Randomized Comparative Study of the Effects of Treatment with Once-Daily, Niacin Extended-Release/Lovastatin and with Simvastatin on Lipid Profile and Fibrinolytic Parameters in Taiwan

Hyperlipidemia can be effectively treated either with niacin or HMG-CoA reductase inhibitor (statin), or a combination of both. Few reports showed the effects of the combination regimen with niacin and statin on hemostatic functions. We conducted a single-center, double-blind, double-dummy, randomized, two-arm study to assess the effects of the niacin extended-release/lovastatin therapy in a fixed-dose formulation and of simvastatin on lipid lowering and two fibrinolytic parameters, fibrinogen and d-dimer. All patients were enrolled according to NCEP-ATP III guidelines and underwent a placebo run-in period of 4 weeks before being randomized to either niacin extended-release/lovastatin tablets (500/20 mg) once daily (n = 36) or simvastatin capsule (20 mg) once daily (n = 34). After 16 weeks of treatment, both groups of patients showed significantly reduced low-density lipoprotein cholesterol and total cholesterol (LDL-C, p < 0.001 and < 0.001, respectively, p = 0.159 between the groups; TC, p < 0.001 and < 0.001, respectively, p = 0.018 between the groups). Both drugs were well tolerated. Only in the group treated with niacin extended-release/lovastatin was fibrinogen concentration significantly reduced after treatment (2.48 ± 0.65 to 1.99 ± 0.62 g/L, p = 0.008). No difference was found with d-dimer in either group. This study shows that both niacin extended-release/ lovastatin and simvastatin are effective and well-tolerated lipid-lowering drugs in Taiwanese patients with dyslipidemia. A combinational treatment with niacin extended-release/lovastatin may provide additional benefit in fibrinolysis

Postchallenge responses of nitrotyrosine and TNF-alpha during 75-g oral glucose tolerance test are associated with the presence of coronary artery diseases in patients with prediabetes

<p>Abstract</p> <p>Background</p> <p>Meta-analysis has demonstrated an exponential relationship between 2-hr postchallenge hyperglycemia and coronary artery disease (CAD). Pulsatile hyperglycemia can acutely increase proinflammatory cytokines by oxidative stress. We hypothesized that postchallenge proinflammatory and nitrosative responses after 75 g oral glucose tolerance tests (75 g-OGTT) might be associated with CAD in patients without previously recognized type 2 diabetes mellitus (T2DM).</p> <p>Methods</p> <p>Serial changes of plasma glucose (PG), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and nitrotyrosine levels were analyzed during 75 g-OGTT in 120 patients (81 male; age 62 ± 11 years) before coronary angiography. Patients were classified as normal (NGT; 42%), impaired (IGT; 34%) and diabetic (T2DM; 24%) glucose tolerance by 75 g-OGTT.</p> <p>Results</p> <p>Postchallenge hyperglycemia elicited TNF-α, IL-6 and nitrotyrosine levels time-dependently, and 2-hr median levels of TNF-α (7.1 versus 6.4 pg/ml; <it>P </it>< 0.05) and nitrotyrosine (1.01 versus 0.83 <it>μ</it>mol/l; <it>P </it>< 0.05), but not IL-6 or PG, were significantly higher in patients with CAD in either IGT or T2DM groups. After adjusting risk factors and glucose tolerance status, 2-hr nitrotyrosine in highest quartiles (OR: 3.1, <it>P </it>< 0.05) remained an independent predictor of CAD by logistic regression analysis.</p> <p>Conclusions</p> <p>These results highlight postchallenge proinflammatory and nitrosative responses by 75 g-OGTT, rather than hyperglycemia <it>per se</it>, are associated with CAD in patients without previous recognized diabetes.</p

Riociguat treatment in patients with chronic thromboembolic pulmonary hypertension: Final safety data from the EXPERT registry

Objective: The soluble guanylate cyclase stimulator riociguat is approved for the treatment of adult patients with pulmonary arterial hypertension (PAH) and inoperable or persistent/recurrent chronic thromboembolic pulmonary hypertension (CTEPH) following Phase

Coronary Artery Aneurysms in a Young Patient with Acute Myocardial Infarction: A Case Report

