Cardiovascular Drugs and Therapy (CARDIOVASC DRUG THER)

Publications in this journal

• Article: Ischaemic Preconditioning and Postconditioning do not Affect Adenosine A1 and A2A Receptor Sensitivity

  Niels P. Riksen, Abigail Wynne, Derek M. Yellon, Derek J. Hausenloy
  Cardiovascular Drugs and Therapy 05/2012; 23(5):415-417.
• Article: Erratum to: Resveratrol: A Multifunctional Compound Improving Endothelial Function

  Huige Li, Ulrich Förstermann
  Cardiovascular Drugs and Therapy 05/2012; 24(1):91-91.
• Article: Beta-Blocker Dose Up-Titration or Addition of Ivabradine in Stable Angina: More is Not Necessarily Better

  Raymond W. Sy, Saul B. Freedman
  Cardiovascular Drugs and Therapy 05/2012; 25(6):501-502.
• Article: Simvastatin Suppresses Apoptosis in Vulnerable Atherosclerotic Plaques Through Regulating the Expression of p53, Bcl-2 and Bcl-xL

  Weiwei Qin, Yonggang Lu, Chengyan Zhan, Tao Shen, Lin Dou, Yong Man, Shu Wang, Chuanshi Xiao, Yunfei Bian, Jian Li
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  ABSTRACT: PurposeSimvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has antioxidant and anti-inflammatory properties that are independent of lipid-lowering abilities. This experiment was carried out to explore the effects of simvastatin on apoptosis in vulnerable atherosclerotic plaques of apoE-deficient mice. Methods and resultsEight weeks-old apoE−/− mice were fed a Western-type diet. Vulnerable atherosclerotic lesions were formed in the branchiocephalic artery at the age of 30-weeks, before simvastatin administration for 8weeks. Simvastatin did neither affect the levels of plasma glucose and lipids, nor the size of atherosclerotic lesions. Analysis of plaque composition showed that simvastatin decreased the area of lipid core and increased the amounts of macrophages and smooth muscle cells in atherosclerotic plaques of apoE−/− mice. In addition, simvastatin down-regulated the expression of vascular cell adhesion molecule-1 (VCAM-1) by both inhibition of nuclear factor kappa B (NF-кB) activation and suppression of the expression of the receptor for advanced glycation end products (RAGE). Moreover, we found that simvastatin administration led to reduced TUNEL-positive cells in the aortic root lesions, accompanied by up-regulation of Bcl-2 and Bcl-xL expression, and decreased P53 expression as shown by Western blot. ConclusionIn the present study, we show novel data to suggest that simvastatin could suppress apoptosis in vulnerable atherosclerotic plaques of apoE−/− mice by regulating the expression of apoptosis-related proteins, such as p53, Bcl-2 and Bcl-xL. Key wordsSimvastatin–Vulnerable lesions–Apoptosis–Bcl-2–Bcl-xL–p53
  Cardiovascular Drugs and Therapy 04/2012; 26(1):23-30.
• Article: Resveratrol Confers Endothelial Protection in Insulin-Dependent Diabetes Mellitus

  Zoltan Ungvari, Anna Csiszar
  Cardiovascular Drugs and Therapy 04/2012; 25(2):111-113.
• Article: President’s Page: ISCP’s Educational Goals

  Jay N. Cohn
  Cardiovascular Drugs and Therapy 04/2012; 24(1):89-89.
• Article: President’s Page: Beijing 2009

  Jay N. Cohn
  Cardiovascular Drugs and Therapy 04/2012; 23(5):419-423.
• Article: The Pleiotropic Effects of Statins in the Prevention of Atherosclerosis

  Wei Kong, Yi Zhu
  Cardiovascular Drugs and Therapy 04/2012; 26(1):5-7.
• Article: Istaroxime: Is the Remedy Better than the Disease?

  Dimitrios Farmakis, Gerasimos Filippatos
  Cardiovascular Drugs and Therapy 04/2012; 25(2):115-117.
• Article: Obituary of Philip Poole-Wilson, Member of the Board of Directors of the International Society of Cardiovascular Pharmacotherapy

  Inder Anand
  Cardiovascular Drugs and Therapy 04/2012; 23(3):257-259.
• Article: Statins and Vitamin D

  David S. Grimes
  Cardiovascular Drugs and Therapy 04/2012; 23(4):261-262.
• Article: Nesiritide, Heart Failure, and Renal Dysfunction: Irrational Exuberance or Throwing the Baby out with the Bathwater

  Ronald M. Witteles
  Cardiovascular Drugs and Therapy 04/2012; 23(3):183-186.
• Article: Secondary Prevention of Coronary Disease with ACE Inhibition-does Blood Pressure Reduction with Perindopril Explain the Benefits in EUROPA?

