamics, which will result in better clinical results through selective coronary interventions.

PURPOSE: This study was designed to investigate the change of peroxisome proliferator-activated receptor gamma (PPARgamma) after the infection of the human coronary artery smooth muscle cells (HCSMCs) with Chlamydia pneumoniae (C. pneumoniae) and the effect of PPARgamma agonist on the expression of PPARgamma of C. pneumoniae-infected HCSMCs. MATERIALS AND METHODS: To determine the effect of PPARgamma agonist on the proliferation of C. pneumoniae-infected HCSMCs, rosiglitazone at various concentrations was applied 1 hour before inoculation of HCSMCs. RESULTS: The expression of PPARgamma mRNA in HCSMCs increased from 3 hours after C. pneumoniae infection and reached that of noninfected HCSMCs at 24 hours (p < 0.05). The expression of PPARgamma protein in HCSMCs also increased from 3 hours after C. pneumoniae and persisted until 24 hours as compared with that of noninfected HCSMCs (p < 0.05). The pretreatment of HCSMCs with rosiglitazone followed by the infection with C. pneumoniae augmented the expression of PPARgamma mRNA and protein (p < 0.05) and decreased cell proliferation. CONCLUSION: Our results showed that the expression of PPARgamma increases in response to C. pneumoniae infection and rosiglitazone further augmented the expression of PPARgamma. It is suggested that rosiglitazone could ameliorate the chronic inflammation in the vessel wall induced by C. pneumoniae by augmenting PPARgamma expression.
Blotting, Western ; Cell Line ; Cell Proliferation/drug effects ; Chlamydophila pneumoniae/growth & development/*physiology ; Gene Expression Regulation/drug effects ; Humans ; Muscle, Smooth, Vascular/cytology/drug effects/metabolism ; Myocytes, Smooth Muscle/drug effects/*metabolism/microbiology ; PPAR gamma/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Thiazolidinediones/pharmacology

Pheochromocytoma is a catecholamine producing tumor. The features that suggest pheochromocytoma in hypertensive patients are paroxysmal headache, palpitation and excessive sweating. Also, specific catecholamine induced dilated cardiomyopathy and acute pancreatitis have been rarely suggested. We recently experienced a case in which pheochromocytoma manifested as both catecholamine-induced cardiomyopathy and acute pancreatitis. A 64-year-old man presented with acute abdomen and ischemic ST-segment changes on EKG. While abdominal pain and elevated P-type amylase on laboratory data suggested acute pancreatitis, rapid recovery of severely depressed left ventricular systolic function suggested a reversible type of cardiomyopathy. Subsequent abdominal CT scan and hormone assays revealed a pheochromocytoma in the left suprarenal area. To the best of our knowledge, the concurrent occurrence of acute pancreatitis and catecholamine-induced cardiomyopathy in a patient with pheochromocytoma has not been previously reported.
Abdomen, Acute ; Abdominal Pain ; Amylases ; Cardiomyopathies* ; Cardiomyopathy, Dilated ; Electrocardiography ; Headache ; Humans ; Middle Aged ; Pancreatitis* ; Pheochromocytoma* ; Sweat ; Sweating ; Tomography, X-Ray Computed

Objective: This study aimed to evaluate the diagnostic efficacy and safety of low-contrast-dose, dual-source dual-energy CT before transcatheter aortic valve replacement (TAVR) in patients with compromised renal function. Materials and Methods: A total of 54 consecutive patients (female:male, 26:38; 81.9 ± 7.3 years) with reduced renal function underwent pre-TAVR dual-energy CT with a 30-mL contrast agent between June 2022 and March 2023. Monochromatic (40- and 50-keV) and conventional (120-kVp) images were reconstructed and analyzed. The subjective quality score, vascular attenuation, contrast-to-noise ratio (CNR), and signal-to-noise ratio (SNR) were compared among the imaging techniques using the Friedman test and post-hoc analysis. Interobserver reliability for aortic annular measurement was assessed using the intraclass correlation coefficient (ICC) and Bland-Altman analysis. The procedural outcomes and incidence of post-contrast acute kidney injury (AKI) were assessed. Results: Monochromatic images achieved diagnostic quality in all patients. The 50-keV images achieved superior vascular attenuation and CNR (P < 0.001 in all) while maintaining a similar SNR compared to conventional CT. For aortic annular measurement, the 50-keV images showed higher interobserver reliability compared to conventional CT: ICC, 0.98 vs. 0.90 for area and 0.97 vs. 0.95 for perimeter; 95% limits of agreement width, 0.63 cm2 vs. 0.92 cm2 for area and 5.78 mm vs. 8.50 mm for perimeter. The size of the implanted device matched CT-measured values in all patients, achieving a procedural success rate of 92.6%. No patient experienced a serum creatinine increase of ≥ 1.5 times baseline in the 48–72 hours following CT. However, one patient had a procedural delay due to gradual renal function deterioration. Conclusion Low-contrast-dose imaging with 50-keV reconstruction enables precise pre-TAVR evaluation with improved image quality and minimal risk of post-contrast AKI. This approach may be an effective and safe option for pre-TAVR evaluation in patients with compromised renal function.