Coronary artery aneurysms are not uncommon. They are usually arteriosclerotic in origin, and may be congenital or secondary to injury, dissection, infection, inflammation, or Kawasaki disease (KD). Herein, we report a case involving a 25-year-old male smoker with acute myocardial infarction (AMI). Coronary angiography showed triple-vessel disease, coronary artery aneurysms, and diffuse ectasia. Coronary artery bypass grafting was performed without complications. Based on his history, serologic examinations, and angiographic findings, we suspected that his coronary artery aneurysms and ectasia were the adult sequelae of KD. This case is a good reminder that KD victims may suffer from young-onset AMI

Unstable Angina with Normal Coronary Angiography in Hyperthyroidism: A Case Report

Hyperthyroidism is associated with an increase in myocardial oxygen consumption that, due to an imbalance of oxygen demand and supply, can cause angina. However, subclinical hyperthyroidism rarely presents as chest pain in the resting state. Herein, we present a case of subclinical hyperthyroidism involving a 58-year-old male who complained of frequent chest tightness and typical electrocardiographic changes while in a resting state. Coronary angiography showed no significant lesion. Laboratory data showed that the patient suffered from hyperthyroidism, for which he was successfully treated with anti-thyroid agents. We are reminded that typical chest pain might be the first symptom of hyperthyroidism

Acute Respiratory Distress Syndrome after Early Successful Primary Percutaneous Coronary Intervention Therapy in Acute Myocardial Infarction: A Case Report

Acute respiratory distress syndrome (ARDS) is characterized by acute-onset dyspnea, diffuse bilateral pulmonary infiltration, low pulmonary capillary wedge pressure (PCWP), and an arterial oxygen tension/ inspired oxygen fraction (PaO2/FiO2) ratio of less than 200 mmHg. Acute myocardial infarction (AMI), whether complicated by circulatory arrest, cardiogenic shock, and hypotension or not, was reported as an etiologic factor in the development of ARDS in the prethrombolytic era. In the thrombolytic era, two cases of AMI complicated with ARDS have been reported. ARDS in these two patients resulted from anaphylactic reaction to the thrombolytic agent and not from the hemodynamic consequences of AMI. Development of ARDS during the AMI period has not been reported after early successful primary percutaneous coronary intervention (PCI). Herein, we report a 61-year-old male patient with persistent chest pain who was diagnosed with Killip II anterior ST-segment elevation AMI. He was treated successfully with primary PCI 2.5 hours after the onset of chest pain. Unfortunately, on the third hospital day, acuteonset dyspnea (respiratory rate, 33 beats/min), fever (38.5°C), leukocytosis (white blood cell count, 18,360/μL), and diffuse bilateral pulmonary infiltration were noted. ARDS was diagnosed from the low PCWP (8 mmHg) and a PaO2/FiO2 of less than 200 mmHg (160 mmHg). No usual causes of ARDS such as infection, aspiration, trauma, shock, or drug reactions were noted. We assumed that, in this particular patient, the systemic inflammatory response syndrome frequently induced by AMI might have caused this episode of ARDS. This may imply that AMI itself is a possible etiology of ARDS

Heparin-Induced Cardiac Tamponade and Life-Threatening Hyperkalemia in a Patient with Chronic Hemodialysis

Heparin, a commonly used anticoagulant agent, is frequently used in patients undergoing hemodialysis. As with most medications, heparin has a significant side effect profile. Two of its most important side effects, major bleeding and hyperkalemia, may be devastating without immediate diagnosis and treatment. Major bleeding such as gastrointestinal, genitourinary or intracranial bleeding is occasionally encountered and rarely neglected. However, heparin-induced cardiac tamponade is rarely encountered and may be easily overlooked. Another side effect, heparin-induced hyperkalemia, an unusual but well-described side effect, is frequently forgotten until life-threatening arrhythmia has occurred. We report a case involving a 40-year-old male patient with uremia, who had received heparin for 10 days for deep vein thrombosis in the left lower extremity. Hemopericardium with cardiac tamponade and life-threatening hyperkalemia were both noted in this patient