  Willem J. Remme, Jaap W. Deckers, Kim M. Fox, Roberto Ferrari, Michel Bertrand, Maarten L. Simoons, EUROPA Investigators
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  ABSTRACT: AimsWe determined whether blood pressure (BP) lowering by perindopril was related to its benefit in the EUROPA study. Methods and resultsTwelve thousand two hundred eighteen patients with documented coronary artery disease received perindopril 8mg once daily or matching placebo after a 4-week run-in period in which all patients received perindopril. Patients were excluded if systolic (S) BP was >180 or <100mmHg. Mean age was 60years (range 26–89). 27% had a history of hypertension. After 4.2years of follow-up, the primary endpoint (cardiovascular death, nonfatal myocardial infarction, or resuscitated cardiac arrest) was observed in 603 (9.9%) placebo versus 488 (8.0%) perindopril patients [20% relative risk reduction (RRR), CI 9–29%, P = 0.003]. There was no interaction between baseline SBP levels (using JNC-7 cutoff values) and treatment effect. If anything, the greatest RRR of the primary endpoint (32%) occurred in patients with the lowest SBP (<120mmHg) in whom perindopril did not reduce SBP. Also, RRR during blinded treatment was comparable, irrespective of whether BP decreased or not or of the extent of BP reduction during perindopril treatment. ConclusionThe treatment benefit in EUROPA cannot be fully explained by baseline BP or BP reduction with perindopril. Other mechanisms including direct anti-atherosclerotic effects of ACE inhibition may play a role.
  Cardiovascular Drugs and Therapy 04/2012; 23(2):161-170.
• Article: Design and Rationale of Japanese Evaluation Between Formula of Azelnidipine and Amlodipine Add on Olmesartan to Get Antialbuminuric Effect Study (J-FLAG)

  Katsuyuki Ando, Masakazu Haneda, Sadayoshi Ito, Naoki Kashihara, Koichi Node, Masaomi Nangaku, Tatsuo Shimosawa, Junji Kishimoto, Toshiro Fujita
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  ABSTRACT: PurposeCalcium channel blockers (CCBs) are recommended second-line antihypertensives for renin-angiotensin system (RAS) inhibitor-treated patients with chronic kidney disease (CKD), but they do not always ameliorate the progression of CKD. However, small clinical studies suggest that sympatholytic CCBs may protect against kidney injury. Therefore, a clinical trial was designed to test whether the sympatholytic CCB azelnidipine decreases the urinary albumin levels of CKD patients treated with the angiotensin receptor blocker olmesartan more potently than the widely-used non-sympatholytic CCB amlodipine. MethodsA multi-center, open-labeled, randomized clinical intervention trial was designed to compare the antialbuminuric effect of azelnidipine (8–16mg/day) and amlodipine (2.5–5mg/day) in olmesartan-treated hypertensive (blood pressure 130–180/80–110mmHg) patients with type 2 diabetes (fasting blood sugar ≥126mg/dL or treatment with antidiabetic agents) and albuminuria (urinary albumin/creatinine ratio ≥30mg/g). The primary study endpoint is the change in the urinary albumin/creatinine ratio after 12months of treatment. ConclusionsThe present trial is expected to clarify whether the sympatholytic CCB azelnidipine is a beneficial second-line choice for RAS inhibitor-treated hypertensive patients with CKD, such as diabetic nephropathy. Key wordsCalcium channel blocker–Urinary albumin–Diabetic nephropathy–Hypertension–Renin-angiotensin system inhibitor
  Cardiovascular Drugs and Therapy 04/2012; 25(4):341-347.
• Article: Granulocyte Colony Stimulating Factor in the Treatment of Cardiac Ischemic Disease. A Decade has Passed: Is it Time to Give Up?

  Ruy Andrade N. Louzada, João Pedro Saar Werneck-de-Castro
  Cardiovascular Drugs and Therapy 04/2012; 25(3):191-195.
• Article: Reduced Thrombin Generation and Soluble P-selectin After Intravenous Enoxaparin During PCI