No abstract available.
Printing, Three-Dimensional* ; Transcatheter Aortic Valve Replacement*

Eosinophilic myocarditis is a disease characterized by eosinophilic infiltration of the myocardium, consisting of acute necrotic stage, thrombotic stage, and fibrotic stage. Although T1 mapping has been increasingly used in various cardiac pathologies, there has been no report of T1 mapping in eosinophilic myocarditis. We report a case of 75-year-old female with eosinophilic myocarditis, whose cardiac magnetic resonance imaging included native T1 mapping, in which apical thrombi were distinctly seen as areas with decreased T1 values, next to areas of inflammation seen as increased T1 value in subendocardium.
Aged ; Churg-Strauss Syndrome* ; Eosinophils* ; Female ; Humans ; Inflammation ; Magnetic Resonance Imaging ; Myocarditis* ; Myocardium ; Necrosis ; Pathology ; Thrombosis

BACKGROUND AND OBJECTIVES: Existing data on the spatiotemporal expression patterns of a variety of galectins in murine atherosclerosis are limited. We investigated the expression levels of galectins, and their in vivo spatiotemporal expression patterns and statin responsiveness in the inflamed atherosclerotic plaques of apolipoprotein E (apoE)-/- mice. MATERIALS AND METHODS: Galectins expression patterns in aortic atherosclerotic plaques and serum galectin-3 levels were investigated in 26-week-old apoE-/- (n=6) and C57BL/6 mice (n=9). To investigate the spatial and temporal patterns of galectin-1 and galectin-3 in plaques, high-cholesterol diet-fed 26-week-old (n=12) and 36-week-old apoE-/- mice (n=6) were sacrificed and their aortas were examined for galectins' expression using immunoblot analysis and immunohistochemical stain. 36-week-old apoE-/- mice were treated with atorvastatin (n=3, 0.57 mg/kg/day) for the evaluation of its effect on aortic galectins' expression. RESULTS: Immunoblot analyses showed that galectin-1 and galectin-3 were the predominant galectins expressed in murine atherosclerosis. The serum galectin-3 level was significantly higher in apoE-/- mice (p<0.001). While galectin-1 was weakly expressed in both intimal plaques and the media of atherosclerotic aortas, galectin-3 was heavily and exclusively accumulated in intimal plaques. Galectin-3 distribution was colocalized with plaque macrophages' distribution (r=0.66). As the degree of plaque extent and inflammation increased, the intraplaque galectin-3 expression levels proportionally elevated (p<0.01 vs. baseline), whereas galectin-1 expression had not elevated (p=0.14 vs. baseline). Atorvastatin treatment markedly reduced intraplaque galectin-3 and macrophage signals (p<0.001 vs. baseline), whereas it failed to reduce galectin-1 expression in the aortas. CONCLUSION: Galectin-3 is the predominant gal and is colocalized with macrophages within atherosclerotic plaques. Intraplaque galectin-3 expression reflects the degree of plaque inflammation.
Animals ; Aorta ; Apolipoproteins ; Atherosclerosis ; Galectin 1 ; Galectin 3 ; Galectins ; Heptanoic Acids ; Inflammation ; Macrophages ; Mice ; Plaque, Atherosclerotic ; Pyrroles ; Atorvastatin Calcium