Ruptured Aneurysm of the Sinus of Valsalva into the Right Atrium without Ventricular Septal Defect: A Case Report and Literature Review

Aneurysm of the sinus of Valsalva (ASV), frequently associated with ventricular septal defect (VSD), is a rare cardiac disease that may be acquired or congenital. Rupture of an ASV, rare in the noncoronary cusp, usually produces serious hemodynamic change and carries poor prognosis if not treated surgically. We present the case of a 55-year-old female who came to us complaining of exertional dyspnea. Transthoracic echocardiography and aortography showed a noncoronary cusp ASV with rupture into the right atrium but without VSD. Because of high left to right shunt flow, she underwent successful surgical intervention with aneurysm repair approached from both the aorta and right atrium with a knitted Dacron patch. This was a rare case of noncoronary cusp involvement in ASV that ruptured into the right atrium without VSD

Association of arterial stiffness and electrocardiography-determined left ventricular hypertrophy with left ventricular diastolic dysfunction.

OBJECTIVES: Increased arterial stiffness is associated with left ventricular diastolic dysfunction (LVDD), but this association may be influenced by left ventricular (LV) performance. Left ventricular hypertrophy (LVH) is not only a significant determinant of LV performance, but is also correlated with LVDD. This study is designed to compare LV diastolic function among patients divided by brachial-ankle pulse wave velocity (baPWV) and electrocardiography (ECG)-determined LVH and to assess whether increased baPWV and ECG-determined LVH are independently associated with LVDD. METHODS: This cross-sectional study enrolled 270 patients and classified them into four groups according to the median value of baPWV and with/without ECG-determined LVH. The baPWV was measured using an ABI-form device. ECG-determined LVH was defined by Sokolow-Lyon criterion. LVDD was defined as impaired relaxation, pseudonormal, and restrictive mitral inflow patterns. Groups 1, 2, 3, and 4 were patients with lower baPWV and without ECG-determined LVH, lower baPWV but with ECG-determined LVH, higher baPWV but without ECG-determined LVH, and higher baPWV and with ECG-determined LVH respectively. RESULTS: Early diastolic mitral velocity (Ea) was gradually decreased from group 1 to group 4 (p≦0.027). Patients in group 4 had the highest prevalence of LVDD (all p<0.001). After multivariate analysis, both baPWV and ECG-determined LVH were independent determinants of Ea (β = -0.02, P<0.001; β = -1.77, P<0.001 respectively) and LVDD (odds ratio = 1.02, P = 0.011 and odds ratio = 3.53, P = 0.013 respectively). CONCLUSION: Our study showed the group with higher baPWV and ECG-determined LVH had the lowest Ea and highest prevalence of LVDD. In addition, both baPWV and ECG-determined LVH were independently associated with Ea and LVDD. Hence, assessment of arterial stiffness by baPWV and LVH by ECG may be useful in identifying the high risk group of LVDD

Lercanidipine and Losartan Effects on Blood Pressure and Fibrinolytic Parameters

Antihypertensive agents may modulate fibrinolysis in addition to reducing blood pressure. We conducted a randomized trial to assess the effects of lercanidipine and losartan on blood pressure (BP) lowering and three fibrinolytic parameters: plasminogen activator inhibitor−1 (PAI-1), D-dimer, and fibrinogen. All patients enrolled had essential hypertension and underwent a placebo run-in period of 2 weeks before randomization to either lercanidipine tablets 10-20 mg once daily or losartan tablets 50-100 mg once daily. Twenty-six patients completed this study. After 8 weeks of treatment, both groups of patients had significantly reduced systolic (SBP) and diastolic BP (DBP) (SBP, p = 0.034 and 0.050, respectively; DBP, p = 0.018 and 0.034 for lercanidipine and losartan, respectively). Both drugs were well tolerated. Only in the group treated with lercanidipine was PAI-1 concentration significantly reduced (57.1 ± 4.7 to 43.1 ± 4.8 ng/ mL, p = 0.047). No difference was found with D-dimer and fibrinogen in either group. This study shows that both lercanidipine and losartan are effective antihypertensive drugs in patients with essential hypertension. Lercanidipine may provide additional benefit in fibrinolysis