  J. Kvasnička, J. Horák, Z. Zenáhlíková, Tomáš Kvasnička, S. Šimek, T. Kovárník, I. Malíková, A. Linhart, M. Aschermann
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  ABSTRACT: PurposeThe objective of our study was to identify changes in the coagulation and serum concentration of soluble P-selectin (sP-sel) after i.v. bolus of 0.75mg/kg enoxaparin in a group of 33 patients during PCI. Methods and resultsAs compared to baseline, i.v. enoxaparin increased anti -Xa activity and FIIa inhibition together with APTT and thrombin time tests within 20min, that persisted for 60min. At 6h, the results of all tests had returned to baseline. In contrast, the level of prothrombin fragments (F1 + 2) decreased persistingly for a period of 6h (baseline 1.19 ± 0.42nmol/l, after 20min 1.03 ± 0.46nmol/l, after 60min 1.06 ± 0.43nmol/l, after 6h 0.95 ± 0.40nmol/l, p < 0.001 vs. baseline for all values). In addition, i.v. enoxaparin decreased serum sP-sel level (baseline 111.80 ± 37.05ng/ml, after 20min 87.80 ± 33.17ng/ml, after 60min 86.45 ± 29.15ng/ml, after 6h 92.24 ± 31.34ng/ml, p < 0.001 vs. baseline value for all). sP-sel level mildly correlated with both F Xa inhibition (r = −0.275, p < 0.05) and F1 + 2 level (r = 0.274, p < 0.05). ConclusionIntravenous enoxaparin induced target F Xa inhibition (>0.6IU/ml) for 60min in 82% of study patients. During the 6h of monitoring, a decrease of thrombin generation (F1 + 2) and sP-selectin levels were observed. Key wordsIntravenous enoxaparin–PCI–F Xa–Thrombin–sP-selectin
  Cardiovascular Drugs and Therapy 04/2012; 25(3):243-250.
• Article: G-CSF and Erythropoietin Combination Therapy for Infarct Repair: Two Plus Two Equals Two?

  Carrie M. Quinn, Buddhadeb Dawn
  Cardiovascular Drugs and Therapy 04/2012; 24(5):369-371.
• Article: Fractalkine as an Important Target of Aspirin in the Prevention of Atherogenesis

  Heidi Noels, Christian Weber
  Cardiovascular Drugs and Therapy 04/2012; 24(1):1-3.
• Article: New Pharmacological Strategies in Chronic Heart Failure

  van de Wal Rma, Voors AA, Plokker HWM, van Gilst WH, van Veldhuisen DJ
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  ABSTRACT: Diuretics, ACE inhibitors and betablockers form the cornerstone of pharmacological treatment of chronic heart failure (CHF), while angiotensin receptor blockers are gaining ground. However, despite optimal treatment CHF remains a syndrome with poor prognosis. For this reason, a large number of new agents have been developed as add-on treatment over the last few years. Vasopeptidase inhibitors, moxonidine, endothelin antagonists, vasopressin antagonists, and selective aldosterone antagonists, are some of the new agents that were designed to interfere with different neurohormonal pathways. Immunomodulating agents, growth hormone, caspase inhibitors, adrenomedullin, and erythropoietin have different modes of action, which in general are less understood. Although most of the agents exhibited efficacy in preclinical trials, the clinical results have not always been similarly positive. The results of trials involving vasopeptidase inhibitors, endothelin antagonists, immunomodulating agents, and growth hormone have been disappointing. Other compounds like caspase inhibitors, adrenomedullin, and vasopressin antagonists are still at the early stages of development. Currently, the two most promising agents seem to be erythropoietin and the selective aldosterone receptor blocker eplerenone. In the present article an overview of new pharmacological developments for CHF is given, and the clinical value of these developments is discussed.
  Cardiovascular Drugs and Therapy 04/2012; 18(6):491-501.
• Article: A Description of the Clinical Characteristics at Baseline of Patients Recruited into the Carvedilol or Metoprolol European Trial (COMET)

  John G.F. Cleland, Kevin Goode, Leif Erhardt, Willem J. Remme, Andrew Charlesworth, Philip A. Poole-Wilson, Andrea Di Lenarda, Peter Hanrath, Michel Komajda, Marco Metra, Karl Swedberg, Christian Torp-Pedersen
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  ABSTRACT: Background & Aims: The COMET trial was a prospective, double-blind, randomised trial comparing carvedilol, a comprehensive adrenergic receptor antagonist, with metoprolol, a beta-1-selective agent in patients with heart failure and left ventricular systolic dysfunction. The trial showed a reduction in mortality with carvedilol that was consistent across subgroups. The purpose of this report is to describe in greater detail the heterogeneity of this population at baseline with particular reference to the impact of symptomatic severity, age and gender on patient characteristics. Methods: A descriptive report using data entered in the COMET study data-base. Results: The characteristics of the population studied were similar to those reported in previous trials of beta-blockers. Almost all patients were receiving diuretics and ACE inhibitors with few patients taking angiotensin receptor blockers. As expected, older patients had more co-morbidity. Older patients and women reported worse symptoms and poorer well-being despite similar ventricular dimensions and systolic dysfunction. NT-proBNP was higher in patients with more severe symptoms and older patients but not in women, although differences in NT-proBNP may have been confounded by differences in renal function. Conclusion: Age and gender, as well as the severity of cardiac dysfunction, appear to have an important effect on the severity of heart failure symptoms and patient ‘well-being’. This could have important implications for the relationship between symptoms and prognosis and therefore the way in which patients are selected for clinical trials and the goals of treatment. This will be the subject of further analyses.
  Cardiovascular Drugs and Therapy 04/2012; 18(2):139-152.